26.1 Introduction

Despite being a relatively common inflammatory disorder, Crohn’s disease (CD) remains an enigma, with the spectrum of disease widely variable, the pathogenesis still unknown, and the treatment strategies continuing to evolve. Early reports in the latter half of the 1800s of CD-like inflammation surfaced that included mostly obstructive symptoms, and were more attributed to ulcerative colitis or intrinsic strictures. Interestingly, the vast majority of pathological findings were located in the colon. ¹ When it finally was described, this disorder may have just as easily been referred to by another eponym had the authors decided against going with the alphabetized listing of its authors (Crohn, Ginzburg, and Oppenheimer) in the 1932 JAMA publication “Regional ileitis: a pathological and clinical entity.” ² In this publication, the authors were able to successfully characterize the inflammatory condition that led to strictures and multiple fistulas; however, they incorrectly felt it was localized to the terminal ileum. Had the authorship proceeded with a more prosurgical angle, the entity may have been named Berg’s disease, as it was the idea of Dr. A.A. Berg, a surgeon, to evaluate the original 52 specimens who were also his patients. ³ Moreover, some readers may not realize that one of the initial descriptions of the condition was actually first made in 1769 by the Italian physician Giovanni Battista Morgagni—the same physician who named anal columns, the aortic sinus, and the space for certain types of congenital diaphragmatic hernias. ⁴ Over time, our understanding of this condition, its epidemiology, and pathogenesis has improved. From Lockhart-Mummery and Morson’s accurate description of CD in the large intestine in 1960 ^{5 , 6} to the identification of the NOD2 genetic abnormality associated with a susceptibility to CD in 2001, ⁷ our knowledge regarding a broad array of aspects of this idiopathic, ulcerogenic, inflammatory condition of the gastrointestinal (GI) tract continues to evolve.

To date, CD remains a predominately medically treated condition, with several new classes of medical therapy available for both primary and recalcitrant disease. Yet, somewhat hidden in this fact is that three-quarters or more of all patients will require at least one operation during their lifetime. ⁶ Furthermore, the waxing and waning of symptoms, propensity for recurrence, and varying intervals between flares result in a lack of a “one-size-fits-all” treatment approach. All physicians, regardless of specialty, must therefore be cognizant of the impact of treatment decisions, as not only must the problem at hand be addressed, but also the patient’s future function must be carefully weighed when considering the proper therapeutic endeavor. Surgeons need to be exceedingly aware of the indications, surgical options, and expected outcomes for patients with CD, as well as have a thorough understanding of the principles guiding both medical and surgical care to maximize outcomes. While operative intervention may be required to address complications of the disease or in the setting of failed medical management, these overriding doctrines need to be balanced with avoiding an overaggressive surgical approach that can dramatically impact the patient’s future course.

26.2 Epidemiology

The true incidence and prevalence of CD is unknown. In part, this data void is secondary to the wide variety of presentations of the disease, for which a patient’s symptoms may be inaccurately attributed to another diagnosis. Yet with improved diagnostic methods and a higher degree of awareness and focus on the disease itself, CD has seen an increase in incidence during the last 50 years. ⁸ Traditionally, CD is described as having a bimodal distribution relative to age of onset, initially between 15 and 30 years, followed by a later, albeit smaller, peak in the sixth to ninth decades. ⁷ More recently, systematic reviews have found an annual incidence of CD ranging from 20.2 per 100,000 person-years in North America and 12.7 per 100,000 person-years in Europe to 5.0 per 100,000 person-years in Asia and the Middle East. ⁹ Looking longitudinally, the mean age at diagnosis has slowly shifted from late teens to late 20 s to early 30 s, although this finding may be more of an indicator that more patients are living longer and being diagnosed later in life—artificially pushing the mean to the right. ¹⁰ Even within regions, variations exist—the incidence in western Europe is almost twice that of eastern Europe, whereas the highest incidence of inflammatory bowel disease (IBD) in the world is in the Faroe Islands. Within England, Hindus and Sikhs have a lower risk than does the general population. While data in developing countries remain relatively sparse, both the incidence and prevalence of CD are increasing in the United States and around the world, including more recently in Asia. There is also an association with latitude, with increased incidences in higher latitude areas (including Canada, Scandinavia, and Australia) compared to regions closer to the equator. Gender has a yet undefined role, with some reports stating a 20 to 30% increased risk of CD in women, and other demonstrating males and females to be equally affected. Ethnicity has a much more established pattern, with whites and certain ethnic groups such as those of Ashkenazi Jewish descent having higher overall rates. ¹¹ In general, Native American Indian and Black populations are affected at much lower rates.

Although CD is not inherited through traditional Mendelian genetics, it appears to have a familial predisposition that leads to higher rates within families. A family history in patients with CD occurs in 2 to 14% of patients. ¹² This statistic translates to 15- to 35-fold increase among family members above the general population. Even closer examination reveals an approximate 5% age-adjusted lifetime risk of a first-degree relative of a CD proband developing IBD (up to 8% for those of Jewish ancestry). ¹³ The concordance rate for monozygotic twins ranges from 20 to 50%, ¹⁴ suggesting that genetics do play a role and that the disease is not entirely dependent on environmental and/or acquired factors. Furthermore, there does not appear to be a genetic concordance with the phenotypical manifestations of fibrostenotic, fistulizing, phlegmonous, or extent of disease among relatives. This risk does not seem to affect second-degree relatives, as they do not appear to have an increased risk association.

26.3 Etiology and Pathogenesis

Despite tremendous progress in the overall understanding of the disease and advancements in the comprehension of the various phenotypical manifestations, the exact etiology of CD remains unknown. Most hypotheses include interplay among the genetic composition of the individual along with environmental, bacteriological, immunological, and epidemiological factors that contribute to its development. Leading theories suggest that CD involves one or more of the following: (1) an antigen or infectious source, (2) a weakened host defense that allows for greater exposure to that source, or (3) an abnormal host response (▶ Table 26.1). ¹⁵ Efforts in each of these areas continue in attempt to determine which are causative factors versus those that are simply associations.

Current theories revolve around the host–microbiome interaction, and the variable response that occurs along several pathways that may ultimately lead to the chronic inflammatory state seen in CD. ¹⁶ In this model, intestinal microorganisms initiate an inappropriately regulated host immune response that results in a cascade of events ranging from altered permeability of the intestinal lumen to autoimmune “attacks” on several host organ systems. ¹⁷ This defective mucosal barrier allows exposure to luminal antigens as well as creates a microenvironment where continuous stimulation of underlying cells upregulates an inflammatory cascade leading to an out-of-proportion and inappropriate proinflammatory response. As such, the fecal and intestinal mucosal bacterial composition is known to be altered in CD patients; however, it is unknown if this occurs as a result of the inflammatory process, or is itself a contributing factor to disease development. ¹⁸ Furthermore, this alteration in mucosal permeability has been demonstrated to be present in up to 10 to 15% of CD family members that do not display any characteristics of the disease. Whether the permeability is a primary causative factor or the end result of another process remains undetermined. What seems more clear through proteomic and metagenomic evaluation of commensal and altered GI microbiota in CD patients is that there is an inappropriate pattern recognition with the microbiota serving as the driver of the disease pathogenesis. ¹⁹

Beginning in 1996, linkage studies of the human genome have helped with the discovery of several IBD genes that signify patients who are susceptible to CD development. ²⁰ Most attention has revolved around the NOD2 (formerly CARD15) gene on chromosome 16, a region felt to be involved in host interactions with bacterial lipopolysaccharide. ²¹ Genetic differences in the pattern-recognition proteins for which NOD2 codes may lead to an impaired sensing and handling of bacteria by the immune system, disrupting the tenuous balance of normal tolerance versus initiating an incorrect immune response. Since then, genome-wide association studies have provided insight that polymorphisms in genes such as ATG16L1 and IRGM play a role in autophagy in patients with CD. This process involves the regulation of cell development and differentiation, senescence, and ultimately the inflammatory system response to what the body deems is normal and abnormal. ²² In addition, other genes such as TLR4, HLA, and IRF5 are involved in the innate and adaptive immune system response seen in CD patients. Other causative immune factors have included overexpression and dysregulation of tumor necrosis factor (TNF), an imbalance between proinflammatory and anti-inflammatory cytokines, and an impaired mucosal susceptibility in sampling gut antigens. ²³ Combined, all these contribute to regulatory mechanisms that may be altered and play a role in CD pathogenesis.

Infectious theories also persist, ²⁴ with specific organisms including Mycobacterium avium subspecies paratuberculosis (i.e., Johne’s disease), Campylobacter concisus, adherent-invasive Escherichia coli (AIEC), and non–H. pylori Helicobacter species among the most common agents cited. Although the beneficial effects of antibiotics in the treatment of CD provide indirect evidence for a bacterial etiology, no distinct organism has been identified to date. Similarly, several viruses have been postulated to have an association with CD, the most common being Epstein–Barr virus (EBV), cytomegalovirus (CMV), and measles. However, systematic reviews have found little evidence to support this notion. ²⁵ Additionally, environmental factors are felt to play a role, highlighted by the well-established link to smoking with both an increased susceptibility and worsened clinical course. Smokers have been shown to have an odds ratio over threefold for the development of the disease, as well as more flares, worse clinical and endoscopic disease severity, higher rate of recurrent disease, and much more apt to undergo resection when compared to nonsmokers. ^{8 , 26 , 27} Food also appears to play a role. While patients with CD frequently have concomitant food intolerances, the role of dietary habits remains debatable. ²⁸ Previously, dietary factors ranging from refined sugar, starches, dietary fats, and low fiber have been described as having an association with the development of CD. However, the dietary theory has not been proven; rather than a causative effect, it is felt that the microbiome in the human GI tract is heavily influenced by dietary intake, leading to a local environment ripe to foster susceptibility to CD. Finally, oral contraceptive use has been shown to increase the risk anywhere from 1.4-fold to fivefold, with higher rates with prolonged use, ^{27 , 29} and something that may be diminished in part or altogether following discontinuation. The mechanism for this association remains unknown.

26.4 Pathology

26.5 Diagnosis

The diagnosis of CD relies upon a combination of clinical, radiological, endoscopic, and laboratory findings. Simple well-known CD facts such as the absence of a “curative” surgery, and a disease hallmarked by lifelong periods of flares and quiescent disease provide some insight but are not enough to make the definitive diagnosis. CD falls under the umbrella of IBD along with ulcerative colitis, as well as indeterminate colitis. In both CD and ulcerative colitis, there is no specific test at present to permit a definitive diagnosis; rather this combination of history and physical examination, laboratory, radiographic, and endoscopic findings is crucial. Unfortunately, approximately 5 to 15% of patients with ulcerative colitis will eventually be diagnosed with CD, and this fact may have widespread ramifications if they have undergone a restorative proctocolectomy. In addition, certain patients are labeled as having indeterminate colitis, due to their expression of manifestations of both diseases. ^{32 , 33}

26.6 Differential Diagnosis

The differential diagnosis in CD is wide and includes both benign and malignant processes (▶ Table 26.2). While CD has certain traits that are more suggestive of its presence such as noncontiguous multisite disease, fistulas, and creeping fat, a variety of abdominal processes may mimic CD. It is not an uncommon scenario for ileocolic CD to be ultimately diagnosed from a clinical picture that may at first resemble acute appendicitis, right-sided diverticulitis, an infectious process, or a perforated malignancy. Radiological studies may demonstrate similar patterns of bowel inflammation, laboratory examination often shows elevated CRP and/or white blood cell counts in each, and the patient demographics are routinely alike. This dilemma occurs intraoperatively; a decision must then be made regarding whether or not to proceed with resection versus closure and medical management alone based on clinical findings. If a resection is performed, questions arise regarding the extent of resection such as whether or not to perform an ileocecectomy versus appendectomy alone and what margins of resection are required for the situation at hand.

When confronted with suspected CD in the operating room, traditional teaching recommends performing an appendectomy if the cecum is normal, or to withhold on resection and undergo medical treatment only. However, data also support performing an ileocolic resection at the time of surgery. One series reported that almost half of patients required no further surgery as a result of their CD, compared to 92% of those undergoing appendectomy only (65% within the next 3 years). ⁵⁶ Hence, early ileocolonic resection may be in the patient’s long-term best interests to avoid recurrent disease and repeated trips to the operating room.

When disease is isolated to the colon, the major differentiation involves distinguishing Crohn’s colitis from ulcerative colitis, though other infectious and inflammatory colitides remain in the differential. As previously noted, many of the same clinical and histopathological traits are shared in both diseases, and contribute to the initial diagnostic dilemma, as well as those patients with indeterminate colitis or those who undergo a change in diagnosis from ulcerative colitis to CD. Ultimately, the entire evaluation includes information taken from laboratory, pathologic, endoscopic, radiologic, and clinical examinations as outlined earlier that will help clarify the picture and aid in diagnosis.

26.7 Classification

Once diagnosed, patients with CD are often categorized in several different manners, the most common of which involves either the site of disease or the patient’s phenotypical manifestations: fibrostenotic, fistulizing, or inflammatory.

26.7.1 Location

By location, the ileum (~60%) has the highest disease incidence. Localized inflammation in the ileocecal region occurs in approximately 45% of patients, whereas approximately 25 to 33% will have colonic involvement, 25% will have more proximal small bowel disease, and less than 10% will have upper GI or perianal disease (▶ Fig. 26.1). In general, patients with concomitant perianal disease tend to have a more severe clinical course, ⁵⁷ and perianal disease in the setting of CD may precede abdominal manifestations in up to 45%. ⁵⁸

Phenotypical Manifestations

When stratifying by disease pattern or phenotype, patients may have fibrostenotic (stricturing), fistulizing (penetrating), or inflammatory (phlegmonous) characteristics. Due to the heterogeneous nature of the disease, these manifestations may occur concomitantly or independently, or may even vary along the longitudinal course of the disease. Fibrostenotic patterns may occur in any location, though these occur most commonly in the terminal ileal region, where patients present with obstructive-type symptoms such as nausea, vomiting, and decreased oral intake. Due to the recurrent chronic nature that results in progressive thickening of the bowel wall, medical management is typically unsuccessful and surgical intervention is required. Inflammatory disease may present with a wide range of symptoms such as abdominal pain, fever, an abdominal mass, and/or weight loss. Bowel movements may either be diarrhea or conversely follow an obstructive pattern due to luminal narrowing or extrinsic compression from the phlegmon. Finally, penetrating or fistulizing disease also has a variable presentation. Patients may be completely asymptomatic, as in the case of many entero-enteral fistulas, present with anorectal abscesses and/or fistulas, or more commonly complain of symptoms mirroring involvement of the secondarily involved organ–recurrent urinary tract infections or pneumaturia, vaginal discharge, diarrhea, cutaneous feculent drainage, and/or hip/back pain from psoas involvement. While medical management continues to be a major component of each of the latter two patterns, surgery is often required for resolution of symptoms.

Montreal Classification

A summary of the revised Montreal classification is shown in ▶ Table 26.3 .

Table 26.3 Montreal classification

Age at diagnosis (A)
A1	16 y or younger
A2	17–40 y
A3	Over 40 y
Location (L)		Upper gastrointestinal modifier (L4)
L1	L1 terminal ileum	L1 + L4
L2	L2 colon	L2 + L4
L3	L3 ileocolon	L3 + L4
L4	L4 Upper gastrointestinal	–
Behavior (B)		Perianal disease modifier (p)
B1	Nonstricturing	B1P
	Nonpenetrating
B2	Stricturing	B2P
B3	Penetrating	B3P

26.7.2 Clinical Evaluation

Small Bowel

The distribution of disease will in large part dictate the clinical presentation. The terminal ileum, including the cecum, is the most commonly affected site, in addition to isolated more proximal small bowel disease. Patients with disease in this location will classically present with abdominal pain, fever, fatigue, nausea, and vomiting. The weight loss seen is a byproduct of both decreased oral intake and the malabsorptive process associated with CD. When the disease is in the terminal ileum and ileocecal region, patients may present with a slow onset of right lower quadrant pain following meals, an abdominal mass, and (when the psoas is involved) pain with hip extension. Obstructive symptoms may also occur in patients with either fibrostenotic or acute inflammation. Diarrhea tends to be nonbloody, though heme-positive stools may occur, and rarely gross blood is a manifestation from a small bowel source.

Colonic

Colonic involvement may occur in isolation in approximately one in four patients, though it is most often seen concomitantly in those with perianal (left-sided) or terminal ileal (cecal and ascending colon) disease. ⁵⁹ Within the colon, the distribution is somewhat variable, with approximately one-third of patients having total colonic involvement, 40% showing segmental disease, and left-sided only in up to 30%. ⁶⁰ Regardless of the exact location within the large intestine, patients with colonic involvement may experience abdominal pain and, in some cases, malnutrition. Diarrhea is often of smaller volume and may be from several sources—salt/water and bile acid malabsorption, infection (CMV), or as a result of an enterocolonic fistula. ^{61 , 62} Unlike ulcerative colitis, rectal bleeding is not routine, and bowel movements are often nonbloody, except in those with moderate-to-severe Crohn’s colitis. In addition, similar to disease in the small bowel, patients can experience hip pain from fistulas, cramping, and obstructive symptoms. Patients with chronic disease may also demonstrate pseudopolyps on endoscopic examination.

Anorectal

Bissell was the first to describe the anorectal component of CD, almost 2 years after the original description of the disease. ⁶³ Despite advances in the understanding of many features of CD, perianal complaints have been recognized as one of its most challenging aspects. Isolated perianal disease is the presenting symptom in approximately 5 to 15% of CD patients; however, over the course of their lifetime, it is seen in 25 to 80%. The perianal area in CD has classically been felt to be a “window” into the abdomen, and perianal involvement is clearly more common in those with concomitant rectal or colonic disease. ^{64 , 65} In addition, active disease in the perineum is felt to act as a harbinger of an overall more virulent course. ⁶⁶ The traditional anorectal complaints witnessed in non-CD patients are similar to those with the disease, including “standard” hemorrhoids, fissures, abscesses, and fistulas. However, CD patients may also manifest edematous (elephant ear) skin tags, blue discoloration of the anus, and abscesses and fistulas that are often recurrent, multiple, and located well away from the anal verge. While fissures due to hypertonicity may be identified, more often CD fissures present as deep-seated, burrowing fissures—more like ulcers—and may be multiple, off the midline, extending in the muscle and associated with large skin tags. Finally, patients with long-standing CD may develop anal stenosis or an anal stricture (▶ Fig. 26.2) at the verge secondary to repeated bouts of chronic inflammation.

Clinical evidence of perianal CD, as manifested by many of these features, is often deemed a hallmark of disease diagnosis, although a biopsy may rarely be considered. Due to local sepsis and perianal tenderness, pain due to one or more fissures or stenosis, patients may need to undergo an examination under anesthesia to fully identify the extent of the disease. Patients presenting with perianal findings consistent with CD should undergo a full alimentary tract evaluation, as previously stated, with endoscopic and radiological evaluation. In addition, a thorough physical examination to identify any extraintestinal manifestations should be performed. A very clinically relevant, easy-to-use septic perianal CD index has been described and is recommended. ⁶⁷

Upper Gastrointestinal Disease

Upper GI CD encompasses disease from the mouth through the jejunum. The incidence of upper tract involvement varies widely, with most studies reporting overall rates of less than 5%. In patients with ileocolic disease, concomitant upper GI manifestations occur in 0.5 to 13%, yet up to 40% of patients will demonstrate early subclinical evidence of CD on radiological and endoscopic evaluation. ⁶⁸ Importantly, when patients have upper GI CD, they almost uniformly have concomitant disease of lower tract and should be evaluated to determine the extent of involvement. Upper tract disease is hallmarked by both obstructive symptoms and fistulas. ⁶⁹ Patients typically present with abdominal pain, cramping, nausea, vomiting, or intolerance of oral intake leading to weight loss. While fistulas may be virtually to any site, the majority involving the proximal tract are gastrocolic or ileogastric in nature. Patients may be asymptomatic or present with diarrhea from high-output and colonic involvement. CD of the esophagus is exceedingly rare, involving less than 0.5% of patients. Most patients will have inflammation or ulcers, though strictures and fistulas have also been reported. As with other upper tract CD, extraesophageal disease is nearly always present. ⁷⁰

26.8 Treatment

26.8.1 Medical Management

First, despite the spectrum of disease presentations, with the exception of isolated perianal CD, the hallmark of CD remains inflammation with abdominal pain and diarrhea. As such, supportive care to include antidiarrheals and antimotility agents, along with a bland diet, is a good first-line approach to provide symptomatic control (▶ Table 26.4). It is important to exclude the concomitant presence of “super-infections” such as CMV or Clostridium difficile infection, as bowel-slowing medications may result in the onset of toxic megacolon (▶ Fig. 26.3) and a rapidly progressive clinical deterioration. Yet, simple over-the-counter, readily available medications such as loperamide, diphenoxylate, and bismuth, along with prescription medications such as codeine and tincture of opium, often provide tremendous relief to abdominal pain, cramping, and loose stools.

Table 26.4 Medical treatment for Crohn’s disease

Class of medication	Examples	Role in therapy
Steroids	Prednisone Prednisolone Methylprednisolone Budesonide a	Induction of remission
Immunomodulators	6-mercaptopurine Methotrexate Azathioprine Tacrolimus Cyclosporine b	Maintenance of remission Induction in select cases
5-ASA	Sulfasalazine Pentasa Mesalamine Olsalazine	Maintenance of remission In mild cases
Biologics	Infliximab Adalimumab Certolizumab Vedolizumab Natalizumab	Induction and maintenance of remission
Antibiotics	Metronidazole Ciprofloxacin	Induction of remission Treatment of infection
Abbreviation: ASA, aminosalicylates. a Budesonide is taken enterally and has only topical effect, no systemic effect. b Cyclosporine can be used as rescue therapy/induction in refractory cases, but has not been supported by evidence in the treatment of Crohn’s disease.

CD has also been traditionally called a “wasting disease,” though increasing numbers of obese patients with CD are observed. Despite this seeming paradox, nutritional support in both groups remains paramount. Ideally, preservation of oral feeding in any form is crucial for maintenance of the absorptive and protective mechanisms provided by the GI mucosal lumen villi and microvilli. However, when enteral feeding is not possible, parenteral nutrition has become invaluable in preserving nutritional stores, aiding in positive nitrogen balance, preventing weight loss, and improving perioperative outcomes. ⁷¹ This must be weighed against the potential complications involved with intravenous routes to include infectious complications and thromboembolic events.

A tiered strategy for medical therapy is often utilized, taking into account the disease activity (flare vs. chronic), pattern (inflammatory vs. fistulizing vs. fibrotic), and location. Antibiotics and aminosalicylates are typically used in the induction and maintenance of remission, respectively, especially for patients with mild-to-moderate disease. Antibiotics are also utilized for the treatment of an acute infection for both the abdominal and perianal locations, with metronidazole and fluoroquinolones among the most commonly used antibiotics. In select cases, antibiotics can be given to patients with perianal disease including fistulas for maintenance of remission as well as decreasing pain. While the exact mechanism of action of antibiotics in CD is debated, by decreasing bacterial load and altering the bacterial milieu of the GI tract, disease activity is lessened. ▶ Table 26.5 lists the class of medications and their role in therapy.

Table 26.5 Class of medications in treatment of Crohn’s disease

Class of medication	Examples	Role in therapy
Biologics	Infliximab Adalimumab Certolizumab Natalizumab	Induction and maintenance of remission
Immunomodulators	6-mercaptopurine Methotrexate Azathioprine Tacrolimus Cyclosporine a	Maintenance of remission Induction in select cases
Steroids	Prednisone Prednisolone Methylprednisolone Budesonide b	Induction of remission
Aminosalicylates	Sulfasalazine Pentasa Mesalamine Olsalazine	Maintenance of remission In mild cases
Antibiotics	Metronidazole Ciprofloxacin	Induction of remission Treatment of infection
a Cyclosporine can be used as rescue therapy/induction in refractory cases, but has not been supported by evidence in the treatment of Crohn’s disease. b Budesonide is taken enterally and has only topical effect, no systemic effect.

Aminosalicylates

Aminosalicylates (5-ASA) are traditionally used as first-line maintenance agents, and are generally well tolerated by patients. Depending on the predominant location of the disease, different moieties can be formulated to allow maximal drug concentration to be targeted at the appropriate site. 5-ASA compounds are not aspirin or nonsteroidal derivatives, though they do work to decrease proinflammatory mediators and function at the mucosal level with reduced systemic absorption. Similar to antibiotics, the mechanism of action in IBD remains unclear, though levels of nuclear factor-κB (NF-κB), TNF, and interleukin-1 have all been shown to decrease, as well as inhibiting both B- and T-cell function. ⁷² Additionally, they can be used in the perioperative period without increasing the risk of postoperative complications. Overall, this class of medications has been shown to prevent disease flares and minimize CD activity index for patients with mild disease, though the results have been inconsistent with questionable clinical benefit. ⁷³ However, at most they have little downside and there are some data to suggest a decrease in disease recurrence following resection.

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