The ‘skinny’ on eosinophilic esophagitis

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The ‘skinny’ on eosinophilic esophagitis

Eosinophilic esophagitis is a new disease defined by specific criteria that include a constellation of symptoms. Consensus guidelines define it as a chronic antigen-mediated esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.1

Ten years ago, a biopsy that revealed eosinophils in the esophagus was diagnostic, because normally eosinophils are not seen in the esophagus. The current definition has evolved to become more comprehensive and includes clinical, demographic, and radiographic criteria.

This article presents an overview of eosinophilic esophagitis­—its pathogenesis, epidemiology, clinical presentation, diagnosis, and management.

ALLERGIC ORIGIN

Eosinophilic esophagitis is best regarded as a systemic rather than a single-organ disease, although current treatments are mostly directed specifically at esophageal inflammation. Evidence is clear that eosinophilic esophagitis is allergy-mediated.

The current “two-hit” etiologic model involves exposure first to aeroallergens that prime the esophagus, followed by food allergens that cause an eosinophilic response with antigen recognition and stimulation of immune cells from the bone marrow. Other allergic avenues may also be present, including those involved with atopy, asthma, eczema, and food allergies, which stimulate the Th2 pathway and lead to esophageal eosinophilia and inflammation.2

Eosinophilic esophagitis is a systemic disease rather than a single-organ problem

The two-hit model is supported experimentally: the disease can be induced in mice by injecting ovalbumin under the skin as a sensitizing agent, then exposing the airway to an aerosol of Aspergillus fumigatus, producing an allergic reaction involving classic Th2 allergy pathways.3 Further evidence is that many patients report that asthma or rhinitis developed years before esophageal disease began.

Patients with eosinophilic esophagitis and their family members have a high prevalence of allergies, and the disease frequently flares up during allergy season. Endoscopic biopsy specimens from patients often reveal increased T cells, mast cells, interleukin (IL)-5, and tumor necrosis factor alpha, all of which stimulate eotaxin and are essential to an allergic reaction. They also have high levels of CD3, CDA, and CD1A antigen-presenting lymphocytes, which are all associated with allergy.

Eosinophilic esophagitis responds to allergy medications, including corticosteroids and IL-5 or IL-13 mast-cell inhibitors. The strongest evidence for an allergic etiology is that withdrawing culpable food allergens leads to resolution of the disease. Peterson et al4 gave 18 adults with eosinophilic esophagitis an elemental diet (ie, a pure amino acid, carbohydrate-based diet in which all suspected allergens have been removed), and in 2 to 4 weeks, the mean number of eosinophils seen histologically fell from 54 to 10 cells per high-power field. The response was nearly complete (≤ 10 eosinophils per high-power field) in 72% of patients. When patients resumed a normal diet, the eosinophil content increased substantially within a few days.

Role of leaky tight junctions

Normally, the junctions between epithelial cells are tight, but many conditions, including allergic and autoimmune diseases, are now believed to involve altered permeability of this tissue. Tight-junction proteins play an important role in regulating antigen delivery and are modulated by cytokines. Activation of cytokines causes the membrane to become more permeable, allowing antigens to get through, leading to an enhanced reaction. In eosinophilic esophagitis, it is postulated that food antigens that pass through the leaky membrane activate CD1-antigen-presenting cells, which then initiate an allergic reaction.5–9

PREVALENCE IS INCREASING

Eosinophilic esophagitis was first described in 1993 with a report of 12 patients who had dysphagia, normal endoscopy, no acid reflux, and intraepithelial eosinophilia.10 The authors recognized that these patients had a distinct disease.

Since then, the disease has increased in prevalence. Kapel et al11 reviewed more than 74,000 endoscopy slides from a national pathology database and found 363 cases, with increasing prevalence during the study period from 2002 to 2005. Looking back further in a similar study, Whitney-Miller et al12 found a 0.3% prevalence from the years 1992 to 2000 vs 3.8% from 2001 to 2004.

Eosinophilic esophagitis is a systemic disease rather than a single-organ problem

Sealock et al13 reviewed the literature to assess the prevalence of eosinophilic esophagitis and found considerable variation depending on the populations sampled. One study from Sweden14 found a prevalence of 0.4% by performing endoscopy in 1,000 randomly selected people from nearly 3,000 responders to a questionnaire on abdominal symptoms. A study based on a Swiss database15 found only a 0.02% prevalence. Other studies show higher rates: a study from Florida that examined biopsy specimens from patients who underwent endoscopy for any reason found a prevalence of 1%.16 Another US study found a 15% prevalence in patients with dysphagia.17 Since these studies were done nearly a decade ago, we can expect the prevalence to be higher today.

Celiac disease has also been increasing in recent decades, as has gluten sensitivity. Allergies in general are on the rise worldwide, including asthma and atopic dermatitis. Theories as to the cause of these increases have focused on ambient antigens, food additives, proton pump inhibitors (PPIs), and the microbiome.18,19

DIAGNOSING EOSINOPHILIC ESOPHAGITIS

Eosinophilic esophagitis is diagnosed with a combination of symptomatic, histologic, and radiographic findings (Table 1). The classic patient is a white male—a child, teenager, or young adult—with dysphagia.

A case series of 23 adult patients20 found a mean age of 35 (age range 18 to 57), with a male preponderance (14:9). There is commonly a history of other allergies, including asthma, allergic rhinitis, and atopic dermatitis. Patients more commonly present with dysphagia than heartburn or other esophageal symptoms.11

Endoscopic findings—eosinophils, later fibrosis

Finding eosinophils in the esophagus is nonspecific and is not sufficient to make the diagnosis. Other systemic diseases can involve esophageal eosinophilia, including Churg-Strauss syndrome, Crohn disease, and helminthic diseases. Whether some are related to eosinophilic esophagitis or are independent is not well understood.

Characteristic findings on endoscopy include a corrugated or ringed appearance and linear furrows, resulting from fibrosis and scarring. “Micro-tears” may also be visible projecting linearly up the esophagus. Multiple white specks are signs of conglomerations of eosinophils and are easily confused with yeast infection. Strictures from scar tissue cause the mucosa to be tight and fragile, making the esophagus very susceptible to tearing during endoscopy.

After years of untreated disease, the esophagus becomes increasingly inflamed and fibrotic. Adult patients with eosinophilic esophagitis who were followed for a decade were found to develop increasing collagen deposition in which the submucosa or even the entire esophageal wall was diffusely fibrotic.21

Radiographic findings—a narrow esophagus

On radiography, the esophagus may appear narrow—not uncommonly one-third to one-quarter the caliber of a normal esophagus. As the esophagus progressively narrows, both eating and treatment become extremely difficult.

Symptoms are different in children and adults

Symptoms reflect the endoscopic changes over time. In children, the condition manifests with feeding difficulties, vomiting, symptoms of gastroesophageal reflux, and abdominal pain as signs of inflammation. As the esophagus becomes fibrotic, teenagers and young adults tend to present with strictures, dysphagia, and food impaction. Of patients who present to an emergency department with food impaction, the major cause is now eosinophilic esophagitis.22

It is important to pay attention to symptoms in children to diagnose the condition and start treatment early to prevent or postpone disease advancement. Medical therapy does not clearly reverse the fibrosis.

As in many chronic benign diseases, patients learn to compensate, so a careful history is essential. Many deny having a swallowing problem, but questioning may reveal that they have always been slow, picky eaters, consuming mostly soft foods and drinking fluids with every bite.

 

 

Distinguishing eosinophilic esophagitis from gastroesophageal reflux disease

Distinguishing eosinophilic esophagitis from gastroesophageal reflux disease can be a challenge, as signs and symptoms overlap.

Veerappan et al23 looked for predictors of eosinophilic esophagitis in 400 adults who underwent routine upper endoscopy, 6.5% of whom had eosinophilic esophagitis. They found significant overlap in medical history for patients with and without the disease; while a higher proportion of patients with eosinophilic esophagitis had a history of asthma, dysphagia, food impactions, dermatitis, and food allergies, these conditions also occurred in other patients.

Similarly, the classic endoscopic findings of eosinophilic esophagitis—rings, furrows, strictures, and plaques—also occur in other conditions.23 Reflux disease can cause scarring from excess acid and may even be associated with eosinophils in the esophagus, indicative of a combination of allergy and reflux. A small-caliber esophagus is also occasionally present in patients with reflux disease.

Long-term PPI therapy is preferable to long-term steroid therapy

Ambulatory pH monitoring has been recommended to help determine if gastroesophageal reflux is the cause of esophageal eosinophilia and to guide therapy. However, in a prospective study of 51 patients,24 neither positive nor negative results of initial pH monitoring accurately predicted response to PPIs or steroid therapy. Another study found that half of patients with an eosinophilic esophagitis profile without evidence of acid reflux by pH monitoring responded to treatment with a PPI.25

This raises the question of whether some patients with eosinophilic esophagitis have more acid reflux than is detected by pH monitoring, or alternatively, whether PPIs have other, less-recognized effects besides reducing acidity. Investigators are now ascribing a host of anti-inflammatory actions to PPIs, including effects on antioxidants, inflammatory cells, endothelial cells, and the gut microflora.26 And PPIs may alleviate eosinophilic esophagitis through anti-inflammatory effects rather than by inhibiting secretion of gastric acid.

THREE TYPES OF THERAPY

In general, three types of therapy are available for patients with eosinophilic esophagitis: medications, allergen avoidance, and esophageal dilation (Table 2).

Medications: Try a PPI first, then a corticosteroid

A PPI should be tried even for patients with a classic presentation of eosinophilic esophagitis because some will respond, and long-term PPI therapy is preferable to long-term steroid treatment. Patients should be put on a 2-month course and should then undergo repeat biopsy.

For patients who do not respond to a PPI, a corticosteroid or montelukast can be tried. Topical therapy is showing promise as both a short- and long-term option to bring about remission.27 For administration, a corticosteroid (budesonide or fluticasone) is mixed with a viscous solution, such as water with honey or chocolate syrup, making it thick so it better coats the esophagus. The therapy can be very effective: in up to 8 weeks some patients have a 90% resolution of esophageal eosinophilia. However, about 5% of patients develop a yeast infection, and adrenal suppression is a concern but appears to be uncommon.

Avoidance of allergens

Because eosinophilic esophagitis is an allergic disease, eliminating allergens should be an effective treatment. Unfortunately, from a practical standpoint, elimination is very difficult. The elemental diet formula is expensive and unpalatable, making it impractical for a prolonged period.

Gonsalves et al28 put 50 adult patients with eosinophilic esophagitis on a diet eliminating the six most common foods believed to trigger the disease—wheat, milk, nuts, eggs, soy, and seafood—and found a marked reduction in eosinophils in the proximal and distal esophagus after 6 weeks. Additional triggers that have been identified include rice, corn, and legumes.29

Eliminating milk alone would benefit 20% of patients

Unfortunately, maintaining a diet without the most commonly identified allergens is not easy. Although some very motivated patients can do it, it is especially hard for teens and young adults. Variations of the diet, such as eliminating just two foods, make following a plan easier. Omitting milk alone would benefit an estimated 20% of patients with eosinophilic esophagitis.

Identifying food triggers is a challenge in itself as there is no good noninvasive method of identifying the allergens. The radioallergosorbent test measures immunoglobulin (Ig) E, and the skin-prick test measures acute hypersensitivity, but neither is very sensitive for the Th2-mediated reaction involved in eosinophilic esophagitis. In early trials, endoscopy and biopsy were painstakingly performed with the removal and reintroduction of every suspected food allergen, requiring multiple biopsies weekly, which is impractical for safety and economic reasons.

Attempts are being made to devise less invasive methods of sampling the esophageal mucosa. Transnasal endoscopy—done as an outpatient procedure with topical anesthesia—is a possibility. Another possibility is the esophageal string test,30 which involves swalling a weighted capsule on a string and then, after an hour, pulling it up again and testing the tissue on the string.

The “cytosponge,” a new device currently under investigation, also uses a string delivery system. The patient swallows a sponge contained in a gelatin capsule and attached to a string. When the capsule dissolves in the stomach—a process that takes only a few minutes—the sponge expands. The string is then pulled up, causing the sponge to sample the esophageal mucosa and thus obtaining a histologic specimen. This method shows promise as an inexpensive and noninvasive way to monitor the disease, although larger studies are needed to establish efficacy.31

Dilation—proceed with caution

Dilation can be an important therapy, especially in teenagers and adults with a fibrotic, narrowed esophagus.

Early on, the procedure often resulted in complications such as deep mucosal tears and perforations. Jung et al32 retrospectively analyzed 293 dilations in 161 patients with eosinophilic esophagitis and found a deep mucosal tear in 27 patients (9%), three perforations, and one incidence of major bleeding. All complications resolved without surgery. Factors associated with increased risk of complications were luminal narrowing in the upper and middle third of the esophagus, a luminal stricture that could not be traversed with a standard upper endoscope, and use of a Savary dilator.

It is critical that dilation be done slowly—a few millimeters at a time. Several sessions may be needed.

TREATMENT DURING REMISSION IS CONTROVERSIAL

Unless the patient with eosinophilic esophagitis can consistently control the disease by avoiding allergens, the question arises of whether to continue treating a patient who is in remission.

On the one hand, there is no known risk of Barrett esophagus or malignancy when the condition is not treated, and weight loss is uncommon because patients tend to accommodate to the condition. However, the long-term consequences are uncertain. Allergies are chronic, and disease progression with more fibrosis should be prevented. Also, food impaction commonly occurs and this requires aggressive dilation, which is risky.

On the other hand, chronic steroid therapy involves risk. The optimum steroid dosage during remission and whether alternate-day dosing is adequate have yet to be determined.

Long-term trials are needed to answer these questions. In the meantime, most physicians tend to aggressively treat this disease, if not with specific food avoidance, then with steroid maintenance therapy.

MONITORING THE DISEASE

Monitoring eosinophilic esophagitis by clinical indicators is difficult. Once fibrosis develops, symptoms often do not reflect underlying pathology. It may turn out that, as in Crohn disease, monitoring mucosal healing rather than symptoms may be best.

Until we know more about this condition, careful monitoring of patients is important. However, it is too early to give specific guidance, such as endoscopy every 2 months or annually. Whether the eosinophil count should be the critical consideration is also unknown.

References
  1. Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol 2011; 128:3–20.
  2. Rothenberg ME. Biology and treatment of eosinophilic esophagitis. Gastroenterology 2009; 137:1238–1249.
  3. Mishra A, Hogan SP, Brandt EB, Rothenberg ME. An etiological role for aeroallergens and eosinophils in experimental esophagitis. J Clin Invest 2001; 107:83–90.
  4. Peterson KA, Byrne KR, Vinson LA, et al. Elemental diet induces histologic response in adult eosinophilic esophagitis. Am J Gastroenterol 2013; 108:759–766.
  5. Steed E, Balda MS, Matter K. Dynamics and functions of tight junctions. Trends Cell Biol 2010; 20:142–149.
  6. Chang F, Anderson S. Clinical and pathological features of eosinophilic oesophagitis: a review. Pathology 2008; 40:3–8.
  7. Orlando LA, Orlando RC. Dilated intercellular spaces as a marker of GERD. Curr Gastroenterol Rep 2009; 11:190–194.
  8. Blanchard C, Wang N, Stringer KF, et al. Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest 2006; 116:536–547.
  9. Rothenberg ME, Spergel JM, Sherrill JD, et al. Common variants at 5q22 associate with pediatric eosinophilic esophagitis. Nat Genet 2010; 42:289–291.
  10. Attwood SE, Smyrk TC, Demeester TR, Jones JB. Esophageal eosinophilia with dysphagia. A distinct clinicopathologic syndrome. Dig Dis Sci 1993; 38:109–116.
  11. Kapel RC, Miller JK, Torres C, Aksoy S, Lash R, Katzka DA. Eosinophilic esophagitis: a prevalent disease in the United States that affects all age groups. Gastroenterology 2008; 134:1316–1321.
  12. Whitney-Miller CL, Katzka D, Furth EE. Eosinophilic esophagitis: a retrospective review of esophageal biopsy specimens from 1992 to 2004 at an adult academic medical center. Am J Clin Pathol 2009; 131:788–792.
  13. Sealock RJ, Rendon G, El-Serag HB. Systematic review: the epidemiology of eosinophilic oesophagitis in adults. Aliment Pharmacol Ther 2010; 32:712–719.
  14.  Ronkainen J, Talley NJ, Aro P, et al. Prevalence of oesophageal eosinophils and eosinophilic oesophagitis in adults: the population-based Kalixanda study. Gut 2007; 56:615–620.
  15. Straumann A, Simon HU. Eosinophilic esophagitis: escalating epidemiology? J Allergy Clin Immunol 2005; 115:418–419.
  16. Almansa C, Krishna M, Buchner AM, et al. Seasonal distribution in newly diagnosed cases of eosinophilic esophagitis in adults. Am J Gastroenterol 2009; 104:828–833.
  17. Prasad GA, Talley NJ, Romero Y, et al. Prevalence and predictive factors of eosinophilic esophagitis in patients presenting with dysphagia: a prospective study. Am J Gastroenterol 2007; 102:2627–2632.
  18. Dellon ES, Peery AF, Shaheen NJ, et al. Inverse association of esophageal eosinophilia with Helicobacter pylori based on analysis of a US pathology database. Gastroenterology 2011; 141:1586–1592.
  19. Björkstén B, Naaber P, Sepp E, Mikelsaar M. The intestinal microflora in allergic Estonian and Swedish 2-year-old children. Clin Exp Allergy 1999; 29:342–346.
  20. Roy-Ghanta S, Larosa DF, Katzka DA. Atopic characteristics of adult patients with eosinophilic esophagitis. Clin Gastroenterol Hepatol 2008; 6:531–535.
  21. Straumann A, Spichtin HP, Grize L, Bucher KA, Beglinger C, Simon HU. Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years. Gastroenterology 2003; 125:1660–1669.
  22. Desai TK, Stecevic V, Chang CH, Goldstein NS, Badizadegan K, Furuta GT. Association of eosinophiic inflammation with esophageal food impaction in adults. Gastrointest Endosc 2005; 61:795–801.
  23. Veerappan GR, Perry JL, Duncan TJ, et al. Prevalence of eosinophilic esophagitis in an adult population undergoing upper endoscopy: a prospective study. Clin Gastroenterol Hepatol 2009; 7:420–426.
  24. Francis DL, Foxx-Orenstein A, Arora AS, et al. Results of ambulatory pH monitoring do not reliably predict response to therapy in patients with eosinophilic oesophagitis. Aliment Pharmacol Ther 2012; 35:300–307.
  25. Molina-Infante J, Ferrando-Lamana L, Ripoll C, et al. Esophageal eosinophilic infiltration responds to proton pump inhibition in most adults. Clin Gastroenterol Hepatol 2011; 9:110–117.
  26. Kedika RR, Souza RF, Spechler SJ. Potential anti-inflammatory effects of proton pump inhibitors: a review and discussion of the clinical implications. Dig Dis Sci 2009; 54:2312–2317.
  27. Straumann A, Conus S, Degen L, et al. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Gastroenterology 2010; 139:1526–1537.
  28. Gonsalves N, Yang GY, Doerfler B, Ritz S, Ditto AM, Hirano I. Elimination diet effectively treats eosinophilic esophagitis in adults; food reintroduction identifies causative factors. Gastroenterology 2012; 142:1451–1459.
  29. Lucendo AJ, Arias Á, González-Cervera J, et al. Empiric 6-food elimination diet induced and maintained prolonged remission in patients with adult eosinophilic esophagitis: a prospective study on the food cause of the disease. J Allergy Clin Immunol 2013; 131:797–804.
  30. Fillon SA, Harris JK, Wagner BD, et al. Novel device to sample the esophageal microbiome—the esophageal string test. PLoS One 2012; 7:e42938.
  31. Katzka DA, Geno DM, Ravi A, et al. Accuracy, safety, and tolerability of tissue collection by Cytosponge vs endoscopy for evaluation of eosinophilic esophagitis. Clin Gastroenterol Hepatol 2014. pii: S1542-3565(14)00933-1. doi: 10.1016/j.cgh.2014.06.026. [Epub ahead of print]
  32. Jung KW, Gundersen N, Kopacova J, et al. Occurrence of and risk factors for complications after endoscopic dilation in eosinophilic esophagitis. Gastrointest Endosc 2011; 73:15–21.
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Medical Grand Rounds articles are based on edited transcripts from Medicine Grand Rounds presentations at Cleveland Clinic. They are approved by the author but are not peer-reviewed.

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Medical Grand Rounds articles are based on edited transcripts from Medicine Grand Rounds presentations at Cleveland Clinic. They are approved by the author but are not peer-reviewed.

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Medical Grand Rounds articles are based on edited transcripts from Medicine Grand Rounds presentations at Cleveland Clinic. They are approved by the author but are not peer-reviewed.

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Related Articles

Eosinophilic esophagitis is a new disease defined by specific criteria that include a constellation of symptoms. Consensus guidelines define it as a chronic antigen-mediated esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.1

Ten years ago, a biopsy that revealed eosinophils in the esophagus was diagnostic, because normally eosinophils are not seen in the esophagus. The current definition has evolved to become more comprehensive and includes clinical, demographic, and radiographic criteria.

This article presents an overview of eosinophilic esophagitis­—its pathogenesis, epidemiology, clinical presentation, diagnosis, and management.

ALLERGIC ORIGIN

Eosinophilic esophagitis is best regarded as a systemic rather than a single-organ disease, although current treatments are mostly directed specifically at esophageal inflammation. Evidence is clear that eosinophilic esophagitis is allergy-mediated.

The current “two-hit” etiologic model involves exposure first to aeroallergens that prime the esophagus, followed by food allergens that cause an eosinophilic response with antigen recognition and stimulation of immune cells from the bone marrow. Other allergic avenues may also be present, including those involved with atopy, asthma, eczema, and food allergies, which stimulate the Th2 pathway and lead to esophageal eosinophilia and inflammation.2

Eosinophilic esophagitis is a systemic disease rather than a single-organ problem

The two-hit model is supported experimentally: the disease can be induced in mice by injecting ovalbumin under the skin as a sensitizing agent, then exposing the airway to an aerosol of Aspergillus fumigatus, producing an allergic reaction involving classic Th2 allergy pathways.3 Further evidence is that many patients report that asthma or rhinitis developed years before esophageal disease began.

Patients with eosinophilic esophagitis and their family members have a high prevalence of allergies, and the disease frequently flares up during allergy season. Endoscopic biopsy specimens from patients often reveal increased T cells, mast cells, interleukin (IL)-5, and tumor necrosis factor alpha, all of which stimulate eotaxin and are essential to an allergic reaction. They also have high levels of CD3, CDA, and CD1A antigen-presenting lymphocytes, which are all associated with allergy.

Eosinophilic esophagitis responds to allergy medications, including corticosteroids and IL-5 or IL-13 mast-cell inhibitors. The strongest evidence for an allergic etiology is that withdrawing culpable food allergens leads to resolution of the disease. Peterson et al4 gave 18 adults with eosinophilic esophagitis an elemental diet (ie, a pure amino acid, carbohydrate-based diet in which all suspected allergens have been removed), and in 2 to 4 weeks, the mean number of eosinophils seen histologically fell from 54 to 10 cells per high-power field. The response was nearly complete (≤ 10 eosinophils per high-power field) in 72% of patients. When patients resumed a normal diet, the eosinophil content increased substantially within a few days.

Role of leaky tight junctions

Normally, the junctions between epithelial cells are tight, but many conditions, including allergic and autoimmune diseases, are now believed to involve altered permeability of this tissue. Tight-junction proteins play an important role in regulating antigen delivery and are modulated by cytokines. Activation of cytokines causes the membrane to become more permeable, allowing antigens to get through, leading to an enhanced reaction. In eosinophilic esophagitis, it is postulated that food antigens that pass through the leaky membrane activate CD1-antigen-presenting cells, which then initiate an allergic reaction.5–9

PREVALENCE IS INCREASING

Eosinophilic esophagitis was first described in 1993 with a report of 12 patients who had dysphagia, normal endoscopy, no acid reflux, and intraepithelial eosinophilia.10 The authors recognized that these patients had a distinct disease.

Since then, the disease has increased in prevalence. Kapel et al11 reviewed more than 74,000 endoscopy slides from a national pathology database and found 363 cases, with increasing prevalence during the study period from 2002 to 2005. Looking back further in a similar study, Whitney-Miller et al12 found a 0.3% prevalence from the years 1992 to 2000 vs 3.8% from 2001 to 2004.

Eosinophilic esophagitis is a systemic disease rather than a single-organ problem

Sealock et al13 reviewed the literature to assess the prevalence of eosinophilic esophagitis and found considerable variation depending on the populations sampled. One study from Sweden14 found a prevalence of 0.4% by performing endoscopy in 1,000 randomly selected people from nearly 3,000 responders to a questionnaire on abdominal symptoms. A study based on a Swiss database15 found only a 0.02% prevalence. Other studies show higher rates: a study from Florida that examined biopsy specimens from patients who underwent endoscopy for any reason found a prevalence of 1%.16 Another US study found a 15% prevalence in patients with dysphagia.17 Since these studies were done nearly a decade ago, we can expect the prevalence to be higher today.

Celiac disease has also been increasing in recent decades, as has gluten sensitivity. Allergies in general are on the rise worldwide, including asthma and atopic dermatitis. Theories as to the cause of these increases have focused on ambient antigens, food additives, proton pump inhibitors (PPIs), and the microbiome.18,19

DIAGNOSING EOSINOPHILIC ESOPHAGITIS

Eosinophilic esophagitis is diagnosed with a combination of symptomatic, histologic, and radiographic findings (Table 1). The classic patient is a white male—a child, teenager, or young adult—with dysphagia.

A case series of 23 adult patients20 found a mean age of 35 (age range 18 to 57), with a male preponderance (14:9). There is commonly a history of other allergies, including asthma, allergic rhinitis, and atopic dermatitis. Patients more commonly present with dysphagia than heartburn or other esophageal symptoms.11

Endoscopic findings—eosinophils, later fibrosis

Finding eosinophils in the esophagus is nonspecific and is not sufficient to make the diagnosis. Other systemic diseases can involve esophageal eosinophilia, including Churg-Strauss syndrome, Crohn disease, and helminthic diseases. Whether some are related to eosinophilic esophagitis or are independent is not well understood.

Characteristic findings on endoscopy include a corrugated or ringed appearance and linear furrows, resulting from fibrosis and scarring. “Micro-tears” may also be visible projecting linearly up the esophagus. Multiple white specks are signs of conglomerations of eosinophils and are easily confused with yeast infection. Strictures from scar tissue cause the mucosa to be tight and fragile, making the esophagus very susceptible to tearing during endoscopy.

After years of untreated disease, the esophagus becomes increasingly inflamed and fibrotic. Adult patients with eosinophilic esophagitis who were followed for a decade were found to develop increasing collagen deposition in which the submucosa or even the entire esophageal wall was diffusely fibrotic.21

Radiographic findings—a narrow esophagus

On radiography, the esophagus may appear narrow—not uncommonly one-third to one-quarter the caliber of a normal esophagus. As the esophagus progressively narrows, both eating and treatment become extremely difficult.

Symptoms are different in children and adults

Symptoms reflect the endoscopic changes over time. In children, the condition manifests with feeding difficulties, vomiting, symptoms of gastroesophageal reflux, and abdominal pain as signs of inflammation. As the esophagus becomes fibrotic, teenagers and young adults tend to present with strictures, dysphagia, and food impaction. Of patients who present to an emergency department with food impaction, the major cause is now eosinophilic esophagitis.22

It is important to pay attention to symptoms in children to diagnose the condition and start treatment early to prevent or postpone disease advancement. Medical therapy does not clearly reverse the fibrosis.

As in many chronic benign diseases, patients learn to compensate, so a careful history is essential. Many deny having a swallowing problem, but questioning may reveal that they have always been slow, picky eaters, consuming mostly soft foods and drinking fluids with every bite.

 

 

Distinguishing eosinophilic esophagitis from gastroesophageal reflux disease

Distinguishing eosinophilic esophagitis from gastroesophageal reflux disease can be a challenge, as signs and symptoms overlap.

Veerappan et al23 looked for predictors of eosinophilic esophagitis in 400 adults who underwent routine upper endoscopy, 6.5% of whom had eosinophilic esophagitis. They found significant overlap in medical history for patients with and without the disease; while a higher proportion of patients with eosinophilic esophagitis had a history of asthma, dysphagia, food impactions, dermatitis, and food allergies, these conditions also occurred in other patients.

Similarly, the classic endoscopic findings of eosinophilic esophagitis—rings, furrows, strictures, and plaques—also occur in other conditions.23 Reflux disease can cause scarring from excess acid and may even be associated with eosinophils in the esophagus, indicative of a combination of allergy and reflux. A small-caliber esophagus is also occasionally present in patients with reflux disease.

Long-term PPI therapy is preferable to long-term steroid therapy

Ambulatory pH monitoring has been recommended to help determine if gastroesophageal reflux is the cause of esophageal eosinophilia and to guide therapy. However, in a prospective study of 51 patients,24 neither positive nor negative results of initial pH monitoring accurately predicted response to PPIs or steroid therapy. Another study found that half of patients with an eosinophilic esophagitis profile without evidence of acid reflux by pH monitoring responded to treatment with a PPI.25

This raises the question of whether some patients with eosinophilic esophagitis have more acid reflux than is detected by pH monitoring, or alternatively, whether PPIs have other, less-recognized effects besides reducing acidity. Investigators are now ascribing a host of anti-inflammatory actions to PPIs, including effects on antioxidants, inflammatory cells, endothelial cells, and the gut microflora.26 And PPIs may alleviate eosinophilic esophagitis through anti-inflammatory effects rather than by inhibiting secretion of gastric acid.

THREE TYPES OF THERAPY

In general, three types of therapy are available for patients with eosinophilic esophagitis: medications, allergen avoidance, and esophageal dilation (Table 2).

Medications: Try a PPI first, then a corticosteroid

A PPI should be tried even for patients with a classic presentation of eosinophilic esophagitis because some will respond, and long-term PPI therapy is preferable to long-term steroid treatment. Patients should be put on a 2-month course and should then undergo repeat biopsy.

For patients who do not respond to a PPI, a corticosteroid or montelukast can be tried. Topical therapy is showing promise as both a short- and long-term option to bring about remission.27 For administration, a corticosteroid (budesonide or fluticasone) is mixed with a viscous solution, such as water with honey or chocolate syrup, making it thick so it better coats the esophagus. The therapy can be very effective: in up to 8 weeks some patients have a 90% resolution of esophageal eosinophilia. However, about 5% of patients develop a yeast infection, and adrenal suppression is a concern but appears to be uncommon.

Avoidance of allergens

Because eosinophilic esophagitis is an allergic disease, eliminating allergens should be an effective treatment. Unfortunately, from a practical standpoint, elimination is very difficult. The elemental diet formula is expensive and unpalatable, making it impractical for a prolonged period.

Gonsalves et al28 put 50 adult patients with eosinophilic esophagitis on a diet eliminating the six most common foods believed to trigger the disease—wheat, milk, nuts, eggs, soy, and seafood—and found a marked reduction in eosinophils in the proximal and distal esophagus after 6 weeks. Additional triggers that have been identified include rice, corn, and legumes.29

Eliminating milk alone would benefit 20% of patients

Unfortunately, maintaining a diet without the most commonly identified allergens is not easy. Although some very motivated patients can do it, it is especially hard for teens and young adults. Variations of the diet, such as eliminating just two foods, make following a plan easier. Omitting milk alone would benefit an estimated 20% of patients with eosinophilic esophagitis.

Identifying food triggers is a challenge in itself as there is no good noninvasive method of identifying the allergens. The radioallergosorbent test measures immunoglobulin (Ig) E, and the skin-prick test measures acute hypersensitivity, but neither is very sensitive for the Th2-mediated reaction involved in eosinophilic esophagitis. In early trials, endoscopy and biopsy were painstakingly performed with the removal and reintroduction of every suspected food allergen, requiring multiple biopsies weekly, which is impractical for safety and economic reasons.

Attempts are being made to devise less invasive methods of sampling the esophageal mucosa. Transnasal endoscopy—done as an outpatient procedure with topical anesthesia—is a possibility. Another possibility is the esophageal string test,30 which involves swalling a weighted capsule on a string and then, after an hour, pulling it up again and testing the tissue on the string.

The “cytosponge,” a new device currently under investigation, also uses a string delivery system. The patient swallows a sponge contained in a gelatin capsule and attached to a string. When the capsule dissolves in the stomach—a process that takes only a few minutes—the sponge expands. The string is then pulled up, causing the sponge to sample the esophageal mucosa and thus obtaining a histologic specimen. This method shows promise as an inexpensive and noninvasive way to monitor the disease, although larger studies are needed to establish efficacy.31

Dilation—proceed with caution

Dilation can be an important therapy, especially in teenagers and adults with a fibrotic, narrowed esophagus.

Early on, the procedure often resulted in complications such as deep mucosal tears and perforations. Jung et al32 retrospectively analyzed 293 dilations in 161 patients with eosinophilic esophagitis and found a deep mucosal tear in 27 patients (9%), three perforations, and one incidence of major bleeding. All complications resolved without surgery. Factors associated with increased risk of complications were luminal narrowing in the upper and middle third of the esophagus, a luminal stricture that could not be traversed with a standard upper endoscope, and use of a Savary dilator.

It is critical that dilation be done slowly—a few millimeters at a time. Several sessions may be needed.

TREATMENT DURING REMISSION IS CONTROVERSIAL

Unless the patient with eosinophilic esophagitis can consistently control the disease by avoiding allergens, the question arises of whether to continue treating a patient who is in remission.

On the one hand, there is no known risk of Barrett esophagus or malignancy when the condition is not treated, and weight loss is uncommon because patients tend to accommodate to the condition. However, the long-term consequences are uncertain. Allergies are chronic, and disease progression with more fibrosis should be prevented. Also, food impaction commonly occurs and this requires aggressive dilation, which is risky.

On the other hand, chronic steroid therapy involves risk. The optimum steroid dosage during remission and whether alternate-day dosing is adequate have yet to be determined.

Long-term trials are needed to answer these questions. In the meantime, most physicians tend to aggressively treat this disease, if not with specific food avoidance, then with steroid maintenance therapy.

MONITORING THE DISEASE

Monitoring eosinophilic esophagitis by clinical indicators is difficult. Once fibrosis develops, symptoms often do not reflect underlying pathology. It may turn out that, as in Crohn disease, monitoring mucosal healing rather than symptoms may be best.

Until we know more about this condition, careful monitoring of patients is important. However, it is too early to give specific guidance, such as endoscopy every 2 months or annually. Whether the eosinophil count should be the critical consideration is also unknown.

Eosinophilic esophagitis is a new disease defined by specific criteria that include a constellation of symptoms. Consensus guidelines define it as a chronic antigen-mediated esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.1

Ten years ago, a biopsy that revealed eosinophils in the esophagus was diagnostic, because normally eosinophils are not seen in the esophagus. The current definition has evolved to become more comprehensive and includes clinical, demographic, and radiographic criteria.

This article presents an overview of eosinophilic esophagitis­—its pathogenesis, epidemiology, clinical presentation, diagnosis, and management.

ALLERGIC ORIGIN

Eosinophilic esophagitis is best regarded as a systemic rather than a single-organ disease, although current treatments are mostly directed specifically at esophageal inflammation. Evidence is clear that eosinophilic esophagitis is allergy-mediated.

The current “two-hit” etiologic model involves exposure first to aeroallergens that prime the esophagus, followed by food allergens that cause an eosinophilic response with antigen recognition and stimulation of immune cells from the bone marrow. Other allergic avenues may also be present, including those involved with atopy, asthma, eczema, and food allergies, which stimulate the Th2 pathway and lead to esophageal eosinophilia and inflammation.2

Eosinophilic esophagitis is a systemic disease rather than a single-organ problem

The two-hit model is supported experimentally: the disease can be induced in mice by injecting ovalbumin under the skin as a sensitizing agent, then exposing the airway to an aerosol of Aspergillus fumigatus, producing an allergic reaction involving classic Th2 allergy pathways.3 Further evidence is that many patients report that asthma or rhinitis developed years before esophageal disease began.

Patients with eosinophilic esophagitis and their family members have a high prevalence of allergies, and the disease frequently flares up during allergy season. Endoscopic biopsy specimens from patients often reveal increased T cells, mast cells, interleukin (IL)-5, and tumor necrosis factor alpha, all of which stimulate eotaxin and are essential to an allergic reaction. They also have high levels of CD3, CDA, and CD1A antigen-presenting lymphocytes, which are all associated with allergy.

Eosinophilic esophagitis responds to allergy medications, including corticosteroids and IL-5 or IL-13 mast-cell inhibitors. The strongest evidence for an allergic etiology is that withdrawing culpable food allergens leads to resolution of the disease. Peterson et al4 gave 18 adults with eosinophilic esophagitis an elemental diet (ie, a pure amino acid, carbohydrate-based diet in which all suspected allergens have been removed), and in 2 to 4 weeks, the mean number of eosinophils seen histologically fell from 54 to 10 cells per high-power field. The response was nearly complete (≤ 10 eosinophils per high-power field) in 72% of patients. When patients resumed a normal diet, the eosinophil content increased substantially within a few days.

Role of leaky tight junctions

Normally, the junctions between epithelial cells are tight, but many conditions, including allergic and autoimmune diseases, are now believed to involve altered permeability of this tissue. Tight-junction proteins play an important role in regulating antigen delivery and are modulated by cytokines. Activation of cytokines causes the membrane to become more permeable, allowing antigens to get through, leading to an enhanced reaction. In eosinophilic esophagitis, it is postulated that food antigens that pass through the leaky membrane activate CD1-antigen-presenting cells, which then initiate an allergic reaction.5–9

PREVALENCE IS INCREASING

Eosinophilic esophagitis was first described in 1993 with a report of 12 patients who had dysphagia, normal endoscopy, no acid reflux, and intraepithelial eosinophilia.10 The authors recognized that these patients had a distinct disease.

Since then, the disease has increased in prevalence. Kapel et al11 reviewed more than 74,000 endoscopy slides from a national pathology database and found 363 cases, with increasing prevalence during the study period from 2002 to 2005. Looking back further in a similar study, Whitney-Miller et al12 found a 0.3% prevalence from the years 1992 to 2000 vs 3.8% from 2001 to 2004.

Eosinophilic esophagitis is a systemic disease rather than a single-organ problem

Sealock et al13 reviewed the literature to assess the prevalence of eosinophilic esophagitis and found considerable variation depending on the populations sampled. One study from Sweden14 found a prevalence of 0.4% by performing endoscopy in 1,000 randomly selected people from nearly 3,000 responders to a questionnaire on abdominal symptoms. A study based on a Swiss database15 found only a 0.02% prevalence. Other studies show higher rates: a study from Florida that examined biopsy specimens from patients who underwent endoscopy for any reason found a prevalence of 1%.16 Another US study found a 15% prevalence in patients with dysphagia.17 Since these studies were done nearly a decade ago, we can expect the prevalence to be higher today.

Celiac disease has also been increasing in recent decades, as has gluten sensitivity. Allergies in general are on the rise worldwide, including asthma and atopic dermatitis. Theories as to the cause of these increases have focused on ambient antigens, food additives, proton pump inhibitors (PPIs), and the microbiome.18,19

DIAGNOSING EOSINOPHILIC ESOPHAGITIS

Eosinophilic esophagitis is diagnosed with a combination of symptomatic, histologic, and radiographic findings (Table 1). The classic patient is a white male—a child, teenager, or young adult—with dysphagia.

A case series of 23 adult patients20 found a mean age of 35 (age range 18 to 57), with a male preponderance (14:9). There is commonly a history of other allergies, including asthma, allergic rhinitis, and atopic dermatitis. Patients more commonly present with dysphagia than heartburn or other esophageal symptoms.11

Endoscopic findings—eosinophils, later fibrosis

Finding eosinophils in the esophagus is nonspecific and is not sufficient to make the diagnosis. Other systemic diseases can involve esophageal eosinophilia, including Churg-Strauss syndrome, Crohn disease, and helminthic diseases. Whether some are related to eosinophilic esophagitis or are independent is not well understood.

Characteristic findings on endoscopy include a corrugated or ringed appearance and linear furrows, resulting from fibrosis and scarring. “Micro-tears” may also be visible projecting linearly up the esophagus. Multiple white specks are signs of conglomerations of eosinophils and are easily confused with yeast infection. Strictures from scar tissue cause the mucosa to be tight and fragile, making the esophagus very susceptible to tearing during endoscopy.

After years of untreated disease, the esophagus becomes increasingly inflamed and fibrotic. Adult patients with eosinophilic esophagitis who were followed for a decade were found to develop increasing collagen deposition in which the submucosa or even the entire esophageal wall was diffusely fibrotic.21

Radiographic findings—a narrow esophagus

On radiography, the esophagus may appear narrow—not uncommonly one-third to one-quarter the caliber of a normal esophagus. As the esophagus progressively narrows, both eating and treatment become extremely difficult.

Symptoms are different in children and adults

Symptoms reflect the endoscopic changes over time. In children, the condition manifests with feeding difficulties, vomiting, symptoms of gastroesophageal reflux, and abdominal pain as signs of inflammation. As the esophagus becomes fibrotic, teenagers and young adults tend to present with strictures, dysphagia, and food impaction. Of patients who present to an emergency department with food impaction, the major cause is now eosinophilic esophagitis.22

It is important to pay attention to symptoms in children to diagnose the condition and start treatment early to prevent or postpone disease advancement. Medical therapy does not clearly reverse the fibrosis.

As in many chronic benign diseases, patients learn to compensate, so a careful history is essential. Many deny having a swallowing problem, but questioning may reveal that they have always been slow, picky eaters, consuming mostly soft foods and drinking fluids with every bite.

 

 

Distinguishing eosinophilic esophagitis from gastroesophageal reflux disease

Distinguishing eosinophilic esophagitis from gastroesophageal reflux disease can be a challenge, as signs and symptoms overlap.

Veerappan et al23 looked for predictors of eosinophilic esophagitis in 400 adults who underwent routine upper endoscopy, 6.5% of whom had eosinophilic esophagitis. They found significant overlap in medical history for patients with and without the disease; while a higher proportion of patients with eosinophilic esophagitis had a history of asthma, dysphagia, food impactions, dermatitis, and food allergies, these conditions also occurred in other patients.

Similarly, the classic endoscopic findings of eosinophilic esophagitis—rings, furrows, strictures, and plaques—also occur in other conditions.23 Reflux disease can cause scarring from excess acid and may even be associated with eosinophils in the esophagus, indicative of a combination of allergy and reflux. A small-caliber esophagus is also occasionally present in patients with reflux disease.

Long-term PPI therapy is preferable to long-term steroid therapy

Ambulatory pH monitoring has been recommended to help determine if gastroesophageal reflux is the cause of esophageal eosinophilia and to guide therapy. However, in a prospective study of 51 patients,24 neither positive nor negative results of initial pH monitoring accurately predicted response to PPIs or steroid therapy. Another study found that half of patients with an eosinophilic esophagitis profile without evidence of acid reflux by pH monitoring responded to treatment with a PPI.25

This raises the question of whether some patients with eosinophilic esophagitis have more acid reflux than is detected by pH monitoring, or alternatively, whether PPIs have other, less-recognized effects besides reducing acidity. Investigators are now ascribing a host of anti-inflammatory actions to PPIs, including effects on antioxidants, inflammatory cells, endothelial cells, and the gut microflora.26 And PPIs may alleviate eosinophilic esophagitis through anti-inflammatory effects rather than by inhibiting secretion of gastric acid.

THREE TYPES OF THERAPY

In general, three types of therapy are available for patients with eosinophilic esophagitis: medications, allergen avoidance, and esophageal dilation (Table 2).

Medications: Try a PPI first, then a corticosteroid

A PPI should be tried even for patients with a classic presentation of eosinophilic esophagitis because some will respond, and long-term PPI therapy is preferable to long-term steroid treatment. Patients should be put on a 2-month course and should then undergo repeat biopsy.

For patients who do not respond to a PPI, a corticosteroid or montelukast can be tried. Topical therapy is showing promise as both a short- and long-term option to bring about remission.27 For administration, a corticosteroid (budesonide or fluticasone) is mixed with a viscous solution, such as water with honey or chocolate syrup, making it thick so it better coats the esophagus. The therapy can be very effective: in up to 8 weeks some patients have a 90% resolution of esophageal eosinophilia. However, about 5% of patients develop a yeast infection, and adrenal suppression is a concern but appears to be uncommon.

Avoidance of allergens

Because eosinophilic esophagitis is an allergic disease, eliminating allergens should be an effective treatment. Unfortunately, from a practical standpoint, elimination is very difficult. The elemental diet formula is expensive and unpalatable, making it impractical for a prolonged period.

Gonsalves et al28 put 50 adult patients with eosinophilic esophagitis on a diet eliminating the six most common foods believed to trigger the disease—wheat, milk, nuts, eggs, soy, and seafood—and found a marked reduction in eosinophils in the proximal and distal esophagus after 6 weeks. Additional triggers that have been identified include rice, corn, and legumes.29

Eliminating milk alone would benefit 20% of patients

Unfortunately, maintaining a diet without the most commonly identified allergens is not easy. Although some very motivated patients can do it, it is especially hard for teens and young adults. Variations of the diet, such as eliminating just two foods, make following a plan easier. Omitting milk alone would benefit an estimated 20% of patients with eosinophilic esophagitis.

Identifying food triggers is a challenge in itself as there is no good noninvasive method of identifying the allergens. The radioallergosorbent test measures immunoglobulin (Ig) E, and the skin-prick test measures acute hypersensitivity, but neither is very sensitive for the Th2-mediated reaction involved in eosinophilic esophagitis. In early trials, endoscopy and biopsy were painstakingly performed with the removal and reintroduction of every suspected food allergen, requiring multiple biopsies weekly, which is impractical for safety and economic reasons.

Attempts are being made to devise less invasive methods of sampling the esophageal mucosa. Transnasal endoscopy—done as an outpatient procedure with topical anesthesia—is a possibility. Another possibility is the esophageal string test,30 which involves swalling a weighted capsule on a string and then, after an hour, pulling it up again and testing the tissue on the string.

The “cytosponge,” a new device currently under investigation, also uses a string delivery system. The patient swallows a sponge contained in a gelatin capsule and attached to a string. When the capsule dissolves in the stomach—a process that takes only a few minutes—the sponge expands. The string is then pulled up, causing the sponge to sample the esophageal mucosa and thus obtaining a histologic specimen. This method shows promise as an inexpensive and noninvasive way to monitor the disease, although larger studies are needed to establish efficacy.31

Dilation—proceed with caution

Dilation can be an important therapy, especially in teenagers and adults with a fibrotic, narrowed esophagus.

Early on, the procedure often resulted in complications such as deep mucosal tears and perforations. Jung et al32 retrospectively analyzed 293 dilations in 161 patients with eosinophilic esophagitis and found a deep mucosal tear in 27 patients (9%), three perforations, and one incidence of major bleeding. All complications resolved without surgery. Factors associated with increased risk of complications were luminal narrowing in the upper and middle third of the esophagus, a luminal stricture that could not be traversed with a standard upper endoscope, and use of a Savary dilator.

It is critical that dilation be done slowly—a few millimeters at a time. Several sessions may be needed.

TREATMENT DURING REMISSION IS CONTROVERSIAL

Unless the patient with eosinophilic esophagitis can consistently control the disease by avoiding allergens, the question arises of whether to continue treating a patient who is in remission.

On the one hand, there is no known risk of Barrett esophagus or malignancy when the condition is not treated, and weight loss is uncommon because patients tend to accommodate to the condition. However, the long-term consequences are uncertain. Allergies are chronic, and disease progression with more fibrosis should be prevented. Also, food impaction commonly occurs and this requires aggressive dilation, which is risky.

On the other hand, chronic steroid therapy involves risk. The optimum steroid dosage during remission and whether alternate-day dosing is adequate have yet to be determined.

Long-term trials are needed to answer these questions. In the meantime, most physicians tend to aggressively treat this disease, if not with specific food avoidance, then with steroid maintenance therapy.

MONITORING THE DISEASE

Monitoring eosinophilic esophagitis by clinical indicators is difficult. Once fibrosis develops, symptoms often do not reflect underlying pathology. It may turn out that, as in Crohn disease, monitoring mucosal healing rather than symptoms may be best.

Until we know more about this condition, careful monitoring of patients is important. However, it is too early to give specific guidance, such as endoscopy every 2 months or annually. Whether the eosinophil count should be the critical consideration is also unknown.

References
  1. Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol 2011; 128:3–20.
  2. Rothenberg ME. Biology and treatment of eosinophilic esophagitis. Gastroenterology 2009; 137:1238–1249.
  3. Mishra A, Hogan SP, Brandt EB, Rothenberg ME. An etiological role for aeroallergens and eosinophils in experimental esophagitis. J Clin Invest 2001; 107:83–90.
  4. Peterson KA, Byrne KR, Vinson LA, et al. Elemental diet induces histologic response in adult eosinophilic esophagitis. Am J Gastroenterol 2013; 108:759–766.
  5. Steed E, Balda MS, Matter K. Dynamics and functions of tight junctions. Trends Cell Biol 2010; 20:142–149.
  6. Chang F, Anderson S. Clinical and pathological features of eosinophilic oesophagitis: a review. Pathology 2008; 40:3–8.
  7. Orlando LA, Orlando RC. Dilated intercellular spaces as a marker of GERD. Curr Gastroenterol Rep 2009; 11:190–194.
  8. Blanchard C, Wang N, Stringer KF, et al. Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest 2006; 116:536–547.
  9. Rothenberg ME, Spergel JM, Sherrill JD, et al. Common variants at 5q22 associate with pediatric eosinophilic esophagitis. Nat Genet 2010; 42:289–291.
  10. Attwood SE, Smyrk TC, Demeester TR, Jones JB. Esophageal eosinophilia with dysphagia. A distinct clinicopathologic syndrome. Dig Dis Sci 1993; 38:109–116.
  11. Kapel RC, Miller JK, Torres C, Aksoy S, Lash R, Katzka DA. Eosinophilic esophagitis: a prevalent disease in the United States that affects all age groups. Gastroenterology 2008; 134:1316–1321.
  12. Whitney-Miller CL, Katzka D, Furth EE. Eosinophilic esophagitis: a retrospective review of esophageal biopsy specimens from 1992 to 2004 at an adult academic medical center. Am J Clin Pathol 2009; 131:788–792.
  13. Sealock RJ, Rendon G, El-Serag HB. Systematic review: the epidemiology of eosinophilic oesophagitis in adults. Aliment Pharmacol Ther 2010; 32:712–719.
  14.  Ronkainen J, Talley NJ, Aro P, et al. Prevalence of oesophageal eosinophils and eosinophilic oesophagitis in adults: the population-based Kalixanda study. Gut 2007; 56:615–620.
  15. Straumann A, Simon HU. Eosinophilic esophagitis: escalating epidemiology? J Allergy Clin Immunol 2005; 115:418–419.
  16. Almansa C, Krishna M, Buchner AM, et al. Seasonal distribution in newly diagnosed cases of eosinophilic esophagitis in adults. Am J Gastroenterol 2009; 104:828–833.
  17. Prasad GA, Talley NJ, Romero Y, et al. Prevalence and predictive factors of eosinophilic esophagitis in patients presenting with dysphagia: a prospective study. Am J Gastroenterol 2007; 102:2627–2632.
  18. Dellon ES, Peery AF, Shaheen NJ, et al. Inverse association of esophageal eosinophilia with Helicobacter pylori based on analysis of a US pathology database. Gastroenterology 2011; 141:1586–1592.
  19. Björkstén B, Naaber P, Sepp E, Mikelsaar M. The intestinal microflora in allergic Estonian and Swedish 2-year-old children. Clin Exp Allergy 1999; 29:342–346.
  20. Roy-Ghanta S, Larosa DF, Katzka DA. Atopic characteristics of adult patients with eosinophilic esophagitis. Clin Gastroenterol Hepatol 2008; 6:531–535.
  21. Straumann A, Spichtin HP, Grize L, Bucher KA, Beglinger C, Simon HU. Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years. Gastroenterology 2003; 125:1660–1669.
  22. Desai TK, Stecevic V, Chang CH, Goldstein NS, Badizadegan K, Furuta GT. Association of eosinophiic inflammation with esophageal food impaction in adults. Gastrointest Endosc 2005; 61:795–801.
  23. Veerappan GR, Perry JL, Duncan TJ, et al. Prevalence of eosinophilic esophagitis in an adult population undergoing upper endoscopy: a prospective study. Clin Gastroenterol Hepatol 2009; 7:420–426.
  24. Francis DL, Foxx-Orenstein A, Arora AS, et al. Results of ambulatory pH monitoring do not reliably predict response to therapy in patients with eosinophilic oesophagitis. Aliment Pharmacol Ther 2012; 35:300–307.
  25. Molina-Infante J, Ferrando-Lamana L, Ripoll C, et al. Esophageal eosinophilic infiltration responds to proton pump inhibition in most adults. Clin Gastroenterol Hepatol 2011; 9:110–117.
  26. Kedika RR, Souza RF, Spechler SJ. Potential anti-inflammatory effects of proton pump inhibitors: a review and discussion of the clinical implications. Dig Dis Sci 2009; 54:2312–2317.
  27. Straumann A, Conus S, Degen L, et al. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Gastroenterology 2010; 139:1526–1537.
  28. Gonsalves N, Yang GY, Doerfler B, Ritz S, Ditto AM, Hirano I. Elimination diet effectively treats eosinophilic esophagitis in adults; food reintroduction identifies causative factors. Gastroenterology 2012; 142:1451–1459.
  29. Lucendo AJ, Arias Á, González-Cervera J, et al. Empiric 6-food elimination diet induced and maintained prolonged remission in patients with adult eosinophilic esophagitis: a prospective study on the food cause of the disease. J Allergy Clin Immunol 2013; 131:797–804.
  30. Fillon SA, Harris JK, Wagner BD, et al. Novel device to sample the esophageal microbiome—the esophageal string test. PLoS One 2012; 7:e42938.
  31. Katzka DA, Geno DM, Ravi A, et al. Accuracy, safety, and tolerability of tissue collection by Cytosponge vs endoscopy for evaluation of eosinophilic esophagitis. Clin Gastroenterol Hepatol 2014. pii: S1542-3565(14)00933-1. doi: 10.1016/j.cgh.2014.06.026. [Epub ahead of print]
  32. Jung KW, Gundersen N, Kopacova J, et al. Occurrence of and risk factors for complications after endoscopic dilation in eosinophilic esophagitis. Gastrointest Endosc 2011; 73:15–21.
References
  1. Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol 2011; 128:3–20.
  2. Rothenberg ME. Biology and treatment of eosinophilic esophagitis. Gastroenterology 2009; 137:1238–1249.
  3. Mishra A, Hogan SP, Brandt EB, Rothenberg ME. An etiological role for aeroallergens and eosinophils in experimental esophagitis. J Clin Invest 2001; 107:83–90.
  4. Peterson KA, Byrne KR, Vinson LA, et al. Elemental diet induces histologic response in adult eosinophilic esophagitis. Am J Gastroenterol 2013; 108:759–766.
  5. Steed E, Balda MS, Matter K. Dynamics and functions of tight junctions. Trends Cell Biol 2010; 20:142–149.
  6. Chang F, Anderson S. Clinical and pathological features of eosinophilic oesophagitis: a review. Pathology 2008; 40:3–8.
  7. Orlando LA, Orlando RC. Dilated intercellular spaces as a marker of GERD. Curr Gastroenterol Rep 2009; 11:190–194.
  8. Blanchard C, Wang N, Stringer KF, et al. Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest 2006; 116:536–547.
  9. Rothenberg ME, Spergel JM, Sherrill JD, et al. Common variants at 5q22 associate with pediatric eosinophilic esophagitis. Nat Genet 2010; 42:289–291.
  10. Attwood SE, Smyrk TC, Demeester TR, Jones JB. Esophageal eosinophilia with dysphagia. A distinct clinicopathologic syndrome. Dig Dis Sci 1993; 38:109–116.
  11. Kapel RC, Miller JK, Torres C, Aksoy S, Lash R, Katzka DA. Eosinophilic esophagitis: a prevalent disease in the United States that affects all age groups. Gastroenterology 2008; 134:1316–1321.
  12. Whitney-Miller CL, Katzka D, Furth EE. Eosinophilic esophagitis: a retrospective review of esophageal biopsy specimens from 1992 to 2004 at an adult academic medical center. Am J Clin Pathol 2009; 131:788–792.
  13. Sealock RJ, Rendon G, El-Serag HB. Systematic review: the epidemiology of eosinophilic oesophagitis in adults. Aliment Pharmacol Ther 2010; 32:712–719.
  14.  Ronkainen J, Talley NJ, Aro P, et al. Prevalence of oesophageal eosinophils and eosinophilic oesophagitis in adults: the population-based Kalixanda study. Gut 2007; 56:615–620.
  15. Straumann A, Simon HU. Eosinophilic esophagitis: escalating epidemiology? J Allergy Clin Immunol 2005; 115:418–419.
  16. Almansa C, Krishna M, Buchner AM, et al. Seasonal distribution in newly diagnosed cases of eosinophilic esophagitis in adults. Am J Gastroenterol 2009; 104:828–833.
  17. Prasad GA, Talley NJ, Romero Y, et al. Prevalence and predictive factors of eosinophilic esophagitis in patients presenting with dysphagia: a prospective study. Am J Gastroenterol 2007; 102:2627–2632.
  18. Dellon ES, Peery AF, Shaheen NJ, et al. Inverse association of esophageal eosinophilia with Helicobacter pylori based on analysis of a US pathology database. Gastroenterology 2011; 141:1586–1592.
  19. Björkstén B, Naaber P, Sepp E, Mikelsaar M. The intestinal microflora in allergic Estonian and Swedish 2-year-old children. Clin Exp Allergy 1999; 29:342–346.
  20. Roy-Ghanta S, Larosa DF, Katzka DA. Atopic characteristics of adult patients with eosinophilic esophagitis. Clin Gastroenterol Hepatol 2008; 6:531–535.
  21. Straumann A, Spichtin HP, Grize L, Bucher KA, Beglinger C, Simon HU. Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years. Gastroenterology 2003; 125:1660–1669.
  22. Desai TK, Stecevic V, Chang CH, Goldstein NS, Badizadegan K, Furuta GT. Association of eosinophiic inflammation with esophageal food impaction in adults. Gastrointest Endosc 2005; 61:795–801.
  23. Veerappan GR, Perry JL, Duncan TJ, et al. Prevalence of eosinophilic esophagitis in an adult population undergoing upper endoscopy: a prospective study. Clin Gastroenterol Hepatol 2009; 7:420–426.
  24. Francis DL, Foxx-Orenstein A, Arora AS, et al. Results of ambulatory pH monitoring do not reliably predict response to therapy in patients with eosinophilic oesophagitis. Aliment Pharmacol Ther 2012; 35:300–307.
  25. Molina-Infante J, Ferrando-Lamana L, Ripoll C, et al. Esophageal eosinophilic infiltration responds to proton pump inhibition in most adults. Clin Gastroenterol Hepatol 2011; 9:110–117.
  26. Kedika RR, Souza RF, Spechler SJ. Potential anti-inflammatory effects of proton pump inhibitors: a review and discussion of the clinical implications. Dig Dis Sci 2009; 54:2312–2317.
  27. Straumann A, Conus S, Degen L, et al. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Gastroenterology 2010; 139:1526–1537.
  28. Gonsalves N, Yang GY, Doerfler B, Ritz S, Ditto AM, Hirano I. Elimination diet effectively treats eosinophilic esophagitis in adults; food reintroduction identifies causative factors. Gastroenterology 2012; 142:1451–1459.
  29. Lucendo AJ, Arias Á, González-Cervera J, et al. Empiric 6-food elimination diet induced and maintained prolonged remission in patients with adult eosinophilic esophagitis: a prospective study on the food cause of the disease. J Allergy Clin Immunol 2013; 131:797–804.
  30. Fillon SA, Harris JK, Wagner BD, et al. Novel device to sample the esophageal microbiome—the esophageal string test. PLoS One 2012; 7:e42938.
  31. Katzka DA, Geno DM, Ravi A, et al. Accuracy, safety, and tolerability of tissue collection by Cytosponge vs endoscopy for evaluation of eosinophilic esophagitis. Clin Gastroenterol Hepatol 2014. pii: S1542-3565(14)00933-1. doi: 10.1016/j.cgh.2014.06.026. [Epub ahead of print]
  32. Jung KW, Gundersen N, Kopacova J, et al. Occurrence of and risk factors for complications after endoscopic dilation in eosinophilic esophagitis. Gastrointest Endosc 2011; 73:15–21.
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KEY POINTS

  • Eosinophilic esophagitis is an allergy-mediated, systemic disease.
  • It is diagnosed by characteristic symptoms, esophageal biopsy (peak value 15 eosinophils per high-power field), and response to allergen avoidance or treatment with steroids.
  • Therapy with a proton pump inhibitor should be tried even for patients with a classic presentation.
  • Strict dietary avoidance of allergens has been shown to resolve the disease but is often impractical.
  • Dilation is indicated for a narrowed esophagus but must be done cautiously because of the risk of tearing.
  • How best to monitor the disease (eg, by annual endoscopy) is still uncertain.
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Diagnostic certainty and the eosinophil

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This issue of the Journal contains an article by Dr. David A. Katzka, titled “The ‘skinny’ on eosinophilic esophagitis.” Reading it, I was struck by two messages, one clinical and one biological.

The clinical message relates to the psychology of diagnosis, or as Dr. Jerome Groopman discussed in his book How Doctors Think, misdiagnosis. In many patients, eosinophilic esophagitis, especially early in its course, can mimic gastroesophageal reflux disease (GERD), causing dysphagia and discomfort with eating that may be relieved at least in part with a proton pump inhibitor. When evaluating a patient who relates a history compatible with a common condition, we instinctively tend to embrace the diagnosis of that common syndrome, in this case GERD, rather than initially explore in depth the possibility of less-common mimics. Once the disease has progressed, with the patient experiencing frequent postprandial emesis or needing to dramatically limit the size of meals despite taking a full dose of a proton pump inhibitor, we will hopefully revisit and reassess our initial diagnosis, often with endoscopy and biopsy. But that may not always occur promptly, because we may have committed (per Groopman) an “anchoring error,” seizing on an initial symptom or finding, allowing it to cloud our clinical judgment, reaching “premature closure,” and not keeping our minds open to alternative diagnoses such as eosinophilic esophagitis. I wonder how many of the younger patients I have diagnosed with GERD who had histories of “food intolerances” actually had eosinophilic esophagitis.

The biological message is that the eosinophil is a fascinating and generally misunderstood cell, not just a marker and mediator of allergy. As an apparent defender against the macro-invaders—worms and other parasites—it carries an arsenal of defensive weapons. But eosinophil-dominant inflammatory reactions started by various molecular triggers and perpetuated by interleukin 5 and other promoters of eosinophil proliferation and chemotaxis have a common histopathologic footprint—fibrosis.

Long-standing significant asthma is characterized as much by airway remodeling and fibrosis as it is by bronchospasm. A myocardial hallmark of hypereosinophilic syndrome is fibrosis. Eosinophilic pneumonia can be followed by local scarring. Eosinophils have been implicated in the pathogenesis of primary biliary cirrhosis and the granulomatous cirrhosis of schistosomiasis. And as Dr. Katzka reminds us, the confluence of food hypersensitivity, gastric acid, and the products of eosinophil activation (likely including transforming growth factor beta) in the esophageal wall can result in a marked fibrotic reaction with dysmotility. It is unclear whether this is a dysregulated attempt at healing with resultant maladaptive “scar” formation, or perhaps a misdirected inflammatory response, with the goal of walling off a perceived invader (an allergen is not a worm).

There are probably many other mimic diseases that we are not recognizing often enough. And tissue eosinophils may portend detrimental fibrotic remodeling.

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This issue of the Journal contains an article by Dr. David A. Katzka, titled “The ‘skinny’ on eosinophilic esophagitis.” Reading it, I was struck by two messages, one clinical and one biological.

The clinical message relates to the psychology of diagnosis, or as Dr. Jerome Groopman discussed in his book How Doctors Think, misdiagnosis. In many patients, eosinophilic esophagitis, especially early in its course, can mimic gastroesophageal reflux disease (GERD), causing dysphagia and discomfort with eating that may be relieved at least in part with a proton pump inhibitor. When evaluating a patient who relates a history compatible with a common condition, we instinctively tend to embrace the diagnosis of that common syndrome, in this case GERD, rather than initially explore in depth the possibility of less-common mimics. Once the disease has progressed, with the patient experiencing frequent postprandial emesis or needing to dramatically limit the size of meals despite taking a full dose of a proton pump inhibitor, we will hopefully revisit and reassess our initial diagnosis, often with endoscopy and biopsy. But that may not always occur promptly, because we may have committed (per Groopman) an “anchoring error,” seizing on an initial symptom or finding, allowing it to cloud our clinical judgment, reaching “premature closure,” and not keeping our minds open to alternative diagnoses such as eosinophilic esophagitis. I wonder how many of the younger patients I have diagnosed with GERD who had histories of “food intolerances” actually had eosinophilic esophagitis.

The biological message is that the eosinophil is a fascinating and generally misunderstood cell, not just a marker and mediator of allergy. As an apparent defender against the macro-invaders—worms and other parasites—it carries an arsenal of defensive weapons. But eosinophil-dominant inflammatory reactions started by various molecular triggers and perpetuated by interleukin 5 and other promoters of eosinophil proliferation and chemotaxis have a common histopathologic footprint—fibrosis.

Long-standing significant asthma is characterized as much by airway remodeling and fibrosis as it is by bronchospasm. A myocardial hallmark of hypereosinophilic syndrome is fibrosis. Eosinophilic pneumonia can be followed by local scarring. Eosinophils have been implicated in the pathogenesis of primary biliary cirrhosis and the granulomatous cirrhosis of schistosomiasis. And as Dr. Katzka reminds us, the confluence of food hypersensitivity, gastric acid, and the products of eosinophil activation (likely including transforming growth factor beta) in the esophageal wall can result in a marked fibrotic reaction with dysmotility. It is unclear whether this is a dysregulated attempt at healing with resultant maladaptive “scar” formation, or perhaps a misdirected inflammatory response, with the goal of walling off a perceived invader (an allergen is not a worm).

There are probably many other mimic diseases that we are not recognizing often enough. And tissue eosinophils may portend detrimental fibrotic remodeling.

This issue of the Journal contains an article by Dr. David A. Katzka, titled “The ‘skinny’ on eosinophilic esophagitis.” Reading it, I was struck by two messages, one clinical and one biological.

The clinical message relates to the psychology of diagnosis, or as Dr. Jerome Groopman discussed in his book How Doctors Think, misdiagnosis. In many patients, eosinophilic esophagitis, especially early in its course, can mimic gastroesophageal reflux disease (GERD), causing dysphagia and discomfort with eating that may be relieved at least in part with a proton pump inhibitor. When evaluating a patient who relates a history compatible with a common condition, we instinctively tend to embrace the diagnosis of that common syndrome, in this case GERD, rather than initially explore in depth the possibility of less-common mimics. Once the disease has progressed, with the patient experiencing frequent postprandial emesis or needing to dramatically limit the size of meals despite taking a full dose of a proton pump inhibitor, we will hopefully revisit and reassess our initial diagnosis, often with endoscopy and biopsy. But that may not always occur promptly, because we may have committed (per Groopman) an “anchoring error,” seizing on an initial symptom or finding, allowing it to cloud our clinical judgment, reaching “premature closure,” and not keeping our minds open to alternative diagnoses such as eosinophilic esophagitis. I wonder how many of the younger patients I have diagnosed with GERD who had histories of “food intolerances” actually had eosinophilic esophagitis.

The biological message is that the eosinophil is a fascinating and generally misunderstood cell, not just a marker and mediator of allergy. As an apparent defender against the macro-invaders—worms and other parasites—it carries an arsenal of defensive weapons. But eosinophil-dominant inflammatory reactions started by various molecular triggers and perpetuated by interleukin 5 and other promoters of eosinophil proliferation and chemotaxis have a common histopathologic footprint—fibrosis.

Long-standing significant asthma is characterized as much by airway remodeling and fibrosis as it is by bronchospasm. A myocardial hallmark of hypereosinophilic syndrome is fibrosis. Eosinophilic pneumonia can be followed by local scarring. Eosinophils have been implicated in the pathogenesis of primary biliary cirrhosis and the granulomatous cirrhosis of schistosomiasis. And as Dr. Katzka reminds us, the confluence of food hypersensitivity, gastric acid, and the products of eosinophil activation (likely including transforming growth factor beta) in the esophageal wall can result in a marked fibrotic reaction with dysmotility. It is unclear whether this is a dysregulated attempt at healing with resultant maladaptive “scar” formation, or perhaps a misdirected inflammatory response, with the goal of walling off a perceived invader (an allergen is not a worm).

There are probably many other mimic diseases that we are not recognizing often enough. And tissue eosinophils may portend detrimental fibrotic remodeling.

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In his monthly podcast for The Journal of Community and Supportive Oncology, Dr David Henry looks at Original Reports on the comparison of atropine-diphenoxylate and hyoscyamine in lowering the rates of irinotecan-related cholinergic syndrome; the effects of age and comorbidities in the management of rectal cancer in elderly patients at an institution in Portugal; the impact of a telehealth intervention on quality of life and symptom distress in patients with head and neck cancer; and the beneficial effects of animal-assisted visits on quality of life during multimodal radiation-chemotherapy regimens. He also discusses a Research Report in which the authors attempt, possibly for the first time, to quantify radiation exposure from diagnostic procedures in patients with newly diagnosed breast cancer, as well as two feature articles – a round-up of some of the presentations at the 2014 San Antonio Breast Cancer Symposium and a Journal Club presentation of therapies for lymphoproliferative disorders.

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In his monthly podcast for The Journal of Community and Supportive Oncology, Dr David Henry looks at Original Reports on the comparison of atropine-diphenoxylate and hyoscyamine in lowering the rates of irinotecan-related cholinergic syndrome; the effects of age and comorbidities in the management of rectal cancer in elderly patients at an institution in Portugal; the impact of a telehealth intervention on quality of life and symptom distress in patients with head and neck cancer; and the beneficial effects of animal-assisted visits on quality of life during multimodal radiation-chemotherapy regimens. He also discusses a Research Report in which the authors attempt, possibly for the first time, to quantify radiation exposure from diagnostic procedures in patients with newly diagnosed breast cancer, as well as two feature articles – a round-up of some of the presentations at the 2014 San Antonio Breast Cancer Symposium and a Journal Club presentation of therapies for lymphoproliferative disorders.

In his monthly podcast for The Journal of Community and Supportive Oncology, Dr David Henry looks at Original Reports on the comparison of atropine-diphenoxylate and hyoscyamine in lowering the rates of irinotecan-related cholinergic syndrome; the effects of age and comorbidities in the management of rectal cancer in elderly patients at an institution in Portugal; the impact of a telehealth intervention on quality of life and symptom distress in patients with head and neck cancer; and the beneficial effects of animal-assisted visits on quality of life during multimodal radiation-chemotherapy regimens. He also discusses a Research Report in which the authors attempt, possibly for the first time, to quantify radiation exposure from diagnostic procedures in patients with newly diagnosed breast cancer, as well as two feature articles – a round-up of some of the presentations at the 2014 San Antonio Breast Cancer Symposium and a Journal Club presentation of therapies for lymphoproliferative disorders.

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Hysteroscopic myomectomy using a mechanical approach

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Uterine fibroids are a common complaint in gynecology, with an incidence of approximately 30% in women aged 25 to 45 years and a cumulative incidence of 70% to 80% by age 50.1,2 They are more prevalent in women of African descent and are a leading indication for ­hysterectomy.

Although they can be asymptomatic, submucosal fibroids are frequently associated with:

 

  • abnormal uterine bleeding (AUB)
  • dysmenorrhea
  • expulsion of an intrauterine device (IUD)
  • leukorrhea
  • pelvic pain
  • urinary frequency
  • infertility
  • premature labor
  • reproductive wastage
  • bleeding during hormone replacement therapy.

In postmenopausal women, the risk of malignancy in a leiomyoma ranges from 0.2% to 0.5%.1 The risk is lower in premenopausal women.

In this article, I describe the technique for hysteroscopic myomectomy using a mechanical approach (Truclear Tissue Removal System, Smith & Nephew, Andover, MA), which offers hysteroscopic morcellation as well as quick resection and efficient fluid ­management. (Note: Unlike open intraperitoneal morcellation, hysteroscopic morcellation carries a low risk of tissue spread.)
 

 

FIGURE 1: Classification of uterine fibroids, ESGE systemAccording to the European Society of Gynaecological Endoscopy system, which considers intramural extension in its categorization, Type 0 myomas have no extension, Type I have less than 50%, and Type II have more than 50%.

Classification of fibroids
Preoperative classification of leiomyomas makes it possible to determine the best route for surgery. The most commonly used classification system was developed by the European Society of Gynaecological Endoscopy (ESGE) (FIGURE 1), which considers the extent of intramural extension. Each fibroid under that system is classified as:

 

  • Type 0 – no intramural extension
  • Type I – less than 50% extension
  • Type II – more than 50% extension.

A second classification system recently was devised to take into account additional features of the fibroid. The STEP-W ­classification considers size, topography, extension, penetration, and the lateral wall (FIGURE 2). In general, the lower the score, the less complex the procedure will be, with a lower risk of fluid intravasation, shorter ­operative time, and a greater likelihood of complete removal of the fibroid.

A multicenter, prospective study of 449 women who underwent hysteroscopic resection of their fibroids correlated the ESGE and STEP-W systems. All 320 fibroids (100%) with a score of 4 or below on the STEP-W classification system were completely removed, compared with 112 of 145 fibroids (77.2%) with a score greater than 4. All 33 cases of incomplete hysteroscopic resection (100%) had a STEP-W score above 4.3

In the same study, 85 of 86 cases (98.9%) with Type 0 fibroids under the ESGE system had complete resection, along with 278 of 298 Type I fibroids (93.3%), and 69 of 81 Type II fibroids (85.2%).3 Complete removal is a goal because it relieves symptoms and averts the need for additional procedures.
 

 

FIGURE 2: Classification of uterine fibroids, STEP-W systemA score of 4 or less is desired for low-complexity hysteroscopic myomectomy.


Patient selection
Proper patient selection for hysteroscopic myomectomy is extremely important. The most common indications are AUB, pelvic pain or discomfort, recurrent pregnancy loss, and infertility. In addition, the patient should have a strong wish for uterine preservation and desire a minimally invasive transcervical approach.

AAGL guidelines on the diagnosis and management of submucous fibroids note that, in general, submucous leiomyomas as large as 4 or 5 cm in diameter can be removed hysteroscopically by experienced surgeons.4

A hysteroscopic approach is not advised for women in whom hysteroscopic surgery is contraindicated, such as women with intrauterine pregnancy, active pelvic infection, active herpes infection, or cervical or uterine cancer. Women who have medical comorbidities such as coronary heart disease, significant renal disease, or bleeding diathesis may need perioperative clearance from anesthesia or hematology prior to hysteroscopic surgery and close fluid monitoring during the procedure.

Consider the leiomyoma
Penetration into the myometrium. Women who have a fibroid that penetrates more than 50% into the myometrium may benefit from hysteroscopic myomectomy, provided the surgeon is highly experienced. A skilled hysteroscopist can ensure complete enucleation of a penetrating fibroid in these cases.

If you are still in the learning process for hysteroscopy, however, start with easier cases—ie, polyps and Type 0 and Type I fibroids. Type II fibroids require longer operative time, are associated with increased fluid absorption and intravasation, carry an increased risk of perioperative complications, and may not always be completely resected.

Size of the fibroid also is relevant. As size increases, so does the volume of tissue needing to be removed, adding to overall operative time.

Presence of other fibroids. When a woman has an intracavitary fibroid as well as myomas in other locations, the surgeon should consider whether hysteroscopic removal of the intracavitary lesion alone can provide significant relief of all fibroid-related symptoms. In such cases, laparoscopic, robotic, or abdominal myomectomy may be preferable, especially if the volume of the additional myomas is considerable.

To determine the optimal surgical route, the physician must consider the symptoms present—is AUB the only symptom, or are other fibroid-related conditions present as well, such as bulk, pelvic pain, and other quality-of-life issues? If multiple symptoms exist, then other approaches may be better.

How fibroids affect fertility
Fibroids are present in 5% to 10% of women with infertility. In this population, fibroids are the only abnormal finding in 1.0% to 2.4% of cases.4

In a meta-analysis of 23 studies evaluating women with fibroids and infertility, Pritts and colleagues found nine studies involving submucosal fibroids.5 These studies included one randomized controlled trial, two prospective studies, and six retrospective analyses. They found that women who had fibroids with a submucosal component had lower pregnancy and implantation rates, compared with their infertile, myoma-free counterparts. Pritts and colleagues concluded that myomectomy is likely to improve fertility in these cases (TABLE).5

Instrumentation
Among the options are monopolar and bipolar resectoscopy and the mechanical approach using the Truclear System, which includes a morcellator. With conventional resectoscopy all chips must be removed, necessitating multiple insertions of the hysteroscope. Monopolar instrumentation, in particular, carries a risk of energy discharge to healthy tissue. The monopolar resectoscope also has a longer learning curve, ­compared with the mechanical approach.6

In contrast, the Truclear System requires fewer insertions, has a short learning curve, and omits the need for capture of individual chips, as the mechanical morcellator suctions and captures them throughout the procedure.7 In addition, because resection is performed mechanically, there is no risk of energy discharge to healthy tissue.

The Truclear system also is associated with a significantly shorter operative time, compared with resectoscopy, which may be advantageous for residents, fellows, and other physicians learning the procedure (­FIGURE 3).7 Shorter operative time also may result in lower fluid deficits. In addition, saline distension may reduce the risk of fluid absorption and hyponatremia. The tissue-capture feature allows evaluation of the entire pathologic specimen.

Besides hysteroscopic myomectomy, the Truclear System is appropriate for visual dilatation and curettage (D&C), adhesiolysis, polypectomy, and evacuation of retained products of conception.
 

 

FIGURE: 3 Operative time, Truclear versus resectoscopyThe Truclear approach involved significantly shorter operative time for both polypectomy and myomectomy.
 

 

Preoperative evaluation
A complete history is vital to document which fibroid-related symptoms are present and how they affect quality of life.

Preoperative imaging also is imperative—using either 2D or 3D saline infusion sonography or a combination of diagnostic hysteroscopy and transvaginal ultrasound—to select patients for hysteroscopy, anticipate blood loss, and ensure that the proper instrumentation is available at the time of surgery. Magnetic resonance imaging, computed tomography, and hysterosalpingo­graphy are either prohibitively expensive or of limited value in the initial preoperative assessment of uterine fibroids.

Any woman who has AUB and a risk for endometrial hyperplasia or cancer should undergo endometrial assessment as well.

Use of preoperative medications
In most cases, prophylactic administration of antibiotics is not warranted to prevent infection or endocarditis.

Although some clinicians give gonadotropin-releasing hormone (GnRH) agonists to reduce the size of large fibroids, the drug complicates dissection of the fibroid from the surrounding capsule. For this reason, and because we lack data demonstrating that GnRH agonists decrease blood loss and limit absorption of distension media, I do not administer them to patients.8–12 Moreover, this drug can cause vasomotor symptoms, cervical stenosis, and vaginal hemorrhage (related to estrogen flare).

GnRH agonists may be of value to stimulate transient amenorrhea for several months preoperatively in order to correct iron-deficiency anemia. Intravenous iron also can be administered during this interval.

The risk of bleeding in hysteroscopic myomectomy is 2% to 3%.1 When the ­mechanical approach is used, rather than resectoscopy, continuous flow coupled with suctioning of the chips during the procedure keeps the image clear. Post-procedure contraction of the uterus stops most bleeding. Intrauterine pressure of the pump can be increased to help tamponade any oozing.

Misoprostol. Cervical stenosis is not ­uncommon in menopausal women. It can also pose a challenge in nulliparous women. Attempting hysteroscopy in the setting of ­cervical stenosis increases the risk of ­cervical laceration, creation of a false passage, and uterine perforation. For this reason, I prescribe oral or vaginal misoprostol 200 to 400 µg nightly for 1 to 2 days before the ­procedure.

Vasopressin can reduce blood loss during hysteroscopic myomectomy when it is injected into the cervical stroma preoperatively. It also reduces absorption of ­distension fluid and facilitates cervical ­dilation.

However, vasopressin must be injected with extreme care, with aspiration to confirm the absence of blood prior to each injection, as intravascular injection can lead to bradycardia, profound hypertension, and even death.13 Always notify the anesthesiologist prior to injection when vasopressin will be administered.

I routinely use vasopressin before hysteroscopic myomectomy (0.5 mg in 20 cc of saline or 20 U in 100 cc), injecting 5 cc of the solution at 3, 6, 9, and 12 o’clock positions.

Anesthesia during hysteroscopic myomectomy typically is “monitored anesthesia care,” or MAC, which consists of local anesthesia with sedation and analgesia. The need for regional or general anesthesia is rare. Consider adding a pericervical block or intravenous ketorolac (Toradol) to provide postoperative analgesia.

Surgical technique
Strict attention to fluid management is required throughout the procedure, preferably in accordance with AAGL guidelines on the management of hysteroscopic distending media.14 With the mechanical approach, because the distension fluid is isotonic (normal saline), it does not increase the risk of hyponatremia but can cause pulmonary edema or congestive heart failure. Intravasation usually is the result of excessive operative time, treatment of deeper myometrial fibroids (Type I or II), or high intrauterine pressure. I operate using intrauterine pressure in the range of 75 to 125 mm Hg.

The steps involved in the mechanical hysteroscopy ­approach are:

 

  • Insert the hysteroscope into the uterus under direct visualization. In general, the greater the number of insertions, the greater the risk of uterine perforation. Preoperative cervical ripening helps facilitate insertion (see “Misoprostol” above).
  • Distend the uterus with saline and inspect the uterine cavity, noting again the size and location of the fibroids and whether they are sessile or pedunculated.
  • Locate the fibroid or other pathology to be removed, and place the morcellator window against it to begin cutting. Use the tip of the morcellator to elevate the fibroid for easier cutting. Enucleation is accomplished largely by varying the intrauterine pressure, which permits uterine decompression and myometrial contraction and renders the fibroid capsule more visible. If necessary, the hysteroscope can be withdrawn to stimulate myometrial ­contraction, which also helps to delineate the fibroid capsule.
  • Reinspect the uterus to rule out perforation and remove any additional intrauterine pathology with a targeted view.
  • Once all designated fibroids have been removed, withdraw the morcellator and hysteroscope from the uterus.
  • Inspect the endocervical landscape to rule out injury and other pathology.

     

 

Best practices for hysteroscopic myomectomy

 

  • Careful preoperative evaluation is important, preferably using diagnostic hysteroscopy or saline infusion sonography, to choose the optimal route of myomectomy and plan the surgical approach.
  • During the myomectomy, pay close attention to fluid management and adhere strictly to predetermined limits.
  • Complete removal of the fibroid is essential to relieve symptoms and avert the need for additional procedures.


Postoperative care
A nonsteroidal anti-inflammatory drug or limited use of narcotics usually is sufficient to relieve any postoperative cramping or vaginal discomfort.

Advise the patient to notify you in the event of increasing pain, foul-smelling vaginal discharge, or fever.

Also counsel her that she can return to most normal activities within 24 to 48 hours. Sexual activity is permissible 1 week after surgery. Early and frequent ambulation is important.

Schedule a follow-up visit 4 to 6 weeks after the procedure.

Share your thoughts on this article! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References

 

1. Perez-Medina T, Font EC, eds. Diagnostic and Operative Hysteroscopy. Tunbridge Wells, Kent, UK: Anshan Publishing; 2007:13.

2. Management of uterine fibroids: an update of the evidence. Agency for Healthcare Research and Quality. http://archive.ahrq.gov/clinic/tp/uteruptp.htm. Published July 2007. Accessed January 14, 2015.

3. Lasmar RB, Zinmei Z, Indman PD, Celeste RK, Di Spiezo Sardo A. Feasibility of a new system of classification of submucous myomas: a multicenter study. Fertil Steril. 2011;95(6):2073–2077.

4. AAGL Practice Report: practice guidelines for the diagnosis and management of submucous leiomyomas. J Minim Invasive Gynecol. 2012;19(2):152–171.

5. Pritts EA, Parker WH, Olive DL. Fibroids and infertility: an updated systematic review of the evidence. Fertil Steril. 2009;91(4):1215–1223.

6. Van Dongen H, Emanuel MH, Wolterbeek R, Trimbos JB, Jansen FW. Hysteroscopic morcellator for removal of intrauterine polyps and myomas: a randomized controlled pilot study among residents in training. J Minim Invasive Gynecol. 2008;15(4):466–471.

7. Emanuel MH, Wamsteker K. The intra uterine morcellator: a new hysteroscopic operating technique to remove intrauterine polyps and myomas. J Minim Invasive Gynecol. 2005;12(1):62–66.

8. Emanuel MH, Hart A, Wamsteker K, Lammes F. An analysis of fluid loss during transcervical resection of submucous myomas. Fertil Steril. 1997;68(5):881–886.

9. Taskin O, Sadik S, Onoglu A, et al. Role of endometrial suppression on the frequency of intrauterine adhesions after resectoscopic surgery. J Am Assoc Gynecol Laparosc. 2000;7(3):351.

10. Propst AM, Liberman RF, Harlow BL, Ginsburg ES. Complications of hysteroscopic surgery: predicting patients at risk. Obstet Gynecol. 2000;96(4):517–520.

11. Perino A, Chianchiano N, Petronio M, Cittadini E. Role of leuprolide acetate depot in hysteroscopic surgery: a controlled study. Fertil Steril. 1993;59(3):507–510.

12. Mencaglia L, Tantini C. GnRH agonist analogs and hysteroscopic resection of myomas. Int J Gynaecol Obstet. 1993;43(3):285–288.

13. Hobo R, Netsu S, Koyasu Y, Tsutsumi O. Bradycardia and cardiac arrest caused by intramyometrial injection of vasopressin during a laparoscopically assisted myomectomy. Obstet Gynecol. 2009;113(2 Pt 2):484–486.

14. Munro MD, Storz K, Abbott JA, et al; AAGL. AAGL Practice Report: practice guidelines for the management of hysteroscopic distending media. J Minim Invasive Gynecol. 2013;20(2):137–148.

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Linda D. Bradley, MD

Dr. Bradley is Professor of Surgery at the Cleveland Clinic College of Medicine, Case Western Reserve University School of Medicine. She also is Vice Chair of Obstetrics and Gynecology, Vice Chair of the Women’s Health Institute, and Director of the Center for Menstrual Disorders, Fibroids, and Hysteroscopic Services at the Cleveland Clinic in Cleveland, Ohio. In addition, she directs Hysteroscopic Education for the Residency Program at Cleveland Clinic Lerner College of Medicine. She is Past President of AAGL and serves on the OBG Management Board of Editors.

Dr. Bradley reports that she serves as a speaker for Bayer HealthCare and as a consultant to Allen ­Medical, BlueSpire, Boston Scientific, Hologic, and Smith & Nephew. She also served as principal investigator and contributor investigator for Bayer Research, is a reviewer for BlueSpire, serves on the Data Safety Monitoring Board of Gynesonics, and holds stock in ­EndoSee.

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Linda D. Bradley MD, hysteroscopic myomectomy, mechanical approach, resectoscopy, hysteroscope, uterine fibroids, minimally invasive gynecologic surgery, MIGS, hysterectomy, abnormal uterine bleeding, AUB, dysmenorrhea, intrauterine device, IUD, leukorrhea, pelvic pain, urinary frequency, infertility, premature labor, hormone replacement therapy, postmenopausal woman, leiomyoma, Truclear Tissue Removal System, Smith & Nephew, hysteroscopic morcellation, fluid management, European Society of Gynaecological Endoscopy, ESGE, classification of fibroids, STEP-W classification, fertility, dilatation and curettage, D&C, adhesiolysis, polypectomy, retained products of conception, 2D or 3D saline infusion sonography, transvaginal ultrasound, magnetic resonance imaging, MRI, computed tomography, CT, hysterosalpingography, antibiotics, gonadotropin-releasing hormone, GnRH, vasomotor symptoms, cervical stenosis, vaginal hemorrhage, anesthesiologist, vasopressin, misoprostol,
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Linda D. Bradley, MD

Dr. Bradley is Professor of Surgery at the Cleveland Clinic College of Medicine, Case Western Reserve University School of Medicine. She also is Vice Chair of Obstetrics and Gynecology, Vice Chair of the Women’s Health Institute, and Director of the Center for Menstrual Disorders, Fibroids, and Hysteroscopic Services at the Cleveland Clinic in Cleveland, Ohio. In addition, she directs Hysteroscopic Education for the Residency Program at Cleveland Clinic Lerner College of Medicine. She is Past President of AAGL and serves on the OBG Management Board of Editors.

Dr. Bradley reports that she serves as a speaker for Bayer HealthCare and as a consultant to Allen ­Medical, BlueSpire, Boston Scientific, Hologic, and Smith & Nephew. She also served as principal investigator and contributor investigator for Bayer Research, is a reviewer for BlueSpire, serves on the Data Safety Monitoring Board of Gynesonics, and holds stock in ­EndoSee.

Author and Disclosure Information

 

Linda D. Bradley, MD

Dr. Bradley is Professor of Surgery at the Cleveland Clinic College of Medicine, Case Western Reserve University School of Medicine. She also is Vice Chair of Obstetrics and Gynecology, Vice Chair of the Women’s Health Institute, and Director of the Center for Menstrual Disorders, Fibroids, and Hysteroscopic Services at the Cleveland Clinic in Cleveland, Ohio. In addition, she directs Hysteroscopic Education for the Residency Program at Cleveland Clinic Lerner College of Medicine. She is Past President of AAGL and serves on the OBG Management Board of Editors.

Dr. Bradley reports that she serves as a speaker for Bayer HealthCare and as a consultant to Allen ­Medical, BlueSpire, Boston Scientific, Hologic, and Smith & Nephew. She also served as principal investigator and contributor investigator for Bayer Research, is a reviewer for BlueSpire, serves on the Data Safety Monitoring Board of Gynesonics, and holds stock in ­EndoSee.

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Uterine fibroids are a common complaint in gynecology, with an incidence of approximately 30% in women aged 25 to 45 years and a cumulative incidence of 70% to 80% by age 50.1,2 They are more prevalent in women of African descent and are a leading indication for ­hysterectomy.

Although they can be asymptomatic, submucosal fibroids are frequently associated with:

 

  • abnormal uterine bleeding (AUB)
  • dysmenorrhea
  • expulsion of an intrauterine device (IUD)
  • leukorrhea
  • pelvic pain
  • urinary frequency
  • infertility
  • premature labor
  • reproductive wastage
  • bleeding during hormone replacement therapy.

In postmenopausal women, the risk of malignancy in a leiomyoma ranges from 0.2% to 0.5%.1 The risk is lower in premenopausal women.

In this article, I describe the technique for hysteroscopic myomectomy using a mechanical approach (Truclear Tissue Removal System, Smith & Nephew, Andover, MA), which offers hysteroscopic morcellation as well as quick resection and efficient fluid ­management. (Note: Unlike open intraperitoneal morcellation, hysteroscopic morcellation carries a low risk of tissue spread.)
 

 

FIGURE 1: Classification of uterine fibroids, ESGE systemAccording to the European Society of Gynaecological Endoscopy system, which considers intramural extension in its categorization, Type 0 myomas have no extension, Type I have less than 50%, and Type II have more than 50%.

Classification of fibroids
Preoperative classification of leiomyomas makes it possible to determine the best route for surgery. The most commonly used classification system was developed by the European Society of Gynaecological Endoscopy (ESGE) (FIGURE 1), which considers the extent of intramural extension. Each fibroid under that system is classified as:

 

  • Type 0 – no intramural extension
  • Type I – less than 50% extension
  • Type II – more than 50% extension.

A second classification system recently was devised to take into account additional features of the fibroid. The STEP-W ­classification considers size, topography, extension, penetration, and the lateral wall (FIGURE 2). In general, the lower the score, the less complex the procedure will be, with a lower risk of fluid intravasation, shorter ­operative time, and a greater likelihood of complete removal of the fibroid.

A multicenter, prospective study of 449 women who underwent hysteroscopic resection of their fibroids correlated the ESGE and STEP-W systems. All 320 fibroids (100%) with a score of 4 or below on the STEP-W classification system were completely removed, compared with 112 of 145 fibroids (77.2%) with a score greater than 4. All 33 cases of incomplete hysteroscopic resection (100%) had a STEP-W score above 4.3

In the same study, 85 of 86 cases (98.9%) with Type 0 fibroids under the ESGE system had complete resection, along with 278 of 298 Type I fibroids (93.3%), and 69 of 81 Type II fibroids (85.2%).3 Complete removal is a goal because it relieves symptoms and averts the need for additional procedures.
 

 

FIGURE 2: Classification of uterine fibroids, STEP-W systemA score of 4 or less is desired for low-complexity hysteroscopic myomectomy.


Patient selection
Proper patient selection for hysteroscopic myomectomy is extremely important. The most common indications are AUB, pelvic pain or discomfort, recurrent pregnancy loss, and infertility. In addition, the patient should have a strong wish for uterine preservation and desire a minimally invasive transcervical approach.

AAGL guidelines on the diagnosis and management of submucous fibroids note that, in general, submucous leiomyomas as large as 4 or 5 cm in diameter can be removed hysteroscopically by experienced surgeons.4

A hysteroscopic approach is not advised for women in whom hysteroscopic surgery is contraindicated, such as women with intrauterine pregnancy, active pelvic infection, active herpes infection, or cervical or uterine cancer. Women who have medical comorbidities such as coronary heart disease, significant renal disease, or bleeding diathesis may need perioperative clearance from anesthesia or hematology prior to hysteroscopic surgery and close fluid monitoring during the procedure.

Consider the leiomyoma
Penetration into the myometrium. Women who have a fibroid that penetrates more than 50% into the myometrium may benefit from hysteroscopic myomectomy, provided the surgeon is highly experienced. A skilled hysteroscopist can ensure complete enucleation of a penetrating fibroid in these cases.

If you are still in the learning process for hysteroscopy, however, start with easier cases—ie, polyps and Type 0 and Type I fibroids. Type II fibroids require longer operative time, are associated with increased fluid absorption and intravasation, carry an increased risk of perioperative complications, and may not always be completely resected.

Size of the fibroid also is relevant. As size increases, so does the volume of tissue needing to be removed, adding to overall operative time.

Presence of other fibroids. When a woman has an intracavitary fibroid as well as myomas in other locations, the surgeon should consider whether hysteroscopic removal of the intracavitary lesion alone can provide significant relief of all fibroid-related symptoms. In such cases, laparoscopic, robotic, or abdominal myomectomy may be preferable, especially if the volume of the additional myomas is considerable.

To determine the optimal surgical route, the physician must consider the symptoms present—is AUB the only symptom, or are other fibroid-related conditions present as well, such as bulk, pelvic pain, and other quality-of-life issues? If multiple symptoms exist, then other approaches may be better.

How fibroids affect fertility
Fibroids are present in 5% to 10% of women with infertility. In this population, fibroids are the only abnormal finding in 1.0% to 2.4% of cases.4

In a meta-analysis of 23 studies evaluating women with fibroids and infertility, Pritts and colleagues found nine studies involving submucosal fibroids.5 These studies included one randomized controlled trial, two prospective studies, and six retrospective analyses. They found that women who had fibroids with a submucosal component had lower pregnancy and implantation rates, compared with their infertile, myoma-free counterparts. Pritts and colleagues concluded that myomectomy is likely to improve fertility in these cases (TABLE).5

Instrumentation
Among the options are monopolar and bipolar resectoscopy and the mechanical approach using the Truclear System, which includes a morcellator. With conventional resectoscopy all chips must be removed, necessitating multiple insertions of the hysteroscope. Monopolar instrumentation, in particular, carries a risk of energy discharge to healthy tissue. The monopolar resectoscope also has a longer learning curve, ­compared with the mechanical approach.6

In contrast, the Truclear System requires fewer insertions, has a short learning curve, and omits the need for capture of individual chips, as the mechanical morcellator suctions and captures them throughout the procedure.7 In addition, because resection is performed mechanically, there is no risk of energy discharge to healthy tissue.

The Truclear system also is associated with a significantly shorter operative time, compared with resectoscopy, which may be advantageous for residents, fellows, and other physicians learning the procedure (­FIGURE 3).7 Shorter operative time also may result in lower fluid deficits. In addition, saline distension may reduce the risk of fluid absorption and hyponatremia. The tissue-capture feature allows evaluation of the entire pathologic specimen.

Besides hysteroscopic myomectomy, the Truclear System is appropriate for visual dilatation and curettage (D&C), adhesiolysis, polypectomy, and evacuation of retained products of conception.
 

 

FIGURE: 3 Operative time, Truclear versus resectoscopyThe Truclear approach involved significantly shorter operative time for both polypectomy and myomectomy.
 

 

Preoperative evaluation
A complete history is vital to document which fibroid-related symptoms are present and how they affect quality of life.

Preoperative imaging also is imperative—using either 2D or 3D saline infusion sonography or a combination of diagnostic hysteroscopy and transvaginal ultrasound—to select patients for hysteroscopy, anticipate blood loss, and ensure that the proper instrumentation is available at the time of surgery. Magnetic resonance imaging, computed tomography, and hysterosalpingo­graphy are either prohibitively expensive or of limited value in the initial preoperative assessment of uterine fibroids.

Any woman who has AUB and a risk for endometrial hyperplasia or cancer should undergo endometrial assessment as well.

Use of preoperative medications
In most cases, prophylactic administration of antibiotics is not warranted to prevent infection or endocarditis.

Although some clinicians give gonadotropin-releasing hormone (GnRH) agonists to reduce the size of large fibroids, the drug complicates dissection of the fibroid from the surrounding capsule. For this reason, and because we lack data demonstrating that GnRH agonists decrease blood loss and limit absorption of distension media, I do not administer them to patients.8–12 Moreover, this drug can cause vasomotor symptoms, cervical stenosis, and vaginal hemorrhage (related to estrogen flare).

GnRH agonists may be of value to stimulate transient amenorrhea for several months preoperatively in order to correct iron-deficiency anemia. Intravenous iron also can be administered during this interval.

The risk of bleeding in hysteroscopic myomectomy is 2% to 3%.1 When the ­mechanical approach is used, rather than resectoscopy, continuous flow coupled with suctioning of the chips during the procedure keeps the image clear. Post-procedure contraction of the uterus stops most bleeding. Intrauterine pressure of the pump can be increased to help tamponade any oozing.

Misoprostol. Cervical stenosis is not ­uncommon in menopausal women. It can also pose a challenge in nulliparous women. Attempting hysteroscopy in the setting of ­cervical stenosis increases the risk of ­cervical laceration, creation of a false passage, and uterine perforation. For this reason, I prescribe oral or vaginal misoprostol 200 to 400 µg nightly for 1 to 2 days before the ­procedure.

Vasopressin can reduce blood loss during hysteroscopic myomectomy when it is injected into the cervical stroma preoperatively. It also reduces absorption of ­distension fluid and facilitates cervical ­dilation.

However, vasopressin must be injected with extreme care, with aspiration to confirm the absence of blood prior to each injection, as intravascular injection can lead to bradycardia, profound hypertension, and even death.13 Always notify the anesthesiologist prior to injection when vasopressin will be administered.

I routinely use vasopressin before hysteroscopic myomectomy (0.5 mg in 20 cc of saline or 20 U in 100 cc), injecting 5 cc of the solution at 3, 6, 9, and 12 o’clock positions.

Anesthesia during hysteroscopic myomectomy typically is “monitored anesthesia care,” or MAC, which consists of local anesthesia with sedation and analgesia. The need for regional or general anesthesia is rare. Consider adding a pericervical block or intravenous ketorolac (Toradol) to provide postoperative analgesia.

Surgical technique
Strict attention to fluid management is required throughout the procedure, preferably in accordance with AAGL guidelines on the management of hysteroscopic distending media.14 With the mechanical approach, because the distension fluid is isotonic (normal saline), it does not increase the risk of hyponatremia but can cause pulmonary edema or congestive heart failure. Intravasation usually is the result of excessive operative time, treatment of deeper myometrial fibroids (Type I or II), or high intrauterine pressure. I operate using intrauterine pressure in the range of 75 to 125 mm Hg.

The steps involved in the mechanical hysteroscopy ­approach are:

 

  • Insert the hysteroscope into the uterus under direct visualization. In general, the greater the number of insertions, the greater the risk of uterine perforation. Preoperative cervical ripening helps facilitate insertion (see “Misoprostol” above).
  • Distend the uterus with saline and inspect the uterine cavity, noting again the size and location of the fibroids and whether they are sessile or pedunculated.
  • Locate the fibroid or other pathology to be removed, and place the morcellator window against it to begin cutting. Use the tip of the morcellator to elevate the fibroid for easier cutting. Enucleation is accomplished largely by varying the intrauterine pressure, which permits uterine decompression and myometrial contraction and renders the fibroid capsule more visible. If necessary, the hysteroscope can be withdrawn to stimulate myometrial ­contraction, which also helps to delineate the fibroid capsule.
  • Reinspect the uterus to rule out perforation and remove any additional intrauterine pathology with a targeted view.
  • Once all designated fibroids have been removed, withdraw the morcellator and hysteroscope from the uterus.
  • Inspect the endocervical landscape to rule out injury and other pathology.

     

 

Best practices for hysteroscopic myomectomy

 

  • Careful preoperative evaluation is important, preferably using diagnostic hysteroscopy or saline infusion sonography, to choose the optimal route of myomectomy and plan the surgical approach.
  • During the myomectomy, pay close attention to fluid management and adhere strictly to predetermined limits.
  • Complete removal of the fibroid is essential to relieve symptoms and avert the need for additional procedures.


Postoperative care
A nonsteroidal anti-inflammatory drug or limited use of narcotics usually is sufficient to relieve any postoperative cramping or vaginal discomfort.

Advise the patient to notify you in the event of increasing pain, foul-smelling vaginal discharge, or fever.

Also counsel her that she can return to most normal activities within 24 to 48 hours. Sexual activity is permissible 1 week after surgery. Early and frequent ambulation is important.

Schedule a follow-up visit 4 to 6 weeks after the procedure.

Share your thoughts on this article! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Uterine fibroids are a common complaint in gynecology, with an incidence of approximately 30% in women aged 25 to 45 years and a cumulative incidence of 70% to 80% by age 50.1,2 They are more prevalent in women of African descent and are a leading indication for ­hysterectomy.

Although they can be asymptomatic, submucosal fibroids are frequently associated with:

 

  • abnormal uterine bleeding (AUB)
  • dysmenorrhea
  • expulsion of an intrauterine device (IUD)
  • leukorrhea
  • pelvic pain
  • urinary frequency
  • infertility
  • premature labor
  • reproductive wastage
  • bleeding during hormone replacement therapy.

In postmenopausal women, the risk of malignancy in a leiomyoma ranges from 0.2% to 0.5%.1 The risk is lower in premenopausal women.

In this article, I describe the technique for hysteroscopic myomectomy using a mechanical approach (Truclear Tissue Removal System, Smith & Nephew, Andover, MA), which offers hysteroscopic morcellation as well as quick resection and efficient fluid ­management. (Note: Unlike open intraperitoneal morcellation, hysteroscopic morcellation carries a low risk of tissue spread.)
 

 

FIGURE 1: Classification of uterine fibroids, ESGE systemAccording to the European Society of Gynaecological Endoscopy system, which considers intramural extension in its categorization, Type 0 myomas have no extension, Type I have less than 50%, and Type II have more than 50%.

Classification of fibroids
Preoperative classification of leiomyomas makes it possible to determine the best route for surgery. The most commonly used classification system was developed by the European Society of Gynaecological Endoscopy (ESGE) (FIGURE 1), which considers the extent of intramural extension. Each fibroid under that system is classified as:

 

  • Type 0 – no intramural extension
  • Type I – less than 50% extension
  • Type II – more than 50% extension.

A second classification system recently was devised to take into account additional features of the fibroid. The STEP-W ­classification considers size, topography, extension, penetration, and the lateral wall (FIGURE 2). In general, the lower the score, the less complex the procedure will be, with a lower risk of fluid intravasation, shorter ­operative time, and a greater likelihood of complete removal of the fibroid.

A multicenter, prospective study of 449 women who underwent hysteroscopic resection of their fibroids correlated the ESGE and STEP-W systems. All 320 fibroids (100%) with a score of 4 or below on the STEP-W classification system were completely removed, compared with 112 of 145 fibroids (77.2%) with a score greater than 4. All 33 cases of incomplete hysteroscopic resection (100%) had a STEP-W score above 4.3

In the same study, 85 of 86 cases (98.9%) with Type 0 fibroids under the ESGE system had complete resection, along with 278 of 298 Type I fibroids (93.3%), and 69 of 81 Type II fibroids (85.2%).3 Complete removal is a goal because it relieves symptoms and averts the need for additional procedures.
 

 

FIGURE 2: Classification of uterine fibroids, STEP-W systemA score of 4 or less is desired for low-complexity hysteroscopic myomectomy.


Patient selection
Proper patient selection for hysteroscopic myomectomy is extremely important. The most common indications are AUB, pelvic pain or discomfort, recurrent pregnancy loss, and infertility. In addition, the patient should have a strong wish for uterine preservation and desire a minimally invasive transcervical approach.

AAGL guidelines on the diagnosis and management of submucous fibroids note that, in general, submucous leiomyomas as large as 4 or 5 cm in diameter can be removed hysteroscopically by experienced surgeons.4

A hysteroscopic approach is not advised for women in whom hysteroscopic surgery is contraindicated, such as women with intrauterine pregnancy, active pelvic infection, active herpes infection, or cervical or uterine cancer. Women who have medical comorbidities such as coronary heart disease, significant renal disease, or bleeding diathesis may need perioperative clearance from anesthesia or hematology prior to hysteroscopic surgery and close fluid monitoring during the procedure.

Consider the leiomyoma
Penetration into the myometrium. Women who have a fibroid that penetrates more than 50% into the myometrium may benefit from hysteroscopic myomectomy, provided the surgeon is highly experienced. A skilled hysteroscopist can ensure complete enucleation of a penetrating fibroid in these cases.

If you are still in the learning process for hysteroscopy, however, start with easier cases—ie, polyps and Type 0 and Type I fibroids. Type II fibroids require longer operative time, are associated with increased fluid absorption and intravasation, carry an increased risk of perioperative complications, and may not always be completely resected.

Size of the fibroid also is relevant. As size increases, so does the volume of tissue needing to be removed, adding to overall operative time.

Presence of other fibroids. When a woman has an intracavitary fibroid as well as myomas in other locations, the surgeon should consider whether hysteroscopic removal of the intracavitary lesion alone can provide significant relief of all fibroid-related symptoms. In such cases, laparoscopic, robotic, or abdominal myomectomy may be preferable, especially if the volume of the additional myomas is considerable.

To determine the optimal surgical route, the physician must consider the symptoms present—is AUB the only symptom, or are other fibroid-related conditions present as well, such as bulk, pelvic pain, and other quality-of-life issues? If multiple symptoms exist, then other approaches may be better.

How fibroids affect fertility
Fibroids are present in 5% to 10% of women with infertility. In this population, fibroids are the only abnormal finding in 1.0% to 2.4% of cases.4

In a meta-analysis of 23 studies evaluating women with fibroids and infertility, Pritts and colleagues found nine studies involving submucosal fibroids.5 These studies included one randomized controlled trial, two prospective studies, and six retrospective analyses. They found that women who had fibroids with a submucosal component had lower pregnancy and implantation rates, compared with their infertile, myoma-free counterparts. Pritts and colleagues concluded that myomectomy is likely to improve fertility in these cases (TABLE).5

Instrumentation
Among the options are monopolar and bipolar resectoscopy and the mechanical approach using the Truclear System, which includes a morcellator. With conventional resectoscopy all chips must be removed, necessitating multiple insertions of the hysteroscope. Monopolar instrumentation, in particular, carries a risk of energy discharge to healthy tissue. The monopolar resectoscope also has a longer learning curve, ­compared with the mechanical approach.6

In contrast, the Truclear System requires fewer insertions, has a short learning curve, and omits the need for capture of individual chips, as the mechanical morcellator suctions and captures them throughout the procedure.7 In addition, because resection is performed mechanically, there is no risk of energy discharge to healthy tissue.

The Truclear system also is associated with a significantly shorter operative time, compared with resectoscopy, which may be advantageous for residents, fellows, and other physicians learning the procedure (­FIGURE 3).7 Shorter operative time also may result in lower fluid deficits. In addition, saline distension may reduce the risk of fluid absorption and hyponatremia. The tissue-capture feature allows evaluation of the entire pathologic specimen.

Besides hysteroscopic myomectomy, the Truclear System is appropriate for visual dilatation and curettage (D&C), adhesiolysis, polypectomy, and evacuation of retained products of conception.
 

 

FIGURE: 3 Operative time, Truclear versus resectoscopyThe Truclear approach involved significantly shorter operative time for both polypectomy and myomectomy.
 

 

Preoperative evaluation
A complete history is vital to document which fibroid-related symptoms are present and how they affect quality of life.

Preoperative imaging also is imperative—using either 2D or 3D saline infusion sonography or a combination of diagnostic hysteroscopy and transvaginal ultrasound—to select patients for hysteroscopy, anticipate blood loss, and ensure that the proper instrumentation is available at the time of surgery. Magnetic resonance imaging, computed tomography, and hysterosalpingo­graphy are either prohibitively expensive or of limited value in the initial preoperative assessment of uterine fibroids.

Any woman who has AUB and a risk for endometrial hyperplasia or cancer should undergo endometrial assessment as well.

Use of preoperative medications
In most cases, prophylactic administration of antibiotics is not warranted to prevent infection or endocarditis.

Although some clinicians give gonadotropin-releasing hormone (GnRH) agonists to reduce the size of large fibroids, the drug complicates dissection of the fibroid from the surrounding capsule. For this reason, and because we lack data demonstrating that GnRH agonists decrease blood loss and limit absorption of distension media, I do not administer them to patients.8–12 Moreover, this drug can cause vasomotor symptoms, cervical stenosis, and vaginal hemorrhage (related to estrogen flare).

GnRH agonists may be of value to stimulate transient amenorrhea for several months preoperatively in order to correct iron-deficiency anemia. Intravenous iron also can be administered during this interval.

The risk of bleeding in hysteroscopic myomectomy is 2% to 3%.1 When the ­mechanical approach is used, rather than resectoscopy, continuous flow coupled with suctioning of the chips during the procedure keeps the image clear. Post-procedure contraction of the uterus stops most bleeding. Intrauterine pressure of the pump can be increased to help tamponade any oozing.

Misoprostol. Cervical stenosis is not ­uncommon in menopausal women. It can also pose a challenge in nulliparous women. Attempting hysteroscopy in the setting of ­cervical stenosis increases the risk of ­cervical laceration, creation of a false passage, and uterine perforation. For this reason, I prescribe oral or vaginal misoprostol 200 to 400 µg nightly for 1 to 2 days before the ­procedure.

Vasopressin can reduce blood loss during hysteroscopic myomectomy when it is injected into the cervical stroma preoperatively. It also reduces absorption of ­distension fluid and facilitates cervical ­dilation.

However, vasopressin must be injected with extreme care, with aspiration to confirm the absence of blood prior to each injection, as intravascular injection can lead to bradycardia, profound hypertension, and even death.13 Always notify the anesthesiologist prior to injection when vasopressin will be administered.

I routinely use vasopressin before hysteroscopic myomectomy (0.5 mg in 20 cc of saline or 20 U in 100 cc), injecting 5 cc of the solution at 3, 6, 9, and 12 o’clock positions.

Anesthesia during hysteroscopic myomectomy typically is “monitored anesthesia care,” or MAC, which consists of local anesthesia with sedation and analgesia. The need for regional or general anesthesia is rare. Consider adding a pericervical block or intravenous ketorolac (Toradol) to provide postoperative analgesia.

Surgical technique
Strict attention to fluid management is required throughout the procedure, preferably in accordance with AAGL guidelines on the management of hysteroscopic distending media.14 With the mechanical approach, because the distension fluid is isotonic (normal saline), it does not increase the risk of hyponatremia but can cause pulmonary edema or congestive heart failure. Intravasation usually is the result of excessive operative time, treatment of deeper myometrial fibroids (Type I or II), or high intrauterine pressure. I operate using intrauterine pressure in the range of 75 to 125 mm Hg.

The steps involved in the mechanical hysteroscopy ­approach are:

 

  • Insert the hysteroscope into the uterus under direct visualization. In general, the greater the number of insertions, the greater the risk of uterine perforation. Preoperative cervical ripening helps facilitate insertion (see “Misoprostol” above).
  • Distend the uterus with saline and inspect the uterine cavity, noting again the size and location of the fibroids and whether they are sessile or pedunculated.
  • Locate the fibroid or other pathology to be removed, and place the morcellator window against it to begin cutting. Use the tip of the morcellator to elevate the fibroid for easier cutting. Enucleation is accomplished largely by varying the intrauterine pressure, which permits uterine decompression and myometrial contraction and renders the fibroid capsule more visible. If necessary, the hysteroscope can be withdrawn to stimulate myometrial ­contraction, which also helps to delineate the fibroid capsule.
  • Reinspect the uterus to rule out perforation and remove any additional intrauterine pathology with a targeted view.
  • Once all designated fibroids have been removed, withdraw the morcellator and hysteroscope from the uterus.
  • Inspect the endocervical landscape to rule out injury and other pathology.

     

 

Best practices for hysteroscopic myomectomy

 

  • Careful preoperative evaluation is important, preferably using diagnostic hysteroscopy or saline infusion sonography, to choose the optimal route of myomectomy and plan the surgical approach.
  • During the myomectomy, pay close attention to fluid management and adhere strictly to predetermined limits.
  • Complete removal of the fibroid is essential to relieve symptoms and avert the need for additional procedures.


Postoperative care
A nonsteroidal anti-inflammatory drug or limited use of narcotics usually is sufficient to relieve any postoperative cramping or vaginal discomfort.

Advise the patient to notify you in the event of increasing pain, foul-smelling vaginal discharge, or fever.

Also counsel her that she can return to most normal activities within 24 to 48 hours. Sexual activity is permissible 1 week after surgery. Early and frequent ambulation is important.

Schedule a follow-up visit 4 to 6 weeks after the procedure.

Share your thoughts on this article! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References

 

1. Perez-Medina T, Font EC, eds. Diagnostic and Operative Hysteroscopy. Tunbridge Wells, Kent, UK: Anshan Publishing; 2007:13.

2. Management of uterine fibroids: an update of the evidence. Agency for Healthcare Research and Quality. http://archive.ahrq.gov/clinic/tp/uteruptp.htm. Published July 2007. Accessed January 14, 2015.

3. Lasmar RB, Zinmei Z, Indman PD, Celeste RK, Di Spiezo Sardo A. Feasibility of a new system of classification of submucous myomas: a multicenter study. Fertil Steril. 2011;95(6):2073–2077.

4. AAGL Practice Report: practice guidelines for the diagnosis and management of submucous leiomyomas. J Minim Invasive Gynecol. 2012;19(2):152–171.

5. Pritts EA, Parker WH, Olive DL. Fibroids and infertility: an updated systematic review of the evidence. Fertil Steril. 2009;91(4):1215–1223.

6. Van Dongen H, Emanuel MH, Wolterbeek R, Trimbos JB, Jansen FW. Hysteroscopic morcellator for removal of intrauterine polyps and myomas: a randomized controlled pilot study among residents in training. J Minim Invasive Gynecol. 2008;15(4):466–471.

7. Emanuel MH, Wamsteker K. The intra uterine morcellator: a new hysteroscopic operating technique to remove intrauterine polyps and myomas. J Minim Invasive Gynecol. 2005;12(1):62–66.

8. Emanuel MH, Hart A, Wamsteker K, Lammes F. An analysis of fluid loss during transcervical resection of submucous myomas. Fertil Steril. 1997;68(5):881–886.

9. Taskin O, Sadik S, Onoglu A, et al. Role of endometrial suppression on the frequency of intrauterine adhesions after resectoscopic surgery. J Am Assoc Gynecol Laparosc. 2000;7(3):351.

10. Propst AM, Liberman RF, Harlow BL, Ginsburg ES. Complications of hysteroscopic surgery: predicting patients at risk. Obstet Gynecol. 2000;96(4):517–520.

11. Perino A, Chianchiano N, Petronio M, Cittadini E. Role of leuprolide acetate depot in hysteroscopic surgery: a controlled study. Fertil Steril. 1993;59(3):507–510.

12. Mencaglia L, Tantini C. GnRH agonist analogs and hysteroscopic resection of myomas. Int J Gynaecol Obstet. 1993;43(3):285–288.

13. Hobo R, Netsu S, Koyasu Y, Tsutsumi O. Bradycardia and cardiac arrest caused by intramyometrial injection of vasopressin during a laparoscopically assisted myomectomy. Obstet Gynecol. 2009;113(2 Pt 2):484–486.

14. Munro MD, Storz K, Abbott JA, et al; AAGL. AAGL Practice Report: practice guidelines for the management of hysteroscopic distending media. J Minim Invasive Gynecol. 2013;20(2):137–148.

References

 

1. Perez-Medina T, Font EC, eds. Diagnostic and Operative Hysteroscopy. Tunbridge Wells, Kent, UK: Anshan Publishing; 2007:13.

2. Management of uterine fibroids: an update of the evidence. Agency for Healthcare Research and Quality. http://archive.ahrq.gov/clinic/tp/uteruptp.htm. Published July 2007. Accessed January 14, 2015.

3. Lasmar RB, Zinmei Z, Indman PD, Celeste RK, Di Spiezo Sardo A. Feasibility of a new system of classification of submucous myomas: a multicenter study. Fertil Steril. 2011;95(6):2073–2077.

4. AAGL Practice Report: practice guidelines for the diagnosis and management of submucous leiomyomas. J Minim Invasive Gynecol. 2012;19(2):152–171.

5. Pritts EA, Parker WH, Olive DL. Fibroids and infertility: an updated systematic review of the evidence. Fertil Steril. 2009;91(4):1215–1223.

6. Van Dongen H, Emanuel MH, Wolterbeek R, Trimbos JB, Jansen FW. Hysteroscopic morcellator for removal of intrauterine polyps and myomas: a randomized controlled pilot study among residents in training. J Minim Invasive Gynecol. 2008;15(4):466–471.

7. Emanuel MH, Wamsteker K. The intra uterine morcellator: a new hysteroscopic operating technique to remove intrauterine polyps and myomas. J Minim Invasive Gynecol. 2005;12(1):62–66.

8. Emanuel MH, Hart A, Wamsteker K, Lammes F. An analysis of fluid loss during transcervical resection of submucous myomas. Fertil Steril. 1997;68(5):881–886.

9. Taskin O, Sadik S, Onoglu A, et al. Role of endometrial suppression on the frequency of intrauterine adhesions after resectoscopic surgery. J Am Assoc Gynecol Laparosc. 2000;7(3):351.

10. Propst AM, Liberman RF, Harlow BL, Ginsburg ES. Complications of hysteroscopic surgery: predicting patients at risk. Obstet Gynecol. 2000;96(4):517–520.

11. Perino A, Chianchiano N, Petronio M, Cittadini E. Role of leuprolide acetate depot in hysteroscopic surgery: a controlled study. Fertil Steril. 1993;59(3):507–510.

12. Mencaglia L, Tantini C. GnRH agonist analogs and hysteroscopic resection of myomas. Int J Gynaecol Obstet. 1993;43(3):285–288.

13. Hobo R, Netsu S, Koyasu Y, Tsutsumi O. Bradycardia and cardiac arrest caused by intramyometrial injection of vasopressin during a laparoscopically assisted myomectomy. Obstet Gynecol. 2009;113(2 Pt 2):484–486.

14. Munro MD, Storz K, Abbott JA, et al; AAGL. AAGL Practice Report: practice guidelines for the management of hysteroscopic distending media. J Minim Invasive Gynecol. 2013;20(2):137–148.

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Linda D. Bradley MD, hysteroscopic myomectomy, mechanical approach, resectoscopy, hysteroscope, uterine fibroids, minimally invasive gynecologic surgery, MIGS, hysterectomy, abnormal uterine bleeding, AUB, dysmenorrhea, intrauterine device, IUD, leukorrhea, pelvic pain, urinary frequency, infertility, premature labor, hormone replacement therapy, postmenopausal woman, leiomyoma, Truclear Tissue Removal System, Smith & Nephew, hysteroscopic morcellation, fluid management, European Society of Gynaecological Endoscopy, ESGE, classification of fibroids, STEP-W classification, fertility, dilatation and curettage, D&C, adhesiolysis, polypectomy, retained products of conception, 2D or 3D saline infusion sonography, transvaginal ultrasound, magnetic resonance imaging, MRI, computed tomography, CT, hysterosalpingography, antibiotics, gonadotropin-releasing hormone, GnRH, vasomotor symptoms, cervical stenosis, vaginal hemorrhage, anesthesiologist, vasopressin, misoprostol,
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Linda D. Bradley MD, hysteroscopic myomectomy, mechanical approach, resectoscopy, hysteroscope, uterine fibroids, minimally invasive gynecologic surgery, MIGS, hysterectomy, abnormal uterine bleeding, AUB, dysmenorrhea, intrauterine device, IUD, leukorrhea, pelvic pain, urinary frequency, infertility, premature labor, hormone replacement therapy, postmenopausal woman, leiomyoma, Truclear Tissue Removal System, Smith & Nephew, hysteroscopic morcellation, fluid management, European Society of Gynaecological Endoscopy, ESGE, classification of fibroids, STEP-W classification, fertility, dilatation and curettage, D&C, adhesiolysis, polypectomy, retained products of conception, 2D or 3D saline infusion sonography, transvaginal ultrasound, magnetic resonance imaging, MRI, computed tomography, CT, hysterosalpingography, antibiotics, gonadotropin-releasing hormone, GnRH, vasomotor symptoms, cervical stenosis, vaginal hemorrhage, anesthesiologist, vasopressin, misoprostol,
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Simple versus radical hysterectomy

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Simple versus radical hysterectomy

Hysterectomy is one of the fundamental surgical procedures in gynecology. Understanding the nuances of both the anatomy and the surgical dissection techniques of this procedure is especially important when approaching complex cases in either benign or oncologic settings.

This month’s surgical video contribution is by my gynecologic oncology colleagues, who highlight the key differences between the simple and radical hysterectomy. They emphasize key surgical principles for the benefit of both benign and oncologic surgeons.

The objectives of this video are to:

  • compare the surgical techniques of a simple versus radical hysterectomy
  • review the relevant anatomy as it relates to the varying types of hysterectomy
  • provide an educational review of the different types of hysterectomy.

This video does an excellent job of achieving its objectives. I hope you share it with your colleagues and residents.

 

Vidyard Video

 

 

Share your thoughts on this video! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

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Dr. George is PGY4 Resident, Department of Obstetrics and Gynecology, Columbia University Medical Center, New York, New York.

Dr. Truong is Fellow in Minimally Invasive Gynecologic Surgery, Columbia University Medical Center.

Dr. Dinkelspiel is Fellow in Gynecologic Oncology, Weill Cornell Medical College, New York, New York.

Dr. Burke is Assistant Clinical Professor, Gynecologic Oncology, Columbia University Medical Center.

Dr. Advincula is Levine Family Professor of Women’s Health, Vice-Chair, Department of Obstetrics and Gynecology, and Chief of Gynecology, Sloane Hospital for Women, Columbia University Medical Center. He also serves on the OBG Management Board of Editors.

Dr. Advincula reports being a consultant to Blue Endo, CooperSurgical, Intuitive Surgical, and SurgiQuest and receiving royalties from CooperSurgical. The other authors report no financial relationships relevant to this article.

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Erin George MD, Mireille Truong MD, Helen Dinkelspiel MD, William Burke MD, Arnold Advincula MD, minimally invasive hysterectomy, Arnold Advincula’s video series, simple versus radical hysterectomy, anatomical nuances, dissection techniques, gynecologic oncology,
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Dr. George is PGY4 Resident, Department of Obstetrics and Gynecology, Columbia University Medical Center, New York, New York.

Dr. Truong is Fellow in Minimally Invasive Gynecologic Surgery, Columbia University Medical Center.

Dr. Dinkelspiel is Fellow in Gynecologic Oncology, Weill Cornell Medical College, New York, New York.

Dr. Burke is Assistant Clinical Professor, Gynecologic Oncology, Columbia University Medical Center.

Dr. Advincula is Levine Family Professor of Women’s Health, Vice-Chair, Department of Obstetrics and Gynecology, and Chief of Gynecology, Sloane Hospital for Women, Columbia University Medical Center. He also serves on the OBG Management Board of Editors.

Dr. Advincula reports being a consultant to Blue Endo, CooperSurgical, Intuitive Surgical, and SurgiQuest and receiving royalties from CooperSurgical. The other authors report no financial relationships relevant to this article.

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Dr. George is PGY4 Resident, Department of Obstetrics and Gynecology, Columbia University Medical Center, New York, New York.

Dr. Truong is Fellow in Minimally Invasive Gynecologic Surgery, Columbia University Medical Center.

Dr. Dinkelspiel is Fellow in Gynecologic Oncology, Weill Cornell Medical College, New York, New York.

Dr. Burke is Assistant Clinical Professor, Gynecologic Oncology, Columbia University Medical Center.

Dr. Advincula is Levine Family Professor of Women’s Health, Vice-Chair, Department of Obstetrics and Gynecology, and Chief of Gynecology, Sloane Hospital for Women, Columbia University Medical Center. He also serves on the OBG Management Board of Editors.

Dr. Advincula reports being a consultant to Blue Endo, CooperSurgical, Intuitive Surgical, and SurgiQuest and receiving royalties from CooperSurgical. The other authors report no financial relationships relevant to this article.

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Related Articles

Hysterectomy is one of the fundamental surgical procedures in gynecology. Understanding the nuances of both the anatomy and the surgical dissection techniques of this procedure is especially important when approaching complex cases in either benign or oncologic settings.

This month’s surgical video contribution is by my gynecologic oncology colleagues, who highlight the key differences between the simple and radical hysterectomy. They emphasize key surgical principles for the benefit of both benign and oncologic surgeons.

The objectives of this video are to:

  • compare the surgical techniques of a simple versus radical hysterectomy
  • review the relevant anatomy as it relates to the varying types of hysterectomy
  • provide an educational review of the different types of hysterectomy.

This video does an excellent job of achieving its objectives. I hope you share it with your colleagues and residents.

 

Vidyard Video

 

 

Share your thoughts on this video! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Hysterectomy is one of the fundamental surgical procedures in gynecology. Understanding the nuances of both the anatomy and the surgical dissection techniques of this procedure is especially important when approaching complex cases in either benign or oncologic settings.

This month’s surgical video contribution is by my gynecologic oncology colleagues, who highlight the key differences between the simple and radical hysterectomy. They emphasize key surgical principles for the benefit of both benign and oncologic surgeons.

The objectives of this video are to:

  • compare the surgical techniques of a simple versus radical hysterectomy
  • review the relevant anatomy as it relates to the varying types of hysterectomy
  • provide an educational review of the different types of hysterectomy.

This video does an excellent job of achieving its objectives. I hope you share it with your colleagues and residents.

 

Vidyard Video

 

 

Share your thoughts on this video! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

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Simple versus radical hysterectomy
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Erin George MD, Mireille Truong MD, Helen Dinkelspiel MD, William Burke MD, Arnold Advincula MD, minimally invasive hysterectomy, Arnold Advincula’s video series, simple versus radical hysterectomy, anatomical nuances, dissection techniques, gynecologic oncology,
Legacy Keywords
Erin George MD, Mireille Truong MD, Helen Dinkelspiel MD, William Burke MD, Arnold Advincula MD, minimally invasive hysterectomy, Arnold Advincula’s video series, simple versus radical hysterectomy, anatomical nuances, dissection techniques, gynecologic oncology,
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LITHOTOMY STIRRUPS FOR PATIENT COMFORT
Frontier Medical Innovations says its new GStirrup® is designed to provide patients stable and comfortable foot positioning for extended periods of time during office-based surgical procedures. The GStirrup is a pair of cushioned lithotomy boots that attach to examination-table foot rests. Straps secure the patient’s feet and legs; weights in the base make it difficult for the patient to lift the boot off the footrest. GStirrups fit most footrests and are helpful for patients who have hip or knee replacement, low back pain, arthritis, or neurologic conditions such as multiple sclerosis or Parkinson’s disease.
FOR MORE INFORMATION, VISIT www.gstirrup.com

PREGNANCY, BIRTH, AND BREASTFEEDING APP
Totally Pregnant, an app for pregnant women and health-care providers, is now partnering with Lamaze International to provide access to online parenting classes for pregnancy, childbirth, and early parenting. By using the Totally Pregnant app, women can personalize their pregnancy experience and clinicians can connect with their patients. Available for iPhone, iPad, Android, and desktop.
FOR MORE INFORMATION, VISIT www.iamtotally.com

PREDICTING IVF SUCCESS
Univfy®offers fertility predictive analytics to help prospective parents understand the probability for the success of in vitro fertilization (IVF) and estimated costs. The PreIVF™ calculator helps to decide whether or when to start IVF; the PredictIVF™ helps determine if another IVF cycle is the right option. The IVF Cost Calculator offers a cost comparison tailored to the patient’s IVF success rate. Your Fertility™ is an interactive multimedia blog offering educational material.
FOR MORE INFORMATION, VISIT www.univfy.com

SECURE WAY TO CARRY MEDS
FusionWrap is a waist/hip wrap with two 7-inch pockets to carry small personal belongings. Besides providing secure space for identification and money, it also allows those with asthma, diabetes, allergies, or other chronic diseases to carry medications at all times. Made of stretch fabric that is moisture wicking and antimicrobial, FusionWrap comes in various colors and sizes for women, men, and children.
FOR MORE INFORMATION, VISIT www.fusion-wrap.com

BREAST IMAGING TOOLS
Volpara Solutions offers multiple volumetric breast-imaging software tools designed to improve clinical decision making and the early detection of breast cancer. Volpara®Density™ is a breast-density assessment tool available for clinical use with 2D mammography  and digital breast tomosynthesis (3D mammography) platforms from multiple manufacturers.
FOR MORE INFORMATION, VISIT www.volparadensity.com

SMOKE EVACUATION PENCIL
The PlumePen® Elite is an electrosurgical smoke pencil with a compact, ergonomic design that is smaller but offers more flow than competitive smoke pencils, claims Buffalo Filter. The adjustable capture port allows for optimum visibility regardless of blade length. The one-piece molded design prevents buttons from sticking and improves grip. The PlumePen Elite connects to most surgical plume evacuators and generators.
FOR MORE INFORMATION, VISIT www.buffalofilter.com

SURGICAL CO2 LASER
Lumenis designed the AcuPulse Smart CO2 Laser with SurgiTouch Automation System for tissue ablation during gynecologic surgery to increase speed, precision, and convenience over other electrosurgical devices. Robotic, computer-controlled laser-beam movement provides more precision than hand-held lasers and offers reproducible outcomes. Brief laser-tissue interaction reduces thermal damage.
FOR MORE INFORMATION, VISIT www.lumenis.com

REUSABLE FORNIX FOR LAP HYSTERECTOMY
The Banyan Colpo-Port Vaginal Fornix Delineator is a reusable uterine elevator/vaginal fornix delineator for laparoscopic hysterectomy. Inserted vaginally, the distal tip has a canted, beveled cup that fits securely in the vaginal fornix. The Calibrated Uterine Elevator (CUE) passes through the inner diameter of the delineator body, through the cervix, and into the uterine cavity. The CUE can be locked at preset depths to prevent uterine perforation. The device is easy to clean using standard sterilization procedures.
FOR MORE INFORMATION, VISIT www.banyanmedllc.com

OVARIAN MALIGNANCY ALGORITHM
The Risk of Ovarian Malignancy Algorithm (ROMA) from Fujirebio is a quantitative serum test intended to assess the risk of finding malignancy at surgery in a premenopausal or postmenopausal woman with an ovarian mass. ROMA, a risk stratification tool, combines the results of human epididymis protein 4 (HE4), cancer antigen 125 (CA125), and menopausal status into a numerical score.
FOR MORE INFORMATION, VISIT www.he4test.com

PORT-SITE CLOSURE DEVICE
neoClose® AnchorGuide facilitates rapid trocar exchange and precise AutoAnchor placement to help prevent port-site hernia. The AnchorGuide design facilitates the delivery of absorbable AutoAnchors through soft tissue during surgery; allows for the VectorX method of port approximation for reduced tension at wound sites; and helps desufflate to remove CO2 at the end of surgery. AnchorGuide comes in 8–15 mm and 5–12 mm sizes compatible with 8 mm robotic ports.
FOR MORE INFORMATION, VISIT www.neosurgical.com

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OBG Management - 27(2)
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49
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Frontier Medical Innovations, GStirrup, lithotomy stirrups, Totally Pregnant, Lamaze International, pregnancy, childbirth, breastfeeding, IVF, Univfy, PreIVF Calculator, Predict IVF, IVF Cost Calculator, Your Fertility, FusionWrap, Volpara Solutions, VolparaDensity, mammography, digital breast tomosynthesis, smoke evacuation pencil, PlumePen Elite, Buffalo Filter, Lumenis, AcuPulse Smart CO2 laser, SurgiTouch Automation System, tissue ablation, Banyan Colpo-Port Vaginal Fornix Delineator, ROMA, Risk of Ovarian Malignancy Algorithm, Fujirebio, neoClose Anchor Guide, AutoAnchor, VectorX, NeoSurgical,
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LITHOTOMY STIRRUPS FOR PATIENT COMFORT
Frontier Medical Innovations says its new GStirrup® is designed to provide patients stable and comfortable foot positioning for extended periods of time during office-based surgical procedures. The GStirrup is a pair of cushioned lithotomy boots that attach to examination-table foot rests. Straps secure the patient’s feet and legs; weights in the base make it difficult for the patient to lift the boot off the footrest. GStirrups fit most footrests and are helpful for patients who have hip or knee replacement, low back pain, arthritis, or neurologic conditions such as multiple sclerosis or Parkinson’s disease.
FOR MORE INFORMATION, VISIT www.gstirrup.com

PREGNANCY, BIRTH, AND BREASTFEEDING APP
Totally Pregnant, an app for pregnant women and health-care providers, is now partnering with Lamaze International to provide access to online parenting classes for pregnancy, childbirth, and early parenting. By using the Totally Pregnant app, women can personalize their pregnancy experience and clinicians can connect with their patients. Available for iPhone, iPad, Android, and desktop.
FOR MORE INFORMATION, VISIT www.iamtotally.com

PREDICTING IVF SUCCESS
Univfy®offers fertility predictive analytics to help prospective parents understand the probability for the success of in vitro fertilization (IVF) and estimated costs. The PreIVF™ calculator helps to decide whether or when to start IVF; the PredictIVF™ helps determine if another IVF cycle is the right option. The IVF Cost Calculator offers a cost comparison tailored to the patient’s IVF success rate. Your Fertility™ is an interactive multimedia blog offering educational material.
FOR MORE INFORMATION, VISIT www.univfy.com

SECURE WAY TO CARRY MEDS
FusionWrap is a waist/hip wrap with two 7-inch pockets to carry small personal belongings. Besides providing secure space for identification and money, it also allows those with asthma, diabetes, allergies, or other chronic diseases to carry medications at all times. Made of stretch fabric that is moisture wicking and antimicrobial, FusionWrap comes in various colors and sizes for women, men, and children.
FOR MORE INFORMATION, VISIT www.fusion-wrap.com

BREAST IMAGING TOOLS
Volpara Solutions offers multiple volumetric breast-imaging software tools designed to improve clinical decision making and the early detection of breast cancer. Volpara®Density™ is a breast-density assessment tool available for clinical use with 2D mammography  and digital breast tomosynthesis (3D mammography) platforms from multiple manufacturers.
FOR MORE INFORMATION, VISIT www.volparadensity.com

SMOKE EVACUATION PENCIL
The PlumePen® Elite is an electrosurgical smoke pencil with a compact, ergonomic design that is smaller but offers more flow than competitive smoke pencils, claims Buffalo Filter. The adjustable capture port allows for optimum visibility regardless of blade length. The one-piece molded design prevents buttons from sticking and improves grip. The PlumePen Elite connects to most surgical plume evacuators and generators.
FOR MORE INFORMATION, VISIT www.buffalofilter.com

SURGICAL CO2 LASER
Lumenis designed the AcuPulse Smart CO2 Laser with SurgiTouch Automation System for tissue ablation during gynecologic surgery to increase speed, precision, and convenience over other electrosurgical devices. Robotic, computer-controlled laser-beam movement provides more precision than hand-held lasers and offers reproducible outcomes. Brief laser-tissue interaction reduces thermal damage.
FOR MORE INFORMATION, VISIT www.lumenis.com

REUSABLE FORNIX FOR LAP HYSTERECTOMY
The Banyan Colpo-Port Vaginal Fornix Delineator is a reusable uterine elevator/vaginal fornix delineator for laparoscopic hysterectomy. Inserted vaginally, the distal tip has a canted, beveled cup that fits securely in the vaginal fornix. The Calibrated Uterine Elevator (CUE) passes through the inner diameter of the delineator body, through the cervix, and into the uterine cavity. The CUE can be locked at preset depths to prevent uterine perforation. The device is easy to clean using standard sterilization procedures.
FOR MORE INFORMATION, VISIT www.banyanmedllc.com

OVARIAN MALIGNANCY ALGORITHM
The Risk of Ovarian Malignancy Algorithm (ROMA) from Fujirebio is a quantitative serum test intended to assess the risk of finding malignancy at surgery in a premenopausal or postmenopausal woman with an ovarian mass. ROMA, a risk stratification tool, combines the results of human epididymis protein 4 (HE4), cancer antigen 125 (CA125), and menopausal status into a numerical score.
FOR MORE INFORMATION, VISIT www.he4test.com

PORT-SITE CLOSURE DEVICE
neoClose® AnchorGuide facilitates rapid trocar exchange and precise AutoAnchor placement to help prevent port-site hernia. The AnchorGuide design facilitates the delivery of absorbable AutoAnchors through soft tissue during surgery; allows for the VectorX method of port approximation for reduced tension at wound sites; and helps desufflate to remove CO2 at the end of surgery. AnchorGuide comes in 8–15 mm and 5–12 mm sizes compatible with 8 mm robotic ports.
FOR MORE INFORMATION, VISIT www.neosurgical.com

LITHOTOMY STIRRUPS FOR PATIENT COMFORT
Frontier Medical Innovations says its new GStirrup® is designed to provide patients stable and comfortable foot positioning for extended periods of time during office-based surgical procedures. The GStirrup is a pair of cushioned lithotomy boots that attach to examination-table foot rests. Straps secure the patient’s feet and legs; weights in the base make it difficult for the patient to lift the boot off the footrest. GStirrups fit most footrests and are helpful for patients who have hip or knee replacement, low back pain, arthritis, or neurologic conditions such as multiple sclerosis or Parkinson’s disease.
FOR MORE INFORMATION, VISIT www.gstirrup.com

PREGNANCY, BIRTH, AND BREASTFEEDING APP
Totally Pregnant, an app for pregnant women and health-care providers, is now partnering with Lamaze International to provide access to online parenting classes for pregnancy, childbirth, and early parenting. By using the Totally Pregnant app, women can personalize their pregnancy experience and clinicians can connect with their patients. Available for iPhone, iPad, Android, and desktop.
FOR MORE INFORMATION, VISIT www.iamtotally.com

PREDICTING IVF SUCCESS
Univfy®offers fertility predictive analytics to help prospective parents understand the probability for the success of in vitro fertilization (IVF) and estimated costs. The PreIVF™ calculator helps to decide whether or when to start IVF; the PredictIVF™ helps determine if another IVF cycle is the right option. The IVF Cost Calculator offers a cost comparison tailored to the patient’s IVF success rate. Your Fertility™ is an interactive multimedia blog offering educational material.
FOR MORE INFORMATION, VISIT www.univfy.com

SECURE WAY TO CARRY MEDS
FusionWrap is a waist/hip wrap with two 7-inch pockets to carry small personal belongings. Besides providing secure space for identification and money, it also allows those with asthma, diabetes, allergies, or other chronic diseases to carry medications at all times. Made of stretch fabric that is moisture wicking and antimicrobial, FusionWrap comes in various colors and sizes for women, men, and children.
FOR MORE INFORMATION, VISIT www.fusion-wrap.com

BREAST IMAGING TOOLS
Volpara Solutions offers multiple volumetric breast-imaging software tools designed to improve clinical decision making and the early detection of breast cancer. Volpara®Density™ is a breast-density assessment tool available for clinical use with 2D mammography  and digital breast tomosynthesis (3D mammography) platforms from multiple manufacturers.
FOR MORE INFORMATION, VISIT www.volparadensity.com

SMOKE EVACUATION PENCIL
The PlumePen® Elite is an electrosurgical smoke pencil with a compact, ergonomic design that is smaller but offers more flow than competitive smoke pencils, claims Buffalo Filter. The adjustable capture port allows for optimum visibility regardless of blade length. The one-piece molded design prevents buttons from sticking and improves grip. The PlumePen Elite connects to most surgical plume evacuators and generators.
FOR MORE INFORMATION, VISIT www.buffalofilter.com

SURGICAL CO2 LASER
Lumenis designed the AcuPulse Smart CO2 Laser with SurgiTouch Automation System for tissue ablation during gynecologic surgery to increase speed, precision, and convenience over other electrosurgical devices. Robotic, computer-controlled laser-beam movement provides more precision than hand-held lasers and offers reproducible outcomes. Brief laser-tissue interaction reduces thermal damage.
FOR MORE INFORMATION, VISIT www.lumenis.com

REUSABLE FORNIX FOR LAP HYSTERECTOMY
The Banyan Colpo-Port Vaginal Fornix Delineator is a reusable uterine elevator/vaginal fornix delineator for laparoscopic hysterectomy. Inserted vaginally, the distal tip has a canted, beveled cup that fits securely in the vaginal fornix. The Calibrated Uterine Elevator (CUE) passes through the inner diameter of the delineator body, through the cervix, and into the uterine cavity. The CUE can be locked at preset depths to prevent uterine perforation. The device is easy to clean using standard sterilization procedures.
FOR MORE INFORMATION, VISIT www.banyanmedllc.com

OVARIAN MALIGNANCY ALGORITHM
The Risk of Ovarian Malignancy Algorithm (ROMA) from Fujirebio is a quantitative serum test intended to assess the risk of finding malignancy at surgery in a premenopausal or postmenopausal woman with an ovarian mass. ROMA, a risk stratification tool, combines the results of human epididymis protein 4 (HE4), cancer antigen 125 (CA125), and menopausal status into a numerical score.
FOR MORE INFORMATION, VISIT www.he4test.com

PORT-SITE CLOSURE DEVICE
neoClose® AnchorGuide facilitates rapid trocar exchange and precise AutoAnchor placement to help prevent port-site hernia. The AnchorGuide design facilitates the delivery of absorbable AutoAnchors through soft tissue during surgery; allows for the VectorX method of port approximation for reduced tension at wound sites; and helps desufflate to remove CO2 at the end of surgery. AnchorGuide comes in 8–15 mm and 5–12 mm sizes compatible with 8 mm robotic ports.
FOR MORE INFORMATION, VISIT www.neosurgical.com

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OBG Management - 27(2)
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Frontier Medical Innovations, GStirrup, lithotomy stirrups, Totally Pregnant, Lamaze International, pregnancy, childbirth, breastfeeding, IVF, Univfy, PreIVF Calculator, Predict IVF, IVF Cost Calculator, Your Fertility, FusionWrap, Volpara Solutions, VolparaDensity, mammography, digital breast tomosynthesis, smoke evacuation pencil, PlumePen Elite, Buffalo Filter, Lumenis, AcuPulse Smart CO2 laser, SurgiTouch Automation System, tissue ablation, Banyan Colpo-Port Vaginal Fornix Delineator, ROMA, Risk of Ovarian Malignancy Algorithm, Fujirebio, neoClose Anchor Guide, AutoAnchor, VectorX, NeoSurgical,
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Frontier Medical Innovations, GStirrup, lithotomy stirrups, Totally Pregnant, Lamaze International, pregnancy, childbirth, breastfeeding, IVF, Univfy, PreIVF Calculator, Predict IVF, IVF Cost Calculator, Your Fertility, FusionWrap, Volpara Solutions, VolparaDensity, mammography, digital breast tomosynthesis, smoke evacuation pencil, PlumePen Elite, Buffalo Filter, Lumenis, AcuPulse Smart CO2 laser, SurgiTouch Automation System, tissue ablation, Banyan Colpo-Port Vaginal Fornix Delineator, ROMA, Risk of Ovarian Malignancy Algorithm, Fujirebio, neoClose Anchor Guide, AutoAnchor, VectorX, NeoSurgical,
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RBC transfusions during CABG increase risk of pneumonia

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RBC transfusions during CABG increase risk of pneumonia

Blood for transfusion

Credit: Elise Amendola

SAN DIEGO—Patients who receive red blood cell (RBC) transfusions during coronary artery bypass grafting (CABG) surgery are at an increased risk of

developing pneumonia, according to research presented at the 51st Annual Meeting of The Society of Thoracic Surgeons.

And the risk appears to increase with the volume of RBCs transfused. Patients who received 6 or more units had a 14 times higher risk of developing pneumonia than their untransfused peers.

“Pneumonia is a known risk following CABG surgery, and developing it has been shown to significantly increase a patient’s risk of morbidity and mortality,” said study investigator Donald S. Likosky, PhD, of the University of Michigan Health System in Ann Arbor.

“Previous research has shown that 1 in every 20 CABG patients develop a major infection, with pneumonia being the most common type of infection.”

For this study, Dr Liksoky and his colleagues examined data on 16,182 patients who underwent CABG between 2011 and 2013 at any of the 33 hospitals participating in the Michigan Society of Thoracic and Cardiovascular Surgeons Quality Collaborative.

They used propensity scoring to match the 4585 patients (32.3%) who received RBCs to the 9612 who did not (total=14,197). The team matched patients based on age, sex, body mass index, history of smoking, congestive heart failure, chronic obstructive pulmonary disease, diabetes, prior cardiac surgery, vascular disease, ejection fraction, preoperative hematocrit, and preoperative pneumonia.

The researchers then calculated adjusted odds ratios (ORs) reflecting the association between the number of RBC units transfused (0 to 6+) and postoperative pneumonia.

In all, 450 patients (3.2%) developed pneumonia. And the analysis revealed a significant association between any RBC transfusion and pneumonia (OR=4.0, P<0.001), as well as associations between the number of units transfused and the odds of developing pneumonia.

The OR was 1.6 (P=0.02) for patients who received 1 RBC unit, 2.1 for those who received 2 units (P<0.001), 4.9 for those who received 3 units (P<0.001), 5.5 for those who received 4 units (P<0.001), 8.9 for those who received 5 units (P<0.001), and 14.4 for patients who received 6 or more units (P<0.001).

“The ability to store and transfuse blood is one of medicine’s greatest accomplishments, but we are continuing to see that receiving a blood transfusion may alter a patient’s ability to fight infection,” said James R. Edgerton, MD, from The Heart Hospital Baylor Plano in Texas, who was not affiliated with this study.

“In their study, Dr Likosky and colleagues have identified an increased risk of pneumonia after transfusion, which is an important breakthrough because it allows physicians to remain vigilant for the onset of pneumonia and initiate therapy early in hopes of shortening its course and severity. It also enables physicians to initiate preventive therapies in patients who have been transfused, which will contribute to better care of our patients.”

“Patients should receive red blood cell transfusions based on clinical need,” Dr Likosky added. “Surgical teams may have opportunities to reduce the need for transfusions among patients, thereby reducing the risk of secondary complications.”

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SAN DIEGO—Patients who receive red blood cell (RBC) transfusions during coronary artery bypass grafting (CABG) surgery are at an increased risk of

developing pneumonia, according to research presented at the 51st Annual Meeting of The Society of Thoracic Surgeons.

And the risk appears to increase with the volume of RBCs transfused. Patients who received 6 or more units had a 14 times higher risk of developing pneumonia than their untransfused peers.

“Pneumonia is a known risk following CABG surgery, and developing it has been shown to significantly increase a patient’s risk of morbidity and mortality,” said study investigator Donald S. Likosky, PhD, of the University of Michigan Health System in Ann Arbor.

“Previous research has shown that 1 in every 20 CABG patients develop a major infection, with pneumonia being the most common type of infection.”

For this study, Dr Liksoky and his colleagues examined data on 16,182 patients who underwent CABG between 2011 and 2013 at any of the 33 hospitals participating in the Michigan Society of Thoracic and Cardiovascular Surgeons Quality Collaborative.

They used propensity scoring to match the 4585 patients (32.3%) who received RBCs to the 9612 who did not (total=14,197). The team matched patients based on age, sex, body mass index, history of smoking, congestive heart failure, chronic obstructive pulmonary disease, diabetes, prior cardiac surgery, vascular disease, ejection fraction, preoperative hematocrit, and preoperative pneumonia.

The researchers then calculated adjusted odds ratios (ORs) reflecting the association between the number of RBC units transfused (0 to 6+) and postoperative pneumonia.

In all, 450 patients (3.2%) developed pneumonia. And the analysis revealed a significant association between any RBC transfusion and pneumonia (OR=4.0, P<0.001), as well as associations between the number of units transfused and the odds of developing pneumonia.

The OR was 1.6 (P=0.02) for patients who received 1 RBC unit, 2.1 for those who received 2 units (P<0.001), 4.9 for those who received 3 units (P<0.001), 5.5 for those who received 4 units (P<0.001), 8.9 for those who received 5 units (P<0.001), and 14.4 for patients who received 6 or more units (P<0.001).

“The ability to store and transfuse blood is one of medicine’s greatest accomplishments, but we are continuing to see that receiving a blood transfusion may alter a patient’s ability to fight infection,” said James R. Edgerton, MD, from The Heart Hospital Baylor Plano in Texas, who was not affiliated with this study.

“In their study, Dr Likosky and colleagues have identified an increased risk of pneumonia after transfusion, which is an important breakthrough because it allows physicians to remain vigilant for the onset of pneumonia and initiate therapy early in hopes of shortening its course and severity. It also enables physicians to initiate preventive therapies in patients who have been transfused, which will contribute to better care of our patients.”

“Patients should receive red blood cell transfusions based on clinical need,” Dr Likosky added. “Surgical teams may have opportunities to reduce the need for transfusions among patients, thereby reducing the risk of secondary complications.”

Blood for transfusion

Credit: Elise Amendola

SAN DIEGO—Patients who receive red blood cell (RBC) transfusions during coronary artery bypass grafting (CABG) surgery are at an increased risk of

developing pneumonia, according to research presented at the 51st Annual Meeting of The Society of Thoracic Surgeons.

And the risk appears to increase with the volume of RBCs transfused. Patients who received 6 or more units had a 14 times higher risk of developing pneumonia than their untransfused peers.

“Pneumonia is a known risk following CABG surgery, and developing it has been shown to significantly increase a patient’s risk of morbidity and mortality,” said study investigator Donald S. Likosky, PhD, of the University of Michigan Health System in Ann Arbor.

“Previous research has shown that 1 in every 20 CABG patients develop a major infection, with pneumonia being the most common type of infection.”

For this study, Dr Liksoky and his colleagues examined data on 16,182 patients who underwent CABG between 2011 and 2013 at any of the 33 hospitals participating in the Michigan Society of Thoracic and Cardiovascular Surgeons Quality Collaborative.

They used propensity scoring to match the 4585 patients (32.3%) who received RBCs to the 9612 who did not (total=14,197). The team matched patients based on age, sex, body mass index, history of smoking, congestive heart failure, chronic obstructive pulmonary disease, diabetes, prior cardiac surgery, vascular disease, ejection fraction, preoperative hematocrit, and preoperative pneumonia.

The researchers then calculated adjusted odds ratios (ORs) reflecting the association between the number of RBC units transfused (0 to 6+) and postoperative pneumonia.

In all, 450 patients (3.2%) developed pneumonia. And the analysis revealed a significant association between any RBC transfusion and pneumonia (OR=4.0, P<0.001), as well as associations between the number of units transfused and the odds of developing pneumonia.

The OR was 1.6 (P=0.02) for patients who received 1 RBC unit, 2.1 for those who received 2 units (P<0.001), 4.9 for those who received 3 units (P<0.001), 5.5 for those who received 4 units (P<0.001), 8.9 for those who received 5 units (P<0.001), and 14.4 for patients who received 6 or more units (P<0.001).

“The ability to store and transfuse blood is one of medicine’s greatest accomplishments, but we are continuing to see that receiving a blood transfusion may alter a patient’s ability to fight infection,” said James R. Edgerton, MD, from The Heart Hospital Baylor Plano in Texas, who was not affiliated with this study.

“In their study, Dr Likosky and colleagues have identified an increased risk of pneumonia after transfusion, which is an important breakthrough because it allows physicians to remain vigilant for the onset of pneumonia and initiate therapy early in hopes of shortening its course and severity. It also enables physicians to initiate preventive therapies in patients who have been transfused, which will contribute to better care of our patients.”

“Patients should receive red blood cell transfusions based on clinical need,” Dr Likosky added. “Surgical teams may have opportunities to reduce the need for transfusions among patients, thereby reducing the risk of secondary complications.”

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Most cardiologists misstep on aspirin in ACS

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SNOWMASS, COLO. – U.S. cardiologists are glaringly out of touch with the guidelines on maintenance aspirin dosing in patients with acute coronary syndrome, American College of Cardiology President Dr. Patrick T. O’Gara said at the Annual Cardiovascular Conference at Snowmass.

The latest AHA/ACC guidelines state that maintenance aspirin therapy at 81 mg/day to be continued indefinitely is preferred over 325 mg/day in patients with ACS, regardless of whether they have received a coronary stent or noninvasive medical management (Circulation 2014 Dec 23;130(25):e344-426).

Dr. Patrick T. O'Gara

“This statement has been out there in the guidelines for several years now. Yet the last time we interrogated the NCDR [National Cardiovascular Data Registry], 70% of patients with ACS were discharged on 325 mg/day of aspirin in the U.S.,” said Dr. O’Gara, professor of medicine at Harvard Medical School and director of clinical cardiology at Brigham and Women’s Hospital, Boston.

The recommendation in the guidelines is based on several solid studies, including OASIS 7, which in more than 25,000 randomized patients showed no difference in outcomes when aspirin at 75-100 mg/day was compared with 300-325 mg/day, but an increased incidence of bleeding at the higher dose (N. Engl. J. Med. 2010;363:930-42).

“Aspirin at 81 mg/day is not inferior with respect to clinical efficacy and it’s superior with respect to its safety outcome. But here in the United States we are still very much wedded to using 325 mg of aspirin. I’m not exactly sure of the reasons for that. Maybe it’s a catch up phenomenon,” Dr. O’Gara commented.

In the setting of percutaneous coronary intervention with a bare metal or drug-eluting stent for patients with either non–ST-elevation ACS or ST-elevation MI, the AHA/ACC guidelines give a class I recommendation for at least 12 months of dual-antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor. Either ticagrelor (Brilinta) at 90 mg twice daily or prasugrel (Effient) once daily at 10 mg is recommended over clopidogrel at 75 mg/day in patients who can take those medications safely; this guidance is based on ticagrelor’s superior efficacy compared with clopidogrel as shown in TRITON TIMI-38 (N. Engl. J. Med. 2007;357:2001-15) and prasugrel’s superiority in the PLATO trial (N. Engl. J. Med. 2009;361:1045-57).

The AHA/ACC guidelines give a relatively tepid level IIb recommendation that continuation of DAPT beyond 12 months may be considered in stent recipients. Many observers expect a stronger endorsement in the next iteration of the guidelines on the strength of the recent DAPT study, which showed that 30 months of DAPT was better than 12 in terms of major adverse cardiac and cerebrovascular events (N. Engl. J. Med. 2014;371:2155-66).

“Interestingly enough, the mechanism of benefit had less to do with prevention of stent thrombosis than it did with prevention of recurrent MI and stroke. This renders into much sharper focus the question of whether we’re treating the patient or we’re treating the stent. This result would imply that we’re treating the patient,” Dr. O’Gara observed.

The guidelines also include a bail-out option which states that if the risk of bleeding outweighs the anticipated benefit, it’s reasonable to discontinue DAPT before 12 months.

“I don’t know a single practitioner who’s not had to withdraw one or both elements of DAPT because of bleeding or because of the need for unanticipated noncardiac surgery. It’s a fact of life, and sometimes you have to just hope for the best,” the cardiologist said.

He reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

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SNOWMASS, COLO. – U.S. cardiologists are glaringly out of touch with the guidelines on maintenance aspirin dosing in patients with acute coronary syndrome, American College of Cardiology President Dr. Patrick T. O’Gara said at the Annual Cardiovascular Conference at Snowmass.

The latest AHA/ACC guidelines state that maintenance aspirin therapy at 81 mg/day to be continued indefinitely is preferred over 325 mg/day in patients with ACS, regardless of whether they have received a coronary stent or noninvasive medical management (Circulation 2014 Dec 23;130(25):e344-426).

Dr. Patrick T. O'Gara

“This statement has been out there in the guidelines for several years now. Yet the last time we interrogated the NCDR [National Cardiovascular Data Registry], 70% of patients with ACS were discharged on 325 mg/day of aspirin in the U.S.,” said Dr. O’Gara, professor of medicine at Harvard Medical School and director of clinical cardiology at Brigham and Women’s Hospital, Boston.

The recommendation in the guidelines is based on several solid studies, including OASIS 7, which in more than 25,000 randomized patients showed no difference in outcomes when aspirin at 75-100 mg/day was compared with 300-325 mg/day, but an increased incidence of bleeding at the higher dose (N. Engl. J. Med. 2010;363:930-42).

“Aspirin at 81 mg/day is not inferior with respect to clinical efficacy and it’s superior with respect to its safety outcome. But here in the United States we are still very much wedded to using 325 mg of aspirin. I’m not exactly sure of the reasons for that. Maybe it’s a catch up phenomenon,” Dr. O’Gara commented.

In the setting of percutaneous coronary intervention with a bare metal or drug-eluting stent for patients with either non–ST-elevation ACS or ST-elevation MI, the AHA/ACC guidelines give a class I recommendation for at least 12 months of dual-antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor. Either ticagrelor (Brilinta) at 90 mg twice daily or prasugrel (Effient) once daily at 10 mg is recommended over clopidogrel at 75 mg/day in patients who can take those medications safely; this guidance is based on ticagrelor’s superior efficacy compared with clopidogrel as shown in TRITON TIMI-38 (N. Engl. J. Med. 2007;357:2001-15) and prasugrel’s superiority in the PLATO trial (N. Engl. J. Med. 2009;361:1045-57).

The AHA/ACC guidelines give a relatively tepid level IIb recommendation that continuation of DAPT beyond 12 months may be considered in stent recipients. Many observers expect a stronger endorsement in the next iteration of the guidelines on the strength of the recent DAPT study, which showed that 30 months of DAPT was better than 12 in terms of major adverse cardiac and cerebrovascular events (N. Engl. J. Med. 2014;371:2155-66).

“Interestingly enough, the mechanism of benefit had less to do with prevention of stent thrombosis than it did with prevention of recurrent MI and stroke. This renders into much sharper focus the question of whether we’re treating the patient or we’re treating the stent. This result would imply that we’re treating the patient,” Dr. O’Gara observed.

The guidelines also include a bail-out option which states that if the risk of bleeding outweighs the anticipated benefit, it’s reasonable to discontinue DAPT before 12 months.

“I don’t know a single practitioner who’s not had to withdraw one or both elements of DAPT because of bleeding or because of the need for unanticipated noncardiac surgery. It’s a fact of life, and sometimes you have to just hope for the best,” the cardiologist said.

He reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

SNOWMASS, COLO. – U.S. cardiologists are glaringly out of touch with the guidelines on maintenance aspirin dosing in patients with acute coronary syndrome, American College of Cardiology President Dr. Patrick T. O’Gara said at the Annual Cardiovascular Conference at Snowmass.

The latest AHA/ACC guidelines state that maintenance aspirin therapy at 81 mg/day to be continued indefinitely is preferred over 325 mg/day in patients with ACS, regardless of whether they have received a coronary stent or noninvasive medical management (Circulation 2014 Dec 23;130(25):e344-426).

Dr. Patrick T. O'Gara

“This statement has been out there in the guidelines for several years now. Yet the last time we interrogated the NCDR [National Cardiovascular Data Registry], 70% of patients with ACS were discharged on 325 mg/day of aspirin in the U.S.,” said Dr. O’Gara, professor of medicine at Harvard Medical School and director of clinical cardiology at Brigham and Women’s Hospital, Boston.

The recommendation in the guidelines is based on several solid studies, including OASIS 7, which in more than 25,000 randomized patients showed no difference in outcomes when aspirin at 75-100 mg/day was compared with 300-325 mg/day, but an increased incidence of bleeding at the higher dose (N. Engl. J. Med. 2010;363:930-42).

“Aspirin at 81 mg/day is not inferior with respect to clinical efficacy and it’s superior with respect to its safety outcome. But here in the United States we are still very much wedded to using 325 mg of aspirin. I’m not exactly sure of the reasons for that. Maybe it’s a catch up phenomenon,” Dr. O’Gara commented.

In the setting of percutaneous coronary intervention with a bare metal or drug-eluting stent for patients with either non–ST-elevation ACS or ST-elevation MI, the AHA/ACC guidelines give a class I recommendation for at least 12 months of dual-antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor. Either ticagrelor (Brilinta) at 90 mg twice daily or prasugrel (Effient) once daily at 10 mg is recommended over clopidogrel at 75 mg/day in patients who can take those medications safely; this guidance is based on ticagrelor’s superior efficacy compared with clopidogrel as shown in TRITON TIMI-38 (N. Engl. J. Med. 2007;357:2001-15) and prasugrel’s superiority in the PLATO trial (N. Engl. J. Med. 2009;361:1045-57).

The AHA/ACC guidelines give a relatively tepid level IIb recommendation that continuation of DAPT beyond 12 months may be considered in stent recipients. Many observers expect a stronger endorsement in the next iteration of the guidelines on the strength of the recent DAPT study, which showed that 30 months of DAPT was better than 12 in terms of major adverse cardiac and cerebrovascular events (N. Engl. J. Med. 2014;371:2155-66).

“Interestingly enough, the mechanism of benefit had less to do with prevention of stent thrombosis than it did with prevention of recurrent MI and stroke. This renders into much sharper focus the question of whether we’re treating the patient or we’re treating the stent. This result would imply that we’re treating the patient,” Dr. O’Gara observed.

The guidelines also include a bail-out option which states that if the risk of bleeding outweighs the anticipated benefit, it’s reasonable to discontinue DAPT before 12 months.

“I don’t know a single practitioner who’s not had to withdraw one or both elements of DAPT because of bleeding or because of the need for unanticipated noncardiac surgery. It’s a fact of life, and sometimes you have to just hope for the best,” the cardiologist said.

He reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

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Your practice moves but your address on the Internet doesn’t

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I moved offices in April 2014, for the first time in my career. Overall, it went quite smoothly.

But one problem persists, thanks to the Internet age.

The majority of search engines and rate-a-doc sites haven’t updated my address. I’ve e-mailed them about it, but get either no response or (even better) a response saying “We’ve reviewed your note and found our information is correct.” Apparently, I don’t know my correct address, in spite of driving there every day.

But what’s even more frustrating is when my patients follow these instructions. My secretary is quite conscientious about giving patients, new and old, the correct location when they make the appointment. My practice website even has a map.

Despite this, we still have a roughly 20% rate of people going to my old office across the street, then calling to see where we went. Worse, this even happens with patients who were never even seen at that office, yet have been to my new one several times.

Then they come in and yell at my staff for giving them the wrong address. They claim my website has the wrong address. It doesn’t, but I can’t control other sites.

The problem is that most don’t trust other people as much as they trust their phones. Rather than writing down my address when talking to my secretary, it’s easier to just tell Siri, “find Dr. Allan Block’s office.” Siri checks the Internet, where the majority of incorrect listings drown out my dinky little practice site. So people follow the phone’s instructions without questioning them. Even those who’ve previously been to this office, or think, “that doesn’t sound right,” will often follow the directions without question. After all, the Internet knows best.

I’m not knocking the rise of the smartphone. They’re awesome. I rely on Siri myself a great deal. But the phone is only as good as the data supplied, and isn’t capable of questioning it. If most sites list an incorrect address, then who am I to argue? I’m just the guy who’s actually renting the place.

The problem is that information itself is often unhelpful and misleading, and the Internet isn’t always right.

When I dictate an EEG report, I often end it with “clinical correlation is advised.” We need to keep that in mind for everyday life, too.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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I moved offices in April 2014, for the first time in my career. Overall, it went quite smoothly.

But one problem persists, thanks to the Internet age.

The majority of search engines and rate-a-doc sites haven’t updated my address. I’ve e-mailed them about it, but get either no response or (even better) a response saying “We’ve reviewed your note and found our information is correct.” Apparently, I don’t know my correct address, in spite of driving there every day.

But what’s even more frustrating is when my patients follow these instructions. My secretary is quite conscientious about giving patients, new and old, the correct location when they make the appointment. My practice website even has a map.

Despite this, we still have a roughly 20% rate of people going to my old office across the street, then calling to see where we went. Worse, this even happens with patients who were never even seen at that office, yet have been to my new one several times.

Then they come in and yell at my staff for giving them the wrong address. They claim my website has the wrong address. It doesn’t, but I can’t control other sites.

The problem is that most don’t trust other people as much as they trust their phones. Rather than writing down my address when talking to my secretary, it’s easier to just tell Siri, “find Dr. Allan Block’s office.” Siri checks the Internet, where the majority of incorrect listings drown out my dinky little practice site. So people follow the phone’s instructions without questioning them. Even those who’ve previously been to this office, or think, “that doesn’t sound right,” will often follow the directions without question. After all, the Internet knows best.

I’m not knocking the rise of the smartphone. They’re awesome. I rely on Siri myself a great deal. But the phone is only as good as the data supplied, and isn’t capable of questioning it. If most sites list an incorrect address, then who am I to argue? I’m just the guy who’s actually renting the place.

The problem is that information itself is often unhelpful and misleading, and the Internet isn’t always right.

When I dictate an EEG report, I often end it with “clinical correlation is advised.” We need to keep that in mind for everyday life, too.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I moved offices in April 2014, for the first time in my career. Overall, it went quite smoothly.

But one problem persists, thanks to the Internet age.

The majority of search engines and rate-a-doc sites haven’t updated my address. I’ve e-mailed them about it, but get either no response or (even better) a response saying “We’ve reviewed your note and found our information is correct.” Apparently, I don’t know my correct address, in spite of driving there every day.

But what’s even more frustrating is when my patients follow these instructions. My secretary is quite conscientious about giving patients, new and old, the correct location when they make the appointment. My practice website even has a map.

Despite this, we still have a roughly 20% rate of people going to my old office across the street, then calling to see where we went. Worse, this even happens with patients who were never even seen at that office, yet have been to my new one several times.

Then they come in and yell at my staff for giving them the wrong address. They claim my website has the wrong address. It doesn’t, but I can’t control other sites.

The problem is that most don’t trust other people as much as they trust their phones. Rather than writing down my address when talking to my secretary, it’s easier to just tell Siri, “find Dr. Allan Block’s office.” Siri checks the Internet, where the majority of incorrect listings drown out my dinky little practice site. So people follow the phone’s instructions without questioning them. Even those who’ve previously been to this office, or think, “that doesn’t sound right,” will often follow the directions without question. After all, the Internet knows best.

I’m not knocking the rise of the smartphone. They’re awesome. I rely on Siri myself a great deal. But the phone is only as good as the data supplied, and isn’t capable of questioning it. If most sites list an incorrect address, then who am I to argue? I’m just the guy who’s actually renting the place.

The problem is that information itself is often unhelpful and misleading, and the Internet isn’t always right.

When I dictate an EEG report, I often end it with “clinical correlation is advised.” We need to keep that in mind for everyday life, too.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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Early initiation of postpartum contraception decreases rapid repeat pregnancy in teens

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In an effort to determine how to curb rapid repeat adolescent pregnancy, researchers at MedStar Washington Hospital Center in Washington, DC, conducted a retrospective cohort study with first-time adolescent mothers, aged 19 years or younger. The repeat pregnancy rate at 2 years was 35% (n = 340). The average (SD) time from delivery to the second pregnancy was 9.9 (6.4) months.

Damle and colleagues found that leaving the hospital after giving birth without initiating any contraception was associated with more than double the risk of repeat pregnancy (odds ratio [OR], 2.447; 95% confidence interval [CI], 1.326–4.515). Follow-up in clinic within an 8-week postpartum period significantly reduced the chance of repeat pregnancy (OR, 0.322; 95% CI, 0.172–0.603). And placement of a long-acting reversible contraception (LARC), including intrauterine device or etonogestrel subdermal implant, by 8 weeks’ postpartum decreased the chance of rapid repeat pregnancy (OR, 0.118; 95% CI, 0.035-0.397).

Researchers Damle and colleagues concluded that adolescent mothers who begin to use a LARC within 8 weeks’ postpartum are less likely to have a repeat pregnancy within 2 years than those who chose another method or no contraception at all.

“First time adolescent mothers should be counseled about this advantage of using LARC,” wrote the authors.

Share your thoughts on this article! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References

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1. Damle LF, Gohari AC, McEvoy AK, Desale SY, Gomez-Lobo V. Early initiation of postpartum contraception: does it decrease rapid repeat pregnancy in adolescents? J Pediatr Adolesc Gynecol. 2015;28(1):57–62.

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In an effort to determine how to curb rapid repeat adolescent pregnancy, researchers at MedStar Washington Hospital Center in Washington, DC, conducted a retrospective cohort study with first-time adolescent mothers, aged 19 years or younger. The repeat pregnancy rate at 2 years was 35% (n = 340). The average (SD) time from delivery to the second pregnancy was 9.9 (6.4) months.

Damle and colleagues found that leaving the hospital after giving birth without initiating any contraception was associated with more than double the risk of repeat pregnancy (odds ratio [OR], 2.447; 95% confidence interval [CI], 1.326–4.515). Follow-up in clinic within an 8-week postpartum period significantly reduced the chance of repeat pregnancy (OR, 0.322; 95% CI, 0.172–0.603). And placement of a long-acting reversible contraception (LARC), including intrauterine device or etonogestrel subdermal implant, by 8 weeks’ postpartum decreased the chance of rapid repeat pregnancy (OR, 0.118; 95% CI, 0.035-0.397).

Researchers Damle and colleagues concluded that adolescent mothers who begin to use a LARC within 8 weeks’ postpartum are less likely to have a repeat pregnancy within 2 years than those who chose another method or no contraception at all.

“First time adolescent mothers should be counseled about this advantage of using LARC,” wrote the authors.

Share your thoughts on this article! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

In an effort to determine how to curb rapid repeat adolescent pregnancy, researchers at MedStar Washington Hospital Center in Washington, DC, conducted a retrospective cohort study with first-time adolescent mothers, aged 19 years or younger. The repeat pregnancy rate at 2 years was 35% (n = 340). The average (SD) time from delivery to the second pregnancy was 9.9 (6.4) months.

Damle and colleagues found that leaving the hospital after giving birth without initiating any contraception was associated with more than double the risk of repeat pregnancy (odds ratio [OR], 2.447; 95% confidence interval [CI], 1.326–4.515). Follow-up in clinic within an 8-week postpartum period significantly reduced the chance of repeat pregnancy (OR, 0.322; 95% CI, 0.172–0.603). And placement of a long-acting reversible contraception (LARC), including intrauterine device or etonogestrel subdermal implant, by 8 weeks’ postpartum decreased the chance of rapid repeat pregnancy (OR, 0.118; 95% CI, 0.035-0.397).

Researchers Damle and colleagues concluded that adolescent mothers who begin to use a LARC within 8 weeks’ postpartum are less likely to have a repeat pregnancy within 2 years than those who chose another method or no contraception at all.

“First time adolescent mothers should be counseled about this advantage of using LARC,” wrote the authors.

Share your thoughts on this article! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References

Reference

1. Damle LF, Gohari AC, McEvoy AK, Desale SY, Gomez-Lobo V. Early initiation of postpartum contraception: does it decrease rapid repeat pregnancy in adolescents? J Pediatr Adolesc Gynecol. 2015;28(1):57–62.

References

Reference

1. Damle LF, Gohari AC, McEvoy AK, Desale SY, Gomez-Lobo V. Early initiation of postpartum contraception: does it decrease rapid repeat pregnancy in adolescents? J Pediatr Adolesc Gynecol. 2015;28(1):57–62.

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Early initiation of postpartum contraception decreases rapid repeat pregnancy in teens
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rapid repeat adolescent pregnancy,MedStar Washington Hospital Center,Washington D.C,adolescent mothers,contraception,long-acting reversible contraception,LARC,intrauterine device,etonogestrel subdermal,
Legacy Keywords
rapid repeat adolescent pregnancy,MedStar Washington Hospital Center,Washington D.C,adolescent mothers,contraception,long-acting reversible contraception,LARC,intrauterine device,etonogestrel subdermal,
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