381878_kelompok 15 Modul 4 No.docx

FACULTY OF MEDICINE BLOK GASTROENTEROHEPATOLOGI UNIVERSITAS MUSLIM INDONESIA

Makassar, 10 Januari 2019

“MODUL 4”

TUTOR : dr. Farah Ekawati Created By : GROUP 15

DEDY KURNIAWAN

(11020170006)

NADIA ROFIFAH ADELIA

(11020170007)

ADIBAH AFRIASTINI WENNI (11020170133) ARDIANSYAH M. ARFA

(11020170160)

YEYEN ANUGRAH. H

(11020170037)

VANIA ALMIRA

(11020170121)

NUR AZIZAH

(11020170154)

MIFTAHUL JANNA

(11020170042)

ANDI AMBAR YUSUFPUTRA

(11020170058)

NURAFNI

(11020170065)

FACULTY OF MEDICINE UNIVERSITAS MUSLIM INDONESIA MAKASSAR 2019

FOREWORD We thank Allah for the blessings and blessings of His grace so that the results of this tutorial can be resolved properly. And do not forget to send greetings and prayers to the Prophet Muhammad SAW that has brought us from a world full of ignorance to a nature full of intelligence. We also thank the parties who helped make this report and the tutors who guided us during the PBL process. Hopefully this tutorial report can be useful for everyone who has read this report and especially for the drafting team itself. Hopefully after reading this report can expand the knowledge of readers.

Makassar, 10 Januari 2019

Group 15

SCENARIO 1 A 60-year-old man comes to the hospital with a difficult bowel complaint in the last 1 month. In the past 1 week, complaints were felt to be burdensome. Stomach feels bloated. Stools are sometimes like goat’s faeces. Last 6 months weight loss history.

DIFFICULT WORDS -

KEYWORDS 

A 60 year old man



Complaint with a difficulty to defecate in the last 1 month and worsit in the past week



Stomach feels bloated



Stools are sometimes like goat’s feces



Weigth loss history in the last month.

QUESTIONS

1. What is the anatomy and histology based on the scenario ? 2. How is the normal mechanism 0of defecation ? 3. What is the relation between all the diagnoses ? 4. How are the steps to support the diagnoses ? 5. What are the differential diagnoses ? 6. How are the treatments and the prevention of the scenario ? 7. What is the perspective Islamic perpestif based on the scenario ?

DISCUSSION 1. The anatomy and histology based on the scenario • Tenue Intestinum The small intestine is a terminal place for food digestion, nutrient absorption.

• Duodenum a) The superior duodeni pars stretch from the ostium pyloricum gaster to collum vesica fellea, right on the right side of the LI vertebrae, and travel anteriorly to the choledochus duct, gastroduodenal artery, porta hepatis vein, and inferior vena cava. b) Pars descendens duodeni is right on the right side of the midline and stretches from collum vesica felle to the bottom of the vertebrae LIII. c) The inferior duodeni pars are the longest part, crossing the inferior vena cava, aorta and vertebral column. This section is crossed anteriorly by arteries and superior mesenteric veins. d) Pars ascendent duodeni runs up on, or on the left side of the aorta to approximately the edge of the LII vertebra and ends as a jejunal duodeno flexura.

Anatomical and histology images of duodenal • Jejenum – Ileum The length of the entire archipelago is 6-7 meters; jejenum is in the proximal part with a length of approximately 2/5 part of it, while the ileum is in the distal section with a length of approximately 3/5 the remaining parts.

Anatomical and histology images of jejenum and ileum • Crassum intestinum

Shorter than the tenue intestine, about 1.5 meters long. The base is wider than the distal end. Consists of : 1) cecum and process vermiform 2) colon 3) rectum. The crassum intestine can be seen as follows: 1. Caecum This building is the beginning of the colon, one end is dead end and facing the caudal. While the other end is open facing cranial. Located inside the dextra iliac fossa, wrapped by peritoneum (intra peritoneal), it is easy to move. 2. Colon 1. Colon ascendens 2. Colon transversum 3. Colon descendens 4. Colon sigmoideum 3. Rectum It is the caudal (anal) part of the crassum intestine, located retroperitoneal, extending from the height of the 3 sacral vertebrae to the anus. Anus is the mouth of the rectum to the outside world.

Anatomical and histology images of rectum 

Anatomy and function of gastrointestinal organs greatly influence the pattern of defecation. Food that enters the body will pass through the digestive tract to reach the rectum where the process of defecation will take place, so it takes gastrointestinal motility to support the movement of food through it to be excreted in the body in the form of feces.



Feces in normal conditions consist of 75% water, the rest are solid materials consisting of 30% dead bacteria, 10-20% fat, 10-20% inorganic ingredients, 23% protein, and undigested food fibers and elements from digestive sap, such as bile pigments and released cells.



The gastrointestinal tract has a nervous system called the enteric nervous system, all located in the intestinal wall, starting from the esophagus extending to the anus. This system mainly regulates gastrointestinal secretion and movements.



Water absorption in the small intestine is caused by the degree of osmolarity that occurs when dissolved material (especially sodium) is actively absorbed from the intestinal lumen by the villous epithelium. Then it is rearranged through an ion pump called Na + K + ATPase to increase its osmolarity and cause other water & electrolytes to flow passively from the lumen of the small intestine through the intercellular tract into the extracellular fluid. This process

maintains the osmotic balance between intraluminer intestinal fluid and extracellular fluid. The next Kimus goes to the large intestine. In the large intestine there is the bacterium Escherichia coli, this bacteria helps in the process of decaying leftover food into feces. The large intestine absorbs almost all of the water that comes from the small intestine and leaves it only about 1% to be excreted into the stool. The sigmoid large intestine functions as a reservoir that accommodates fecal mass which has reduced its fluid content until the defecation process takes place. Referensi :  

E-jurnal.Kebutuhan Dasar Manusia.Fakultas Kedokteran Universitas Padjadjaran Sobotta Jilid 2.Atlas Anatomi Manusia (Organ-Organ Dalam).

2. The normal mechanism of defecation: 

Defecation`Physiology Approximately 1,500 ml of chimus normally passes through the ileocecal

valve into the large intestine every day. Most of the water and electrolytes in this cimus are absorbed in the colon, usually leaving less than 100 ml of fluid to be excreted in the stool. Also, basically all ions are absorbed, leaving only 1 to 5 meq of

each

sodium

and

chloride

ion

to

be

lost

in

the

stool.

Most absorption in the large intestine is lodged in the middle of the proximal colon, so this part is called the absorbing colon, while the distal colon in principle functions as a place for storing feces to the right time for faecal excretion and is thereforecalledthestoragecolon. The mucosa of the large intestine, such as the intestinal mucosa, has the ability to absorb sodium and also causes absorption of chloride. The tight link between the large intestinal epithelial and epithelial cells is much tighter than the link of the large fine intestine to absorb sodium is much more perfect, that is, passing a much higher concentration gradient - than in the small intestine. This is

especially true when there is a large amount of aldosterone larena aldosterone which greatly enhances

sodium

transportcapability.

In addition, as it occurs in the distal portion of the small intestine, the large intestinal mucosa secretes bicarbonate ions while simultaneously absorbing the same amount of chloride ion in the exchange transport process described earlier. Bicarbonate helps neutralize acidic end products and work bacteria in the large intestine. Absorption of sodium and chloride ions creates an osmotic gradient along the mucosa of the large intestine, which then causes water absorption. The large intestine can absorb a maximum of 5 to 8 L of fluid and electrolytes every day. If the total amount of fluid entering the large intestine through the ileocecal valve or through the secretion of the large intestine exceeds this amount, excess fluid will appear in the faeces as diarrhea. As noted earlier in this chapter, cholera toxins or certain other bacterial infections often cause crypts in the terminal ileum and the large intestine to secrete 10 L or more fluid every day, causing severe diarrhea and frequent death. Many bacteria, especially colon bacilli, even occur normally in the absorbing colon. These bacteria are capable of digesting small amounts of cellulose, in this way providing several calories of additional nutrients for the body. In herbivorous animals, this energy source is very significant, although this is not important to humans. Other substances formed as a result of bacterial activity are vitamin K, vitamin B12, thiamine, riboflavin, and various kinds of money gases causing flatus in the colon, especially carbon dioxide, hydrogen gas, and methane. Vitamin K formed by bacteria is very important because the amount of this vitamin in food consumed daily is normally lacking to maintain adequate blood coagulation. Normally, stool consists of three quarters of water and a quarter of solid materials composed of 30% dead bacteria, 10-20% fat, 10-20% inorganic ingredients, 2-3% protein, 30% food fibers that are not digested and dry elements of digestive sap, such as bile pigments and released epithelial cells. Stool brown is caused by sterkobilin and urobilin, which are derived from bilirubin. Stool odor is

mainly caused by bacterial work products; this product varies from one person to another, depending on the bacterial flora of each person's colon and on the type of food eaten. Products that actually emit odors include indole, skatol, mercaptan and hydrogen sulfide. The process of defecation begins with the mass movement of the descending large intestine which pushes the stool into the rectum. Mass movements arise +/- 15 minutes after eating and only occur several times a day. The presence of feces in the rectum causes rectal stretching and stooling towards the anal sphincter. Reflex Defecation Reflexes arise when stool enters the rectum, then stretching the rectum then creates sensory stimulation of the intestinal and pelvic walls, giving rise to peristaltic waves in the descending large intestine, sigmoid and rectum, pushing the stool towards the anus. Rectal distension causes impulses in the ascending sensory fibers which are then brought to the cortex which raises awareness about the presence of distension. While there is a temporary contraction of the external sphincter muscle, the pubicectal sling (part of the levator ani muscle). Thus there is a reflex called inflation reflex. Delivery of nerve impulses distally through the myenteric plexus in the caudal part of the rectal wall will cause reflex inhibition of smooth muscle internal sphincter muscle. This event is called the rectoshinging relaxation reflex. This internal sphincter relaxation occurs proportionally to the volume and speed of rectal distension. This condition is followed by inhibition of the external anal spingter, which involves reflex pathways and cortical facilitation. Puborektalis reflexes will result in anorectal angle widening (normal 60 - 105 ° to 140 °) causing the anal path to not be blocked. Increased abdominal pressure is associated with peristalsis in the abdominal wall, causing discharge of feces resulting in emptying of the rectum. After the stool comes out, then a closure reflex occurs immediately, this activity occurs very quickly, namely the return of the pelvic floor muscle, the anorectal angle and spingter tone to its original position.

Reference:  Guyton, Arthur C. dan Hall, John E. 2007. Buku Ajar Fisiology Kedokteran Ed. 11. Jakarta: Penerbit Buku Kedokteran EGC.  Tehuteru ES, Hegar B, Firmansyah A. Pola Defekasi pada Anak. Sari Pediatri 2001;3: 129 – 33.  Barrett KE. Lange Gastrointestinal Physiology Philadelpia: The McGrawHill Companies; 2007 3. The relation between all the diagnoses

 Relation between all the symptoms The patient felt difficulty to defecate becase there is a mass at colon descendens . If the mass at colon is going bigger that can make accumulation of feses that why the patient stomach feels bloated. But when the patient trying to defecate , feces will be slowly going through the mass so that why the feces looks like goat’s feces. Reference : 

Slide pengampuh, dr. Andi Irwansyah Achmad,Sp.B, karsinoma kolo. 2017

4. The steps to support the diagnoses  Anamnesis 1. Patient identity 2. Main complaint 

Since when does constipation occur? How long? Repeated, new cases, or long ago (born)?



To see the severity and stage (acute or chronic) When was the last bowel movement?



How many times the frequency of defecation in a week?



What is the shape and consistency of the stool?



Does it need to push harder when defecating?



Does it take longer when defecating?



Has it been accompanied by bleeding? if "yes", the blood comes out together with feces or not?



Is it accompanied by mucus? CHAPTER with mucus usually occurs in diarrhea How does it smell? (Fishy, sour, rotten)



Does pain during defecation / bowel movements?



To show whether the malignancy has occurred, what is the shape and color of the stool? In the malignancy, the shape of the small stool is black (like goat's faeces)



Does the anus feel painful? If "yes" what does it feel like (hot, burning)? what is the feeling at what time?



How is the food pattern that is often consumed (low fiber, a little drink)? Eating patterns or eating history are very important to ask because patients are often too little to drink and eat foods that are low in fiber, this is one of the causes of the occurrence of constipation. If food that is often consumed is a food that is low in fiber, it will cause an intraluminal defect. Have you treated or not? What medicine is given?

Accompanying complaint 

Is there a fever? To get rid of DD, because there is no fever in constipation. Fever usually occurs because of an infection such as diarrhea.



Is there a feeling of bloating?



Is there an enlarged stomach?



Are there complaints about the fart (frequency, difficult / not)?



Does the patient have a problem? If "yes" then it is not a serious illness



Does the patient feel abdominal pain?



Is there a weight loss?



To identify symptoms of malignancy



Is there a history of frequent hunger, thirst, drowsiness, and BAK? To identify the typical symptoms of diabetes mellitus



Is there a urinary problem (difficult)?



Does the patient's anus feel hot, especially when sitting? To identify hemorrhoids



Is the patient having a visual impairment (blurred, diplopia / squint)? To identify symptoms of diabetes mellitus, namely retinopathy with typical symptoms of vision or symptoms of multiple sclerosis accompanied by diplopia / squint eyes.



What is the patient's physical activity (often exercising or not)? To identify whether patients often or rarely exercise or similar physical activity.



Is accompanied by nausea? In hemorrhoids accompanied by nausea. Is accompanied by vomiting? In intestinal obstruction accompanied by vomiting

Past medical history 

Have you ever had the same symptoms?



To find out if symptoms of constipation have been suffered before.



Is there a history of cancer? To find out whether the patient has or has cancer, especially previous intestinal cancer. Possible diagnosis in the direction of lower gastrointestinal obstruction by cancer.



Is there a history of abdominal surgery? To identify paralytic ileo symptoms. One of the complications after abdominal surgery.

Family history 

Is there a history of intestinal malignancy in the family? To find out a familial history that might be reduced, namely malignancy, especially intestinal malignancy.

Physical Examination

Step

Position

Inspection

Supine, head and knees supported

Auscultation

Supine, head and knees supported

Palpation

Supine, head and knees supported

Percussion

Supine, head and knees supported

Check for ascites

Supine, may need to roll patient for shifting dullness

Rectal examination

Left lateral decubitus

Inguinal

Standing

examination

Anatomical structure

Abnormality

Common condition

Umbilicus

Mass or protrusion

Hernia Sister Mary Joseph's node

Stomach

Prominent veins

Portal hypertension

Mass in left upper quadrant

Gastric

carcinoma

Gastric

outlet

obstruction

Pancreas

Mass in right upper quadrant

Pancreatic

carcinoma

Pancreatic pseudocyst

Anatomical structure

Abnormality

Common condition

Gallbladder

Mass in right upper quadrant

Cholecystitis

Carcinoma

of

gallbladder Hydrops of gallbladder

Tenderness and guarding in right upper Acute cholecystitis quadrant

Small intestine

Decreased bowel sounds

Ileus

Increased bowel sounds

Obstruction

Colon

Abdominal mass

Carcinoma

Liver

Increased size

Hepatitis Metastatic Cirrhosis

Decreased size

Cirrhosis

carcinoma

Anatomical structure

Abnormality

Common condition

Nodularity

Metastatic

carcinoma

Cirrhosis

Spleen

Increased size

Acute viral infections Portal

hypertension

Hemolytic anemia

Peritoneal space

Presence of ascites

Portal

hypertension

Metastatic

carcinoma

Congestive

heart

failure

Anus and rectum

Anal mass

Hemorrhoid Anal carcinoma

Anal inflammatory lesion

Fissure Fistula

Rectal mass

Rectal

carcinoma

Benign rectal ulcer

Anatomical structure

Abnormality

Common condition

Inguinal canal

Reducible mass

Direct

hernia

Indirect

hernia

Femoral hernia

Supporting investigation 

Blood tests. doctor will look for a systemic condition such as low thyroid (hypothyroidism).



Examination

of

the

rectum

and

lower,

or

sigmoid,

colon

(sigmoidoscopy). In this procedure, your doctor inserts a lighted, flexible tube into your anus to examine your rectum and the lower portion of your colon. 

Examination of the rectum and entire colon (colonoscopy). This diagnostic procedure allows your doctor to examine the entire colon with a flexible, camera-equipped tube.



Evaluation of anal sphincter muscle function (anorectal manometry). In this procedure, your doctor inserts a narrow, flexible tube into your anus and rectum and then inflates a small balloon at the tip of the tube. The device is then pulled back through the sphincter muscle. This procedure allows your doctor to measure the coordination of the muscles you use to move your bowels.



Evaluation of anal sphincter muscle speed (balloon expulsion test). Often used along with anorectal manometry, this test measures the amount of time it takes for you to push out a balloon that has been filled with water and placed in your rectum.



Evaluation of how well food moves through the colon (colonic transit study).In this procedure, you may swallow a capsule that contains either a radiopaque marker or a wireless recording device. The progress of the capsule through your colon will be recorded over several days and be visible on X-rays. In some cases, you may eat radiocarbon-activated food and a special camera will record its progress (scintigraphy). Your doctor will look for signs of intestinal muscle dysfunction and how well food moves through your colon.



An X-ray of the rectum during defecation (defecography). During this procedure, your doctor inserts a soft paste made of barium into your rectum. You then pass the barium paste as you would stool. The barium shows up on X-rays and may reveal a prolapse or problems with muscle function and muscle coordination.



MRI defecography. During this procedure, as in barium defecography, a doctor will insert contrast gel into your rectum. You then pass the gel. The MRI scanner can visualize and assess the function of the defecation muscles. This test also can diagnose problems that can cause constipation, such as rectocele or rectal prolapse.

Reference : 

At A glance: Anamnesis dan pemeriksaan fisis oleh jonathan glade

5. The differential diagnoses Inflammatory Bowel Disease Inflammatory bowel disease (IBD) is an idiopathic disease caused by a dysregulated immune response to host intestinal microflora. The two major types of inflammatory bowel disease are ulcerative colitis (UC), which is limited to the colonic mucosa, and Crohn disease (CD), which can affect any segment of the gastrointestinal tract from the mouth to the anus, involves "skip

lesions," and is transmural. There is a genetic predisposition for IBD, and patients with this condition are more prone to the development of malignancy. Ulcerative colitis and Crohn disease share many extraintestinal manifestations, although some of these tend to occur more commonly Eyeskin-mouth-joint extraintestinal manifestations (eg, oral aphthae, erythema nodosum, large-joint arthritis, and episcleritis) reflect active disease, whereas pyoderma gangrenosum, primary sclerosing cholangitis (PSC), ankylosing spondylitis, uveitis, kidney stones, and gallstones may occur in quiescent disease. Although both ulcerative colitis and Crohn disease have distinct pathologic findings, approximately 10%-15% of patients cannot be classified definitively into either type; in such patients, the disease is labeled as indeterminate colitis. Systemic symptoms are common in IBD and include fever, sweats, malaise, and arthralgias. Pathophysiology The common end pathway of ulcerative colitis is inflammation of the mucosa of the intestinal tract, causing ulceration, edema, bleeding, and fluid and electrolyte loss. In several studies, genetic factors appeared to influence the risk of inflammatory bowel disease (IBD) by causing a disruption of epithelial barrier integrity, deficits in autophagy, deficiencies in innate pattern recognition receptors, and problems with lymphocyte differentiation, especially in Crohn disease. Inflammatory mediators have been identified in IBD, and considerable evidence suggests that these mediators play an important role in the pathologic and clinical characteristics of these disorders. Cytokines, which are released by macrophages in response to various antigenic stimuli, bind to different receptors and produce autocrine, paracrine, and endocrine effects. Cytokines differentiate lymphocytes into different types of T cells. Helper T cells, type 1 (Th-1), are associated principally with Crohn disease, whereas Th-2 cells are associated principally with ulcerative colitis.

The immune response disrupts the intestinal mucosa and leads to a chronic inflammatory process. In animal studies, a local irritant (acetic acid, trinitrobenzene sulfonic acid) can be inserted via an enema into the colon of rats or rabbits to induce a chemical colitis. An interleukin-10 (IL-10) knockout mouse has been genetically engineered to have some characteristics similar to those of a human with IBD. The cotton-top marmoset, a South American primate, develops colitis very similar to ulcerative colitis when the animal is subjected to stress. A. Ulcerative colitis In ulcerative colitis, the inflammation begins in the rectum and extends proximally in an uninterrupted fashion to the proximal colon and could eventually involve the entire length of the large intestine. The rectum is always involved in ulcerative colitis; and unlike in Crohn disease, there are no "skip areas" (ie, normal areas of the bowel interspersed with diseased areas), unless pretreated with topical rectal therapy (ie, a steroid or 5-aminosalicylic acid [5-ASA] enema). The disease remains confined to the rectum in approximately 25% of cases, and in the remainder of cases, ulcerative colitis spreads proximally and contiguously. Pancolitis occurs in 10% of patients. The distal terminal ileum may become inflamed in a superficial manner, referred to as backwash ileitis. Even with less than total colonic involvement, the disease is strikingly and uniformly continuous. As ulcerative colitis becomes chronic, the colon becomes a rigid foreshortened tube that lacks its usual haustral markings, leading to the lead-pipe appearance observed on barium enema.

Figure 1. Inflamed colonic mucosa in a patient with ulcerative colitis A. Crohn disease Crohn disease can affect any portion of the gastrointestinal tract, from the mouth to the anus, and causes 3 patterns of involvement: inflammatory disease, strictures, and fistulas. This disease consists of segmental involvement by a nonspecific granulomatous inflammatory process. The most important pathologic feature of Crohn disease is that it is transmural, involving all layers of the bowel, not just the mucosa and the submucosa, which is characteristic of ulcerative colitis. Furthermore, Crohn disease is discontinuous, with skip areas interspersed between 2 or more involved areas. Late in the disease, the mucosa develops a cobblestone appearance, which results from deep, longitudinal ulcerations interlaced with intervening normal mucosa (see the images below). In 35% of cases, Crohn disease occurs in the ileum and colon; in 32%, solely in the colon; in 28%, in the small bowel; and in 5%, in the gastroduodenal region. Diarrhea, cramping, and abdominal pain are common symptoms of Crohn disease in all of the above locations, except for the gastroduodenal region, in which anorexia, nausea, and vomiting are more common. Rectal sparing is a typical but not constant feature of Crohn disease. However, anorectal complications (fistulas, abscesses) are common. Much less commonly, Crohn disease involves the more proximal parts of the GI tract, including the mouth, tongue, esophagus, stomach, and duodenum.

Figure 2. Cobblestone change of the mucosa of the termina ileum in a patient with Crohn disease.

Figure 3. The mucosal barrier in health, in Crohn’s disease, and in ulcerative colitis.

Etiology Several environmental risk factors have been proposed as contributing to the IBD pathogenesis, but the results are inconsistent, and the limitations of the studies preclude drawing firm conclusions. The most consistent association described has been smoking, which increases the risk of Crohn disease. However, current smoking protects against ulcerative colitis, whereas former

smoking increases the risk of ulcerative colitis. Dietary factors have also been inconsistently described. In some studies, high fiber intake and high intake of fruits and vegetables appear protective against IBD. The E3N prospective study found that high animal protein intake (meat or fish) carried a higher risk of IBD. 1. Genetics Persons with IBD have a genetic susceptibility for the disease, and considerable research over the past decade has improved our understanding of the role of these genes. Note that these genes appear to be permissive (ie, allow IBD to occur), but they are not causative (just because the gene is present does not necessarily mean the disease will develop). First-degree relatives have a 5- to 20-fold increased risk of developing IBD, as compared with persons from unaffected families. The child of a parent with IBD has a 5% risk of developing IBD. Twin studies show a concordance of approximately 70% in identical twins, versus 5%-10% in nonidentical twins. Of patients with IBD, 10%-25% are estimated to have a first-degree relative with the disease. Monozygous twin studies show a high concordance for Crohn disease but less so for ulcerative colitis. 2. Smoking The risk of developing ulcerative colitis is higher in nonsmokers and former smokers than in current smokers. The onset of ulcerative colitis occasionally appears to coincide with smoking cessation; however, this does not imply that smoking would improve the symptoms of ulcerative colitis. There has been limited success with the use of nicotine patches. Crohn disease patients have a higher incidence of smoking than the general population, and smoking appears to lessen the response to medical therapy.

Epidemiology International statistics The highest rates of IBD are assumed to be in developed countries, and the lowest are considered to be in developing regions; colder-climate regions and

urban areas have a greater rate of IBD than those of warmer climates and rural areas. Internationally, the incidence of IBD is approximately 0.5-24.5 cases per 100,000 person-years for ulcerative colitis and 0.1-16 cases per 100,000 personyears for Crohn disease. Overall, the prevalence for IBD is 396 cases per 100,000 persons annually. Diagnostic evaluation

The (initial) diagnosis of IBD is made on the basis of history and physical examination, along with the laboratory values and the findings of endoscopic, histological, and radiological studies. No single feature establishes the diagnosis. Chronic diarrhea is a characteristic manifestation, with bloody diarrhea typifying ulcerative colitis; abdominal pain and weight loss are also typical. For differential diagnosis, the patient should be specifically asked about food intolerance, drugs taken (including nonsteroidal anti-inflammatory drugs [NSAID]), travel abroad, and cigarette smoking. IBD should be considered as a possible diagnosis in children with unexplained failure to thrive, nutritional deficiencies (particularly vitamin B12 deficiency), certain skin changes (erythema nodosum, pyoderma gangrenosum), and seronegative rheumatic joint pain (a possible extra-intestinal manifestation of IBD) Endoscopy is the gold standard for the initial diagnosis of IBD. If Crohn’s disease is suspected, the terminal ileum must be intubated, because most patients have mucosal changes there. In severe exacerbations of ulcerative colitis, with

maximum inflammation nearly always in the rectum, sigmoidoscopy often suffices for the acute evaluation. Histological examination yields important additional information; architectonic abnormalities confirm the diagnosis. In some cases, the two kinds of IBD can be distinguished from each other, and from other types of bowel disease (infection) only on further follow-up, but over 90% of patients have a definite diagnosis 5 years after presentation. The upper gastrointestinal tract should be evaluated by esophagogastroduodenoscopy with biopsy at the time of initial diagnosis, because extensive involvement with Crohn’s disease confers a worse prognosis. Ultrasonography and magnetic resonance enterography of the small intestine complete the initial diagnostic evaluation for the extent of disease. We also often use ultrasonography to monitor the course of disease, although MRI (or, in emergency cases, CT) is superior to ultrasonography for the demonstration of fistulae and abscesses. MRI is also suitable for the evaluation of stenoses, showing not only their extent and prestenotic dilatation, but also wall thickening and perfusion (which can help distinguish fibrotic from inflammatory stenoses). This, in turn, is helpful in treatment planning, the decision whether to treat with anti-inflammatory drugs or to perform dilatation. Toxic megacolon can be a serious acute manifestation of ulcerative colitis; a plain abdominal x-ray demonstrating colonic dilatation over 6 cm without any distal stenosis is diagnostic. The treatment of IBD The pharmacotherapy of IBD as recommended in current guidelines is wholly based on the findings of controlled trials and meta-analyses. The treatment should always be adapted to the site, extent, and course of disease in the individual patient, with further adaptations guided by the clinical response; there is inadequate evidence to support basing treatment escalations on endoscopic findings alone. A strategy of immediate, maximal immunosuppression, including antibody administration, at the time of diagnosis has not been incorporated into the guidelines, as this would constitute overtreatment for many patients, with frequent adverse effects. Thus, the standard therapeutic strategy is clinically

guided, stepwise treatment, beginning with relatively well-tolerated drugs and proceeding incrementally toward aggressive immunosuppression. As the individual course of disease is unpredictable, clinical follow-up should be frequent, and the treatment should be escalated whenever there has been an unsatisfactory response. This strategy enables the early detection of disease complications, while avoiding the costly and unnecessary provision of antibody therapy to uncomplicated patients. Table 1 Evidence levels of treatment recommendations for chronic inflammatory bowel disease Crohn’s disease Involvement/c

Ulcerative colitis Treatment

ourse

Evide

Involvement/c

nce

ourse

Treatment* Eviden cD

level Ileocecal

Budesonide I

involvement

Mesalazine

Proctitis

II

Topical

II

mesalazine

II

Glucocortic I

Plus topical II

oids (syst.)

steroids Topical tacrolimus

Colonic

Sulfasalazin I

Left

involvement

e

if

I

Glucocortic

colitis, Mesalazine mesalazine- (topical

resistant

oids

II

+ III

systemic) then glucocortico ids

Small-bowel

Glucocortic II

Widespread

Mesalazine

involvement

oids

involvement,

(topical

I

+ III

Crohn’s disease Involvement/c

Ulcerative colitis Treatment

ourse

Evide

Involvement/c

nce

ourse

Treatment* Eviden cD

level if

mesalazine- systemic)

resistant

then glucocortico ids

Steroid-

Anti-TNFα

resistant course

or

I

Severe course

anti- I

Glucocortic

II

oids i. v.

integrin Antibodies Maintenance of Azathioprin I

Steroid-

remission(steroi e

II

resistant course e

d-dependent)

6-

II

Infliximab

mercaptopu

I

Tacrolimus

rine

I

I II

I

Methotrexat

Maintenance of M esalazine I

e

remission

Anti- TNFα

then E. coli I

if

Nissle

I

antibodies

mesalazine-

then

Anti-

intolerant

azathioprine

integrin antibodies

if

/6-

mesalazineresistant steroiddependent

Laboratory

Cyclosporin I

mercaptopu or

rine, TNFα

anti-

Hematologic tests - Complete blood cell count The components of the complete blood cell (CBC) count can be useful indicators of disease activity and iron or vitamin deficiency. An elevated white blood cell (WBC) count is common in patients with active inflammatory disease and does not necessarily indicate infection. Anemia is common and may be either an anemia of chronic disease (usually normal mean corpuscular volume [MCV]) or an iron deficiency anemia (MCV is often low). Anemia may result from acute or chronic blood loss, malabsorption (iron, folate, and vitamin B12) or may reflect the chronic disease state. Note that the MCV can be elevated in patients taking azathioprine (Imuran) or 6-mercaptopurine (6-MP). Generally, the platelet count is normal, or it may be elevated in the setting of active inflammation. - Nutritional evaluation: Vitamin B12 evaluation, iron studies, RBC folate, nutritional markers Serology - ANCA and ASCA tests Perinuclear antineutrophil cytoplasmic antibodies (pANCA) have been identified in some patients with ulcerative colitis, and anti-Saccharomyces cerevisiae antibodies (ASCA) have been found in patients with Crohn disease. The combination of positive pANCA and negative ASCA has high specificity for ulcerative colitis, whereas the inverse pattern—positive ASCA, negative pANCA—is more specific for Crohn disease. [1] However, false-positive (and false-negative) results are not uncommon; therefore, at this time, serologic markers cannot be used to definitively rule in or exclude inflammatory bowel disease (IBD). Radiography - Upright chest and abdominal radiography Ultrasonography Ultrasonography (US) is a non-invasive technique in diagnosing Crohn

disease. Although this technique has a sensitivity of 84% and a specificity of 92%, it has less accuracy when disease is located proximal to the terminal ilium. Colonoscopy Colonoscopy with ileoscopy in the assessment of Crohn disease has a sensitivity of 74% and a specificity of 100%, leading to a positive predictive value of 100% as a diagnostic test. [67] When paired with small bowel followthrough, the sensitivity of this pair of diagnostic tests is increased to 78%, with a continued positive predictive value of 100%. Upper GI Endoscopy Esophagogastroduodenoscopy (EGD) is used for the evaluation of upper gastrointestinal tract symptoms, particularly in patients with Crohn disease. Aphthous ulceration occurs in the stomach and duodenum in 5%-10% of patients with Crohn disease. The diagnosis of Crohn disease may be made after gastric or duodenal ulcers fail to heal with acid suppression alone but is usually accompanied by ileal or ileocolonic Crohn disease. Reference: 

Molodecky NA, Soon IS,Rabi DM, et al. Increasing incidence and prevalence of the inflammatory bowel disease based on systematic review. Gastroenterohepatology.2014

Colon Cancer  Background Invasive colorectal cancer is a preventable disease. Early detection through widely applied screening programs is the most important factor in the recent decline of colorectal cancer in developed countries (see Deterrence/Prevention). In the past 10 years, an unprecedented advance in systemic therapy for colorectal cancer has dramatically improved outcome for patients with metastatic disease.

Until the mid-1990s, the only approved agent for colorectal cancer was 5fluorouracil. Since then, new agents in a variety of classes have become available, including the following: 

Cytotoxic agents (eg, irinotecan, oxaliplatin)



Oral fluoropyrimidines (ie, capecitabine)



Biologic

agents

(eg,

bevacizumab,

cetuximab,

panitumumab,

pembrolizumab, nivolumab) [7] 

Most recently, anti-angiogenic agents (ie, ziv-aflibercept, regorafenib)

Although surgery remains the definitive treatment modality, these new agents will likely translate into improved cure rates for patients with early-stage disease (stage II and III) and prolonged survival for those with stage IV disease.  Etiology Colorectal cancer is a multifactorial disease process. Genetic factors, environmental exposures (including diet), and inflammatory conditions of digestive tract are all involved in the development of colorectal cancer. Although much about colorectal cancer genetics remains unknown, current research indicates that genetic factors have the greatest correlation to colorectal cancer. Hereditary mutation of the APC gene is the cause of familial adenomatous polyposis (FAP), in which affected individuals carry an almost 100% risk of developing colon cancer by age 40 years. The risk factor; 

Hereditary nonpolyposis colon cancer syndrome (HNPCC, Lynch syndrome) poses about a 40% lifetime risk for developing colorectal cancer. Lynch syndrome is characterized by deficient mismatch repair (dMMR) due to inherited mutation in one of the mismatch repair genes, such as hMLH1, hMSH2, hMSH6, hPMS1, hPMS2, and possibly other undiscovered genes. HNPCC is a cause of about 6% of all colon cancers. Although the use of aspirin may reduce the risk of colorectal neoplasia in some populations, a study by Burn et al found no effect on the incidence of colorectal cancer in carriers of Lynch syndrome with use of aspirin, resistant starch, or both.



Dietary factors are the subject of intense and ongoing investigations. Epidemiologic studies have linked increased risk of colorectal cancer with a diet high in red meat and animal fat, low-fiber diets, and low overall intake of fruits and vegetables. A study by Aune et al found that a high intake of fiber was associated with a reduced risk of colorectal cancer. In particular, cereal fiber and whole grains were found to be effective. A study by Pala et al found that high yogurt intake was also associated with a decreased risk for colorectal cancer.



Obesity and lifestyle choices such as cigarette smoking, alcohol consumption, and sedentary habits have also been associated with increased risk for colorectal cancer. A meta-analysis of prospective cohort studies found a modest but significant elevation of colorectal cancer risk in current smokers; risk was higher for men and for rectal cancers than colon cancers, and persisting in former smokers. Activation of the WNT signaling pathway, which most often results from APC loss, plays a critical role in the development of colorectal cancer, and CTNNB1 (βcatenin) is a major mediator of the WNT pathway. WNT-CTNNB1 signaling also appears to be involved in obesity, glucose metabolism, and metabolic diseases such as obesity and type II diabetes. Consequently, Morikawa et al hypothesized that the association of obesity and physical activity with colorectal cancer risk might differ by tumor subtypes according to CTNNB1 status.



Inflammatory bowel diseases such as ulcerative colitis and Crohn disease also carry an increased risk of developing colorectal adenocarcinoma.



Epidemiology Worldwide, colorectal cancer is the second most common in cancer in women

(614,000 cases, 9.2% of all cancers) and the third most common in men (746,000 cases, 10.0% of the total). Geographically, the incidence varies as much as 10fold. The highest estimated rates are in Australia/New Zealand (per 100,000

population, 44.8 in men and 32.2 in women), and the lowest in Western Africa (per 100,000 population, 4.5 in men and 3.8 in women). Colorectal cancer causes approximately 694,000 deaths annually, accounting for 8.5% of cancer mortality overall. More deaths (52%) occur in the lessdeveloped regions of the world, reflecting a poorer survival in these regions. Geographically, mortality rates worldwide vary six-fold in men and four-fold in women, with the highest estimated mortality rates in both sexes in Central and Eastern Europe (20.3 per 100,000 for men, 11.7 per 100,000 for women), and the lowest in Western Africa (3.5 and 3.0, respectively). Racial, sexual, and agerelated disparities in incidence 

Pathophysiology

Genetically, colorectal cancer represents a complex disease, and genetic alterations are often associated with progression from premalignant lesion (adenoma) to invasive adenocarcinoma. Sequence of molecular and genetic events leading to transformation from adenomatous polyps to overt malignancy has been characterized by Vogelstein and Fearon. [8] The early event is a mutation of APC (adenomatous polyposis gene), which was first discovered in individuals with familial adenomatous polyposis (FAP). The protein encoded by APC is important in the activation of oncogene c-myc and cyclin D1, which drives the progression to malignant phenotype. Although FAP is a rare hereditary syndrome accounting for only about 1% of cases of colon cancer, APC mutations are very frequent in sporadic colorectal cancers. In addition to mutations, epigenetic events such as abnormal DNA methylation can also cause silencing of tumor suppressor genes or activation of oncogenes. These events compromise the genetic balance and ultimately lead to malignant transformation. Other important genes in colon carcinogenesis include the KRAS oncogene, chromosome 18 loss of heterozygosity (LOH) leading to inactivation of SMAD4 (DPC4), and DCC (deleted in colon cancer) tumor suppression genes. Chromosome arm 17p deletion and mutations affecting the

p53 tumor suppressor gene confer resistance to programmed cell death (apoptosis) and are thought to be late events in colon carcinogenesis. A subset of colorectal cancers is characterized with deficient DNA mismatch repair. This phenotype has been linked to mutations of genes such as MSH2, MLH1, and PMS2. These mutations result in so-called high frequency microsatellite

instability

(H-MSI),

which

can

be

detected

with

an

immunocytochemistry assay. H-MSI is a hallmark of hereditary nonpolyposis colon cancer syndrome (HNPCC, Lynch syndrome), which accounts for about 6% of all colon cancers. H-MSI is also found in about 20% of sporadic colon cancers. Practice Essentials Colon cancer is the most common type of gastrointestinal cancer. It is a multifactorial disease process, with etiology encompassing genetic factors, environmental exposures (including diet), and inflammatory conditions of the digestive tract. Surgery currently is the definitive treatment modality. The image below depicts standard colectomies for adenocarcinoma of the colon.  Signs and symptoms Colon cancer is now often detected during screening procedures. Other common clinical presentations include the following: 

Iron-deficiency anemia



Rectal bleeding



Abdominal pain



Change in bowel habits



Intestinal obstruction or perforation

 Physical findings may include the following: 

Early disease: Nonspecific findings (fatigue, weight loss) or none at all



More advanced disease: Abdominal tenderness, macroscopic rectal bleeding, palpable abdominal mass, hepatomegaly, ascites

 Diagnosis Laboratory studies that may be helpful include the following: 

Complete blood count



Chemistries and liver function tests



Serum carcinoembryonic antigen

Imaging studies that may facilitate staging include the following: 

Chest radiography



Chest computed tomography



Abdominal barium study



Abdominal/pelvic CT



Contrast ultrasonography of the abdomen and liver



Abdominal/pelvic MRI



Positron emission tomography, including fusion PET-CT scan

Other procedures that may be warranted include the following: 

Colonoscopy



Sigmoidoscopy



Biopsy of suspicious lesions



Double-contrast barium enema

Current TNM classification is as follows: 

Tx – Primary tumor cannot be assessed



T0 – No evidence of primary tumor



Tis – Carcinoma in situ: intraepithelial or or intramucosal carcinoma (involvement of lamina propria with no extension through the muscularis mucosa)



T1 – Tumor invades submucosa (through the muscularis mucosa but not into the muscularis propria)



T2 – Tumor invades muscularis propria



T3 – Tumor invades through the muscularis propria into the pericolorectal tissues



T4a – Tumor invades through the visceral peritoneum (including gross perforation of the bowel through tumor and continuous invasion of tumor through areas of inflammation to the surface of the visceral peritoneum)



T4b – Tumor directly invades or is adherent to other organs or structures

 Management

Surgery is the only curative modality for localized colon cancer (stage I-III). Surgical resection potentially provides the only curative option for patients with limited metastatic disease in liver and/or lung (stage IV disease). Surgical options include the following: 

Right hemicolectomy: For lesions in the cecum and right colon



Extended right hemicolectomy: For lesions in the proximal or middle transverse colon



Left hemicolectomy: For lesions in the splenic flexure and left colon



Sigmoid colectomy: For sigmoid colon lesions



Total abdominal colectomy with ileorectal anastomosis: For selected patients with hereditary nonpolyposis colon cancer, attenuated familial adenomatous polyposis, metachronous cancers in separate colon segments, or acute malignant colon obstructions with unknown status of the proximal bowel.

Other therapeutic options for patients who are not surgical candidates include the following: 

Cryotherapy



Radiofrequency ablation



Hepatic arterial infusion of chemotherapeutic agents

Regimens used for systemic chemotherapy may include the following: 

5-Fluorouracil (5-FU)



Capecitabine



Oxaliplatin



Irinotecan



Combinations of multiple agents (eg, capecitabine or 5-FU with oxaliplatin, 5-FU with leucovorin and oxaliplatin)

 Physical Examination Physical examination findings can be very nonspecific (eg, fatigue, weight loss) or normal early in the course of colon cancer. In more advanced cases, any of the following may be present: 

Abdominal tenderness



Macroscopic rectal bleeding



Palpable abdominal mass



Hepatomegaly



Ascites



 Treatment 

Surgical care



Laparoscopic surgery



Metastatic colorectal cancer



Ablation

 Prognosis The approximate 5-year survival rate for colorectal cancer patients in the United States (all stages included) is 65%. Survival is inversely related to stage: approximate 5-year survival rates are 95% for patients with stage I disease, 60% for those with stage III disease, and 10% for those with stage IV (metastatic) disease (see Staging). A study by Chua et al found that approximately one in every three patients who undergo resection for colorectal liver metastases become actual 5-year survivors. Of those, approximately half survive 10 years and are cured of colorectal liver metastases. A multivariate analysis of 1001 patients who underwent potentially curative resection of liver metastases identified five factors as independent predictors of worse outcome :



Size greater than 5 cm



Disease-free interval of less than a year



More than one tumor



Primary lymph-node positivity



Carcinoembryonic antigen (CEA) level greater than 200 ng/mL

Reference: Tomislav Dragovich, MD, PhD. 2018.

Colon Cancer,

Drugs &

Diseases. Medscape

INTUSSUSCEPTION  Pathogenesis Intussusception is the invagination of one portion of the intestine into another and is the most common form of intestinal obstruction in infancy. Intussusception begins as a proximal segment of intestine, the intussusceptum, telescopes into a more distal one, the intussuscipiens. The intussusceptum is propagated distally by the action of peristalsis. This leads to compression and angulation of the mesenteric vessels to the invaginated bowel with subsequent obstruction, ischemia, and, eventually, necrosis. Necrosis begins at the apex of the intussusceptum

and

extends

proximally.

Secondary

pressure

on

the

intussuscipiens may cause ischemic necrosis of its outer layer resulting in free perforation or prolapse of the intussusceptum into the peritoneal cavity.

Greater than 80% of intussusception involves the ileocecal region with ileoileal, colocolic. and jejujojenal variations progressively less common. Eighty percent of ileocolic intussusceptions have their apex in the ascending or transverse colon. Isolated retrograde small bowel intussusception has been described. "’ Gastroduodenal and duodenogastric invaginalions have been reported as complications of gastroslomy tubes and in association with gastric polyps. The wall of the terminal ileum of infants is rich in lymphoid tissue, and in approximately 90% of cases there is no obvious cause other than hyperplasia of this lymphoid tissue. In the remaining 10%. there is a distinct pathological lead point or other underlying abnormality.| Under the age of 2 years. lead points occur in less than 4%; after the age of 2 years, a pathological lead point is found in one third of patients. One half of children with recurrent intussusception will have lead points. In contrast to the 10% incidence of lead points in children, adults with intussusception have pathological lead points greater than 90% of the time. Adult intussusceptions are of the small bowel variety over 75% of the time, and are associated with malignant lesions 50% of the time.

There are many different pathological lead points for intussusception in children (Table l). The most common lead point is Meckel’s diverticulum. which can cause intussusception throughout childhood. Duplication cysts also seem to be independent of age. whereas intestinal polyps and lymphomas affect older childrenFl‘x-M Small bowel tumors are rare in children but most often present with intussusception.48 Over the age of 3 years. ileal lymphoma or lymphosarcoma should be considered. In older children with cystic fibrosis, abnormally viscous bowel contents are thought to play a role in subacute ileocolie intussusception. Postoperative intussusception accounts for only l% to 2% of all cases and is associated with both abdominal and nonabdominal procedures.Intriguing studies suggest hypergastiinemia may play a role in the pathogenesis of intussusception.  Clinical Presentation Classically, infants with intussusception are previously healthy and present with intermittent, severe cramping abdominal pain. Episodes are characterized by screaming, drawing up of the legs. and flexing at the waist and last anywhere from several seconds to several minutes. The time between attacks ranges from 5 to 30 minutes during which infants are generally calm with normal appearance and activity. Some infants are somnolent or lethargic between attacks. Vomiting is a very common feature, initially of undigested food. then bilious. Early in the course of the illness, stools appear normal but may eventually become dark red and mucoid resembling “currant jelly,” a sign of intestinal ischemia and mucosal sloughing. Although blood in the stool (occult or gross) is quite common, signihcant or ongoing hemorrhage from intussusception is unusual.  Symptoms A thorough review of the literature by Stringer et all indicates the following mean occurrence of symptoms: abdominal pain, 83%; vomiting, 85%; blood in stool (occult or gross), 53%; abdominal mass, 63%. The classic triad of colicky. intermittent abdominal pain; vomiting; and currant jelly stool appears in only 10%

to 20% of cases. Changing the triad to pain, vomiting, and gross or occult blood increases the average incidence of the triad to 32%. Clinical signs with significant positive predictive value (PPV) for intussusception include right upper quadrant abdominal mass (PPV 94%), gross blood in stool (PPV 80%), blood on rectal examination (PPV 78%), the triad of intermittent abdominal pain, vomiting and right upper quadrant mass (PPV 93%). And the triad with occult or gross blood per rectum (PPV 100%).  Additional Examination 

Abdominal Radiograph

Although rarely definitive, the plain abdominal film can be helpful for the diagnosis. The most specific and sensitive sign is a soft-tissue mass with 2 concentric circles of fat density. the so-called “target sign” (Fig 1). Other findings include the absence of cecal gas and stool, loss of visualization of the tip of the liver, and paucity of bowel of gas, particularly in the right lower quadrant. Overall. the plain abdominal radiograph identities intussusception only about 50% of the time. 

Sonography

The sonographic appearance of intussusception was first described in the l980s.Characteristic findings include the target sign seen on transverse section and the pseudokidney sign seen on longitudinal section (Fig 2). This appearance makes the sonographic diagnosis or exclusion of intussusception straightforward. In 1987, Pracos et al82 reported l00% accuracy of sonography for the diagnosis and exclusion of intussusception in 426 children, including I45 with intussusception. A 97% to 100% accuracy rate has been verified since by others. In addition to the positive predictive value of ultrasonography, large, prospective studies also have shown a l00% negative predictive value. In these studies, no patients with a negative sonogram had intussusception at enema.Additional advantages

of

sonography include

the

ability to

document

ileo-ileal

intussusception, the absence of ionizing radiation to the patient, and identification of lead points.



Diagnostic Enema

Barium study of the colon has been the gold standard in many parts of the world until the mid 1980s when it was recognized that sonography could accurately diagnose intussusception (Fig 3). It was also around this time that the benefits of air contrast enema both for diagnosis and treatment of intussusception became evident. Many institutions still consider air enema the quickest method of excluding or confirming the presence of intussusception. It also can be more cost effective. Particularly with an affirmative finding of intussusception in which the condition can be both diagnosed and treated with a single procedure.  Treatment Successful management of intussusception depends on early diagnosis, adequate resuscitation, and prompt reduction. This is best achieved through close cooperation between surgeon and radiologist. Nanoperarive Reduction It is now generally accepted that nonoperative reduction of intussusception should be attempted in most patients. Absolute contraindications to nonoperative reduction include peritonitis, perforation, or profound shock. Relative contraindications to nonoperative reduction include chronic and neonatal intussusceptions, history greater than 48 hours, small bowel obstruction on plain radiograph,and children older than 2 years.In these situations there is a lower likelihood of success, a higher incidence of pathological lead points, and an increased risk of complications. Nonoperative reduction in these circumstances should be considered in the context of the patient history and clinical condition. The first reports of barium enema reduction of intussusception under huoroscopic control occurred in 1927,In the 1980s, pneumatic reduction using air as the contrast agent was reported in China with high success rates in series of greater than 6,000 patients.” In recent years, pneumatic reduction has become the procedure ofchoice.

Air contrast enema with huoroscopic guidance has several advantages over enema reduction with barium 0r water-soluble contrast. Air enema is quicker, less messy, easier to perform, and therefore delivers less radiation to the patients who appear to be more comfortable during the procedure?Although perforation rates for both air and barium are less than 1%, the morbidity in the event of perforation with air versus barium clearly favors pneumatic reduction.ml The review of Stringer et al” of the literature from 1980 to 1991 found that reduction rates with barium 0r water-soluble contrast were 50% to 78% versus 75% to 94% success with pneumatic reduction. Review of more recent series (1995 through 1998) shows barium reduction success rates at 50% to 85% and pneumatic reduction success rates at 81% to 91 %.Although these data have led to air contrast enema being

the

current

procedure

ofchoice

for

nonoperative

reduction

of

intussusception, to date there is still no large,prospective study comparing the use and success of pneumatic and barium or water soluble enemas under fiuoroscopic guidance.  Opemtive Reduction Operative reduction is necessary when radiological techniques are contraindicated or have failed, when a pathological lead point is suspected, or in the case of multiple recurrences (Fig 4). The operative approach is generally through a right-sided transverse incision slightly above or below the umbilicus. Gentle, steady pressure at the apex of the intussusception usually will achieve reduction, after which, bowel is allowed to reperfuse and is then inspected for viability. Necrotic areas, persistently ischemic areas, or intussuscepted areas that cannot be reduced require prompt resection and primary anastomosis.

Many surgeons perform appendectomy to avoid future confusion regarding its presence. With recurrence rates for operative reduction only to 1% to 4%, appendectomy should not pose a significant risk with respect to the need for reduction enema in acute postoperative reintussusception. In the event that acute postoperative intussusception does occur, successful barium enema reduction of intussusception without disruption of the appendiceal stump has been reported as early as 6 days status post open reduction ofintussusception with appendectomy. Reference : 

Difiore, John. W.B.Saunders Company .2011.Intussusception. Transaction of the society for improvement of medical and chirurgical knowledge page 214-218.

Colorectal polyps A polyp is defined as any mass protruding into the lumen of a hollow viscus. Colorectal polyps may be classified by their macroscopic appearance as sessile (flat, arising directly from the mucosal layer) or pedunculated (extending from the mucosa through a fibrovascular stalk). Colorectal polyps may also be histologically classified as neoplastic or as non-neoplastic (hyperplastic, hamartomatous, or inflammatory). The neoplastic polyps are of primary importance because they harbor a malignant potential, which represents a stage in the development of colorectal cancer. For this reason, it is essential to identify these polyps at a sufficiently early stage, when a simple outpatient procedure to

remove them can interrupt the development of colorectal cancer and prevent disease and death. When invasive carcinoma arises in a polyp, careful consideration must be given to ensuring the adequacy of treatment. Although most neoplastic polyps do not evolve into cancer, it is well accepted that the majority of colorectal carcinomas evolve from adenomatous polyps; the sequence of events leading to this transformation is referred to as the adenoma-to-carcinoma sequence. The presence of a systemic process that promotes the development of multiple gastro-intestinal polyps is termed ‘polyposis’. Hereditary gastrointestinal polyposis syndromes account for approximately 1% of all cases of colorectal cancer and are associated with a broad spectrum of extra-colonic tumors. Early detection and accurate classification of these syndromes are essential, in order to initiate a surveillance program for the early detection of cancer. Several polyposis syndromes have been described, each having its own genetic basis and characteristic polyp distribution, clinical presentation, and malignancy risk.  Colorectal Polyps ‘Polyp’ is a term derived from the Greek word polypous, which means ‘morbid lump.’ Generally, this term describes any mass protruding into the lumen of a hollow vessel, anywhere in the gastro-intestinal, genito-urinary or respiratory tracts. Usually, polyps arise from the mucosal layer of these organs, although some submucosal pathologies may cause mucosal protrusion into the lumen and resemble mucosal polyps. Not all polyps necessarily exhibit neoplastic behavior. Colorectal polyps may be histologically classified as neoplastic, hyperplastic, hamartomatous, or inflammatory. The neoplastic polyps are of primary importance because they harbor a malignant potential, which represents a stage in the development of colorectal cancer. For this reason, it is essential to identify these polyps at a sufficiently early stage, when a simple office procedure to remove them can stop the development of colorectal cancer and prevent disease and death.

Colorectal polyps may be classified by their colonoscopic appearance as sessile (flat, arising directly from the mucosal layer) or pedunculated (extending from the mucosa through a fibrovascular stalk)

Colonoscopic display of sessile polyps (1a) and pedunculated (1b).  Diagnosis And Treatment Colorectal polyps can be diagnosed by endoscopy or bar- ium radiography. When there is an indication to examine the entire large bowel, colonoscopy is the diagnostic pro- cedure of choice. It is the most accurate method of detecting polyps of all sizes and it allows immediate biopsy or polypectomy. Most polyps found during colonoscopy can be completely and safely resected, usually using electrocautery techniques. Scientific studies now conclusively show that resecting adenomatous polyps prevents colorectal cancer. Colonic polyps can be diagnosed either by endoscopy or barium radiography. Because most polyps are asymptom- atic, they are usually found incidentally or as the result of screening. Colonoscopy is the procedure of choice for di- agnosing colorectal polyps. It is the most accurate method for detecting polyps of all sizes, and it allows biopsy of lesions and resection of most polyps. An earlier controlled, single-blinded comparison study of colonoscopy and double-contrast barium enema performed by expert examiners reported an accuracy of 94% and 67% for diag- nosing polyps for colonoscopy and radiographic studies, respectively. More recently, the National Polyp Study reported the results of a similar controlled comparison of colonoscopy and double-contrast barium enema performed in a

large cohort of patients undergoing postpolypectomy surveillance. The barium enema study missed 52% of pol- yps that were 1 cm. In two other recently controlled investigations, tandem colonoscopies performed by two ex- perienced examiners indicated an appreciable miss rate for polyps measuring 10 mm in diameter, but very few polyps 10 mm were undetected by the first examination. Most polyps found during colonoscopy can be completely and safely removed by electrocautery . Despite its advantages for the diagnosis and treatment of polyps, colonoscopy has some limitations. Areas adjacent to acute angulations or flexures and the ileocecal valve may be difficult to observe. Furthermore, in 5–10% of patients, usually those with diverticulosis or previous pelvic surgery, the endoscopist may not be able to pass the instrument comfortably and safely to the cecum. The single-contrast barium enema examination is an in- accurate method for detecting polyps in most patients. In one large screening study, single-contrast barium enemas found only 40% of neoplastic polyps detected on subsequent colonoscopy. Double-contrast techniques greatly im- prove the accuracy of radiological methods for detecting polyps. However, even when double-contrast methods are employed, barium enema examinations as they are cur- rently performed in most community hospitals are insuff- iently sensitive for the reliable detection of colorectal polyps. The other main limitations of barium enema is that it does not allow biopsy or polypectomy, and it has relatively low specificity (many false-positives) for polyps.

References : 

Siegel R, Naishadham D, Jemal A. Cancer statistics, 2013. CA Cancer J Clin. 2013;63:11–30. Bujanda L, Cosme A, Gil I, Arenas-Mirave JI. Malignant colorectal polyps. World J Gastroenterol. 2010

6. The treatments and the prevention of the scenario 7. The perspective Islamic perpestif based on the scenario Islam teaches to keep the menu schedule eating well. Humans are taught to consume a variety of foods with sufficient and not excessive. Both the Qur'an and the Hadith discuss a lot about this, before science discovered the concept of a high dietary allowance. The Qur'an states repeatedly that it is prohibited to overeat. Humans simply consume food according to the nutritional adequacy rate. Allah says in Surah Thaha Ayat 81:

[Saying], "Eat from the good things with which We have provided you and do not transgress [or oppress others] therein, lest My anger should descend upon you. And he upon whom My anger descends has certainly fallen." Based on the hadith narrated from Miqdam, that the Prophet ordered us to eat enough and not fill our whole stomach with food. But it is divided into three parts, one per third for food, one per third for water, and one per third for air. Thus, Islam has taught a balanced diet. Excessive eating is something that is forbidden by God. It has been proven in the health literature that excessive food is the basis of various diseases. Excess food

can make obesity increase the risk of various diseases such as diabetes, hypertension, heart disease, and others. To keep accustomed to not overeating, Islam also regulates the obligatory fasting in Ramadan and fasting circumcision on other days.