Cirurgia

#Incontinencia anal: el silencio impide un tratamiento eficaz

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Perder la capacidad de continencia fecal es mucho más frecuente de lo que se piensa. La falta de consulta aleja a muchos pacientes de las terapias eficaces.

Neuromodulación de raíces sacra, en el Hospital Universitario de La Princesa.
Luis Camacho

La continencia o la capacidad para que los esfínteres retengan las heces y la orina es determinante en la calidad de vida, pero el pudor que rodea a la función excretora es la principal barrera para pedir ayuda cuando esa función falla. En especial sucede con la incontinencia anal, un trastorno que se estima en el 10% de la población general, pero del que no se habla lo suficiente en la consulta del médico.

Superar ese muro de vergüenza es el primer paso para acceder a una terapia adecuada: desde las sencillas pautas de dieta y ejercicios de fortalecimiento del esfínter anal a la más sofisticada neuromodulación de raíces sacras. “Un buen tratamiento conservador, con dieta, ejercicio dirigido (biofeedback) y en ocasiones apoyado en fármacos, puede ser suficiente para mejorar la situación en la mitad de los pacientes. Por eso es tan importante que se divulgue este trastorno, también entre los profesionales sanitarios”, afirma Elena Bermejo, de la Unidad de Coloproctología del Servicio de Cirugía General y del Aparato Digestivo que dirige Elena Martín en el Hospital Universitario de la Princesa, en Madrid.

En ello coincide Javier García Septiem, también cirujano en la citada unidad: “Es importante que en la atención primaria, que es la puerta de entrada a la asistencia sanitaria, se conozca que hay salidas para este trastorno, que se conozca el tratamiento de inicio y, en los casos más graves, a qué unidades con especialistas implicados en esta enfermedad pueden derivarse a los pacientes”.
En concreto, la Unidad de Coloproctología de La Princesa está integrada por estos dos especialistas, el cirujano Adolfo Alonso y la enfermera estomaterapeuta Inmaculada Pérez. Todos ellos se coordinan a su vez con especialistas de los Servicios de Aparato Digestivo, Urología (en los casos asociados a incontinencia urinaria), Radiología y Rehabilitación, “de forma que se aplica un abordaje multidisciplinar absolutamente necesario para alcanzar el tratamiento correcto”, enfatiza Bermejo.

Los cirujanos Javier García Septiem, Elena Bermejo Marcos, Adolfo Alonso Casado y la enfermera estomaterapeuta Inmaculada Pérez Salazar, todos de la Unidad de Coloproctología del Servicio de Cirugía General y del Aparato Digestivo del Hospital Universitario de La Princesa, en Madrid.

El Hospital de La Princesa se ha implicado en la celebración estos días de la Semana Mundial de la Continencia, con el apoyo de la Asociación de la Incontinencia Anal (Asia). El objetivo de la iniciativa, impulsada por la Federación Mundial de Pacientes con Incontinencia (WFIP) y bajo el lema Deja de escapar,es visibilizar una enfermedad de la que apenas se habla. Precisamente sobre la importancia del lenguaje en una patología silenciada, Bermejo puntualiza que “en realidad debemos referirnos a la incontinencia anal, no fecal, porque con ese término se engloba todo el problema, que puede ser solo escapes para gases, al margen de la urgencia defecatoria o de las deposiciones involuntarias”.

Paradójicamente para un trastorno tan oculto, abundan mensajes que no se corresponden con la realidad: “No es solo una enfermedad de ancianos y mujeres, también puede aparecer en niños y jóvenes, así como en varones”, recalca Bermejo. No obstante, es más frecuente entre las féminas -por el traumatismo asociado al parto- y se ha establecido una prevalencia del 20-50% en las residencias de ancianos.

Tampoco hay que contemplar siempre como solución una dieta astringente; de hecho, el estreñimiento puede causar incontinencia por rebosamiento, al producirse impactación fecal. Las pautas alimentarias en estos pacientes buscan modificar las características de las heces, sin llegar a estreñir, así como modular el hábito defecatorio. A eso se pueden añadir fármacos compactadores de heces, que también inciden en las características fecales para mejorar la continencia.

Las causas de la incontinencia anal son tan diversas como las personas que la sufren y abarcan desde las lesiones derivadas en los partos a las secuelas de una cirugía colorrectal, sin olvidar enfermedades neurológicas como la esclerosis múltiple. “Además, los pacientes incontinentes suelen tener otras patologías de suelo pélvico y las causas aparecen con frecuencia mezcladas”, recuerda García Septiem. La diabetes mellitus y la enfermedad inflamatoria intestinal, entre otras, también pueden disparar este problema, e incluso hay pacientes en los que aparece por causa idiopática.

Algoritmo terapéutico

Una manera simplificada de clasificación es la incontinencia pasiva y la de urgencia. Adolfo Alonso explica que “en la incontinencia pasiva, el escape de heces no se siente, mientras que en la de urgencia, el esfínter no responde y al paciente no le da tiempo a llegar al baño. Según el caso, puede haber o no una lesión estructural del esfínter. Si existe una lesión grave, lo ideal es repararla quirúrgicamente con esfinteroplastia, que obtiene muy buenos resultados, pero en ocasiones, aun reparada la lesión, si el paciente no mejora lo suficiente es necesario recurrir a tratamientos más avanzados como la neuromodulación de raíces sacras”. Con todo, siempre hay que intentar primero un abordaje conservador basado en pautas higienicodietéticas y biofeedback.

Para determinar la causa y gravedad en cada caso, es esencial la anamnesis, apoyada en la relación de confianza con el paciente y en herramientas como las escalas de Wexner y la visual de Bristol. “De esta forma, conocemos no solo el número de escapes y las características de las heces, sino en qué medida los pacientes se sienten seguros y ven comprometida su vida social y familiar”, afirma García Septiem. Hace hincapié en la escucha al enfermo. Para muchos de ellos, la consulta es el primer lugar donde cuentan lo que les está pasando, ni siquiera lo comentan en su entorno familiar. “La incontinencia genera gran aislamiento familiar y social, pero hay estrategias terapéuticas eficaces. En nuestra mano está difundirlas, para que cada vez más pacientes mejoren su calidad de vida”.

Neuromodulación de raíces sacras

La neuromodulación de raíces sacras es una técnica avanzada empleada en la incontinencia urinaria y la anal. Su eficacia está bien contrastada, aunque se desconocen todas las vías implicadas. Antes se denominaba neuroestimulación, pero se cambió al comprobarse que el paciente mejora no solo por el estímulo eléctrico de las fibras musculares, sino por la modulación de toda la inervación pélvica.

 

 

 

Mediante abordaje percutáneo, con anestesia local, se localiza la raíz sacra que inerva la zona anal y perianal (raíz S3). Con el paciente despierto, una aguja conectada a un estimulador eléctrico permite evaluar la respuesta motora y sensitiva. Una vez ubicada la mejor respuesta, se coloca el electrodo, que se mantendrá unas semanas conectado a un estimulador externo para comprobar su eficacia. Cuando se ha asegurado la mejoría de la continencia, se programa la intervención con la que se implanta el neuromodulador de forma permanente. El dispositivo es, en esencia, un marcapasos que funciona conectado a una batería y se puede programar desde fuera, por bluetooth.

 

#Efficacy of #gastric bypass surgery for #reflux symptoms

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  •  Univadis Medical News

Researchers have suggested the efficacy of gastric bypass in the treatment of reflux symptoms may have been overestimated, with a new study showing around half of operated patients require continuous anti‐reflux medication.

Researchers assessed the long‐term risk of remaining/recurring reflux symptoms after gastric bypass in 2,454 adults in Sweden with preoperative reflux who underwent gastric bypass between 2006 and 2015, with complete follow‐up through 2016. Participants were followed for a median of 4.6 years. The main outcome was remaining/recurring reflux defined by the dispensing of proton pump inhibitors (PPI) and histamine‐2 receptor antagonists (H2RA) after gastric bypass.

The researchers found reflux symptoms remained/recurred in around 48 per cent of participants in the second year of gastric bypass and remained stable up to 10 years after surgery. The risk of reflux was similar comparing laparoscopic with open gastric bypass.

Risk factors for recurring reflux included high preoperative dose of anti‐reflux medication, older age, female sex and comorbidity.

Writing in Alimentary Pharmacology & Therapeutics, the authors said: “Physicians and patients should be aware of the limited effect of gastric bypass on reflux in patients with severe obesity, particularly in those with risk factors for post‐operative reflux.”

#Cholecystectomy may reduce #stroke risk in patients with #gallstones

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  •  Univadis Medical News

New research suggests cholecystectomy may be associated with a reduced stroke risk in patients with gallstones.

Researchers examined data from Taiwan’s National Health Insurance Research Database on 310,712 gallstone patients divided into two groups: those who underwent cholecystectomy (intervention group) and those who did not (controls).

During the study period (2000-2012), 19,098 controls and 11,913 gallstone patients who underwent cholecystectomy had a stroke, translating to incidence rates of 17.8/1,000 person-years and 10.6/1,000 person-years, respectively.

After adjustment for age, sex and major co-morbidities, the researchers found cholecystectomy patients had significantly lower risks of overall stroke (HR 0.60; 95% CI 0.59-0.62), ischaemic stroke (HR 0.60; 95% CI 0.58-0.61) and haemorrhagic stroke (HR 0.55; 95% CI 0.51-0.58) than the non-cholecystectomy patients. Both asymptomatic and symptomatic gallstone patients had lower overall stroke risk after cholecystectomy.

Writing in the Journal of Gastroenterology and Hepatology, the authors said the findings provide evidence that gallstones may be one of the potential risk factors in stroke.

“Our findings require gastroenterologists and gastrointestinal surgeons to pay closer attention to the gallstone patients to implement stroke preventive measures, particularly in cases with conventional stroke risk factor(s),” the authors concluded.

#EEA issues new guideline on #gynaecomastia

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  •  Univadis Medical News

The European Academy of Andrology (EAA) has published new clinical guidelines which include 15 recommendations on the assessment and management of gynaecomastia (GM).

The recommendations are:

  • Consider underlying pathology in GM of adulthood
  • GP or another non-specialist should rule out lipomastia, obvious breast cancer or testicular cancer
  • Thorough diagnostic workup, when warranted, should be performed by a specialist
  • Medical history should include information on onset and duration, sexual development and function and use of substances associated with GM
  • Examine for signs of under-virilisation or systemic disease
  • Breast exam should confirm the presence of palpable glandular tissue
  • Physical examination should include examination of the genitalia
  • Genitalia examination should be aided by testicular ultrasound
  • Testosterone (T), oestradiol (E2), sex hormone-binding globulin (SHBG), luteinising hormone (LH), follicular stimulating hormone (FSH), thyroid stimulating hormone (TSH), prolactin, human chorionic gonadotropin (hCG), alpha-foetal protein (AFP) and liver and renal function tests are appropriate
  • Breast imaging may offer assistance
  • Core needle biopsy for suspicious lesions
  • Watchful waiting after treatment of underlying pathology or discontinuation of substances associated with GM
  • T therapy only for men with proven deficiency
  • Avoid selective oestrogen receptor modulators (SERMs), aromatase inhibitors (AIs) or non-aromatisable androgens, in general
  • Surgical treatment only for patients with long-lasting GM

#Crohn´s Disease

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Resultado de imagem para Crohn Disease

Overview

Crohn disease (CD) is an idiopathic, chronic regional enteritis that most commonly affects the terminal ileum but has the potential to affect any part of the gastrointestinal tract from mouth to anus. This condition was first described by Crohn, Ginzburg, and Oppenheimer in 1932, but it was not clinically, histologically, or radiographically distinguished from ulcerative colitis (UC) until 1959. [12]

Untreated CD is characterized by transmural (full-thickness) inflammation, involvement of discontinuous segments of the intestine (skip areas), and, in a proportion of cases, by non-necrotizing granulomas composed of epithelioid histiocytes. Patients present with a range of symptoms, including crampy abdominal pain and diarrhea, which may be complicated by intestinal fistulas, particularly after surgical intervention, by intramural abscesses, and by bowel obstruction.

The diagnosis of CD can be difficult, and the proper clinical separation of this entity from UC has important therapeutic implications. [3Consequently, a thorough understanding of the clinical, radiologic, endoscopic, and pathologic features of CD, as well as effective communication between the pathologist and the managing clinicians, is essential to diagnostic accuracy.

Below are examples of some gross features of Crohn disease.

Mucosal pseudopolyps (inflammatory pseudopolyps) oMucosal pseudopolyps (inflammatory pseudopolyps) of the terminal ileum in a patient with Crohn disease. These polyps can reach giant proportions, up to 5 cm in maximum dimension, and are often seen on the proximal side of an ulcerated stricture (a “sentinel” inflammatory polyp).

Cobblestone change of the mucosa of the terminal iCobblestone change of the mucosa of the terminal ileum in a patient with Crohn disease. Communicating fissures and crevices in the mucosa separate islands of more intact, edematous epithelium.

Etiology

The precise etiology of Crohn disease (CD) is unknown, but there are several known risk factors, including family history, smoking, use of oral contraceptives, diet, and ethnicity. A combination of factors, including aberrant mucosal immune responses, intestinal epithelial dysfunction, and defects of host interactions with intestinal microbes likely contribute to CD. [78]

Genetics

There is a clear genetic predisposition for Crohn disease. First-degree relatives have a 13-18% increase in incidence, and there are concordance rates of 50% in monozygotic twins. Classic Mendelian inheritance is not seen, implying a polygenic basis of the disease. [910]

Molecular linkage analyses of affected families have identified NOD2 (nucleotide-binding domain 2) as a susceptibility gene in CD. [1112NOD2 encodes a protein that binds to intracellular bacterial peptidoglycans, subsequently activates NF-kB (nuclear factor-kappaB), and may be involved both in preventing excessive immune activation and in combating luminal microbes. However, fewer than 10% of individuals carrying NOD2 mutations develop the disease, and genomic screening has identified linkage to multiple chromosomes, including chromosomes 3, 7, 12, and 16. [131415]

Other genes of interest include ATG16L1 (autophagy-related 16-like) and IRGM(immunity-related GTPase M), both of which are involved in autophagy and the clearance of intracellular bacteria. IL23R (interleukin-23 receptor) may also be involved, as it is a regulatory cytokine receptor that plays a role in the initiation of the innate and adaptive immune activation in the intestinal mucosa. [16171819]

Environment

Environmental factors, especially cigarette smoking and diet, are also clearly involved in this disease. Tobacco smoking doubles the risk of both initial and recurrent Crohn disease (CD), unlike the apparent protective effect of tobacco seen in ulcerative colitis. Improved food storage conditions and decreased food contamination may also contribute to the increase in incidence. [20]

This so-called “hygiene hypothesis” suggests that the reduction in enteric infections in developed countries has resulted in inadequate development of the regulatory processes that limit mucosal immune responses. [21Pathogens that otherwise might cause only self-limited disease instead may trigger overwhelming inflammatory responses in susceptible individuals. Although more data are required, the observations that episodes of acute gastritis often precede the onset of CD in humans and that helminthic infections can prevent disease development in animal models lend support to this idea. [21]

Infective agents

Given the success of treatment of peptic ulcer disease with the discovery of Helicobacter pylori as the causative agent, there have been multiple studies attempting to link an infectious agent with inflammatory bowel disease (IBD). [22]Although decreased numbers of native lactobacilli and overgrowth of enteric bacteria are postulated to trigger excessive inflammation seen in Crohn disease (CD), a single causative infectious agent has not been identified. Mycobacteria have been studied extensively in this context, given the histopathologic similarities between intestinal tuberculosis and CD, but the suggestion that mycobacteria play an etiologic role has been largely disputed. [2324]

Similarly, although both a measleslike virus and the measles vaccine have been implicated in the pathogenesis of CD, epidemiologic evidence has failed to support either as a causative agent. [25262728The search for an infectious cause of IBD continues, but it seems more likely that the ultimate cause is polyfactorial. [7]

Mucosal immune response and epithelial damage

A variety of epithelial defects have been described in both Crohn disease (CD) and ulcerative colitis, including tight junction barrier function, defective transepithelial transport, extracellular matrix barrier proteins, and Paneth cell antibacterial peptides. [29In addition, polarization of T cells to the T-helper cell type 1 (TH1) type is a well-recognized feature of CD, and emerging data indicate that TH17 cells also contribute to disease pathogenesis, whereas IL-23 receptor polymorphisms may confer protection from CD. [30318]

It has also been proposed that neutrophil dysfunction may play a role in altered innate immunity early in the development of CD. [3233At this point in time, the exact defects and mechanisms involved in disease pathogenesis are yet to be elucidated, and research is ongoing. Immunosuppression remains the mainstay of CD therapy, and it is likely that a combination of derangements that alter mucosal immunity and suppress immunoregulation is crucial in the development of this disease.

Affected Anatomic Sites

Unlike ulcerative colitis, Crohn disease (CD) can occur at any point along the gastrointestinal tract. The most commonly involved sites at presentation are the terminal ileum, ileocecal valve, and cecum.

Disease is limited to the small intestine in approximately 40-50% of cases, whereas another 30-40% of cases involve both the small intestine and the colon. The remaining cases involve only the colon. [34]

Aphthoid ulcers in the mouth and anal fissures, skin tags, and abscesses are frequently seen, whereas involvement of the esophagus and stomach is much less common. [3536]

Extraintestinal features are common and include the following:

  • Ocular manifestations (uveitis, recurrent iritis, and episcleritis)

  • Dermal manifestations (erythema nodosum, pyoderma gangrenosum, and Sweet syndrome)

  • Inflammatory seronegative arthropathies (sacroiliitis, ankylosing spondylitis, psoriatic arthritis, and reactive arthritis) [37]

The liver and bile ducts can be also be involved; the incidence of primary sclerosing cholangitis is increased by approximately 10% in patients with a history of CD. [38]

 

Clinical Features

Regardless of the location of disease, Crohn disease (CD) usually follows a chronic, indolent course and tends to relapse and remit. Patients commonly present with symptoms due to ileocecal inflammation, [3940including the following:

  • Crampy, lower right quadrant or periumbilical pain that is often relieved by defecation – Some patients report more diffuse and constant pain.

  • Prolonged nonbloody diarrhea with accompanying weight loss and possible malabsorption syndromes – If the colon is involved, the diarrhea may contain blood, mucus, and pus.

  • Low-grade fever and feeling of general fatigue and malaise

  • In pediatric patients, unexplained growth failure in addition to the above symptoms

Fissures, fistulas, and abscesses

Chronic, transmural inflammation can lead to fissures in the bowel wall with ensuing fistulas and abscesses. Fistulas may develop between the bowel and other organs, including enteroenteric fistulas, enterogastric, enterovaginal, enterocutaneous, and enterovesical fistulas. These can present as feculent vomiting or vaginal discharge, frequent urinary tract infections, pneumouria, fecaluria, and feculent soiling of skin lesions. Fistulas are significantly more common in postsurgical patients, an important reason why surgical intervention is deferred in favor of medical intervention, whenever possible. Retroperitoneal, intraperitoneal, and perianal/perirectal abscesses are common.

A retrospective study evaluated the clinico-pathological characteristics of patients who underwent surgery due to stricturing or non-perineal fistulizing Crohn’s disease. The study concluded that no specific clinical feature was found to differentiate patients with the stricturing form of Crohn’s disease from the fistulizing form. However, the authors also add that histopathological analysis of the resected specimens revealed significant differences in some parameters between the two disease forms. The L3 localization (Montreal Classification) was detected significantly more often in the non-perineal fistulizing group than in the stricturing group. [41]

Obstruction

Patients may also present with symptoms of obstruction, including the following:

  • Cramping, borborygmus, and postprandial bloating due to edema of the bowel wall

  • Possible ensuing constipation and obstipation, as the bowel wall becomes chronically thickened and the lumen narrows

  • Occurrence of complete obstruction as the result of stricture formation and progressive bowel wall thickening

Extraintestinal involvement

Extraintestinal features may involve the mouth, anus, eyes, skin, joints, liver, and bile ducts. Aphthoid ulcers and erosions of the mouth, anal fissures, abscesses, ulceration around stomas and skin tags are common features of the disease. Uveitis and episcleritis as well as pyoderma gangrenosum and constitutional eczema are also quite common. [4243The arthropathies tend to be migratory and asymmetrical, and there may be an associated ankylosing spondylitis. [4445]

Liver function test abnormalities are common, but severe hepatic pathology such as pericholangitis and primary sclerosing cholangitis are not as clearly associated with Crohn disease as with ulcerative colitis. [38]

Dysplasia and carcinoma

Patients with Crohn colitis are at increased risk to develop intraepithelial neoplasia, also known as dysplasia, and colonic adenocarcinoma. [46Patients should begin periodic regular colonoscopic surveillance for dysplasia and carcinoma beginning approximately 8-10 years after the diagnosis of Crohn colitis. Patients with concomitant primary sclerosing cholangitis are thought to be at increased risk for colorectal neoplasia compared with other Crohn patients, but the relative risk is better defined for patients with ulcerative colitis and primary sclerosing cholangitis.[47In addition, strictures may harbor malignancy.

The biopsy strategy for surveillance includes 4-quadrant biopsies taken at intervals of every 10 cm of colon involved by the colitis, beginning 10 cm proximal to the area of involvement, and extending 10 cm distally. If there is pancolitis, at least 33 biopsies are recommended, and biopsies at 5-cm intervals of the rectum are included. Biopsies should also include any nodules or masses, as well as the flat mucosa adjacent to the masses, clearly designated as such, and submitted separately. [46]

NOTE: Extreme care should be taken to avoid labeling the patient with Crohn disease at first biopsy. It is preferable in this clinical context to provide a descriptive diagnosis with a differential diagnosis. Appropriate clinical follow-up and subsequent biopsies will usually resolve the diagnostic dilemma.

Differential Diagnosis

Several conditions should be considered when evaluating a patient for Crohn disease. These are discussed below, as follows:

  • Crohn disease versus ulcerative colitis

  • Infectious disease

  • Drugs-induced colitis

  • Conditions with small bowel fissuring ulcers

  • Diverticular disease

  • Ischemic changes

Crohn disease versus ulcerative colitis

The main differential diagnosis is between Crohn disease (CD) and ulcerative colitis (UC). The distinction between these 2 conditions is important, as both increase the risk of developing adenocarcinoma, and the response to surgical treatment vary dramatically between them. [6162]

Although CD and UC each carry an increased risk of neoplastic transformation, the risk is higher and surgical intervention is better tolerated in UC. In CD, as noted earlier, there is a higher risk of recurrence and ulceration, fissure, and fistula formation at sites of reanastomosis or stoma formation. [6364]

The main features of CD that separate it from UC include the presence of skip lesions, granulomas, transmural inflammation, fissures, and/or involvement of any part of the gastrointestinal tract. UC is generally limited to the colon, apart from minimal distal “back-wash” ileitis; however, this condition may also manifest cecal or appendiceal patches of involvement that can simulate the “skip” lesions of CD. More typically, ulcerative colitis in its untreated state is a continuous process, worse distally, with increased span of involvement distal to proximal, as the disease progresses. Moreover, ulcerative colitis usually involves only the mucosal layer of the bowel, and, in some cases, superficial submucosa, unless there is fulminant colitis (toxic megacolon).

Nonetheless, the distinction between the 2 processes can be challenging, as CD can occasionally affect only the distal colon, granulomas may be present in UC (although typically adjacent to ruptured crypts, whereas CD granulomas have no necessary spatial relationship to injured crypts), and the regional involvement/skip lesions of CD may not be apparent endoscopically or in small mucosal biopsies. [52]

In addition, treatment can markedly alter the apparent pattern of involvement by location. For example, steroid enema treatment of UC may eradicate endoscopic and histologic evidence of rectal injury and inflammation, leaving more severe inflammation in the proximal colon. Without complete clinical information regarding the endoscopic appearance and the history of treatment, the pathologist may misconstrue the biopsy findings and render an incorrect diagnosis.

When the distinction between CD and UC is impossible, some pathologists choose to render a diagnosis of “indeterminate colitis.” [52656667In time, most cases will declare themselves as CD or UC, but approximately 30% may remain indeterminate. [5265]

It is critical for the pathologist and the managing physician to recognize that “indeterminate colitis” is not a third category of disease, but that it is a diagnosis of idiopathic inflammatory bowel disease (IIBD), not otherwise specified, pending additional information. Features that assist in defining CD in this setting are the presence of granulomas, transmural lymphoid aggregates, and creeping fat; however, these findings may be noted only in resection specimens. [68]Classification of the type of IIBD may be possible with additional clinical history, with biopsies of small intestine or stomach, or with disease recurrence and progression.

Infectious disease

Infectious etiologies, especially yersiniosis and tuberculosis, can lead to a similar clinical and histopathologic picture as Crohn disease (CD) and must be considered.[39695762This is particularly important, given the risk for systemic infection if the patient is placed on immunosuppressive treatment for presumed CD. Therefore, it is strongly recommended that the endoscopic and managing physicians consider special studies, including special histologic stains for microorganisms, and even including polymerase chain reaction (PCR), to exclude infection, if there is any significant travel or exposure history, even remote.

Conversely, early or treated CD may manifest regionally as microscopic disease (focal active colitis) in a pattern otherwise typical of infectious or so-called “acute self-limited colitis.”

Drug-inducted colitis

Drug-induced colitis—particularly nonsteroidal anti-inflammatory drug (NSAID) toxicity, methyldopa, gold, and penicillins—can produce mucosal changes that lead to full-thickness ulcers and resultant chronic crypt architectural remodeling that can mimic Crohn disease. Drugs may also cause a granulomatous reaction. [5770]

Conditions with small bowel fissuring ulcers

Fissuring ulcers in the small intestine may also be seen in Behçet disease, malignant lymphoma, and “ulcerative jejunitis.” The latter represents early lymphomatous transformation in celiac sprue. [2957]

Diverticular disease

Diverticular disease may be associated with active crypt injury in peridiverticular mucosa in a pattern that is indistinguishable from active Crohn disease (CD). Concomitant active or active chronic injury in nearby mucosa unassociated with diverticular ostia favors a diagnosis of CD.

Crohnlike changes, including erosions, fistulae, granulomas, crypt architectural distortion, and intraepithelial neutrophilic inflammation, may be seen in the vicinity of diverticulitis. Caution should be used in making a diagnosis of CD in the sigmoid colon or in the vicinity of diverticular disease, unless there is evidence of Crohnlike histologic changes in parts of the bowel uninvolved by diverticula. [71]

Ischemic changes

Ischemia may result in histologic changes that mimic Crohn disease, including full-thickness mucosal ulcerations and injury, with crypt architectural remodeling and pseudopyloric metaplasia, also known as “ulcer-associated changes” or “ulcer-associated cell lineage” (UACL).

 

 

emedicine

Updated: Apr 04, 2017
  • Author: Mara Rendi, MD, PhD; Chief Editor: Mamoun Younes, MD  more…

#Cirugía colorrectal: el #protocolo ERAS estricto reduce complicaciones

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Un estudio en ‘JAMA Surgery’ confirma que adherirse a las pautas de recuperación temprana favorece un mejor resultado postquirúrgico.

El primer firmante del estudio, Javier Ripollés, del Servicio de Anestesiología y Reanimación del Hospital Universitario Infanta Leonor, en Vallecas (Madrid).
Luis Camacho

Los protocolos de recuperación temprana tras la cirugía (más conocidos por sus siglas en inglés, ERAS) recogen una veintena de pautas en torno al momento de la intervención, muchas de las cuales han supuesto una revolución en comparación con el manejo tradicional del paciente quirúrgico, tales como evitar el ayuno perioperatorio prolongado y el uso de drenajes y sondas, así como utilizar una analgesia regional e introducir lo antes posible la alimentación oral y la movilización precoz tras la cirugía.

Con estas medidas se intenta reducir al mínimo las complicaciones derivadas de una cirugía que, en el ámbito colorrectal, aparecen en un 25% de los casos y se relacionan con una menor supervivencia a largo plazo de los pacientes con este tipo de cáncer.

Para determinar la relación entre la implantación de los protocolos ERAS y la evolución de los pacientes que han recibido una cirugía colorrectal, un grupo de investigadores, encabezados por Javier Ripollés Melchor, facultativo especialista del Servicio de Anestesiología y Reanimación del Hospital Universitario Infanta Leonor, con apoyo del Grupo Español de Rehabilitación Multimodal (RedGERM), ha llevado a cabo un estudio observacional prospectivo cuyos resultados publica la revista JAMA Surgery. Junto a Ripollés como primer firmante, también figuran como autores Ane Abad Motos y Alfredo Abad Gurumeta, jefa de Sección y jefe de Servicio de Anestesiología y Reanimación del citado hospital madrileño.

El trabajo asocia una mayor adherencia a los protocolos ERAS con menores complicaciones después de la cirugía colorrectal. Como destaca a DM su primer firmante, Javier Ripollés, “las diferencias en el grado de cumplimiento suponen una variación muy importante en las complicaciones que presentan los pacientes de un centro a otro”. En el estudio Power (Postoperative Outcomes Within Enhanced Recovery After Surgery Protocol) han participado 80 hospitales españoles, independientemente de si tenían o no un protocolo ERAS. En total, se reclutaron a 2.084 pacientes: todos intervenidos de cirugía colorrectal programada de manera consecutiva durante dos meses a finales de 2017, con 30 días de seguimiento.

El estudio, sobre 2.084 pacientes en 80 centros, muestra una falta de adherencia a los ERAS y a ciertas medidas de tratamiento estándar

La muestra completa de todos los pacientes (independientemente de su adscripción a un protocolo ERAS) fue dividida en cuartiles de cumplimiento. Así se encontró una reducción del 19% en el número de complicaciones moderadas graves en el grupo de mayor cumplimiento en comparación con el de menor cumplimiento. Asimismo la estancia hospitalaria resultó ser menor en el grupo de mayor cumplimiento (8 frente a 5 días) comparando los grupos de menor y mayor cumplimiento.

Para Ripollés, el estudio refleja que el cumplimiento de estos protocolos aún es bajo, así como el de otras prácticas que teóricamente son un tratamiento estándar: “Nos ha llamado la atención, por ejemplo, que una recomendación de la Organización Mundial de la Salud (OMS) sobre la administración de antibiótico previa a la incisión quirúrgica no se cumpla siempre, lo que se asocia a un 17% más de riesgo de complicaciones postoperatorias. Y también que más del 45% de los pacientes llegan anémicos a quirófano, una cifra muy elevada”.

Estudio destacado en Europa

La evidencia que avala la implantación de los programas ERAS procede fundamentalmente de metanálisis y estudios observacionales. El estudio Power es el segundo en número de pacientes que se publica -el mayor fue un trabajo llevado a cabo en hospitales escandinavos que incluía a unos 2.600 pacientes durante cinco años-, y tiene el aliciente de haberse realizado durante un periodo de tiempo muy corto (dos meses de reclutamiento).

El presente trabajo, que además fue nominado en 2018 a los premios europeos de investigación (Castor Research Awards), es el primer fruto de una línea estable de investigación sobre los beneficios de los protocolos ERAS tras la cirugía, coordinada por Ripollés y RedGERM, que tendrá continuidad con otros tres estudios, en los que se seguirá una filosofía similar de reclutamiento de pacientes y seguimiento.

El siguiente estudio (Power-2), actualmente en proceso de análisis de datos, está enfocado en pacientes operados de prótesis total de cadera y rodilla. Se desarrolla en colaboración con Óliver Marín-Peña, del Servicio de Cirugía Ortopédica y Traumatología del Hospital Infanta Leonor, y participan 850 colaboradores de 131 hospitales españoles, con una muestra de 6.100 pacientes. El Power-3 estará centrado en la cirugía bariátrica y se hará en colaboración con la Sociedad Española de Cirugía de la Obesidad (SECO). Por su parte, el Power-4 pondrá el foco en cirugía de cáncer gástrico.

Una ‘vía’ en vías de expansión

El concepto de la recuperación intensificada tras la cirugía tiene su origen a finales de la década de 1990, cuando el cirujano danés Henrik Kehlet postula sus teorías sobre cómo una serie de medidas basadas en la evidencia a lo largo de todo el periodo perioperatorio pueden disminuir el estrés quirúrgico al que se ve sometido el paciente y mantenerle en un estado fisiológico adecuado, de forma que vuelva al estado previo a la cirugía en el menor tiempo posible y se disminuyan las complicaciones tras la operación.

En España, se han cumplido ya tres años desde la presentación de la Vía Clínica de Recuperación Intensificada en Cirugía Abdominal (RICA), un documento basado en ERAS, elaborado por profesionales de enfermería y medicina de diferentes especialidades, con el apoyo del Ministerio de Sanidad, cuyo objetivo es expandir esta forma de trabajo en todo el Sistema Nacional de Salud.

#Doença de Crohn poderá ser tratada com as próprias células do doente

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Fonte de imagem: Pain Resource

Uma equipa de investigadores desenvolveu uma técnica que emprega as próprias células do paciente para tratar a doença de Crohn. 

A doença de Crohn é uma doença vitalícia e debilitante em que partes do sistema digestivo sofrem inflamação severa, causando diarreia, dores de estômago, cansaço, entre outros sintomas. Embora não se conheçam as causas da doença, sabe-se que tem alguma ligação com o sistema imunitário.

A nova técnica, que demonstrou ter sido eficaz em experiências com células humanas, poderá entrar em ensaio clínico nos próximos seis meses.

Os investigadores do Centro de Investigação Biomédica dos Hospitais Guy and St Thomas, Londres, Reino Unido, desenvolveram a inovadora técnica recorrendo a glóbulos brancos, conhecidos como linfócitos T reguladores, recolhidos de pacientes com a doença de Crohn e comparados com linfócitos de indivíduos saudáveis.

A comparação entre os linfócitos T reguladores de pacientes com Crohn e os de pacientes saudáveis permitiu apurar que os doentes com Crohn produziam menos integrina α4β7, uma proteína específica do sistema gastrointestinal.

Este achado foi a base para o desenvolvimento de uma técnica de terapia celular. A técnica envolve a manipulação de células de pacientes com Crohn com uma molécula conhecida como RAR568 que repõe níveis saudáveis de integrina α4β7.

As células tratadas são novamente injetadas no paciente através de infusão intravenosa.

“Isto é o próximo patamar da terapia celular, na medida em que estamos a ir além do tratamento dos sintomas da doença de Crohn e a tentar reprogramar o sistema imunitário para tratar a doença”, explicou Graham Lord, investigador que liderou este estudo.