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What is the most likely cause of this patient’s fever?
A 63-year-old man undergoes cardiac bypass surgery. He is able to be extubated at 8 hours. The next morning he has a fever to 38.5° C His exam shows no redness at the surgical site, or at his IV sites. His lung exam is unremarkable. His urinalysis is without white blood cells. His white blood cell count is 8,500, and his chest x-ray shows atelectasis without other abnormalities.
One of the earliest things I was taught in my clinical years were the causes of postoperative fever, or the 5Ws, which are wind, water, wound, walk, and wonder drug.
Atelectasis was touted as the cause of early postoperative fever. This became clear fact in my medical student mind, not something that I had ever questioned. But investigation into whether there is evidence of this shows it is only a myth. In actuality, there is scant evidence, if any, for atelectasis causing fever. Frequently, no cause of postoperative fever has been found, despite aggressive attempts to look for one.
What the research says
Fanning and colleagues prospectively looked at 537 women who were undergoing major gynecologic surgery.1 Postoperative fever occurred in 211 of them. In 92% of these patients, no cause for fever was found.
Atelectasis is frequently seen postoperatively. Schlenker and colleagues reported that, in patients with postoperative atelectasis, temperature elevation on the first postoperative day was directly related to the degree of atelectasis, but the white blood cell count elevation was inversely related.2
In this study, atelectasis was diagnosed by auscultation, with chest x-rays ordered at the discretion of the physician. There was little correlation with the auscultatory findings and presence or absence of atelectasis in the patients who did receive chest x-rays.
Engoren did a study to prospectively evaluate 100 postoperative patients with daily chest x-rays and continuous temperature monitoring.3 Results from the day of surgery (day 0) to the second postoperative day showed an increase in presence of atelectasis from 43% on the day of surgery to 79% by day 2.
Fever, defined as temperature greater than 38° C, fell from 37% on the day of surgery to 17% by day 2. Engoren found no association between fever and degree of atelectasis.
Mavros and colleagues did a comprehensive review to determine whether there was evidence to support atelectasis causing fever.4 They concluded that there was no clinical evidence supporting the concept that atelectasis is associated with early postoperative fever.
A possible cause of fever
Mavros and colleagues’ paper suggested that early postoperative fever was caused by stress derived by surgery, which can increase the patient’s interleukin-6 levels and thermostatic set point. This was demonstrated in a small study by Wortel and colleagues, who measured IL-6 levels in the portal and peripheral blood of patients following pancreaticoduodenectomy.5 They found IL-6 levels correlated strongly with peak body temperature.
In conclusion, atelectasis is not a well-established cause of postoperative fever.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Fanning J et al. Infect Dis Obstet Gynecol. 1998; 6(6):252-5 .
2. Schlenker JD and Hubay CA. Arch Surg 1973;107:846-50
3. Engoren M. Chest. 1995;107(1):81-4 .
4. Michael N et al. Chest. 2011;140(2):418-24
5. Wortel CH et al. Surgery. 1993;114(3):564-70 .
A 63-year-old man undergoes cardiac bypass surgery. He is able to be extubated at 8 hours. The next morning he has a fever to 38.5° C His exam shows no redness at the surgical site, or at his IV sites. His lung exam is unremarkable. His urinalysis is without white blood cells. His white blood cell count is 8,500, and his chest x-ray shows atelectasis without other abnormalities.
One of the earliest things I was taught in my clinical years were the causes of postoperative fever, or the 5Ws, which are wind, water, wound, walk, and wonder drug.
Atelectasis was touted as the cause of early postoperative fever. This became clear fact in my medical student mind, not something that I had ever questioned. But investigation into whether there is evidence of this shows it is only a myth. In actuality, there is scant evidence, if any, for atelectasis causing fever. Frequently, no cause of postoperative fever has been found, despite aggressive attempts to look for one.
What the research says
Fanning and colleagues prospectively looked at 537 women who were undergoing major gynecologic surgery.1 Postoperative fever occurred in 211 of them. In 92% of these patients, no cause for fever was found.
Atelectasis is frequently seen postoperatively. Schlenker and colleagues reported that, in patients with postoperative atelectasis, temperature elevation on the first postoperative day was directly related to the degree of atelectasis, but the white blood cell count elevation was inversely related.2
In this study, atelectasis was diagnosed by auscultation, with chest x-rays ordered at the discretion of the physician. There was little correlation with the auscultatory findings and presence or absence of atelectasis in the patients who did receive chest x-rays.
Engoren did a study to prospectively evaluate 100 postoperative patients with daily chest x-rays and continuous temperature monitoring.3 Results from the day of surgery (day 0) to the second postoperative day showed an increase in presence of atelectasis from 43% on the day of surgery to 79% by day 2.
Fever, defined as temperature greater than 38° C, fell from 37% on the day of surgery to 17% by day 2. Engoren found no association between fever and degree of atelectasis.
Mavros and colleagues did a comprehensive review to determine whether there was evidence to support atelectasis causing fever.4 They concluded that there was no clinical evidence supporting the concept that atelectasis is associated with early postoperative fever.
A possible cause of fever
Mavros and colleagues’ paper suggested that early postoperative fever was caused by stress derived by surgery, which can increase the patient’s interleukin-6 levels and thermostatic set point. This was demonstrated in a small study by Wortel and colleagues, who measured IL-6 levels in the portal and peripheral blood of patients following pancreaticoduodenectomy.5 They found IL-6 levels correlated strongly with peak body temperature.
In conclusion, atelectasis is not a well-established cause of postoperative fever.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Fanning J et al. Infect Dis Obstet Gynecol. 1998; 6(6):252-5 .
2. Schlenker JD and Hubay CA. Arch Surg 1973;107:846-50
3. Engoren M. Chest. 1995;107(1):81-4 .
4. Michael N et al. Chest. 2011;140(2):418-24
5. Wortel CH et al. Surgery. 1993;114(3):564-70 .
A 63-year-old man undergoes cardiac bypass surgery. He is able to be extubated at 8 hours. The next morning he has a fever to 38.5° C His exam shows no redness at the surgical site, or at his IV sites. His lung exam is unremarkable. His urinalysis is without white blood cells. His white blood cell count is 8,500, and his chest x-ray shows atelectasis without other abnormalities.
One of the earliest things I was taught in my clinical years were the causes of postoperative fever, or the 5Ws, which are wind, water, wound, walk, and wonder drug.
Atelectasis was touted as the cause of early postoperative fever. This became clear fact in my medical student mind, not something that I had ever questioned. But investigation into whether there is evidence of this shows it is only a myth. In actuality, there is scant evidence, if any, for atelectasis causing fever. Frequently, no cause of postoperative fever has been found, despite aggressive attempts to look for one.
What the research says
Fanning and colleagues prospectively looked at 537 women who were undergoing major gynecologic surgery.1 Postoperative fever occurred in 211 of them. In 92% of these patients, no cause for fever was found.
Atelectasis is frequently seen postoperatively. Schlenker and colleagues reported that, in patients with postoperative atelectasis, temperature elevation on the first postoperative day was directly related to the degree of atelectasis, but the white blood cell count elevation was inversely related.2
In this study, atelectasis was diagnosed by auscultation, with chest x-rays ordered at the discretion of the physician. There was little correlation with the auscultatory findings and presence or absence of atelectasis in the patients who did receive chest x-rays.
Engoren did a study to prospectively evaluate 100 postoperative patients with daily chest x-rays and continuous temperature monitoring.3 Results from the day of surgery (day 0) to the second postoperative day showed an increase in presence of atelectasis from 43% on the day of surgery to 79% by day 2.
Fever, defined as temperature greater than 38° C, fell from 37% on the day of surgery to 17% by day 2. Engoren found no association between fever and degree of atelectasis.
Mavros and colleagues did a comprehensive review to determine whether there was evidence to support atelectasis causing fever.4 They concluded that there was no clinical evidence supporting the concept that atelectasis is associated with early postoperative fever.
A possible cause of fever
Mavros and colleagues’ paper suggested that early postoperative fever was caused by stress derived by surgery, which can increase the patient’s interleukin-6 levels and thermostatic set point. This was demonstrated in a small study by Wortel and colleagues, who measured IL-6 levels in the portal and peripheral blood of patients following pancreaticoduodenectomy.5 They found IL-6 levels correlated strongly with peak body temperature.
In conclusion, atelectasis is not a well-established cause of postoperative fever.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Fanning J et al. Infect Dis Obstet Gynecol. 1998; 6(6):252-5 .
2. Schlenker JD and Hubay CA. Arch Surg 1973;107:846-50
3. Engoren M. Chest. 1995;107(1):81-4 .
4. Michael N et al. Chest. 2011;140(2):418-24
5. Wortel CH et al. Surgery. 1993;114(3):564-70 .
Does optimal iron absorption include vitamin C?
Her blood work shows a hematocrit level of 32, a mean corpuscular volume of 77, a platelet count of 390,000, and a ferritin level of 5.
What would you recommend for iron replacement?
A. FeSO4 325 mg three times a day with vitamin C
B. FeSO4 325 mg daily with vitamin C
C. FeSO4 325 mg every other day
Recommendations and supporting research
I think I would start with choice C, FeSO4 every other day.
Treatment of iron deficiency with oral iron has traditionally been done by giving 150-200 mg of elemental iron (which is equal to three 325 mg tablets of iron sulfate).1 This dosing regimen has considerable gastrointestinal side effects. Recent evidence has shown that iron absorption is diminished the more frequently it is given.
Stoffel and colleagues found that fractional iron absorption was higher in iron-deficient women who were given iron every other day, compared with those who received daily iron.2 They also found that the more frequently iron was administered, the higher the hepcidin levels were, and the lower the iron absorption.
Karacok and colleagues studied every other day iron versus daily iron for the treatment of iron-deficiency anemia of pregnancy.3 A total of 217 women completed randomization and participated in the study, with all women receiving 100 mg of elemental iron, either daily (111) or every other day (106). There was no significant difference in increase in ferritin levels, or hemoglobin increase between the groups. The daily iron group had more gastrointestinal symptoms (41.4%) than the every other day iron group (15.1%) (P < .0057).
Düzen Oflas and colleagues looked at the same question in nonpregnant women with iron deficiency anemia.4 Study patients either received 80 mg iron sulfate twice a day, 80 mg once a day, or 80 mg every other day. There was no statistically significant difference in hemoglobin improvement between groups, but the group that received twice a day dosing of iron had statistically significantly higher ferritin levels than the daily or every other day iron groups. This improvement in ferritin levels came at a cost, though, as 68% of patients in the twice daily iron group had gastrointestinal symptoms, compared with only 10% in the every other day iron group (P < .01).
Vitamin C is often recommended to be taken with iron to promote absorption. The evidence for this practice is scant, and dates back almost 50 years.5,6
Cook and Reddy found there was no significant difference in mean iron absorption among the three dietary periods studied in 12 patients despite a range of mean daily intakes of dietary vitamin C of 51-247 mg/d.7
Hunt and colleagues studied 25 non pregnant, healthy women with low ferritin levels.8 The women’s meals were supplemented with vitamin C (500 mg, three times a day) for 5 of the 10 weeks, in a double-blind, crossover design. Vitamin C supplementation did not lead to a difference in iron absorption, lab indices of iron deficiency, or the biological half-life of iron.
Li and colleagues looked at the effect of vitamin C supplementation on iron levels in women with iron deficiency anemia.9 A total of 440 women were recruited, with 432 completing the trial. Women were randomized to receive iron supplements plus vitamin C or iron supplements only. Their findings were that oral iron supplements alone were equivalent to oral iron supplements plus vitamin C in improving hemoglobin recovery and iron absorption.
Bottom line
Less frequent administration of iron supplements (every other day) is as effective as more frequent administration, with less GI symptoms. Also, adding vitamin C does not appear to improve absorption of iron supplements.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. 1. Fairbanks VF and Beutler E. Iron deficiency, in “Williams Textbook of Hematology, 6th ed.” (New York: McGraw-Hill, 2001).
2. Stoffel N et al. Lancet Haematology. 2017;4: e524-33.
3. Karakoc G et al. J Matern Fetal Neonatal Med. 2021 Apr 18:1-5
4. Düzen Oflas N et al. Intern Med J. 2020 Jul;50(7):854-8
5. Cook JD and Monsen ER. Am J Clin Nutr. 1977;30:235-41.
6. Hallberg L etal. Hum Nutr Appl Nutr. 1986;40: 97-113.
7. Cook JD and Reddy M. Am J Clin Nutr. 2001;73:93-8.
8. Hunt JR et al. Am J Clin Nutr. 1994 Jun;59(6):1381-5.
9. Li N et al. JAMA Netw Open. 2020 Nov 2;3(11):e2023644.
Her blood work shows a hematocrit level of 32, a mean corpuscular volume of 77, a platelet count of 390,000, and a ferritin level of 5.
What would you recommend for iron replacement?
A. FeSO4 325 mg three times a day with vitamin C
B. FeSO4 325 mg daily with vitamin C
C. FeSO4 325 mg every other day
Recommendations and supporting research
I think I would start with choice C, FeSO4 every other day.
Treatment of iron deficiency with oral iron has traditionally been done by giving 150-200 mg of elemental iron (which is equal to three 325 mg tablets of iron sulfate).1 This dosing regimen has considerable gastrointestinal side effects. Recent evidence has shown that iron absorption is diminished the more frequently it is given.
Stoffel and colleagues found that fractional iron absorption was higher in iron-deficient women who were given iron every other day, compared with those who received daily iron.2 They also found that the more frequently iron was administered, the higher the hepcidin levels were, and the lower the iron absorption.
Karacok and colleagues studied every other day iron versus daily iron for the treatment of iron-deficiency anemia of pregnancy.3 A total of 217 women completed randomization and participated in the study, with all women receiving 100 mg of elemental iron, either daily (111) or every other day (106). There was no significant difference in increase in ferritin levels, or hemoglobin increase between the groups. The daily iron group had more gastrointestinal symptoms (41.4%) than the every other day iron group (15.1%) (P < .0057).
Düzen Oflas and colleagues looked at the same question in nonpregnant women with iron deficiency anemia.4 Study patients either received 80 mg iron sulfate twice a day, 80 mg once a day, or 80 mg every other day. There was no statistically significant difference in hemoglobin improvement between groups, but the group that received twice a day dosing of iron had statistically significantly higher ferritin levels than the daily or every other day iron groups. This improvement in ferritin levels came at a cost, though, as 68% of patients in the twice daily iron group had gastrointestinal symptoms, compared with only 10% in the every other day iron group (P < .01).
Vitamin C is often recommended to be taken with iron to promote absorption. The evidence for this practice is scant, and dates back almost 50 years.5,6
Cook and Reddy found there was no significant difference in mean iron absorption among the three dietary periods studied in 12 patients despite a range of mean daily intakes of dietary vitamin C of 51-247 mg/d.7
Hunt and colleagues studied 25 non pregnant, healthy women with low ferritin levels.8 The women’s meals were supplemented with vitamin C (500 mg, three times a day) for 5 of the 10 weeks, in a double-blind, crossover design. Vitamin C supplementation did not lead to a difference in iron absorption, lab indices of iron deficiency, or the biological half-life of iron.
Li and colleagues looked at the effect of vitamin C supplementation on iron levels in women with iron deficiency anemia.9 A total of 440 women were recruited, with 432 completing the trial. Women were randomized to receive iron supplements plus vitamin C or iron supplements only. Their findings were that oral iron supplements alone were equivalent to oral iron supplements plus vitamin C in improving hemoglobin recovery and iron absorption.
Bottom line
Less frequent administration of iron supplements (every other day) is as effective as more frequent administration, with less GI symptoms. Also, adding vitamin C does not appear to improve absorption of iron supplements.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. 1. Fairbanks VF and Beutler E. Iron deficiency, in “Williams Textbook of Hematology, 6th ed.” (New York: McGraw-Hill, 2001).
2. Stoffel N et al. Lancet Haematology. 2017;4: e524-33.
3. Karakoc G et al. J Matern Fetal Neonatal Med. 2021 Apr 18:1-5
4. Düzen Oflas N et al. Intern Med J. 2020 Jul;50(7):854-8
5. Cook JD and Monsen ER. Am J Clin Nutr. 1977;30:235-41.
6. Hallberg L etal. Hum Nutr Appl Nutr. 1986;40: 97-113.
7. Cook JD and Reddy M. Am J Clin Nutr. 2001;73:93-8.
8. Hunt JR et al. Am J Clin Nutr. 1994 Jun;59(6):1381-5.
9. Li N et al. JAMA Netw Open. 2020 Nov 2;3(11):e2023644.
Her blood work shows a hematocrit level of 32, a mean corpuscular volume of 77, a platelet count of 390,000, and a ferritin level of 5.
What would you recommend for iron replacement?
A. FeSO4 325 mg three times a day with vitamin C
B. FeSO4 325 mg daily with vitamin C
C. FeSO4 325 mg every other day
Recommendations and supporting research
I think I would start with choice C, FeSO4 every other day.
Treatment of iron deficiency with oral iron has traditionally been done by giving 150-200 mg of elemental iron (which is equal to three 325 mg tablets of iron sulfate).1 This dosing regimen has considerable gastrointestinal side effects. Recent evidence has shown that iron absorption is diminished the more frequently it is given.
Stoffel and colleagues found that fractional iron absorption was higher in iron-deficient women who were given iron every other day, compared with those who received daily iron.2 They also found that the more frequently iron was administered, the higher the hepcidin levels were, and the lower the iron absorption.
Karacok and colleagues studied every other day iron versus daily iron for the treatment of iron-deficiency anemia of pregnancy.3 A total of 217 women completed randomization and participated in the study, with all women receiving 100 mg of elemental iron, either daily (111) or every other day (106). There was no significant difference in increase in ferritin levels, or hemoglobin increase between the groups. The daily iron group had more gastrointestinal symptoms (41.4%) than the every other day iron group (15.1%) (P < .0057).
Düzen Oflas and colleagues looked at the same question in nonpregnant women with iron deficiency anemia.4 Study patients either received 80 mg iron sulfate twice a day, 80 mg once a day, or 80 mg every other day. There was no statistically significant difference in hemoglobin improvement between groups, but the group that received twice a day dosing of iron had statistically significantly higher ferritin levels than the daily or every other day iron groups. This improvement in ferritin levels came at a cost, though, as 68% of patients in the twice daily iron group had gastrointestinal symptoms, compared with only 10% in the every other day iron group (P < .01).
Vitamin C is often recommended to be taken with iron to promote absorption. The evidence for this practice is scant, and dates back almost 50 years.5,6
Cook and Reddy found there was no significant difference in mean iron absorption among the three dietary periods studied in 12 patients despite a range of mean daily intakes of dietary vitamin C of 51-247 mg/d.7
Hunt and colleagues studied 25 non pregnant, healthy women with low ferritin levels.8 The women’s meals were supplemented with vitamin C (500 mg, three times a day) for 5 of the 10 weeks, in a double-blind, crossover design. Vitamin C supplementation did not lead to a difference in iron absorption, lab indices of iron deficiency, or the biological half-life of iron.
Li and colleagues looked at the effect of vitamin C supplementation on iron levels in women with iron deficiency anemia.9 A total of 440 women were recruited, with 432 completing the trial. Women were randomized to receive iron supplements plus vitamin C or iron supplements only. Their findings were that oral iron supplements alone were equivalent to oral iron supplements plus vitamin C in improving hemoglobin recovery and iron absorption.
Bottom line
Less frequent administration of iron supplements (every other day) is as effective as more frequent administration, with less GI symptoms. Also, adding vitamin C does not appear to improve absorption of iron supplements.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. 1. Fairbanks VF and Beutler E. Iron deficiency, in “Williams Textbook of Hematology, 6th ed.” (New York: McGraw-Hill, 2001).
2. Stoffel N et al. Lancet Haematology. 2017;4: e524-33.
3. Karakoc G et al. J Matern Fetal Neonatal Med. 2021 Apr 18:1-5
4. Düzen Oflas N et al. Intern Med J. 2020 Jul;50(7):854-8
5. Cook JD and Monsen ER. Am J Clin Nutr. 1977;30:235-41.
6. Hallberg L etal. Hum Nutr Appl Nutr. 1986;40: 97-113.
7. Cook JD and Reddy M. Am J Clin Nutr. 2001;73:93-8.
8. Hunt JR et al. Am J Clin Nutr. 1994 Jun;59(6):1381-5.
9. Li N et al. JAMA Netw Open. 2020 Nov 2;3(11):e2023644.
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 [email protected].
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 [email protected].
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 [email protected].
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 [email protected].
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 [email protected].
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 [email protected].
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 [email protected].
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 [email protected].
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 [email protected].
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.
Cellulitis treatment recommendations
He noticed discomfort today and saw that his left lower leg had redness and was warm. He does not recall scratches or injury to his leg. He has not had fever or chills. He has no other symptoms. His diabetes has been well controlled with diet and metformin.
On exam, his blood pressure is 120/70, pulse is 80, temperature is 37 degrees Celsius.
In the left lower extremity, the patient had 1+ edema at the ankle, with a 14-cm x 20-cm warm, erythematous area just above the ankle and extending proximally.
His labs found an HCT of 44 and a WBC of 12,000. What do you recommend?
A) Vascular duplex exam
B) 1st generation cephalosporin
C) 1st generation cephalosporin + TMP/Sulfa
D) Oral clindamycin
E) IV vancomycin
This patient has cellulitis and should receive a beta lactam antibiotic, which will have the best coverage and lowest minimal inhibitory concentration for the likely organism, beta hemolytic streptococci. Clindamycin would likely work, but it has greater side effects. This patient does not need coverage for methicillin-resistant staphylococcus aureus (MRSA). I know many of you, if not most, know this, but I want to go through relevant data and formal recommendations, because of a recent call I received from a patient.
My patient had a full body rash after receiving cephalexin + TMP/sulfa [trimethoprim-sulfamethoxazole] treatment for cellulitis. In recent years the addition of TMP/sulfa to strep treatment to also cover MRSA has become popular, especially in emergency department and urgent care settings.
Moran and colleagues studied cephalexin + TMP/sulfa vs. cephalexin and placebo in patients with uncomplicated cellulitis.1 The outcome measured was clinical cure, and there was no difference between groups; clinical cure occurred in 182 (83.5%) of 218 participants in the cephalexin plus TMP/sulfa group vs. 165 (85.5%) of 193 in the cephalexin group (difference, −2.0%; 95% confidence interval, −9.7% to 5.7%; P = .50).
Jeng and colleagues studied patients admitted for a cellulitis, and evaluated the patients’ response to beta-lactam antibiotics.2 Patients had acute and convalescent serologies for beta hemolytic strep. Almost all evaluable patients with positive strep studies (97%) responded to beta-lactams, and 21 of 23 (91%) with negative studies responded to beta-lactams (overall response rate 95%). This study was done during a time of high MRSA prevalence.
The most recent Infectious Diseases Society of America guidelines for skin and soft tissue infections, recommend oral penicillin, cephalexin, dicloxacillin, or clindamycin for mild cellulitis, and IV equivalent if patients have moderate cellulitis.3 If abscesses are present, then drainage is recommended and MRSA coverage. Kamath and colleagues reported on how closely guidelines for skin and soft tissue infections were followed.4 In patients with mild cellulitis, only 36% received guideline-suggested antibiotics. The most common antibiotic prescribed that was outside the guidelines was trimethoprim-sulfamethoxazole.
Myth: Cellulitis treatment should include MRSA coverage.
My advice: Stick with beta-lactam antibiotics, unless an abscess is present. There is no need to add MRSA coverage for initial treatment of mild to moderate cellulitis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Moran GJ et al. Effect of cephalexin plus trimethoprim-sulfamethoxazole vs. cephalexin alone on clinical cure of uncomplicated cellulitis: A randomized clinical trial. JAMA 2017 May 23;317(20):2088-96.
2. Jeng Arthur et al. The role of beta-hemolytic streptococci in causing diffuse, nonculturable cellulitis. Medicine. 2010;July;89(4):217-26.
3. Stevens DL et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-e52.
4. Kamath RS et al. Guidelines vs. actual management of skin and soft tissue infections in the emergency department. Open Forum Infect Dis. 2018 Jan 12;5(1):ofx188.
He noticed discomfort today and saw that his left lower leg had redness and was warm. He does not recall scratches or injury to his leg. He has not had fever or chills. He has no other symptoms. His diabetes has been well controlled with diet and metformin.
On exam, his blood pressure is 120/70, pulse is 80, temperature is 37 degrees Celsius.
In the left lower extremity, the patient had 1+ edema at the ankle, with a 14-cm x 20-cm warm, erythematous area just above the ankle and extending proximally.
His labs found an HCT of 44 and a WBC of 12,000. What do you recommend?
A) Vascular duplex exam
B) 1st generation cephalosporin
C) 1st generation cephalosporin + TMP/Sulfa
D) Oral clindamycin
E) IV vancomycin
This patient has cellulitis and should receive a beta lactam antibiotic, which will have the best coverage and lowest minimal inhibitory concentration for the likely organism, beta hemolytic streptococci. Clindamycin would likely work, but it has greater side effects. This patient does not need coverage for methicillin-resistant staphylococcus aureus (MRSA). I know many of you, if not most, know this, but I want to go through relevant data and formal recommendations, because of a recent call I received from a patient.
My patient had a full body rash after receiving cephalexin + TMP/sulfa [trimethoprim-sulfamethoxazole] treatment for cellulitis. In recent years the addition of TMP/sulfa to strep treatment to also cover MRSA has become popular, especially in emergency department and urgent care settings.
Moran and colleagues studied cephalexin + TMP/sulfa vs. cephalexin and placebo in patients with uncomplicated cellulitis.1 The outcome measured was clinical cure, and there was no difference between groups; clinical cure occurred in 182 (83.5%) of 218 participants in the cephalexin plus TMP/sulfa group vs. 165 (85.5%) of 193 in the cephalexin group (difference, −2.0%; 95% confidence interval, −9.7% to 5.7%; P = .50).
Jeng and colleagues studied patients admitted for a cellulitis, and evaluated the patients’ response to beta-lactam antibiotics.2 Patients had acute and convalescent serologies for beta hemolytic strep. Almost all evaluable patients with positive strep studies (97%) responded to beta-lactams, and 21 of 23 (91%) with negative studies responded to beta-lactams (overall response rate 95%). This study was done during a time of high MRSA prevalence.
The most recent Infectious Diseases Society of America guidelines for skin and soft tissue infections, recommend oral penicillin, cephalexin, dicloxacillin, or clindamycin for mild cellulitis, and IV equivalent if patients have moderate cellulitis.3 If abscesses are present, then drainage is recommended and MRSA coverage. Kamath and colleagues reported on how closely guidelines for skin and soft tissue infections were followed.4 In patients with mild cellulitis, only 36% received guideline-suggested antibiotics. The most common antibiotic prescribed that was outside the guidelines was trimethoprim-sulfamethoxazole.
Myth: Cellulitis treatment should include MRSA coverage.
My advice: Stick with beta-lactam antibiotics, unless an abscess is present. There is no need to add MRSA coverage for initial treatment of mild to moderate cellulitis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Moran GJ et al. Effect of cephalexin plus trimethoprim-sulfamethoxazole vs. cephalexin alone on clinical cure of uncomplicated cellulitis: A randomized clinical trial. JAMA 2017 May 23;317(20):2088-96.
2. Jeng Arthur et al. The role of beta-hemolytic streptococci in causing diffuse, nonculturable cellulitis. Medicine. 2010;July;89(4):217-26.
3. Stevens DL et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-e52.
4. Kamath RS et al. Guidelines vs. actual management of skin and soft tissue infections in the emergency department. Open Forum Infect Dis. 2018 Jan 12;5(1):ofx188.
He noticed discomfort today and saw that his left lower leg had redness and was warm. He does not recall scratches or injury to his leg. He has not had fever or chills. He has no other symptoms. His diabetes has been well controlled with diet and metformin.
On exam, his blood pressure is 120/70, pulse is 80, temperature is 37 degrees Celsius.
In the left lower extremity, the patient had 1+ edema at the ankle, with a 14-cm x 20-cm warm, erythematous area just above the ankle and extending proximally.
His labs found an HCT of 44 and a WBC of 12,000. What do you recommend?
A) Vascular duplex exam
B) 1st generation cephalosporin
C) 1st generation cephalosporin + TMP/Sulfa
D) Oral clindamycin
E) IV vancomycin
This patient has cellulitis and should receive a beta lactam antibiotic, which will have the best coverage and lowest minimal inhibitory concentration for the likely organism, beta hemolytic streptococci. Clindamycin would likely work, but it has greater side effects. This patient does not need coverage for methicillin-resistant staphylococcus aureus (MRSA). I know many of you, if not most, know this, but I want to go through relevant data and formal recommendations, because of a recent call I received from a patient.
My patient had a full body rash after receiving cephalexin + TMP/sulfa [trimethoprim-sulfamethoxazole] treatment for cellulitis. In recent years the addition of TMP/sulfa to strep treatment to also cover MRSA has become popular, especially in emergency department and urgent care settings.
Moran and colleagues studied cephalexin + TMP/sulfa vs. cephalexin and placebo in patients with uncomplicated cellulitis.1 The outcome measured was clinical cure, and there was no difference between groups; clinical cure occurred in 182 (83.5%) of 218 participants in the cephalexin plus TMP/sulfa group vs. 165 (85.5%) of 193 in the cephalexin group (difference, −2.0%; 95% confidence interval, −9.7% to 5.7%; P = .50).
Jeng and colleagues studied patients admitted for a cellulitis, and evaluated the patients’ response to beta-lactam antibiotics.2 Patients had acute and convalescent serologies for beta hemolytic strep. Almost all evaluable patients with positive strep studies (97%) responded to beta-lactams, and 21 of 23 (91%) with negative studies responded to beta-lactams (overall response rate 95%). This study was done during a time of high MRSA prevalence.
The most recent Infectious Diseases Society of America guidelines for skin and soft tissue infections, recommend oral penicillin, cephalexin, dicloxacillin, or clindamycin for mild cellulitis, and IV equivalent if patients have moderate cellulitis.3 If abscesses are present, then drainage is recommended and MRSA coverage. Kamath and colleagues reported on how closely guidelines for skin and soft tissue infections were followed.4 In patients with mild cellulitis, only 36% received guideline-suggested antibiotics. The most common antibiotic prescribed that was outside the guidelines was trimethoprim-sulfamethoxazole.
Myth: Cellulitis treatment should include MRSA coverage.
My advice: Stick with beta-lactam antibiotics, unless an abscess is present. There is no need to add MRSA coverage for initial treatment of mild to moderate cellulitis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Moran GJ et al. Effect of cephalexin plus trimethoprim-sulfamethoxazole vs. cephalexin alone on clinical cure of uncomplicated cellulitis: A randomized clinical trial. JAMA 2017 May 23;317(20):2088-96.
2. Jeng Arthur et al. The role of beta-hemolytic streptococci in causing diffuse, nonculturable cellulitis. Medicine. 2010;July;89(4):217-26.
3. Stevens DL et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-e52.
4. Kamath RS et al. Guidelines vs. actual management of skin and soft tissue infections in the emergency department. Open Forum Infect Dis. 2018 Jan 12;5(1):ofx188.
Colonoscopy prep suggestions for those who hate it
A 61-year-old man is seen for a primary care visit. He has a history of colonic polyps (tubular adenoma) on two previous colonoscopies (at age 50 and 55). He has been on an appropriate 5-year schedule, but is overdue for his colonoscopy. He did not follow up with messages from his gastroenterologist for scheduling his colonoscopy last year. He explains he really hates the whole preparation for colonoscopy, but does realize he needs to follow up, and is willing to do so now. What do you recommend for colonoscopy prep?
A) Diet as usual until 5 p.m. day before, then clear liquid diet. Start GoLYTELY (1 gallon) night before procedure.
B) Low-fiber diet X2 days, clear liquid diet day before procedure, GoLYTELY (1 gallon) night before procedure.
C) Low residue diet X3 days, SUPREP the night before the procedure.
D) Low residue diet X2 days, followed by clear liquid diet the day before the procedure, SUPREP the night before the procedure.
It is common for patients to be reluctant to follow recommendations for colonoscopy due to dreading the prep. I would recommend choice C here, as the least difficult bowel preparation for colonoscopy.
Gastroenterologists are usually the ones to recommend the bowel prep that they want their patients to follow.
Major diet change for several days before colonoscopy is difficult for many patients. Standard advice is that patients eat only low-fiber foods starting 3 days before the procedure. Patients are advised to switch to a completely clear liquid diet 1-2 days before the colonoscopy.
Are there more tolerable diets to offer patients?
Soweid and colleagues randomized 200 patients to a low residue diet for the three meals the day before colonoscopy vs. clear liquid diet.1 The low residue diet allowed patients to eat meat, eggs, cheese, bread, rice, and ice cream. Not surprisingly, patients tolerated the low residue diet better with statistically significantly less nausea, vomiting, weakness, headache, sleep difficulties, and hunger. The patients in the low residue diet group also had better bowel prep than did those in the clear liquid diet group (81% vs. 52%, P less than 0.001).1
In a recent meta- analysis, low residue diets were comparable to clear liquid diets in regard to adequacy of bowel prep and for detection of polyps.2 Patients who followed low residue diets had statistically significantly less headaches, nausea, vomiting, and hunger. Very importantly, patients who followed low residue diets showed an increased willingness to repeat it, compared with those who followed a clear liquid diet (P less than .005; odds ratio, 2.23; 95% confidence interval, 1.28-3.89).2
What alternatives to GoLYTELY exist?
Another part of the bowel prep that patients struggle with is drinking a gallon of GoLYTELY (polyethylene glycol/electrolytes). Drinking that amount of this nasty stuff is never welcome.
There are a number of lower-volume alternatives that are as effective as GoLYTELY. Sarvepalli and colleagues did a retrospective study of 75,874 patients who had a colonoscopy in the Cleveland Clinic health system.3 The choice of bowel prep was not associated with adenoma detection.
Patients who lower volume preparations (2 quarts) SUPREP, MoviPrep, Osmoprep and HalfLytely had varying results of rates of inadequate bowel prep compared with patients who took GoLYTELY. Results for patients taking SUPREP and MoviPrep were statistically significantly better than for patients taking GoLYTELY. Results for patients taking OsmoPrep were not statistically different from those for patients taking GoLYTELY. Rates of inadequate bowel prep were statistically higher, meaning worse, for patients taking HalfLytely vs. patients taking GoLYTELY.3
Gu and colleagues did a prospective study of bowel prep outcomes from 4,339 colonoscopies, involving 75 different endoscopists.4 There was a wide range of bowel preps used, including low- and high-volume bowel preps. The low-volume preparations, SUPREP (P less than .001), MoviPrep (P less than .004) and MiraLAX with Gatorade (P less than .001), were superior to GoLYTELY for bowel cleansing. This was based on scoring via the Boston Bowel Preparation Scale. All were better tolerated than GoLYTELY.
Myth: All patients need a clear liquid diet and GoLYTELY for their bowel prep.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Soweid AM et al. A randomized single-blind trial of standard diet versus fiber-free diet with polyethylene glycol electrolyte solution for colonoscopy preparation. Endoscopy 2010;42:633-8.
2. Zhang X et al. Low-[residue] diet versus clear-liquid diet for bowel preparation before colonoscopy: meta-analysis and trial sequential analysis of randomized controlled trials. Gastrointest Endosc. 2020 Sep;92(3):508-18.
3. Sarvepalli S et al. Comparative effectiveness of commercial bowel preparations in ambulatory patients presenting for screening or surveillance colonoscopy. Dig Dis Sci. 2020 Jul 20. doi: 10.1007/s10620-020-06492-z.
4. Gu P et al. Comparing the real-world effectiveness of competing colonoscopy preparations: results of a prospective trial. Am J Gastroenterol. 2019;114(2):305-14.
A 61-year-old man is seen for a primary care visit. He has a history of colonic polyps (tubular adenoma) on two previous colonoscopies (at age 50 and 55). He has been on an appropriate 5-year schedule, but is overdue for his colonoscopy. He did not follow up with messages from his gastroenterologist for scheduling his colonoscopy last year. He explains he really hates the whole preparation for colonoscopy, but does realize he needs to follow up, and is willing to do so now. What do you recommend for colonoscopy prep?
A) Diet as usual until 5 p.m. day before, then clear liquid diet. Start GoLYTELY (1 gallon) night before procedure.
B) Low-fiber diet X2 days, clear liquid diet day before procedure, GoLYTELY (1 gallon) night before procedure.
C) Low residue diet X3 days, SUPREP the night before the procedure.
D) Low residue diet X2 days, followed by clear liquid diet the day before the procedure, SUPREP the night before the procedure.
It is common for patients to be reluctant to follow recommendations for colonoscopy due to dreading the prep. I would recommend choice C here, as the least difficult bowel preparation for colonoscopy.
Gastroenterologists are usually the ones to recommend the bowel prep that they want their patients to follow.
Major diet change for several days before colonoscopy is difficult for many patients. Standard advice is that patients eat only low-fiber foods starting 3 days before the procedure. Patients are advised to switch to a completely clear liquid diet 1-2 days before the colonoscopy.
Are there more tolerable diets to offer patients?
Soweid and colleagues randomized 200 patients to a low residue diet for the three meals the day before colonoscopy vs. clear liquid diet.1 The low residue diet allowed patients to eat meat, eggs, cheese, bread, rice, and ice cream. Not surprisingly, patients tolerated the low residue diet better with statistically significantly less nausea, vomiting, weakness, headache, sleep difficulties, and hunger. The patients in the low residue diet group also had better bowel prep than did those in the clear liquid diet group (81% vs. 52%, P less than 0.001).1
In a recent meta- analysis, low residue diets were comparable to clear liquid diets in regard to adequacy of bowel prep and for detection of polyps.2 Patients who followed low residue diets had statistically significantly less headaches, nausea, vomiting, and hunger. Very importantly, patients who followed low residue diets showed an increased willingness to repeat it, compared with those who followed a clear liquid diet (P less than .005; odds ratio, 2.23; 95% confidence interval, 1.28-3.89).2
What alternatives to GoLYTELY exist?
Another part of the bowel prep that patients struggle with is drinking a gallon of GoLYTELY (polyethylene glycol/electrolytes). Drinking that amount of this nasty stuff is never welcome.
There are a number of lower-volume alternatives that are as effective as GoLYTELY. Sarvepalli and colleagues did a retrospective study of 75,874 patients who had a colonoscopy in the Cleveland Clinic health system.3 The choice of bowel prep was not associated with adenoma detection.
Patients who lower volume preparations (2 quarts) SUPREP, MoviPrep, Osmoprep and HalfLytely had varying results of rates of inadequate bowel prep compared with patients who took GoLYTELY. Results for patients taking SUPREP and MoviPrep were statistically significantly better than for patients taking GoLYTELY. Results for patients taking OsmoPrep were not statistically different from those for patients taking GoLYTELY. Rates of inadequate bowel prep were statistically higher, meaning worse, for patients taking HalfLytely vs. patients taking GoLYTELY.3
Gu and colleagues did a prospective study of bowel prep outcomes from 4,339 colonoscopies, involving 75 different endoscopists.4 There was a wide range of bowel preps used, including low- and high-volume bowel preps. The low-volume preparations, SUPREP (P less than .001), MoviPrep (P less than .004) and MiraLAX with Gatorade (P less than .001), were superior to GoLYTELY for bowel cleansing. This was based on scoring via the Boston Bowel Preparation Scale. All were better tolerated than GoLYTELY.
Myth: All patients need a clear liquid diet and GoLYTELY for their bowel prep.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Soweid AM et al. A randomized single-blind trial of standard diet versus fiber-free diet with polyethylene glycol electrolyte solution for colonoscopy preparation. Endoscopy 2010;42:633-8.
2. Zhang X et al. Low-[residue] diet versus clear-liquid diet for bowel preparation before colonoscopy: meta-analysis and trial sequential analysis of randomized controlled trials. Gastrointest Endosc. 2020 Sep;92(3):508-18.
3. Sarvepalli S et al. Comparative effectiveness of commercial bowel preparations in ambulatory patients presenting for screening or surveillance colonoscopy. Dig Dis Sci. 2020 Jul 20. doi: 10.1007/s10620-020-06492-z.
4. Gu P et al. Comparing the real-world effectiveness of competing colonoscopy preparations: results of a prospective trial. Am J Gastroenterol. 2019;114(2):305-14.
A 61-year-old man is seen for a primary care visit. He has a history of colonic polyps (tubular adenoma) on two previous colonoscopies (at age 50 and 55). He has been on an appropriate 5-year schedule, but is overdue for his colonoscopy. He did not follow up with messages from his gastroenterologist for scheduling his colonoscopy last year. He explains he really hates the whole preparation for colonoscopy, but does realize he needs to follow up, and is willing to do so now. What do you recommend for colonoscopy prep?
A) Diet as usual until 5 p.m. day before, then clear liquid diet. Start GoLYTELY (1 gallon) night before procedure.
B) Low-fiber diet X2 days, clear liquid diet day before procedure, GoLYTELY (1 gallon) night before procedure.
C) Low residue diet X3 days, SUPREP the night before the procedure.
D) Low residue diet X2 days, followed by clear liquid diet the day before the procedure, SUPREP the night before the procedure.
It is common for patients to be reluctant to follow recommendations for colonoscopy due to dreading the prep. I would recommend choice C here, as the least difficult bowel preparation for colonoscopy.
Gastroenterologists are usually the ones to recommend the bowel prep that they want their patients to follow.
Major diet change for several days before colonoscopy is difficult for many patients. Standard advice is that patients eat only low-fiber foods starting 3 days before the procedure. Patients are advised to switch to a completely clear liquid diet 1-2 days before the colonoscopy.
Are there more tolerable diets to offer patients?
Soweid and colleagues randomized 200 patients to a low residue diet for the three meals the day before colonoscopy vs. clear liquid diet.1 The low residue diet allowed patients to eat meat, eggs, cheese, bread, rice, and ice cream. Not surprisingly, patients tolerated the low residue diet better with statistically significantly less nausea, vomiting, weakness, headache, sleep difficulties, and hunger. The patients in the low residue diet group also had better bowel prep than did those in the clear liquid diet group (81% vs. 52%, P less than 0.001).1
In a recent meta- analysis, low residue diets were comparable to clear liquid diets in regard to adequacy of bowel prep and for detection of polyps.2 Patients who followed low residue diets had statistically significantly less headaches, nausea, vomiting, and hunger. Very importantly, patients who followed low residue diets showed an increased willingness to repeat it, compared with those who followed a clear liquid diet (P less than .005; odds ratio, 2.23; 95% confidence interval, 1.28-3.89).2
What alternatives to GoLYTELY exist?
Another part of the bowel prep that patients struggle with is drinking a gallon of GoLYTELY (polyethylene glycol/electrolytes). Drinking that amount of this nasty stuff is never welcome.
There are a number of lower-volume alternatives that are as effective as GoLYTELY. Sarvepalli and colleagues did a retrospective study of 75,874 patients who had a colonoscopy in the Cleveland Clinic health system.3 The choice of bowel prep was not associated with adenoma detection.
Patients who lower volume preparations (2 quarts) SUPREP, MoviPrep, Osmoprep and HalfLytely had varying results of rates of inadequate bowel prep compared with patients who took GoLYTELY. Results for patients taking SUPREP and MoviPrep were statistically significantly better than for patients taking GoLYTELY. Results for patients taking OsmoPrep were not statistically different from those for patients taking GoLYTELY. Rates of inadequate bowel prep were statistically higher, meaning worse, for patients taking HalfLytely vs. patients taking GoLYTELY.3
Gu and colleagues did a prospective study of bowel prep outcomes from 4,339 colonoscopies, involving 75 different endoscopists.4 There was a wide range of bowel preps used, including low- and high-volume bowel preps. The low-volume preparations, SUPREP (P less than .001), MoviPrep (P less than .004) and MiraLAX with Gatorade (P less than .001), were superior to GoLYTELY for bowel cleansing. This was based on scoring via the Boston Bowel Preparation Scale. All were better tolerated than GoLYTELY.
Myth: All patients need a clear liquid diet and GoLYTELY for their bowel prep.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Soweid AM et al. A randomized single-blind trial of standard diet versus fiber-free diet with polyethylene glycol electrolyte solution for colonoscopy preparation. Endoscopy 2010;42:633-8.
2. Zhang X et al. Low-[residue] diet versus clear-liquid diet for bowel preparation before colonoscopy: meta-analysis and trial sequential analysis of randomized controlled trials. Gastrointest Endosc. 2020 Sep;92(3):508-18.
3. Sarvepalli S et al. Comparative effectiveness of commercial bowel preparations in ambulatory patients presenting for screening or surveillance colonoscopy. Dig Dis Sci. 2020 Jul 20. doi: 10.1007/s10620-020-06492-z.
4. Gu P et al. Comparing the real-world effectiveness of competing colonoscopy preparations: results of a prospective trial. Am J Gastroenterol. 2019;114(2):305-14.
Patient with CKD: Contrast or no contrast?
A 67-year-old man with stage 3 chronic kidney disease (CKD) develops abdominal pain over 24 hours. He has had low grade fevers and nausea. He has a history of colon cancer and had a resection four years ago. Abdominal exam reveals tenderness to palpation, including rebound tenderness in his right lower quadrant. Labs: hemoglobin: 13; hematocrit: 39; white blood cells: 18,000; platelets: 333; blood urea nitrogen: 28; creatinine: 1.8 (estimated glomerular filtration rate: 37); sodium: 136; potassium: 3.9; bicarbonate: 24; chlorine: 105; and lipase: 10.
What testing would you recommend?
A) Ultrasound
B) Non contrast computed tomography (CT)
C) Contrast CT
D) MRI without gadolinium
The correct answer here is to get a contrast CT scan, as it will give you the most appropriate diagnostic information.
For years, we have hesitated to order contrast studies in our patients with CKD, for fear of causing contrast-induced nephrotoxicity. We might choose less helpful studies that avoid contrast, or might not obtain imaging that is needed. Over the years I have especially seen this in the case of avoiding computed tomography angiography (CTA) for evaluation of pulmonary embolus and choosing the much less useful ventilation/perfusion scan. The problem arises with the fact that patients with CKD are more likely to develop worsening renal function when they get sick.
Lee and colleagues performed an analysis of six retrospective studies involving a total of 55,963 participants. They found that patients with CKD receiving contrast material did not have an increased risk of deteriorating renal function compared with those without CKD (odds ratio, 1.07; 95% confidence interval, 0.98-1.17).1
The early studies reporting contrast-induced renal disease were in patients who received high osmolality contrast agents.2 Most patients now receive low osmolality agents, with less nephrotoxicity.3
Key points of guidelines
This year, the American College of Radiology and the National Kidney Foundation put out joint guidelines that helped clarify why there is a diminished concern for contrast-induced kidney disease in the modern era.4 Below are some of the key points of these guidelines:
- The risk of contrast-induced acute kidney injury (AKI) from intravenous iodinated contrast media is lower than previously thought.
- Necessary contrast material–enhanced CT without a suitable alternative should not be avoided solely on the basis of contrast-induced chronic kidney insufficiency risk.
- Contrast-induced AKI risk should be determined primarily by using CKD stage and AKI.
- Patients at high risk for contrast-induced kidney injury include those with recent AKI and those with estimated glomerular filtration rate (eGFR) less than 30 mL/min per 1.73 m2.
Data supporting guidelines
The data from several studies used to support these recommendations were impressive, showing just how low the risk for contrast-induced AKI is in most patients. In these studies, the risk of contrast-induced AKI has been estimated to be near 0% for patients with an eGFR greater than or equal to 45 and 0%-2% for patients with an eGFR of 30-44.5-7 This information and recommendations make imaging much easier. In most of our patients, we can get contrast studies when we need them. The group to be concerned about are patients with eGFRs less than 30. The guidelines single out this group as the patients where risk/benefit needs to be calculated before proceeding with the study, and to use prophylactic saline hydration in patients not undergoing dialysis.
Myth: Contrast-induced renal disease is common.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Lee YC et al. Contrast-induced acute kidney injury among patients with chronic kidney disease undergoing imaging studies: A meta-analysis. Am J Roentgenol. 2019 Oct;213(4):728-35.
2. Luk L et al. Intravenous contrast-induced nephropathy: The rise and fall of a threatening idea. Adv Chronic Kidney Dis. 2017 May;24(3):169-75.
3. Goldfarb S et al. Low-osmolality contrast media and the risk of contrast-associated nephrotoxicity. Invest Radiol. 1993;28(Suppl 5):7-10.
4. Davenport MS, et al. Use of intravenous iodinated contrast media in patients with kidney disease: Consensus statements from the American College of Radiology and the National Kidney Foundation. Kidney Med. 2020 Jan 22;2(1):85-93.
5. Davenport MS et al. Contrast material–induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology. 2013;267(1):94-105.
6. McDonald RJ et al. Intravenous contrast material–induced nephropathy: Causal or coincident phenomenon? Radiology. 2013;267(1):106-18.
7. McDonald JS et al. Risk of intravenous contrast material–mediated acute kidney injury: A propensity scorematched study stratified by baseline-estimated glomerular filtration rate. Radiology. 2014;271(1):65-73.
A 67-year-old man with stage 3 chronic kidney disease (CKD) develops abdominal pain over 24 hours. He has had low grade fevers and nausea. He has a history of colon cancer and had a resection four years ago. Abdominal exam reveals tenderness to palpation, including rebound tenderness in his right lower quadrant. Labs: hemoglobin: 13; hematocrit: 39; white blood cells: 18,000; platelets: 333; blood urea nitrogen: 28; creatinine: 1.8 (estimated glomerular filtration rate: 37); sodium: 136; potassium: 3.9; bicarbonate: 24; chlorine: 105; and lipase: 10.
What testing would you recommend?
A) Ultrasound
B) Non contrast computed tomography (CT)
C) Contrast CT
D) MRI without gadolinium
The correct answer here is to get a contrast CT scan, as it will give you the most appropriate diagnostic information.
For years, we have hesitated to order contrast studies in our patients with CKD, for fear of causing contrast-induced nephrotoxicity. We might choose less helpful studies that avoid contrast, or might not obtain imaging that is needed. Over the years I have especially seen this in the case of avoiding computed tomography angiography (CTA) for evaluation of pulmonary embolus and choosing the much less useful ventilation/perfusion scan. The problem arises with the fact that patients with CKD are more likely to develop worsening renal function when they get sick.
Lee and colleagues performed an analysis of six retrospective studies involving a total of 55,963 participants. They found that patients with CKD receiving contrast material did not have an increased risk of deteriorating renal function compared with those without CKD (odds ratio, 1.07; 95% confidence interval, 0.98-1.17).1
The early studies reporting contrast-induced renal disease were in patients who received high osmolality contrast agents.2 Most patients now receive low osmolality agents, with less nephrotoxicity.3
Key points of guidelines
This year, the American College of Radiology and the National Kidney Foundation put out joint guidelines that helped clarify why there is a diminished concern for contrast-induced kidney disease in the modern era.4 Below are some of the key points of these guidelines:
- The risk of contrast-induced acute kidney injury (AKI) from intravenous iodinated contrast media is lower than previously thought.
- Necessary contrast material–enhanced CT without a suitable alternative should not be avoided solely on the basis of contrast-induced chronic kidney insufficiency risk.
- Contrast-induced AKI risk should be determined primarily by using CKD stage and AKI.
- Patients at high risk for contrast-induced kidney injury include those with recent AKI and those with estimated glomerular filtration rate (eGFR) less than 30 mL/min per 1.73 m2.
Data supporting guidelines
The data from several studies used to support these recommendations were impressive, showing just how low the risk for contrast-induced AKI is in most patients. In these studies, the risk of contrast-induced AKI has been estimated to be near 0% for patients with an eGFR greater than or equal to 45 and 0%-2% for patients with an eGFR of 30-44.5-7 This information and recommendations make imaging much easier. In most of our patients, we can get contrast studies when we need them. The group to be concerned about are patients with eGFRs less than 30. The guidelines single out this group as the patients where risk/benefit needs to be calculated before proceeding with the study, and to use prophylactic saline hydration in patients not undergoing dialysis.
Myth: Contrast-induced renal disease is common.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Lee YC et al. Contrast-induced acute kidney injury among patients with chronic kidney disease undergoing imaging studies: A meta-analysis. Am J Roentgenol. 2019 Oct;213(4):728-35.
2. Luk L et al. Intravenous contrast-induced nephropathy: The rise and fall of a threatening idea. Adv Chronic Kidney Dis. 2017 May;24(3):169-75.
3. Goldfarb S et al. Low-osmolality contrast media and the risk of contrast-associated nephrotoxicity. Invest Radiol. 1993;28(Suppl 5):7-10.
4. Davenport MS, et al. Use of intravenous iodinated contrast media in patients with kidney disease: Consensus statements from the American College of Radiology and the National Kidney Foundation. Kidney Med. 2020 Jan 22;2(1):85-93.
5. Davenport MS et al. Contrast material–induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology. 2013;267(1):94-105.
6. McDonald RJ et al. Intravenous contrast material–induced nephropathy: Causal or coincident phenomenon? Radiology. 2013;267(1):106-18.
7. McDonald JS et al. Risk of intravenous contrast material–mediated acute kidney injury: A propensity scorematched study stratified by baseline-estimated glomerular filtration rate. Radiology. 2014;271(1):65-73.
A 67-year-old man with stage 3 chronic kidney disease (CKD) develops abdominal pain over 24 hours. He has had low grade fevers and nausea. He has a history of colon cancer and had a resection four years ago. Abdominal exam reveals tenderness to palpation, including rebound tenderness in his right lower quadrant. Labs: hemoglobin: 13; hematocrit: 39; white blood cells: 18,000; platelets: 333; blood urea nitrogen: 28; creatinine: 1.8 (estimated glomerular filtration rate: 37); sodium: 136; potassium: 3.9; bicarbonate: 24; chlorine: 105; and lipase: 10.
What testing would you recommend?
A) Ultrasound
B) Non contrast computed tomography (CT)
C) Contrast CT
D) MRI without gadolinium
The correct answer here is to get a contrast CT scan, as it will give you the most appropriate diagnostic information.
For years, we have hesitated to order contrast studies in our patients with CKD, for fear of causing contrast-induced nephrotoxicity. We might choose less helpful studies that avoid contrast, or might not obtain imaging that is needed. Over the years I have especially seen this in the case of avoiding computed tomography angiography (CTA) for evaluation of pulmonary embolus and choosing the much less useful ventilation/perfusion scan. The problem arises with the fact that patients with CKD are more likely to develop worsening renal function when they get sick.
Lee and colleagues performed an analysis of six retrospective studies involving a total of 55,963 participants. They found that patients with CKD receiving contrast material did not have an increased risk of deteriorating renal function compared with those without CKD (odds ratio, 1.07; 95% confidence interval, 0.98-1.17).1
The early studies reporting contrast-induced renal disease were in patients who received high osmolality contrast agents.2 Most patients now receive low osmolality agents, with less nephrotoxicity.3
Key points of guidelines
This year, the American College of Radiology and the National Kidney Foundation put out joint guidelines that helped clarify why there is a diminished concern for contrast-induced kidney disease in the modern era.4 Below are some of the key points of these guidelines:
- The risk of contrast-induced acute kidney injury (AKI) from intravenous iodinated contrast media is lower than previously thought.
- Necessary contrast material–enhanced CT without a suitable alternative should not be avoided solely on the basis of contrast-induced chronic kidney insufficiency risk.
- Contrast-induced AKI risk should be determined primarily by using CKD stage and AKI.
- Patients at high risk for contrast-induced kidney injury include those with recent AKI and those with estimated glomerular filtration rate (eGFR) less than 30 mL/min per 1.73 m2.
Data supporting guidelines
The data from several studies used to support these recommendations were impressive, showing just how low the risk for contrast-induced AKI is in most patients. In these studies, the risk of contrast-induced AKI has been estimated to be near 0% for patients with an eGFR greater than or equal to 45 and 0%-2% for patients with an eGFR of 30-44.5-7 This information and recommendations make imaging much easier. In most of our patients, we can get contrast studies when we need them. The group to be concerned about are patients with eGFRs less than 30. The guidelines single out this group as the patients where risk/benefit needs to be calculated before proceeding with the study, and to use prophylactic saline hydration in patients not undergoing dialysis.
Myth: Contrast-induced renal disease is common.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Lee YC et al. Contrast-induced acute kidney injury among patients with chronic kidney disease undergoing imaging studies: A meta-analysis. Am J Roentgenol. 2019 Oct;213(4):728-35.
2. Luk L et al. Intravenous contrast-induced nephropathy: The rise and fall of a threatening idea. Adv Chronic Kidney Dis. 2017 May;24(3):169-75.
3. Goldfarb S et al. Low-osmolality contrast media and the risk of contrast-associated nephrotoxicity. Invest Radiol. 1993;28(Suppl 5):7-10.
4. Davenport MS, et al. Use of intravenous iodinated contrast media in patients with kidney disease: Consensus statements from the American College of Radiology and the National Kidney Foundation. Kidney Med. 2020 Jan 22;2(1):85-93.
5. Davenport MS et al. Contrast material–induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology. 2013;267(1):94-105.
6. McDonald RJ et al. Intravenous contrast material–induced nephropathy: Causal or coincident phenomenon? Radiology. 2013;267(1):106-18.
7. McDonald JS et al. Risk of intravenous contrast material–mediated acute kidney injury: A propensity scorematched study stratified by baseline-estimated glomerular filtration rate. Radiology. 2014;271(1):65-73.
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 [email protected].
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 [email protected].
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 [email protected].
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.
Geriatric patients: My three rules for them
I have been in practice for 31 years, so many of my patients are now in their 80s and 90s. Practices age with us, and I have been seeing many of these patients for 25-30 years.
Absolutely, positively make sure you move!
Our older patients often have many reasons not to move, including pain from arthritis, deconditioning, muscle weakness, fatigue, and depression. “Keeping moving” is probably the most important thing a patient can do for their health.
Holme and Anderssen studied a large cohort of men for cardiovascular risk in 1972 and again in 2000. The surviving men were followed over an additional 12 years.1 They found that 30 minutes of physical activity 6 days a week was associated with a 40% reduction in mortality. Sedentary men had a reduced life expectancy of about 5 years, compared with men who were moderately to vigorously physically active.
Stewart etal. studied the benefit of physical activity in people with stable coronary disease.2 They concluded that, in patients with stable coronary heart disease, more physical activity was associated with lower mortality, and the largest benefit occurred in the sedentary patient groups and the highest cardiac risk groups.
Saint-Maurice et al. studied the effects of total daily step count and step intensity on mortality risk.3 They found that the risk of all-cause mortality decreases as the total number of daily steps increases, but that the speed of those steps did not make a difference. This is very encouraging data for our elderly patients. Moving is the secret, even if it may not be moving at a fast pace!
Never, ever get on a ladder!
This one should be part of every geriatric’s assessment and every Medicare wellness exam. I first experienced the horror of what can happen when elderly people climb when a 96-year-old healthy patient of mine fell off his roof and died. I never thought to tell him climbing on the roof was an awful idea.
Akland et al. looked at the epidemiology and outcomes of ladder-related falls that required ICU admission.4 Hospital mortality was 26%, and almost all of the mortalities occurred in older males in domestic falls, who died as a result of traumatic brain injury. Fewer than half of the survivors were living independently 1 year after the fall.
Valmuur et al. studied ladder related falls in Australia.5 They found that rates of ladder related falls requiring hospitalization rose from about 20/100,000 for men ages 15-29 years to 78/100,000 for men aged over 60 years. Of those who died from fall-related injury, 82% were over the age of 60, with more than 70% dying from head injuries.
Schaffarczyk et al. looked at the impact of nonoccupational falls from ladders in men aged over 50 years.6 The mean age of the patients in the study was 64 years (range, 50-85), with 27% suffering severe trauma. There was a striking impact on long-term function occurring in over half the study patients. The authors did interviews with patients in follow-up long after the falls and found that most never thought of themselves at risk for a fall, and after the experience of a bad fall, would never consider going on a ladder again. I think it is important for health care professionals to discuss the dangers of ladder use with our older patients, pointing out the higher risk of falling and the potential for the fall to be a life-changing or life-ending event.
Let them eat!
Many patients have a reduced appetite as they age. We work hard with our patients to choose a healthy diet throughout their lives, to help ward off obesity, treat hypertension, prevent or control diabetes, or provide heart health. Many patients just stop being interested in food, reduce intake, and may lose weight and muscle mass. When my patients pass the age of 85, I change my focus to encouraging them to eat for calories, socialization, and joy. I think the marginal benefits of more restrictive diets are small, compared with the benefits of helping your patients enjoy eating again. I ask patients what their very favorite foods are and encourage them to have them.
Pearl
Keep your patients eating and moving, except not onto a ladder!
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 [email protected].
References
1. Holme I, Anderssen SA. Increases in physical activity is as important as smoking cessation for reduction in total mortality in elderly men: 12 years of follow-up of the Oslo II study. Br J Sports Med. 2015; 49:743-8.
2. Stewart RAH et al. Physical activity and mortality in patients with stable coronary heart disease. J Am Coll Cardiol. 2017 Oct 3;70(14):1689-1700..
3. Saint-Maurice PF et al. Association of daily step count and step intensity with mortality among U.S. adults. JAMA 2020;323:1151-60.
4. Ackland HM et al. Danger at every rung: Epidemiology and outcomes of ICU-admitted ladder-related trauma. Injury. 2016;47:1109-117.
5. Vallmuur K et al. Falls from ladders in Australia: comparing occupational and nonoccupational injuries across age groups. Aust N Z J Public Health. 2016 Dec;40(6):559-63.
6. Schaffarczyk K et al. Nonoccupational falls from ladders in men 50 years and over: Contributing factors and impact. Injury. 2020 Aug;51(8):1798-1804.
I have been in practice for 31 years, so many of my patients are now in their 80s and 90s. Practices age with us, and I have been seeing many of these patients for 25-30 years.
Absolutely, positively make sure you move!
Our older patients often have many reasons not to move, including pain from arthritis, deconditioning, muscle weakness, fatigue, and depression. “Keeping moving” is probably the most important thing a patient can do for their health.
Holme and Anderssen studied a large cohort of men for cardiovascular risk in 1972 and again in 2000. The surviving men were followed over an additional 12 years.1 They found that 30 minutes of physical activity 6 days a week was associated with a 40% reduction in mortality. Sedentary men had a reduced life expectancy of about 5 years, compared with men who were moderately to vigorously physically active.
Stewart etal. studied the benefit of physical activity in people with stable coronary disease.2 They concluded that, in patients with stable coronary heart disease, more physical activity was associated with lower mortality, and the largest benefit occurred in the sedentary patient groups and the highest cardiac risk groups.
Saint-Maurice et al. studied the effects of total daily step count and step intensity on mortality risk.3 They found that the risk of all-cause mortality decreases as the total number of daily steps increases, but that the speed of those steps did not make a difference. This is very encouraging data for our elderly patients. Moving is the secret, even if it may not be moving at a fast pace!
Never, ever get on a ladder!
This one should be part of every geriatric’s assessment and every Medicare wellness exam. I first experienced the horror of what can happen when elderly people climb when a 96-year-old healthy patient of mine fell off his roof and died. I never thought to tell him climbing on the roof was an awful idea.
Akland et al. looked at the epidemiology and outcomes of ladder-related falls that required ICU admission.4 Hospital mortality was 26%, and almost all of the mortalities occurred in older males in domestic falls, who died as a result of traumatic brain injury. Fewer than half of the survivors were living independently 1 year after the fall.
Valmuur et al. studied ladder related falls in Australia.5 They found that rates of ladder related falls requiring hospitalization rose from about 20/100,000 for men ages 15-29 years to 78/100,000 for men aged over 60 years. Of those who died from fall-related injury, 82% were over the age of 60, with more than 70% dying from head injuries.
Schaffarczyk et al. looked at the impact of nonoccupational falls from ladders in men aged over 50 years.6 The mean age of the patients in the study was 64 years (range, 50-85), with 27% suffering severe trauma. There was a striking impact on long-term function occurring in over half the study patients. The authors did interviews with patients in follow-up long after the falls and found that most never thought of themselves at risk for a fall, and after the experience of a bad fall, would never consider going on a ladder again. I think it is important for health care professionals to discuss the dangers of ladder use with our older patients, pointing out the higher risk of falling and the potential for the fall to be a life-changing or life-ending event.
Let them eat!
Many patients have a reduced appetite as they age. We work hard with our patients to choose a healthy diet throughout their lives, to help ward off obesity, treat hypertension, prevent or control diabetes, or provide heart health. Many patients just stop being interested in food, reduce intake, and may lose weight and muscle mass. When my patients pass the age of 85, I change my focus to encouraging them to eat for calories, socialization, and joy. I think the marginal benefits of more restrictive diets are small, compared with the benefits of helping your patients enjoy eating again. I ask patients what their very favorite foods are and encourage them to have them.
Pearl
Keep your patients eating and moving, except not onto a ladder!
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 [email protected].
References
1. Holme I, Anderssen SA. Increases in physical activity is as important as smoking cessation for reduction in total mortality in elderly men: 12 years of follow-up of the Oslo II study. Br J Sports Med. 2015; 49:743-8.
2. Stewart RAH et al. Physical activity and mortality in patients with stable coronary heart disease. J Am Coll Cardiol. 2017 Oct 3;70(14):1689-1700..
3. Saint-Maurice PF et al. Association of daily step count and step intensity with mortality among U.S. adults. JAMA 2020;323:1151-60.
4. Ackland HM et al. Danger at every rung: Epidemiology and outcomes of ICU-admitted ladder-related trauma. Injury. 2016;47:1109-117.
5. Vallmuur K et al. Falls from ladders in Australia: comparing occupational and nonoccupational injuries across age groups. Aust N Z J Public Health. 2016 Dec;40(6):559-63.
6. Schaffarczyk K et al. Nonoccupational falls from ladders in men 50 years and over: Contributing factors and impact. Injury. 2020 Aug;51(8):1798-1804.
I have been in practice for 31 years, so many of my patients are now in their 80s and 90s. Practices age with us, and I have been seeing many of these patients for 25-30 years.
Absolutely, positively make sure you move!
Our older patients often have many reasons not to move, including pain from arthritis, deconditioning, muscle weakness, fatigue, and depression. “Keeping moving” is probably the most important thing a patient can do for their health.
Holme and Anderssen studied a large cohort of men for cardiovascular risk in 1972 and again in 2000. The surviving men were followed over an additional 12 years.1 They found that 30 minutes of physical activity 6 days a week was associated with a 40% reduction in mortality. Sedentary men had a reduced life expectancy of about 5 years, compared with men who were moderately to vigorously physically active.
Stewart etal. studied the benefit of physical activity in people with stable coronary disease.2 They concluded that, in patients with stable coronary heart disease, more physical activity was associated with lower mortality, and the largest benefit occurred in the sedentary patient groups and the highest cardiac risk groups.
Saint-Maurice et al. studied the effects of total daily step count and step intensity on mortality risk.3 They found that the risk of all-cause mortality decreases as the total number of daily steps increases, but that the speed of those steps did not make a difference. This is very encouraging data for our elderly patients. Moving is the secret, even if it may not be moving at a fast pace!
Never, ever get on a ladder!
This one should be part of every geriatric’s assessment and every Medicare wellness exam. I first experienced the horror of what can happen when elderly people climb when a 96-year-old healthy patient of mine fell off his roof and died. I never thought to tell him climbing on the roof was an awful idea.
Akland et al. looked at the epidemiology and outcomes of ladder-related falls that required ICU admission.4 Hospital mortality was 26%, and almost all of the mortalities occurred in older males in domestic falls, who died as a result of traumatic brain injury. Fewer than half of the survivors were living independently 1 year after the fall.
Valmuur et al. studied ladder related falls in Australia.5 They found that rates of ladder related falls requiring hospitalization rose from about 20/100,000 for men ages 15-29 years to 78/100,000 for men aged over 60 years. Of those who died from fall-related injury, 82% were over the age of 60, with more than 70% dying from head injuries.
Schaffarczyk et al. looked at the impact of nonoccupational falls from ladders in men aged over 50 years.6 The mean age of the patients in the study was 64 years (range, 50-85), with 27% suffering severe trauma. There was a striking impact on long-term function occurring in over half the study patients. The authors did interviews with patients in follow-up long after the falls and found that most never thought of themselves at risk for a fall, and after the experience of a bad fall, would never consider going on a ladder again. I think it is important for health care professionals to discuss the dangers of ladder use with our older patients, pointing out the higher risk of falling and the potential for the fall to be a life-changing or life-ending event.
Let them eat!
Many patients have a reduced appetite as they age. We work hard with our patients to choose a healthy diet throughout their lives, to help ward off obesity, treat hypertension, prevent or control diabetes, or provide heart health. Many patients just stop being interested in food, reduce intake, and may lose weight and muscle mass. When my patients pass the age of 85, I change my focus to encouraging them to eat for calories, socialization, and joy. I think the marginal benefits of more restrictive diets are small, compared with the benefits of helping your patients enjoy eating again. I ask patients what their very favorite foods are and encourage them to have them.
Pearl
Keep your patients eating and moving, except not onto a ladder!
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 [email protected].
References
1. Holme I, Anderssen SA. Increases in physical activity is as important as smoking cessation for reduction in total mortality in elderly men: 12 years of follow-up of the Oslo II study. Br J Sports Med. 2015; 49:743-8.
2. Stewart RAH et al. Physical activity and mortality in patients with stable coronary heart disease. J Am Coll Cardiol. 2017 Oct 3;70(14):1689-1700..
3. Saint-Maurice PF et al. Association of daily step count and step intensity with mortality among U.S. adults. JAMA 2020;323:1151-60.
4. Ackland HM et al. Danger at every rung: Epidemiology and outcomes of ICU-admitted ladder-related trauma. Injury. 2016;47:1109-117.
5. Vallmuur K et al. Falls from ladders in Australia: comparing occupational and nonoccupational injuries across age groups. Aust N Z J Public Health. 2016 Dec;40(6):559-63.
6. Schaffarczyk K et al. Nonoccupational falls from ladders in men 50 years and over: Contributing factors and impact. Injury. 2020 Aug;51(8):1798-1804.