Colorectal cancer screening: Colonoscopy has disadvantages

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Colorectal cancer screening: Colonoscopy has disadvantages

To the Editor: In the article, “Colorectal cancer screening: Choosing the right test,” the authors offer an excellent review, but restrict the discussion to just 2 of the many options. Screening compliance improves when clinicians and patients can select their preferred screening approach, and other noninvasive or minimally invasive approaches also deserve consideration and may well be superior. It is important that both the patient and the healthcare provider be fully aware of the advantages and disadvantages of each method.

The article is overly generous in its description of the accuracy and sensitivity of optical colonoscopy. The statement that colonoscopy visualizes the entire colon in more than 98% of cases is not supported by the biomedical literature or clinical experience. The measure of colonoscopy accuracy is best quantified by a review of more than 15,000 tandem colonoscopies that showed an average polyp miss rate of 22% using standard colonoscopes, and a 69% polyp miss rate compared with full-spectrum colonoscopes with greater fields of view.1–3 Between 5% and 10% of colonoscopies are technically incomplete and do not reach the cecum. Only 35% of colonoscopy bowel preps are excellent, and 21% are so poor that the procedure cannot be completed.4–8 Colorectal cancers are frequently missed at colonoscopy, with a rate of 7% quoted in the literature for interval cancer development.9–16 Studies of computed tomography colonography (virtual colonoscopy) have confirmed that between 10% and 20% of the colonic mucosa is hidden from view on optical colonoscopy by tall haustral mucosal folds.17,18 The operator variation measured by adenoma detection rates can exceed a 10-fold differential.

Colonoscopy is an important and valuable diagnostic and therapeutic tool. The disadvantages include significant cancer and polyp miss rates, high discomfort, high expense, potentially life-threatening complications, time- and resource-intensive utilization, high loss of patient work productivity, challenging and frequently inadequate preparation, higher risk of metachronous cancer and polyp spread, and high operator variability of quality.19–24 Unfortunately, while colonoscopy is an important tool, it does not come anywhere close to a score of 98% and should not be considered the gold standard for colorectal cancer screening.25

References
  1. Zhao S, Wang S, Pan P, et al. Magnitude, risk factors, and factors associated with adenoma miss rate of tandem colonoscopy: a systemic review and meta-analysis. Gastroenterology 2019; 156(6):1661–1674. doi:10.1053/j.gastro.2019.01.260
  2. van Rijn JC, Reitsma JB, Stoker J, Bossuyt PM, van Deventer SJ, Dekker E. Polyp miss rate determined by tandem colonoscopy: a systematic review. Am J Gastroenterol 2006; 101(2):343–350. doi:10.1111/j.1572-0241.2006.00390.x
  3. Gralnek IM, Siersema PD, Halpern Z, et al. Standard forward-viewing colonoscopy versus full-spectrum endoscopy: an international, multicenter, randomised, tandem colonoscopy trial. Lancet Oncol 2014; 15(3):353–360. doi:10.1016/S1470-2045(14)70020-8
  4. Ness RM, Manam R, Hoen H, Chalasani N. Predictors of inadequate bowel preparation for colonoscopy. Am J Gastroenterol 2001; 96(6):1797–1802. doi:10.1111/j.1572-0241.2001.03874.x 
  5. Kluge M, Williams J, Wu C, et al. Inadequate Boston Bowel Preparation Scale scores predict the risk of missed neoplasia on the next colonoscopy. Gastrointest Endosc 2018; 87(3):744–751. doi:10.1016/j.gie.2017.06.012
  6. Gagneja H, Parekh P, Burleson D, et al. HyGIeaCare® preparation for colonoscopy – a technical update for success. J Gastrointest Dig Syst 2016; 6:4. doi:10.4172/2161-069X.1000458
  7. Das A, Parekh P, Bekal P, et al. Bowel preparation for colonoscopy: a comparative cost-effective analysis of traditional per os purgatory prep versus a novel method using high-volume colonic water irrigation. Gastroenterol Hepatol Int J 2017; 2(4):000132.
  8. D’Souza SM, Parekh PJ, Johnson DA. The dirty side of colonoscopy: predictors of poor bowel preparation and novel approaches to overcome the shortcomings. Br J Gastroenterol 2019: 1:1. https://hygieacare.com/wp-content/uploads/2019/06/The-Dirty-Side-of-Colonoscopy-PDF.pdf. Accessed October 23, 2019.
  9. Mouchli M, Ouk L, Scheitel M. Colonoscopy surveillance for high risk polyps does not always prevent colorectal cancer. World J Gastroenterol 2018; 24(8):905–916. doi:10.3748/wjg.v24.i8.905
  10. Adler J, Robertson DJ. Interval colorectal cancer after colonoscopy: exploring explanations and solutions. Am J Gastroenterol 2015; 110(12):1657–1664. doi:10.1038/ajg.2015.365
  11. Robertson DJ, Lieberman DA, Winawer SJ, et al. Colorectal cancers soon after colonoscopy: a pooled multi-cohort analysis. Gut 2014; 63(6):949–956. doi:10.1136/gutjnl-2012-303796
  12. Brenner H, Chang-Claude J, Seiler CM, Rickert A, Hoffmeister M. Protection from colorectal cancer after colonoscopy: a population-based, case-control study. Ann Intern Med 2011; 154(1):22–30. doi:10.7326/0003-4819-154-1-201101040-00004
  13. Brenner H, Chang-Claude J, Seiler CM, Hoffmeister M. Long-term risk of colorectal cancer after negative colonoscopy. J Clin Oncol 2011; 29(28):3761–3767. doi:10.1200/JCO.2011.35.9307
  14. Pohl H, Robertson DJ. Colorectal cancers detected after colonoscopy frequently result from missed lesions. Clin Gastroenterol Hepatol 2010; 8(10):858–864. doi:10.1016/j.cgh.2010.06.028
  15. Singh H, Nugent Z, Demers AA, Bernstein CN. Rate and predictors of early/missed colorectal cancers after colonoscopy in Manitoba: a population-based study. Am J Gastroenterol 2010; 105(12):2588–2596. doi:10.1038/ajg.2010.390
  16. Nishihara R, Wu K, Lochhead P, et al. Long-term colorectal-cancer incidence and mortality after lower endoscopy. N Engl J Med 2013; 369(12):1095–1105. doi:10.1056/NEJMoa1301969
  17. Thompson A, Jones R, Pou P, et al. Taller haustral folds in the proximal colon: a potential factor contributing to interval colorectal cancer. J Colon Rectal Cancer 2016; 1(1):45–54. doi:10.14302/issn.2471-7061.jcrc-15-899
  18. Zhu H, Barish M, Pickhardt P, et al. Haustral fold segmentation with curvature-guided level set evolution. IEEE Trans Biomed Eng 2013; 60(2):321–331. doi:10.1109/TBME.2012.2226242
  19. Chukmaitov A, Bradley CJ, Dahman B, Siangphoe U, Warren JL, Klabunde CN. Association of polypectomy techniques, endoscopist volume, and facility type with colonoscopy complications. Gastrointest Endosc 2013; 77(3):436–446. doi:10.1016/j.gie.2012.11.012
  20. Reumkens A, Rondagh EJ, Bakker CM, et al. Post-colonoscopy complications: a systematic review, time trends, and meta-analysis of population-based studies. Am J Gastroenterol 2016; 111(8):1092–1101. doi:10.1038/ajg.2016.234
  21. ASGE Standards of Practice Committee, Fisher DA, Maple JT, Ben-Menachem T, et al. Complications of colonoscopy. Gastrointest Endosc 2011; 74(4):745–752. doi:10.1016/j.gie.2011.07.025
  22. Warren JL, Klabunde CN, Mariotto AB, et al. Adverse events after outpatient colonoscopy in the Medicare population. Ann Intern Med 2009; 150(12):849–857. doi:10.7326/0003-4819-150-12-200906160-00008
  23. Whitlock EP, Lin JS, Liles E, et al. Screening for colorectal cancer: a targeted, updated systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2008; 149(9):638–658. doi:10.7326/0003-4819-149-9-200811040-00245
  24. Backes Y, Seerden T, van Gestel R, et al. Tumor seeding during colonoscopy as a possible cause for metachronous colorectal cancer. Gastroenterology 2019; Aug 13. pii: S0016-5085(19)41229-8. [Epub ahead of print] doi:10.1053/j.gastro.2019.07.062
  25. Lin JS, Piper MA, Perdue LA, et al. Screening for colorectal cancer: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA 2016; 315(23):2576–2594. doi:10.1001/jama.2016.3332
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University of California San Diego

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To the Editor: In the article, “Colorectal cancer screening: Choosing the right test,” the authors offer an excellent review, but restrict the discussion to just 2 of the many options. Screening compliance improves when clinicians and patients can select their preferred screening approach, and other noninvasive or minimally invasive approaches also deserve consideration and may well be superior. It is important that both the patient and the healthcare provider be fully aware of the advantages and disadvantages of each method.

The article is overly generous in its description of the accuracy and sensitivity of optical colonoscopy. The statement that colonoscopy visualizes the entire colon in more than 98% of cases is not supported by the biomedical literature or clinical experience. The measure of colonoscopy accuracy is best quantified by a review of more than 15,000 tandem colonoscopies that showed an average polyp miss rate of 22% using standard colonoscopes, and a 69% polyp miss rate compared with full-spectrum colonoscopes with greater fields of view.1–3 Between 5% and 10% of colonoscopies are technically incomplete and do not reach the cecum. Only 35% of colonoscopy bowel preps are excellent, and 21% are so poor that the procedure cannot be completed.4–8 Colorectal cancers are frequently missed at colonoscopy, with a rate of 7% quoted in the literature for interval cancer development.9–16 Studies of computed tomography colonography (virtual colonoscopy) have confirmed that between 10% and 20% of the colonic mucosa is hidden from view on optical colonoscopy by tall haustral mucosal folds.17,18 The operator variation measured by adenoma detection rates can exceed a 10-fold differential.

Colonoscopy is an important and valuable diagnostic and therapeutic tool. The disadvantages include significant cancer and polyp miss rates, high discomfort, high expense, potentially life-threatening complications, time- and resource-intensive utilization, high loss of patient work productivity, challenging and frequently inadequate preparation, higher risk of metachronous cancer and polyp spread, and high operator variability of quality.19–24 Unfortunately, while colonoscopy is an important tool, it does not come anywhere close to a score of 98% and should not be considered the gold standard for colorectal cancer screening.25

To the Editor: In the article, “Colorectal cancer screening: Choosing the right test,” the authors offer an excellent review, but restrict the discussion to just 2 of the many options. Screening compliance improves when clinicians and patients can select their preferred screening approach, and other noninvasive or minimally invasive approaches also deserve consideration and may well be superior. It is important that both the patient and the healthcare provider be fully aware of the advantages and disadvantages of each method.

The article is overly generous in its description of the accuracy and sensitivity of optical colonoscopy. The statement that colonoscopy visualizes the entire colon in more than 98% of cases is not supported by the biomedical literature or clinical experience. The measure of colonoscopy accuracy is best quantified by a review of more than 15,000 tandem colonoscopies that showed an average polyp miss rate of 22% using standard colonoscopes, and a 69% polyp miss rate compared with full-spectrum colonoscopes with greater fields of view.1–3 Between 5% and 10% of colonoscopies are technically incomplete and do not reach the cecum. Only 35% of colonoscopy bowel preps are excellent, and 21% are so poor that the procedure cannot be completed.4–8 Colorectal cancers are frequently missed at colonoscopy, with a rate of 7% quoted in the literature for interval cancer development.9–16 Studies of computed tomography colonography (virtual colonoscopy) have confirmed that between 10% and 20% of the colonic mucosa is hidden from view on optical colonoscopy by tall haustral mucosal folds.17,18 The operator variation measured by adenoma detection rates can exceed a 10-fold differential.

Colonoscopy is an important and valuable diagnostic and therapeutic tool. The disadvantages include significant cancer and polyp miss rates, high discomfort, high expense, potentially life-threatening complications, time- and resource-intensive utilization, high loss of patient work productivity, challenging and frequently inadequate preparation, higher risk of metachronous cancer and polyp spread, and high operator variability of quality.19–24 Unfortunately, while colonoscopy is an important tool, it does not come anywhere close to a score of 98% and should not be considered the gold standard for colorectal cancer screening.25

References
  1. Zhao S, Wang S, Pan P, et al. Magnitude, risk factors, and factors associated with adenoma miss rate of tandem colonoscopy: a systemic review and meta-analysis. Gastroenterology 2019; 156(6):1661–1674. doi:10.1053/j.gastro.2019.01.260
  2. van Rijn JC, Reitsma JB, Stoker J, Bossuyt PM, van Deventer SJ, Dekker E. Polyp miss rate determined by tandem colonoscopy: a systematic review. Am J Gastroenterol 2006; 101(2):343–350. doi:10.1111/j.1572-0241.2006.00390.x
  3. Gralnek IM, Siersema PD, Halpern Z, et al. Standard forward-viewing colonoscopy versus full-spectrum endoscopy: an international, multicenter, randomised, tandem colonoscopy trial. Lancet Oncol 2014; 15(3):353–360. doi:10.1016/S1470-2045(14)70020-8
  4. Ness RM, Manam R, Hoen H, Chalasani N. Predictors of inadequate bowel preparation for colonoscopy. Am J Gastroenterol 2001; 96(6):1797–1802. doi:10.1111/j.1572-0241.2001.03874.x 
  5. Kluge M, Williams J, Wu C, et al. Inadequate Boston Bowel Preparation Scale scores predict the risk of missed neoplasia on the next colonoscopy. Gastrointest Endosc 2018; 87(3):744–751. doi:10.1016/j.gie.2017.06.012
  6. Gagneja H, Parekh P, Burleson D, et al. HyGIeaCare® preparation for colonoscopy – a technical update for success. J Gastrointest Dig Syst 2016; 6:4. doi:10.4172/2161-069X.1000458
  7. Das A, Parekh P, Bekal P, et al. Bowel preparation for colonoscopy: a comparative cost-effective analysis of traditional per os purgatory prep versus a novel method using high-volume colonic water irrigation. Gastroenterol Hepatol Int J 2017; 2(4):000132.
  8. D’Souza SM, Parekh PJ, Johnson DA. The dirty side of colonoscopy: predictors of poor bowel preparation and novel approaches to overcome the shortcomings. Br J Gastroenterol 2019: 1:1. https://hygieacare.com/wp-content/uploads/2019/06/The-Dirty-Side-of-Colonoscopy-PDF.pdf. Accessed October 23, 2019.
  9. Mouchli M, Ouk L, Scheitel M. Colonoscopy surveillance for high risk polyps does not always prevent colorectal cancer. World J Gastroenterol 2018; 24(8):905–916. doi:10.3748/wjg.v24.i8.905
  10. Adler J, Robertson DJ. Interval colorectal cancer after colonoscopy: exploring explanations and solutions. Am J Gastroenterol 2015; 110(12):1657–1664. doi:10.1038/ajg.2015.365
  11. Robertson DJ, Lieberman DA, Winawer SJ, et al. Colorectal cancers soon after colonoscopy: a pooled multi-cohort analysis. Gut 2014; 63(6):949–956. doi:10.1136/gutjnl-2012-303796
  12. Brenner H, Chang-Claude J, Seiler CM, Rickert A, Hoffmeister M. Protection from colorectal cancer after colonoscopy: a population-based, case-control study. Ann Intern Med 2011; 154(1):22–30. doi:10.7326/0003-4819-154-1-201101040-00004
  13. Brenner H, Chang-Claude J, Seiler CM, Hoffmeister M. Long-term risk of colorectal cancer after negative colonoscopy. J Clin Oncol 2011; 29(28):3761–3767. doi:10.1200/JCO.2011.35.9307
  14. Pohl H, Robertson DJ. Colorectal cancers detected after colonoscopy frequently result from missed lesions. Clin Gastroenterol Hepatol 2010; 8(10):858–864. doi:10.1016/j.cgh.2010.06.028
  15. Singh H, Nugent Z, Demers AA, Bernstein CN. Rate and predictors of early/missed colorectal cancers after colonoscopy in Manitoba: a population-based study. Am J Gastroenterol 2010; 105(12):2588–2596. doi:10.1038/ajg.2010.390
  16. Nishihara R, Wu K, Lochhead P, et al. Long-term colorectal-cancer incidence and mortality after lower endoscopy. N Engl J Med 2013; 369(12):1095–1105. doi:10.1056/NEJMoa1301969
  17. Thompson A, Jones R, Pou P, et al. Taller haustral folds in the proximal colon: a potential factor contributing to interval colorectal cancer. J Colon Rectal Cancer 2016; 1(1):45–54. doi:10.14302/issn.2471-7061.jcrc-15-899
  18. Zhu H, Barish M, Pickhardt P, et al. Haustral fold segmentation with curvature-guided level set evolution. IEEE Trans Biomed Eng 2013; 60(2):321–331. doi:10.1109/TBME.2012.2226242
  19. Chukmaitov A, Bradley CJ, Dahman B, Siangphoe U, Warren JL, Klabunde CN. Association of polypectomy techniques, endoscopist volume, and facility type with colonoscopy complications. Gastrointest Endosc 2013; 77(3):436–446. doi:10.1016/j.gie.2012.11.012
  20. Reumkens A, Rondagh EJ, Bakker CM, et al. Post-colonoscopy complications: a systematic review, time trends, and meta-analysis of population-based studies. Am J Gastroenterol 2016; 111(8):1092–1101. doi:10.1038/ajg.2016.234
  21. ASGE Standards of Practice Committee, Fisher DA, Maple JT, Ben-Menachem T, et al. Complications of colonoscopy. Gastrointest Endosc 2011; 74(4):745–752. doi:10.1016/j.gie.2011.07.025
  22. Warren JL, Klabunde CN, Mariotto AB, et al. Adverse events after outpatient colonoscopy in the Medicare population. Ann Intern Med 2009; 150(12):849–857. doi:10.7326/0003-4819-150-12-200906160-00008
  23. Whitlock EP, Lin JS, Liles E, et al. Screening for colorectal cancer: a targeted, updated systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2008; 149(9):638–658. doi:10.7326/0003-4819-149-9-200811040-00245
  24. Backes Y, Seerden T, van Gestel R, et al. Tumor seeding during colonoscopy as a possible cause for metachronous colorectal cancer. Gastroenterology 2019; Aug 13. pii: S0016-5085(19)41229-8. [Epub ahead of print] doi:10.1053/j.gastro.2019.07.062
  25. Lin JS, Piper MA, Perdue LA, et al. Screening for colorectal cancer: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA 2016; 315(23):2576–2594. doi:10.1001/jama.2016.3332
References
  1. Zhao S, Wang S, Pan P, et al. Magnitude, risk factors, and factors associated with adenoma miss rate of tandem colonoscopy: a systemic review and meta-analysis. Gastroenterology 2019; 156(6):1661–1674. doi:10.1053/j.gastro.2019.01.260
  2. van Rijn JC, Reitsma JB, Stoker J, Bossuyt PM, van Deventer SJ, Dekker E. Polyp miss rate determined by tandem colonoscopy: a systematic review. Am J Gastroenterol 2006; 101(2):343–350. doi:10.1111/j.1572-0241.2006.00390.x
  3. Gralnek IM, Siersema PD, Halpern Z, et al. Standard forward-viewing colonoscopy versus full-spectrum endoscopy: an international, multicenter, randomised, tandem colonoscopy trial. Lancet Oncol 2014; 15(3):353–360. doi:10.1016/S1470-2045(14)70020-8
  4. Ness RM, Manam R, Hoen H, Chalasani N. Predictors of inadequate bowel preparation for colonoscopy. Am J Gastroenterol 2001; 96(6):1797–1802. doi:10.1111/j.1572-0241.2001.03874.x 
  5. Kluge M, Williams J, Wu C, et al. Inadequate Boston Bowel Preparation Scale scores predict the risk of missed neoplasia on the next colonoscopy. Gastrointest Endosc 2018; 87(3):744–751. doi:10.1016/j.gie.2017.06.012
  6. Gagneja H, Parekh P, Burleson D, et al. HyGIeaCare® preparation for colonoscopy – a technical update for success. J Gastrointest Dig Syst 2016; 6:4. doi:10.4172/2161-069X.1000458
  7. Das A, Parekh P, Bekal P, et al. Bowel preparation for colonoscopy: a comparative cost-effective analysis of traditional per os purgatory prep versus a novel method using high-volume colonic water irrigation. Gastroenterol Hepatol Int J 2017; 2(4):000132.
  8. D’Souza SM, Parekh PJ, Johnson DA. The dirty side of colonoscopy: predictors of poor bowel preparation and novel approaches to overcome the shortcomings. Br J Gastroenterol 2019: 1:1. https://hygieacare.com/wp-content/uploads/2019/06/The-Dirty-Side-of-Colonoscopy-PDF.pdf. Accessed October 23, 2019.
  9. Mouchli M, Ouk L, Scheitel M. Colonoscopy surveillance for high risk polyps does not always prevent colorectal cancer. World J Gastroenterol 2018; 24(8):905–916. doi:10.3748/wjg.v24.i8.905
  10. Adler J, Robertson DJ. Interval colorectal cancer after colonoscopy: exploring explanations and solutions. Am J Gastroenterol 2015; 110(12):1657–1664. doi:10.1038/ajg.2015.365
  11. Robertson DJ, Lieberman DA, Winawer SJ, et al. Colorectal cancers soon after colonoscopy: a pooled multi-cohort analysis. Gut 2014; 63(6):949–956. doi:10.1136/gutjnl-2012-303796
  12. Brenner H, Chang-Claude J, Seiler CM, Rickert A, Hoffmeister M. Protection from colorectal cancer after colonoscopy: a population-based, case-control study. Ann Intern Med 2011; 154(1):22–30. doi:10.7326/0003-4819-154-1-201101040-00004
  13. Brenner H, Chang-Claude J, Seiler CM, Hoffmeister M. Long-term risk of colorectal cancer after negative colonoscopy. J Clin Oncol 2011; 29(28):3761–3767. doi:10.1200/JCO.2011.35.9307
  14. Pohl H, Robertson DJ. Colorectal cancers detected after colonoscopy frequently result from missed lesions. Clin Gastroenterol Hepatol 2010; 8(10):858–864. doi:10.1016/j.cgh.2010.06.028
  15. Singh H, Nugent Z, Demers AA, Bernstein CN. Rate and predictors of early/missed colorectal cancers after colonoscopy in Manitoba: a population-based study. Am J Gastroenterol 2010; 105(12):2588–2596. doi:10.1038/ajg.2010.390
  16. Nishihara R, Wu K, Lochhead P, et al. Long-term colorectal-cancer incidence and mortality after lower endoscopy. N Engl J Med 2013; 369(12):1095–1105. doi:10.1056/NEJMoa1301969
  17. Thompson A, Jones R, Pou P, et al. Taller haustral folds in the proximal colon: a potential factor contributing to interval colorectal cancer. J Colon Rectal Cancer 2016; 1(1):45–54. doi:10.14302/issn.2471-7061.jcrc-15-899
  18. Zhu H, Barish M, Pickhardt P, et al. Haustral fold segmentation with curvature-guided level set evolution. IEEE Trans Biomed Eng 2013; 60(2):321–331. doi:10.1109/TBME.2012.2226242
  19. Chukmaitov A, Bradley CJ, Dahman B, Siangphoe U, Warren JL, Klabunde CN. Association of polypectomy techniques, endoscopist volume, and facility type with colonoscopy complications. Gastrointest Endosc 2013; 77(3):436–446. doi:10.1016/j.gie.2012.11.012
  20. Reumkens A, Rondagh EJ, Bakker CM, et al. Post-colonoscopy complications: a systematic review, time trends, and meta-analysis of population-based studies. Am J Gastroenterol 2016; 111(8):1092–1101. doi:10.1038/ajg.2016.234
  21. ASGE Standards of Practice Committee, Fisher DA, Maple JT, Ben-Menachem T, et al. Complications of colonoscopy. Gastrointest Endosc 2011; 74(4):745–752. doi:10.1016/j.gie.2011.07.025
  22. Warren JL, Klabunde CN, Mariotto AB, et al. Adverse events after outpatient colonoscopy in the Medicare population. Ann Intern Med 2009; 150(12):849–857. doi:10.7326/0003-4819-150-12-200906160-00008
  23. Whitlock EP, Lin JS, Liles E, et al. Screening for colorectal cancer: a targeted, updated systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2008; 149(9):638–658. doi:10.7326/0003-4819-149-9-200811040-00245
  24. Backes Y, Seerden T, van Gestel R, et al. Tumor seeding during colonoscopy as a possible cause for metachronous colorectal cancer. Gastroenterology 2019; Aug 13. pii: S0016-5085(19)41229-8. [Epub ahead of print] doi:10.1053/j.gastro.2019.07.062
  25. Lin JS, Piper MA, Perdue LA, et al. Screening for colorectal cancer: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA 2016; 315(23):2576–2594. doi:10.1001/jama.2016.3332
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In reply: Colorectal cancer screening

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In Reply: We thank the readers for their interest in our paper.

Drs. Goldstein, Mascitelli, and Rauf point out the concerning epidemiologic increase in the incidence of colorectal cancer (CRC) among individuals under the age of 50 and suggest folate as a potential cause.1

The underlying cause of the rise in incidence is unknown, and many environmental and lifestyle risk factors have been proposed.2–4 Black men have historically had and continue to have the highest incidence of and stage-adjusted mortality from CRC, but the rise of CRC in the young is a phenomenon in whites.1 Furthermore, these cancers are left-sided. Other known and proposed risk factors associated with this phenomenon include dietary and lifestyle factors such as alcohol consumption, smoking, obesity, and consumption of processed and red meat.5–7

The cohort effect of rising colon and rectal cancer incidence in younger individuals is likely due to changes in the microbiome. Antibiotic exposure is widespread and has been conjectured as a cause, as has folate supplementation, which began in the United States in 1998. Folic acid has been shown to be associated with both protective and harmful effects on colorectal neoplasia.8,9 While Goldstein et al recommend CRC screening starting at an early age in countries with folate supplementation, countries without folate supplementation have also noted a rise in early-onset CRC. For example, in Azerbaijan, the mean age at diagnosis of CRC in 546 individuals was 55.2 ± 11.5, and 23% had an age lower than 40 years. Nearly 60% presented at an advanced stage, and the majority of lesions were in the rectum.10

The impact of the confounding variables and risk factors resulting in the epidemiologic shift in young patients with CRC, along with the biology of the cancers, should be teased out. Once these are known, population screening guidelines can be adjusted. Until then, practitioners should personalize recommendations based on individual risk factors and promptly investigate colonic symptoms, no matter the age of the patient.

We also thank Drs. Joseph Weiss, Nancy Cetel, and Danielle Weiss for their thoughtful analysis of our article. Our intent was to highlight 2 of the most utilized options available for CRC screening and surveillance in the United States. As we pointed out, the choice of test depends on patient preference, family history, and the likelihood of compliance. The goal of any screening program is outreach and adherence, which is optimized when patients are offered a choice of tests.11–13Table 1 from our article shows the options available.14

When discussing these options with patients, several factors should be taken into consideration. It is important that patients have an understanding of how tests are performed: stool-based vs imaging, bowel prep vs no prep, and frequency of testing.15 Any screening test short of colonoscopy that is positive leads to colonoscopy. Also, programmatic noncolonoscopic screening tests require a system of patient navigation for both positive and negative results. An individual may be more likely to complete 1 test such as screening colonoscopy every 10 years vs another test annually.

A common misconception about computed tomography colonography is that it is similar to computed tomography of the abdomen with a focus on the colon. Individuals may still have to undergo a bowel preparation and dietary restrictions before the procedure. Furthermore, a rectal catheter is used to insufflate and distend the colon prior to capturing images, which many patients find uncomfortable.16 Finally, the incidental discovery of extracolonic lesions may result in unnecessary testing.17

The sensitivity and specificity of each test and operator variability in accuracy and quality should also be highlighted. For example, the sensitivity of a one-time fecal immunochemical test to detect an advanced adenoma may be as low as 25%.18 All testing modalities are diagnostic, but only colonoscopy is therapeutic.

We agree that clinicians who perform CRC screening have an armamentarium of tests to offer, and the advantages and disadvantages of each should be carefully considered and individualized.

References
  1. Siegel RL, Fedewa SA, Anderson WF, et al. Colorectal cancer incidence patterns in the United States, 1974–2013. J Natl Cancer Inst 2017:109(8). doi:10.1093/jnci/djw322
  2. Rosato V, Bosetti C, Levi F, et al. Risk factors for young-onset colorectal cancer. Cancer Causes Control 2013; 24(2):335–341. doi:10.1007/s10552-012-0119-3
  3. Pearlman R, Frankel WL, Swanson B, et al. Prevalence and spectrum of germline cancer susceptibility gene mutations among patients with early-onset colorectal cancer. JAMA Oncol 2017; 3(4):464–471. doi:10.1001/jamaoncol.2016.5194
  4. Stoffel EM, Koeppe E, Everett J, et al. Germline genetic features of young individuals with colorectal cancer. Gastroenterology 2018; 154(4):897–905. doi:10.1053/j.gastro.2017.11.004
  5. Huxley RR, Ansary-Moghaddam A, Clifton P, Czernichow S, Parr CL, Woodward M. The impact of dietary and lifestyle risk factors on risk of colorectal cancer: a quantitative overview of the epidemiological evidence. Int J Cancer 2009; 125(1):171–180. doi:10.1002/ijc.24343
  6. Yuhara H, Steinmaus C, Cohen SE, et al. Is diabetes mellitus an independent risk factor for colon cancer and rectal cancer? Am J Gastroenterol 2011; 106(11):1911–1921. doi:10.1038/ajg.2011.301
  7. Chan DS, Lau R, Aune D, et al. Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies. PLoS ONE 2011; 6(6):e20456. doi:10.1371/journal.pone.0020456
  8. Lee JE, Willett WC, Fuchs CS, et al. Folate intake and risk of colorectal cancer and adenoma: modification by time. Am J Clin Nutr 2011; 93(4):817–825. doi:10.3945/ajcn.110.007781
  9. Cole BF, Baron JA, Sandler RS, et al. Folic acid for the prevention of colorectal adenomas: a randomized clinical trial. JAMA 2007; 297(21):2351–2359. doi:10.1001/jama.297.21.2351
  10. Mahmodlou R, Mohammadi P, Sepehrvand N. Colorectal cancer in northwestern Iran. ISRN Gastroenterol 2012; 2012:968560. doi:10.5402/2012/968560
  11. Inadomi JM, Vijan S, Janz NK, et al. Adherence to colorectal cancer screening: a randomized clinical trial of competing strategies. Arch Intern Med 2012; 172(7):575–582. doi:10.1001/archinternmed.2012.332
  12. Steinwachs D, Allen JD, Barlow WE, et al. National Institutes of Health state-of-the-science conference statement: enhancing use and quality of colorectal cancer screening. Ann Intern Med 2010; 152(10):663–667. doi:10.7326/0003-4819-152-10-201005180-00237
  13. Subramanian S, Klosterman M, Amonkar MM, Hunt TL. Adherence with colorectal cancer screening guidelines: a review. Prev Med 2004; 38(5):536–550. doi:10.1016/j.ypmed.2003.12.011
  14. Mankaney G, Sutton RA, Burke CA. Colorectal cancer screening: choosing the right test. Cleve Clin J Med 2019; 86(6):385–392. doi:10.3949/ccjm.86a.17125
  15. Tiro JA, Kamineni A, Levin TR, et al. The colorectal cancer screening process in community settings: a conceptual model for the population-based research optimizing screening through personalized regimens consortium. Cancer Epidemiol Biomarkers Prev 2014; 23(7):1147–1158. doi:10.1158/1055-9965.EPI-13-1217
  16. Plumb A, Ghanouni A, Rees CJ, et al. Patient experience of CT colonography and colonoscopy after fecal occult blood test in a national screening programme. Eur Radiol 2017; 27(3):1052–1063. doi:10.1007/s00330-016-4428-x
  17. Macari M, Nevsky G, Bonavita J, Kim DC, Megibow AJ, Babb JS. CT colonography in senior versus nonsenior patients: extracolonic findings, recommendations for additional imaging, and polyp prevalence. Radiology 2011; 259(3):767–774. doi:10.1148/radiol.11102144
  18. Robertson DJ, Lee JK, Boland CR, et al. Recommendations on fecal immunochemical testing to screen for colorectal neoplasia: a consensus statement by the US Multi-Society Task Force on Colorectal Cancer. Gastrointest Endosc 2017; 85(1):2–21.e3. doi:10.1016/j.gie.2016.09.025
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Department of Gastroenterology and Hepatology, Cleveland Clinic

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Department of Gastroenterology and Hepatology, Cleveland Clinic

Richard Andrew Sutton, DO
University of Kansas Medical Center, Kansas City, KS

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University of Kansas Medical Center, Kansas City, KS

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In Reply: We thank the readers for their interest in our paper.

Drs. Goldstein, Mascitelli, and Rauf point out the concerning epidemiologic increase in the incidence of colorectal cancer (CRC) among individuals under the age of 50 and suggest folate as a potential cause.1

The underlying cause of the rise in incidence is unknown, and many environmental and lifestyle risk factors have been proposed.2–4 Black men have historically had and continue to have the highest incidence of and stage-adjusted mortality from CRC, but the rise of CRC in the young is a phenomenon in whites.1 Furthermore, these cancers are left-sided. Other known and proposed risk factors associated with this phenomenon include dietary and lifestyle factors such as alcohol consumption, smoking, obesity, and consumption of processed and red meat.5–7

The cohort effect of rising colon and rectal cancer incidence in younger individuals is likely due to changes in the microbiome. Antibiotic exposure is widespread and has been conjectured as a cause, as has folate supplementation, which began in the United States in 1998. Folic acid has been shown to be associated with both protective and harmful effects on colorectal neoplasia.8,9 While Goldstein et al recommend CRC screening starting at an early age in countries with folate supplementation, countries without folate supplementation have also noted a rise in early-onset CRC. For example, in Azerbaijan, the mean age at diagnosis of CRC in 546 individuals was 55.2 ± 11.5, and 23% had an age lower than 40 years. Nearly 60% presented at an advanced stage, and the majority of lesions were in the rectum.10

The impact of the confounding variables and risk factors resulting in the epidemiologic shift in young patients with CRC, along with the biology of the cancers, should be teased out. Once these are known, population screening guidelines can be adjusted. Until then, practitioners should personalize recommendations based on individual risk factors and promptly investigate colonic symptoms, no matter the age of the patient.

We also thank Drs. Joseph Weiss, Nancy Cetel, and Danielle Weiss for their thoughtful analysis of our article. Our intent was to highlight 2 of the most utilized options available for CRC screening and surveillance in the United States. As we pointed out, the choice of test depends on patient preference, family history, and the likelihood of compliance. The goal of any screening program is outreach and adherence, which is optimized when patients are offered a choice of tests.11–13Table 1 from our article shows the options available.14

When discussing these options with patients, several factors should be taken into consideration. It is important that patients have an understanding of how tests are performed: stool-based vs imaging, bowel prep vs no prep, and frequency of testing.15 Any screening test short of colonoscopy that is positive leads to colonoscopy. Also, programmatic noncolonoscopic screening tests require a system of patient navigation for both positive and negative results. An individual may be more likely to complete 1 test such as screening colonoscopy every 10 years vs another test annually.

A common misconception about computed tomography colonography is that it is similar to computed tomography of the abdomen with a focus on the colon. Individuals may still have to undergo a bowel preparation and dietary restrictions before the procedure. Furthermore, a rectal catheter is used to insufflate and distend the colon prior to capturing images, which many patients find uncomfortable.16 Finally, the incidental discovery of extracolonic lesions may result in unnecessary testing.17

The sensitivity and specificity of each test and operator variability in accuracy and quality should also be highlighted. For example, the sensitivity of a one-time fecal immunochemical test to detect an advanced adenoma may be as low as 25%.18 All testing modalities are diagnostic, but only colonoscopy is therapeutic.

We agree that clinicians who perform CRC screening have an armamentarium of tests to offer, and the advantages and disadvantages of each should be carefully considered and individualized.

In Reply: We thank the readers for their interest in our paper.

Drs. Goldstein, Mascitelli, and Rauf point out the concerning epidemiologic increase in the incidence of colorectal cancer (CRC) among individuals under the age of 50 and suggest folate as a potential cause.1

The underlying cause of the rise in incidence is unknown, and many environmental and lifestyle risk factors have been proposed.2–4 Black men have historically had and continue to have the highest incidence of and stage-adjusted mortality from CRC, but the rise of CRC in the young is a phenomenon in whites.1 Furthermore, these cancers are left-sided. Other known and proposed risk factors associated with this phenomenon include dietary and lifestyle factors such as alcohol consumption, smoking, obesity, and consumption of processed and red meat.5–7

The cohort effect of rising colon and rectal cancer incidence in younger individuals is likely due to changes in the microbiome. Antibiotic exposure is widespread and has been conjectured as a cause, as has folate supplementation, which began in the United States in 1998. Folic acid has been shown to be associated with both protective and harmful effects on colorectal neoplasia.8,9 While Goldstein et al recommend CRC screening starting at an early age in countries with folate supplementation, countries without folate supplementation have also noted a rise in early-onset CRC. For example, in Azerbaijan, the mean age at diagnosis of CRC in 546 individuals was 55.2 ± 11.5, and 23% had an age lower than 40 years. Nearly 60% presented at an advanced stage, and the majority of lesions were in the rectum.10

The impact of the confounding variables and risk factors resulting in the epidemiologic shift in young patients with CRC, along with the biology of the cancers, should be teased out. Once these are known, population screening guidelines can be adjusted. Until then, practitioners should personalize recommendations based on individual risk factors and promptly investigate colonic symptoms, no matter the age of the patient.

We also thank Drs. Joseph Weiss, Nancy Cetel, and Danielle Weiss for their thoughtful analysis of our article. Our intent was to highlight 2 of the most utilized options available for CRC screening and surveillance in the United States. As we pointed out, the choice of test depends on patient preference, family history, and the likelihood of compliance. The goal of any screening program is outreach and adherence, which is optimized when patients are offered a choice of tests.11–13Table 1 from our article shows the options available.14

When discussing these options with patients, several factors should be taken into consideration. It is important that patients have an understanding of how tests are performed: stool-based vs imaging, bowel prep vs no prep, and frequency of testing.15 Any screening test short of colonoscopy that is positive leads to colonoscopy. Also, programmatic noncolonoscopic screening tests require a system of patient navigation for both positive and negative results. An individual may be more likely to complete 1 test such as screening colonoscopy every 10 years vs another test annually.

A common misconception about computed tomography colonography is that it is similar to computed tomography of the abdomen with a focus on the colon. Individuals may still have to undergo a bowel preparation and dietary restrictions before the procedure. Furthermore, a rectal catheter is used to insufflate and distend the colon prior to capturing images, which many patients find uncomfortable.16 Finally, the incidental discovery of extracolonic lesions may result in unnecessary testing.17

The sensitivity and specificity of each test and operator variability in accuracy and quality should also be highlighted. For example, the sensitivity of a one-time fecal immunochemical test to detect an advanced adenoma may be as low as 25%.18 All testing modalities are diagnostic, but only colonoscopy is therapeutic.

We agree that clinicians who perform CRC screening have an armamentarium of tests to offer, and the advantages and disadvantages of each should be carefully considered and individualized.

References
  1. Siegel RL, Fedewa SA, Anderson WF, et al. Colorectal cancer incidence patterns in the United States, 1974–2013. J Natl Cancer Inst 2017:109(8). doi:10.1093/jnci/djw322
  2. Rosato V, Bosetti C, Levi F, et al. Risk factors for young-onset colorectal cancer. Cancer Causes Control 2013; 24(2):335–341. doi:10.1007/s10552-012-0119-3
  3. Pearlman R, Frankel WL, Swanson B, et al. Prevalence and spectrum of germline cancer susceptibility gene mutations among patients with early-onset colorectal cancer. JAMA Oncol 2017; 3(4):464–471. doi:10.1001/jamaoncol.2016.5194
  4. Stoffel EM, Koeppe E, Everett J, et al. Germline genetic features of young individuals with colorectal cancer. Gastroenterology 2018; 154(4):897–905. doi:10.1053/j.gastro.2017.11.004
  5. Huxley RR, Ansary-Moghaddam A, Clifton P, Czernichow S, Parr CL, Woodward M. The impact of dietary and lifestyle risk factors on risk of colorectal cancer: a quantitative overview of the epidemiological evidence. Int J Cancer 2009; 125(1):171–180. doi:10.1002/ijc.24343
  6. Yuhara H, Steinmaus C, Cohen SE, et al. Is diabetes mellitus an independent risk factor for colon cancer and rectal cancer? Am J Gastroenterol 2011; 106(11):1911–1921. doi:10.1038/ajg.2011.301
  7. Chan DS, Lau R, Aune D, et al. Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies. PLoS ONE 2011; 6(6):e20456. doi:10.1371/journal.pone.0020456
  8. Lee JE, Willett WC, Fuchs CS, et al. Folate intake and risk of colorectal cancer and adenoma: modification by time. Am J Clin Nutr 2011; 93(4):817–825. doi:10.3945/ajcn.110.007781
  9. Cole BF, Baron JA, Sandler RS, et al. Folic acid for the prevention of colorectal adenomas: a randomized clinical trial. JAMA 2007; 297(21):2351–2359. doi:10.1001/jama.297.21.2351
  10. Mahmodlou R, Mohammadi P, Sepehrvand N. Colorectal cancer in northwestern Iran. ISRN Gastroenterol 2012; 2012:968560. doi:10.5402/2012/968560
  11. Inadomi JM, Vijan S, Janz NK, et al. Adherence to colorectal cancer screening: a randomized clinical trial of competing strategies. Arch Intern Med 2012; 172(7):575–582. doi:10.1001/archinternmed.2012.332
  12. Steinwachs D, Allen JD, Barlow WE, et al. National Institutes of Health state-of-the-science conference statement: enhancing use and quality of colorectal cancer screening. Ann Intern Med 2010; 152(10):663–667. doi:10.7326/0003-4819-152-10-201005180-00237
  13. Subramanian S, Klosterman M, Amonkar MM, Hunt TL. Adherence with colorectal cancer screening guidelines: a review. Prev Med 2004; 38(5):536–550. doi:10.1016/j.ypmed.2003.12.011
  14. Mankaney G, Sutton RA, Burke CA. Colorectal cancer screening: choosing the right test. Cleve Clin J Med 2019; 86(6):385–392. doi:10.3949/ccjm.86a.17125
  15. Tiro JA, Kamineni A, Levin TR, et al. The colorectal cancer screening process in community settings: a conceptual model for the population-based research optimizing screening through personalized regimens consortium. Cancer Epidemiol Biomarkers Prev 2014; 23(7):1147–1158. doi:10.1158/1055-9965.EPI-13-1217
  16. Plumb A, Ghanouni A, Rees CJ, et al. Patient experience of CT colonography and colonoscopy after fecal occult blood test in a national screening programme. Eur Radiol 2017; 27(3):1052–1063. doi:10.1007/s00330-016-4428-x
  17. Macari M, Nevsky G, Bonavita J, Kim DC, Megibow AJ, Babb JS. CT colonography in senior versus nonsenior patients: extracolonic findings, recommendations for additional imaging, and polyp prevalence. Radiology 2011; 259(3):767–774. doi:10.1148/radiol.11102144
  18. Robertson DJ, Lee JK, Boland CR, et al. Recommendations on fecal immunochemical testing to screen for colorectal neoplasia: a consensus statement by the US Multi-Society Task Force on Colorectal Cancer. Gastrointest Endosc 2017; 85(1):2–21.e3. doi:10.1016/j.gie.2016.09.025
References
  1. Siegel RL, Fedewa SA, Anderson WF, et al. Colorectal cancer incidence patterns in the United States, 1974–2013. J Natl Cancer Inst 2017:109(8). doi:10.1093/jnci/djw322
  2. Rosato V, Bosetti C, Levi F, et al. Risk factors for young-onset colorectal cancer. Cancer Causes Control 2013; 24(2):335–341. doi:10.1007/s10552-012-0119-3
  3. Pearlman R, Frankel WL, Swanson B, et al. Prevalence and spectrum of germline cancer susceptibility gene mutations among patients with early-onset colorectal cancer. JAMA Oncol 2017; 3(4):464–471. doi:10.1001/jamaoncol.2016.5194
  4. Stoffel EM, Koeppe E, Everett J, et al. Germline genetic features of young individuals with colorectal cancer. Gastroenterology 2018; 154(4):897–905. doi:10.1053/j.gastro.2017.11.004
  5. Huxley RR, Ansary-Moghaddam A, Clifton P, Czernichow S, Parr CL, Woodward M. The impact of dietary and lifestyle risk factors on risk of colorectal cancer: a quantitative overview of the epidemiological evidence. Int J Cancer 2009; 125(1):171–180. doi:10.1002/ijc.24343
  6. Yuhara H, Steinmaus C, Cohen SE, et al. Is diabetes mellitus an independent risk factor for colon cancer and rectal cancer? Am J Gastroenterol 2011; 106(11):1911–1921. doi:10.1038/ajg.2011.301
  7. Chan DS, Lau R, Aune D, et al. Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies. PLoS ONE 2011; 6(6):e20456. doi:10.1371/journal.pone.0020456
  8. Lee JE, Willett WC, Fuchs CS, et al. Folate intake and risk of colorectal cancer and adenoma: modification by time. Am J Clin Nutr 2011; 93(4):817–825. doi:10.3945/ajcn.110.007781
  9. Cole BF, Baron JA, Sandler RS, et al. Folic acid for the prevention of colorectal adenomas: a randomized clinical trial. JAMA 2007; 297(21):2351–2359. doi:10.1001/jama.297.21.2351
  10. Mahmodlou R, Mohammadi P, Sepehrvand N. Colorectal cancer in northwestern Iran. ISRN Gastroenterol 2012; 2012:968560. doi:10.5402/2012/968560
  11. Inadomi JM, Vijan S, Janz NK, et al. Adherence to colorectal cancer screening: a randomized clinical trial of competing strategies. Arch Intern Med 2012; 172(7):575–582. doi:10.1001/archinternmed.2012.332
  12. Steinwachs D, Allen JD, Barlow WE, et al. National Institutes of Health state-of-the-science conference statement: enhancing use and quality of colorectal cancer screening. Ann Intern Med 2010; 152(10):663–667. doi:10.7326/0003-4819-152-10-201005180-00237
  13. Subramanian S, Klosterman M, Amonkar MM, Hunt TL. Adherence with colorectal cancer screening guidelines: a review. Prev Med 2004; 38(5):536–550. doi:10.1016/j.ypmed.2003.12.011
  14. Mankaney G, Sutton RA, Burke CA. Colorectal cancer screening: choosing the right test. Cleve Clin J Med 2019; 86(6):385–392. doi:10.3949/ccjm.86a.17125
  15. Tiro JA, Kamineni A, Levin TR, et al. The colorectal cancer screening process in community settings: a conceptual model for the population-based research optimizing screening through personalized regimens consortium. Cancer Epidemiol Biomarkers Prev 2014; 23(7):1147–1158. doi:10.1158/1055-9965.EPI-13-1217
  16. Plumb A, Ghanouni A, Rees CJ, et al. Patient experience of CT colonography and colonoscopy after fecal occult blood test in a national screening programme. Eur Radiol 2017; 27(3):1052–1063. doi:10.1007/s00330-016-4428-x
  17. Macari M, Nevsky G, Bonavita J, Kim DC, Megibow AJ, Babb JS. CT colonography in senior versus nonsenior patients: extracolonic findings, recommendations for additional imaging, and polyp prevalence. Radiology 2011; 259(3):767–774. doi:10.1148/radiol.11102144
  18. Robertson DJ, Lee JK, Boland CR, et al. Recommendations on fecal immunochemical testing to screen for colorectal neoplasia: a consensus statement by the US Multi-Society Task Force on Colorectal Cancer. Gastrointest Endosc 2017; 85(1):2–21.e3. doi:10.1016/j.gie.2016.09.025
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Gastroparesis

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To the Editor: We read with great pleasure the article by Sharayah et al about acute gastro­paresis in a patient with diabetic ketoacidosis.1 However, in the case description, the authors reached a diagnosis of gastroparesis secondary to diabetic ketoacidosis without aptly ruling out some of its most common causes such as hypokalemia and other electrolyte imbalances seen in diabetic patients (in the setting of recurrent vomiting).

The authors also did not include the patient’s duration of diabetes or hemoglobin A1c level, both of which are linked with gastroparesis in diabetic patients.2 Pertinent biochemical information that can help readers formulate a rational approach and journey to making a diagnosis appears elusive in their article.

References
  1. Sharayah AM, Hajjaj N, Osman R, Livornese D. Gastroparesis in a patient with diabetic ketoacidosis. Cleve Clin J Med 2019; 86(4):238–239. doi:10.3949/ccjm.86a.18116
  2. Bharucha AE, Kudva Y, Basu A, et al. Relationship between glycemic control and gastric emptying in poorly controlled type 2 diabetes. Clin Gastroenterol Hepatol 2015; 13(3):466–476.e461. doi:10.1016/j.cgh.2014.06.034
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Saint Vincent Hospital, Worcester, MA

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To the Editor: We read with great pleasure the article by Sharayah et al about acute gastro­paresis in a patient with diabetic ketoacidosis.1 However, in the case description, the authors reached a diagnosis of gastroparesis secondary to diabetic ketoacidosis without aptly ruling out some of its most common causes such as hypokalemia and other electrolyte imbalances seen in diabetic patients (in the setting of recurrent vomiting).

The authors also did not include the patient’s duration of diabetes or hemoglobin A1c level, both of which are linked with gastroparesis in diabetic patients.2 Pertinent biochemical information that can help readers formulate a rational approach and journey to making a diagnosis appears elusive in their article.

To the Editor: We read with great pleasure the article by Sharayah et al about acute gastro­paresis in a patient with diabetic ketoacidosis.1 However, in the case description, the authors reached a diagnosis of gastroparesis secondary to diabetic ketoacidosis without aptly ruling out some of its most common causes such as hypokalemia and other electrolyte imbalances seen in diabetic patients (in the setting of recurrent vomiting).

The authors also did not include the patient’s duration of diabetes or hemoglobin A1c level, both of which are linked with gastroparesis in diabetic patients.2 Pertinent biochemical information that can help readers formulate a rational approach and journey to making a diagnosis appears elusive in their article.

References
  1. Sharayah AM, Hajjaj N, Osman R, Livornese D. Gastroparesis in a patient with diabetic ketoacidosis. Cleve Clin J Med 2019; 86(4):238–239. doi:10.3949/ccjm.86a.18116
  2. Bharucha AE, Kudva Y, Basu A, et al. Relationship between glycemic control and gastric emptying in poorly controlled type 2 diabetes. Clin Gastroenterol Hepatol 2015; 13(3):466–476.e461. doi:10.1016/j.cgh.2014.06.034
References
  1. Sharayah AM, Hajjaj N, Osman R, Livornese D. Gastroparesis in a patient with diabetic ketoacidosis. Cleve Clin J Med 2019; 86(4):238–239. doi:10.3949/ccjm.86a.18116
  2. Bharucha AE, Kudva Y, Basu A, et al. Relationship between glycemic control and gastric emptying in poorly controlled type 2 diabetes. Clin Gastroenterol Hepatol 2015; 13(3):466–476.e461. doi:10.1016/j.cgh.2014.06.034
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In Reply: We thank the readers for their letter. Our patient’s laboratory values at the time of presentation were as follows:

  • Corrected sodium 142 mmol/L
  • Potassium 5.5 mmol/L
  • Phosphorus 6.6 mmol/L.

The rest of the electrolyte levels were within normal limits.

These reported electrolyte levels were unlikely to cause such gastroparesis. The patient’s hemoglobin A1c was 8.7% at the time of presentation, with no previous values available. However, since abdominal computed tomography done 1 year before this presentation did not show stomach dilation and the patient was asymptomatic, his gastroparesis was presumed to be acute.

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Monmouth Medical Center, Long Branch, NJ

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Monmouth Medical Center, Long Branch, NJ

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Monmouth Medical Center, Long Branch, NJ

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Monmouth Medical Center, Long Branch, NJ

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In Reply: We thank the readers for their letter. Our patient’s laboratory values at the time of presentation were as follows:

  • Corrected sodium 142 mmol/L
  • Potassium 5.5 mmol/L
  • Phosphorus 6.6 mmol/L.

The rest of the electrolyte levels were within normal limits.

These reported electrolyte levels were unlikely to cause such gastroparesis. The patient’s hemoglobin A1c was 8.7% at the time of presentation, with no previous values available. However, since abdominal computed tomography done 1 year before this presentation did not show stomach dilation and the patient was asymptomatic, his gastroparesis was presumed to be acute.

In Reply: We thank the readers for their letter. Our patient’s laboratory values at the time of presentation were as follows:

  • Corrected sodium 142 mmol/L
  • Potassium 5.5 mmol/L
  • Phosphorus 6.6 mmol/L.

The rest of the electrolyte levels were within normal limits.

These reported electrolyte levels were unlikely to cause such gastroparesis. The patient’s hemoglobin A1c was 8.7% at the time of presentation, with no previous values available. However, since abdominal computed tomography done 1 year before this presentation did not show stomach dilation and the patient was asymptomatic, his gastroparesis was presumed to be acute.

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We commend Gottenborg and Pierce on their well-written summary of the 2013 National Institutes of Care Excellence (NICE) guidelines on intravenous fluids (IV) for adults.1 One area of the guidelines that we believe should be modified is the outdated recommendation for prescribing 1 mmol/kg/day of sodium.2 At the guideline recommended rate of 25-30 mL/kg/day, a 75 kg adult would be prescribed a solution of 25-30 mmol/L of sodium or 0.18% saline, which is in stark contrast to the more recent recommendations of isotonic fluids from the 2018 American Academy of Pediatrics and 2015 NICE pediatric guidelines.3,4 0.18% saline is extremely hypotonic compared to plasma sodium and would place hospitalized patients at significant risk for developing hospital-acquired hyponatremia.

The recommendations for hypotonic solutions were largely developed from theoretical research in the 1950s before the first description of the syndrome of inappropriate secretion of antidiuretic hormone.5 Hospitalized patients are at significant risk for nonosmotic stimuli for antidiuretic hormone secretion, and hypotonic fluids increase the risk of hyponatremia, which can have catastrophic complications. We believe the pediatric evidence should be extrapolated and included with the supporting (albeit limited) adult evidence, and that when indicated, isotonic fluids should be the maintenance fluid for most hospitalized adults.3-4,6

Disclosures

We have no relevant conflicts of interest to report. No payment or services from a third party were received for any aspect of this submitted work. We have no financial relationships with entities in the bio-medical arena that could be perceived to influence, or that give the appearance of potentially influencing, what was written in this submitted work.


 

References

1. Gottenborg E, Pierce R. Clinical Guideline Highlights for the Hospitalist: The Use of Intravenous Fluids in the Hospitalized Adult. J Hosp Med. 2019;14(3):172-173. https://doi.org/10.12788/jhm.3178
2. National Clinical Guideline Centre. Intravenous Fluid Therapy: Intravenous Fluid Therapy in Adults in Hospital, London: Royal College of Physicians (UK); 2013 Dec. Updated May 3, 2017. https://www.nice.org.uk/guidance/g174. Accessed April 6, 2019.
3. Feld LG, Neuspiel DR, Foster BA, et al. Clinical practice guideline: maintenance intravenous fluids in children. Pediatrics. 2018;142(6):170-171. https://doi.org/10.1542/peds.2018-3083.
4. Neilson J, O’Neill F, Dawoud D, Crean P, Guideline Development G. Intravenous fluids in children and young people: summary of NICE guidance. BMJ. 2015;351:h6388. https://doi.org/10.1136/bmj.h6388
5. Talbot NB, Crawford DJ, Butler AM. Medical progress; homeostatic limits to safe parenteral fluid therapy. N Engl J Med. 1953;248:1100-1108. https://doi.org/10.1056/NEJM195306252482605
6. Okada M, Egi M, Yokota Y, et al. Comparison of the incidences of hyponatremia in adult postoperative critically ill patients receiving intravenous maintenance fluids with 140 mmol/L or 35 mmol/L of sodium: retrospective before/after observational study. J Anesth. 2017;31(5):657-663 PubMed

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We commend Gottenborg and Pierce on their well-written summary of the 2013 National Institutes of Care Excellence (NICE) guidelines on intravenous fluids (IV) for adults.1 One area of the guidelines that we believe should be modified is the outdated recommendation for prescribing 1 mmol/kg/day of sodium.2 At the guideline recommended rate of 25-30 mL/kg/day, a 75 kg adult would be prescribed a solution of 25-30 mmol/L of sodium or 0.18% saline, which is in stark contrast to the more recent recommendations of isotonic fluids from the 2018 American Academy of Pediatrics and 2015 NICE pediatric guidelines.3,4 0.18% saline is extremely hypotonic compared to plasma sodium and would place hospitalized patients at significant risk for developing hospital-acquired hyponatremia.

The recommendations for hypotonic solutions were largely developed from theoretical research in the 1950s before the first description of the syndrome of inappropriate secretion of antidiuretic hormone.5 Hospitalized patients are at significant risk for nonosmotic stimuli for antidiuretic hormone secretion, and hypotonic fluids increase the risk of hyponatremia, which can have catastrophic complications. We believe the pediatric evidence should be extrapolated and included with the supporting (albeit limited) adult evidence, and that when indicated, isotonic fluids should be the maintenance fluid for most hospitalized adults.3-4,6

Disclosures

We have no relevant conflicts of interest to report. No payment or services from a third party were received for any aspect of this submitted work. We have no financial relationships with entities in the bio-medical arena that could be perceived to influence, or that give the appearance of potentially influencing, what was written in this submitted work.


 

We commend Gottenborg and Pierce on their well-written summary of the 2013 National Institutes of Care Excellence (NICE) guidelines on intravenous fluids (IV) for adults.1 One area of the guidelines that we believe should be modified is the outdated recommendation for prescribing 1 mmol/kg/day of sodium.2 At the guideline recommended rate of 25-30 mL/kg/day, a 75 kg adult would be prescribed a solution of 25-30 mmol/L of sodium or 0.18% saline, which is in stark contrast to the more recent recommendations of isotonic fluids from the 2018 American Academy of Pediatrics and 2015 NICE pediatric guidelines.3,4 0.18% saline is extremely hypotonic compared to plasma sodium and would place hospitalized patients at significant risk for developing hospital-acquired hyponatremia.

The recommendations for hypotonic solutions were largely developed from theoretical research in the 1950s before the first description of the syndrome of inappropriate secretion of antidiuretic hormone.5 Hospitalized patients are at significant risk for nonosmotic stimuli for antidiuretic hormone secretion, and hypotonic fluids increase the risk of hyponatremia, which can have catastrophic complications. We believe the pediatric evidence should be extrapolated and included with the supporting (albeit limited) adult evidence, and that when indicated, isotonic fluids should be the maintenance fluid for most hospitalized adults.3-4,6

Disclosures

We have no relevant conflicts of interest to report. No payment or services from a third party were received for any aspect of this submitted work. We have no financial relationships with entities in the bio-medical arena that could be perceived to influence, or that give the appearance of potentially influencing, what was written in this submitted work.


 

References

1. Gottenborg E, Pierce R. Clinical Guideline Highlights for the Hospitalist: The Use of Intravenous Fluids in the Hospitalized Adult. J Hosp Med. 2019;14(3):172-173. https://doi.org/10.12788/jhm.3178
2. National Clinical Guideline Centre. Intravenous Fluid Therapy: Intravenous Fluid Therapy in Adults in Hospital, London: Royal College of Physicians (UK); 2013 Dec. Updated May 3, 2017. https://www.nice.org.uk/guidance/g174. Accessed April 6, 2019.
3. Feld LG, Neuspiel DR, Foster BA, et al. Clinical practice guideline: maintenance intravenous fluids in children. Pediatrics. 2018;142(6):170-171. https://doi.org/10.1542/peds.2018-3083.
4. Neilson J, O’Neill F, Dawoud D, Crean P, Guideline Development G. Intravenous fluids in children and young people: summary of NICE guidance. BMJ. 2015;351:h6388. https://doi.org/10.1136/bmj.h6388
5. Talbot NB, Crawford DJ, Butler AM. Medical progress; homeostatic limits to safe parenteral fluid therapy. N Engl J Med. 1953;248:1100-1108. https://doi.org/10.1056/NEJM195306252482605
6. Okada M, Egi M, Yokota Y, et al. Comparison of the incidences of hyponatremia in adult postoperative critically ill patients receiving intravenous maintenance fluids with 140 mmol/L or 35 mmol/L of sodium: retrospective before/after observational study. J Anesth. 2017;31(5):657-663 PubMed

References

1. Gottenborg E, Pierce R. Clinical Guideline Highlights for the Hospitalist: The Use of Intravenous Fluids in the Hospitalized Adult. J Hosp Med. 2019;14(3):172-173. https://doi.org/10.12788/jhm.3178
2. National Clinical Guideline Centre. Intravenous Fluid Therapy: Intravenous Fluid Therapy in Adults in Hospital, London: Royal College of Physicians (UK); 2013 Dec. Updated May 3, 2017. https://www.nice.org.uk/guidance/g174. Accessed April 6, 2019.
3. Feld LG, Neuspiel DR, Foster BA, et al. Clinical practice guideline: maintenance intravenous fluids in children. Pediatrics. 2018;142(6):170-171. https://doi.org/10.1542/peds.2018-3083.
4. Neilson J, O’Neill F, Dawoud D, Crean P, Guideline Development G. Intravenous fluids in children and young people: summary of NICE guidance. BMJ. 2015;351:h6388. https://doi.org/10.1136/bmj.h6388
5. Talbot NB, Crawford DJ, Butler AM. Medical progress; homeostatic limits to safe parenteral fluid therapy. N Engl J Med. 1953;248:1100-1108. https://doi.org/10.1056/NEJM195306252482605
6. Okada M, Egi M, Yokota Y, et al. Comparison of the incidences of hyponatremia in adult postoperative critically ill patients receiving intravenous maintenance fluids with 140 mmol/L or 35 mmol/L of sodium: retrospective before/after observational study. J Anesth. 2017;31(5):657-663 PubMed

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WHAT IS YOUR APPROACH TO THE PERSISTENT OCCIPUT POSTERIOR MALPOSITION?

ROBERT L. BARBIERI, MD

(EDITORIAL; MARCH 2019)

A classic approach for managing fetal malposition

For those of us who trained and practiced obstetrics in the days of the 6% primary cesarean delivery (CD) rate, we never considered the management of the persistent occiput posterior (OP) position to be particularly difficult. I outline below a method that requires no unusual level of skill or dexterity.

  1. The cervix must be fully dilated.
  2. Dense regional anesthesia must be achieved.
  3. The vertex must have reached +1 station.
  4. The position must be clearly established, and this does not require anything other than the ability to palpate an ear, as it can be pointed only in one direction. If you feel ultrasonography is needed, be my guest.
  5. Use an obstetric lubricant to reduce resistance and minimize lacerations.
  6. While a trial of manual rotation is reasonable, it commonly will not succeed and requires that an operator’s hand be inserted rather than a slender and less traumatic device (forceps).
  7. Next, palpate the sagittal suture to determine whether the position is straight OP versus left OP or right OP. This should not be difficult unless the poor woman has gone through 2 or 3 hours of unproductive pushing, thereby creating caput.
  8. After proper forceps application is confirmed, gently apply upward pressure. This will make rotation easier.
  9. Dr. Irving’s recommendations notwithstanding, the forceps handles are not carried in a wide sweep. One should use Kielland’s forceps, which do not have a pelvic curve and were invented for this precise indication. The forceps are simply rotated.
  10. Try to avoid delivery as an OP, as this pulls a much larger diameter deflexed head through the pelvis and usually results in significant lacerations.
  11. Episiotomy is not always required if rotation has succeeded.
  12. Once descent to the outlet has been achieved, it is probably best to switch to a forceps with a pelvic curve to achieve easier extension.
  13. This should complete the delivery, but as a general rule, if more than minimal resistance is met in any of the above steps, abandon the procedure and move to CD.
  14. This process should result in at least a 70% success rate.

As is most likely understood by the current generation of obstetricians who appear to be satisfied with a 30% to 40% primary CD rate, the above reflects the views of a long-retired ObGyn (whose CD rate never exceeded 10%) and may be inappropriate for those who are not adequately trained in or comfortable with vaginal obstetrics.

David M. Priver, MD

San Diego, California

 

Continue to: HOW DO YOU FEEL ABOUT EXPECTANTLY MANAGING A WELL-DATED PREGNANCY PAST 41 WEEKS’ GESTATION?

 

 

HOW DO YOU FEEL ABOUT EXPECTANTLY MANAGING A WELL-DATED PREGNANCY PAST 41 WEEKS’ GESTATION?

ROBERT L. BARBIERI, MD

(EDITORIAL; FEBRUARY 2019)

Membrane stripping can be problematic

The recent discussion on stripping membranes to facilitate the initiation of labor and delivery was intriguing. This practice was reviewed extensively during my training in the 1960s and abandoned when the results were disappointing or contradictory. Although the practice has been revitalized recently, I am concerned that potential risks and the absence of a recommended protocol of safeguards may allow new problems to develop.

In a metropolitan community where I provide consultative services, the only patients I see for evaluation of pregnancies beyond 40 to 41 weeks come from providers who are non-physicians. Apparently, they are concerned that they may have to turn their patients over to physician providers for interventions that they are not capable of doing. My advice to them is simply that nothing good happens after 40 to 41 weeks.

Well-grown babies may continue to grow if they are healthy, and they may incur greater risks of dystotic labor and delivery resulting in injury or the need for physician-administered surgical assistance. If, on the other hand, growth markedly diminishes or ceases, fetal harm or neonatal complications may occur through asphyxia, meconium aspiration, or trauma. In either event, physician-based assistance is strongly encouraged, as long as due diligence in determining gestational age has been done.

Promoting membrane stripping without having a protocol for ascertainment of risk factors is worrisome to me. In my opinion, large population studies that fail to demonstrate increased risks of infection may fail to demonstrate that membrane stripping may induce a degree of perinatal infection comparable to that of prolonged labor with multiple internal examinations with or without ultimate cesarean birth. Prior to considering membrane stripping as a strategy, one should recognize certain important considerations, namely:

  • Patients most in need of active intervention may have the least favorable cervical findings, and as a result they are potentially at risk for the greatest discomfort.
  • The frequency of group B streptococcal colonization of the vagina at term should be recognized, and a culture should be obtained immediately prior to intervention. When a culture is a positive, membrane stripping should be avoided, or at least a sober consideration of its use and appropriate antibiotic coverage should occur.
  • Consider performing transvaginal ultrasonography prior to membrane stripping to exclude the possibility of a placental edge close enough to be encountered and compromised, with resultant hemorrhage in an outpatient venue ill equipped to provide adequate emergency support.
  • The comparative effectiveness of other direct cervical conditioning therapies, including use of a Foley catheter or regional prostaglandin medication, has been well explored and found effective. Also, if one takes seriously the need for any intervention, admission to the hospital for overnight cervical conditioning allows for surveillance and avoids the patient experience of being sent home cramping, bleeding, brooding infection, and questioning her trust in the provider.

Continue to: I am concerned that the promotion...

 

 

I am concerned that the promotion of this potentially rather brutish practice by highly reputable advisors can result in its growing utilization by providers some of whom may be least qualified to apply proper judgment and sensitivity to its selection. In the most primitive of circumstances, it may have utility. Personally, however, I feel that medically based strategies initiated and monitored by professionals capable of dealing with any untoward departures from the expected results must be considered in the best traditions of what we do. The appeal of simplicity must not encourage the adoption of interventions that lack the proper application of thought and plan and whose only appeal is that of simplicity.

Richard P. Perkins, MD

Fort Myers, Florida; Stockton, California

 

Dr. Barbieri responds

I thank Dr. Priver for his excellent description of how to use forceps to resolve a persistent occiput posterior position. I also thank Dr. Perkins for his valuable comments and agree with him that in the United States among the options available for outpatient cervical ripening, misoprostol or a balloon are more commonly used than membrane stripping. Membrane stripping is an outpatient cervical ripening technique that is commonly used in the United Kingdom.

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WHAT IS YOUR APPROACH TO THE PERSISTENT OCCIPUT POSTERIOR MALPOSITION?

ROBERT L. BARBIERI, MD

(EDITORIAL; MARCH 2019)

A classic approach for managing fetal malposition

For those of us who trained and practiced obstetrics in the days of the 6% primary cesarean delivery (CD) rate, we never considered the management of the persistent occiput posterior (OP) position to be particularly difficult. I outline below a method that requires no unusual level of skill or dexterity.

  1. The cervix must be fully dilated.
  2. Dense regional anesthesia must be achieved.
  3. The vertex must have reached +1 station.
  4. The position must be clearly established, and this does not require anything other than the ability to palpate an ear, as it can be pointed only in one direction. If you feel ultrasonography is needed, be my guest.
  5. Use an obstetric lubricant to reduce resistance and minimize lacerations.
  6. While a trial of manual rotation is reasonable, it commonly will not succeed and requires that an operator’s hand be inserted rather than a slender and less traumatic device (forceps).
  7. Next, palpate the sagittal suture to determine whether the position is straight OP versus left OP or right OP. This should not be difficult unless the poor woman has gone through 2 or 3 hours of unproductive pushing, thereby creating caput.
  8. After proper forceps application is confirmed, gently apply upward pressure. This will make rotation easier.
  9. Dr. Irving’s recommendations notwithstanding, the forceps handles are not carried in a wide sweep. One should use Kielland’s forceps, which do not have a pelvic curve and were invented for this precise indication. The forceps are simply rotated.
  10. Try to avoid delivery as an OP, as this pulls a much larger diameter deflexed head through the pelvis and usually results in significant lacerations.
  11. Episiotomy is not always required if rotation has succeeded.
  12. Once descent to the outlet has been achieved, it is probably best to switch to a forceps with a pelvic curve to achieve easier extension.
  13. This should complete the delivery, but as a general rule, if more than minimal resistance is met in any of the above steps, abandon the procedure and move to CD.
  14. This process should result in at least a 70% success rate.

As is most likely understood by the current generation of obstetricians who appear to be satisfied with a 30% to 40% primary CD rate, the above reflects the views of a long-retired ObGyn (whose CD rate never exceeded 10%) and may be inappropriate for those who are not adequately trained in or comfortable with vaginal obstetrics.

David M. Priver, MD

San Diego, California

 

Continue to: HOW DO YOU FEEL ABOUT EXPECTANTLY MANAGING A WELL-DATED PREGNANCY PAST 41 WEEKS’ GESTATION?

 

 

HOW DO YOU FEEL ABOUT EXPECTANTLY MANAGING A WELL-DATED PREGNANCY PAST 41 WEEKS’ GESTATION?

ROBERT L. BARBIERI, MD

(EDITORIAL; FEBRUARY 2019)

Membrane stripping can be problematic

The recent discussion on stripping membranes to facilitate the initiation of labor and delivery was intriguing. This practice was reviewed extensively during my training in the 1960s and abandoned when the results were disappointing or contradictory. Although the practice has been revitalized recently, I am concerned that potential risks and the absence of a recommended protocol of safeguards may allow new problems to develop.

In a metropolitan community where I provide consultative services, the only patients I see for evaluation of pregnancies beyond 40 to 41 weeks come from providers who are non-physicians. Apparently, they are concerned that they may have to turn their patients over to physician providers for interventions that they are not capable of doing. My advice to them is simply that nothing good happens after 40 to 41 weeks.

Well-grown babies may continue to grow if they are healthy, and they may incur greater risks of dystotic labor and delivery resulting in injury or the need for physician-administered surgical assistance. If, on the other hand, growth markedly diminishes or ceases, fetal harm or neonatal complications may occur through asphyxia, meconium aspiration, or trauma. In either event, physician-based assistance is strongly encouraged, as long as due diligence in determining gestational age has been done.

Promoting membrane stripping without having a protocol for ascertainment of risk factors is worrisome to me. In my opinion, large population studies that fail to demonstrate increased risks of infection may fail to demonstrate that membrane stripping may induce a degree of perinatal infection comparable to that of prolonged labor with multiple internal examinations with or without ultimate cesarean birth. Prior to considering membrane stripping as a strategy, one should recognize certain important considerations, namely:

  • Patients most in need of active intervention may have the least favorable cervical findings, and as a result they are potentially at risk for the greatest discomfort.
  • The frequency of group B streptococcal colonization of the vagina at term should be recognized, and a culture should be obtained immediately prior to intervention. When a culture is a positive, membrane stripping should be avoided, or at least a sober consideration of its use and appropriate antibiotic coverage should occur.
  • Consider performing transvaginal ultrasonography prior to membrane stripping to exclude the possibility of a placental edge close enough to be encountered and compromised, with resultant hemorrhage in an outpatient venue ill equipped to provide adequate emergency support.
  • The comparative effectiveness of other direct cervical conditioning therapies, including use of a Foley catheter or regional prostaglandin medication, has been well explored and found effective. Also, if one takes seriously the need for any intervention, admission to the hospital for overnight cervical conditioning allows for surveillance and avoids the patient experience of being sent home cramping, bleeding, brooding infection, and questioning her trust in the provider.

Continue to: I am concerned that the promotion...

 

 

I am concerned that the promotion of this potentially rather brutish practice by highly reputable advisors can result in its growing utilization by providers some of whom may be least qualified to apply proper judgment and sensitivity to its selection. In the most primitive of circumstances, it may have utility. Personally, however, I feel that medically based strategies initiated and monitored by professionals capable of dealing with any untoward departures from the expected results must be considered in the best traditions of what we do. The appeal of simplicity must not encourage the adoption of interventions that lack the proper application of thought and plan and whose only appeal is that of simplicity.

Richard P. Perkins, MD

Fort Myers, Florida; Stockton, California

 

Dr. Barbieri responds

I thank Dr. Priver for his excellent description of how to use forceps to resolve a persistent occiput posterior position. I also thank Dr. Perkins for his valuable comments and agree with him that in the United States among the options available for outpatient cervical ripening, misoprostol or a balloon are more commonly used than membrane stripping. Membrane stripping is an outpatient cervical ripening technique that is commonly used in the United Kingdom.

 

WHAT IS YOUR APPROACH TO THE PERSISTENT OCCIPUT POSTERIOR MALPOSITION?

ROBERT L. BARBIERI, MD

(EDITORIAL; MARCH 2019)

A classic approach for managing fetal malposition

For those of us who trained and practiced obstetrics in the days of the 6% primary cesarean delivery (CD) rate, we never considered the management of the persistent occiput posterior (OP) position to be particularly difficult. I outline below a method that requires no unusual level of skill or dexterity.

  1. The cervix must be fully dilated.
  2. Dense regional anesthesia must be achieved.
  3. The vertex must have reached +1 station.
  4. The position must be clearly established, and this does not require anything other than the ability to palpate an ear, as it can be pointed only in one direction. If you feel ultrasonography is needed, be my guest.
  5. Use an obstetric lubricant to reduce resistance and minimize lacerations.
  6. While a trial of manual rotation is reasonable, it commonly will not succeed and requires that an operator’s hand be inserted rather than a slender and less traumatic device (forceps).
  7. Next, palpate the sagittal suture to determine whether the position is straight OP versus left OP or right OP. This should not be difficult unless the poor woman has gone through 2 or 3 hours of unproductive pushing, thereby creating caput.
  8. After proper forceps application is confirmed, gently apply upward pressure. This will make rotation easier.
  9. Dr. Irving’s recommendations notwithstanding, the forceps handles are not carried in a wide sweep. One should use Kielland’s forceps, which do not have a pelvic curve and were invented for this precise indication. The forceps are simply rotated.
  10. Try to avoid delivery as an OP, as this pulls a much larger diameter deflexed head through the pelvis and usually results in significant lacerations.
  11. Episiotomy is not always required if rotation has succeeded.
  12. Once descent to the outlet has been achieved, it is probably best to switch to a forceps with a pelvic curve to achieve easier extension.
  13. This should complete the delivery, but as a general rule, if more than minimal resistance is met in any of the above steps, abandon the procedure and move to CD.
  14. This process should result in at least a 70% success rate.

As is most likely understood by the current generation of obstetricians who appear to be satisfied with a 30% to 40% primary CD rate, the above reflects the views of a long-retired ObGyn (whose CD rate never exceeded 10%) and may be inappropriate for those who are not adequately trained in or comfortable with vaginal obstetrics.

David M. Priver, MD

San Diego, California

 

Continue to: HOW DO YOU FEEL ABOUT EXPECTANTLY MANAGING A WELL-DATED PREGNANCY PAST 41 WEEKS’ GESTATION?

 

 

HOW DO YOU FEEL ABOUT EXPECTANTLY MANAGING A WELL-DATED PREGNANCY PAST 41 WEEKS’ GESTATION?

ROBERT L. BARBIERI, MD

(EDITORIAL; FEBRUARY 2019)

Membrane stripping can be problematic

The recent discussion on stripping membranes to facilitate the initiation of labor and delivery was intriguing. This practice was reviewed extensively during my training in the 1960s and abandoned when the results were disappointing or contradictory. Although the practice has been revitalized recently, I am concerned that potential risks and the absence of a recommended protocol of safeguards may allow new problems to develop.

In a metropolitan community where I provide consultative services, the only patients I see for evaluation of pregnancies beyond 40 to 41 weeks come from providers who are non-physicians. Apparently, they are concerned that they may have to turn their patients over to physician providers for interventions that they are not capable of doing. My advice to them is simply that nothing good happens after 40 to 41 weeks.

Well-grown babies may continue to grow if they are healthy, and they may incur greater risks of dystotic labor and delivery resulting in injury or the need for physician-administered surgical assistance. If, on the other hand, growth markedly diminishes or ceases, fetal harm or neonatal complications may occur through asphyxia, meconium aspiration, or trauma. In either event, physician-based assistance is strongly encouraged, as long as due diligence in determining gestational age has been done.

Promoting membrane stripping without having a protocol for ascertainment of risk factors is worrisome to me. In my opinion, large population studies that fail to demonstrate increased risks of infection may fail to demonstrate that membrane stripping may induce a degree of perinatal infection comparable to that of prolonged labor with multiple internal examinations with or without ultimate cesarean birth. Prior to considering membrane stripping as a strategy, one should recognize certain important considerations, namely:

  • Patients most in need of active intervention may have the least favorable cervical findings, and as a result they are potentially at risk for the greatest discomfort.
  • The frequency of group B streptococcal colonization of the vagina at term should be recognized, and a culture should be obtained immediately prior to intervention. When a culture is a positive, membrane stripping should be avoided, or at least a sober consideration of its use and appropriate antibiotic coverage should occur.
  • Consider performing transvaginal ultrasonography prior to membrane stripping to exclude the possibility of a placental edge close enough to be encountered and compromised, with resultant hemorrhage in an outpatient venue ill equipped to provide adequate emergency support.
  • The comparative effectiveness of other direct cervical conditioning therapies, including use of a Foley catheter or regional prostaglandin medication, has been well explored and found effective. Also, if one takes seriously the need for any intervention, admission to the hospital for overnight cervical conditioning allows for surveillance and avoids the patient experience of being sent home cramping, bleeding, brooding infection, and questioning her trust in the provider.

Continue to: I am concerned that the promotion...

 

 

I am concerned that the promotion of this potentially rather brutish practice by highly reputable advisors can result in its growing utilization by providers some of whom may be least qualified to apply proper judgment and sensitivity to its selection. In the most primitive of circumstances, it may have utility. Personally, however, I feel that medically based strategies initiated and monitored by professionals capable of dealing with any untoward departures from the expected results must be considered in the best traditions of what we do. The appeal of simplicity must not encourage the adoption of interventions that lack the proper application of thought and plan and whose only appeal is that of simplicity.

Richard P. Perkins, MD

Fort Myers, Florida; Stockton, California

 

Dr. Barbieri responds

I thank Dr. Priver for his excellent description of how to use forceps to resolve a persistent occiput posterior position. I also thank Dr. Perkins for his valuable comments and agree with him that in the United States among the options available for outpatient cervical ripening, misoprostol or a balloon are more commonly used than membrane stripping. Membrane stripping is an outpatient cervical ripening technique that is commonly used in the United Kingdom.

Issue
OBG Management - 31(7)
Issue
OBG Management - 31(7)
Page Number
8-10
Page Number
8-10
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