Bloody StoolCase II

A 2-year and 6 month-old boy was admitted to the hospital with a chief compalint of bloody

diarrhea associated with tenesmus for 5 days. The boy also had high-grade, sustained fever,

episodes of vomiting, and mild abdominal distension.

Keyword :

A 2-year and 6 month-old boy

bloody diarrhea associated with tenesmus for 5 days

high-grade, sustained fever

episodes of vomiting mild abdominal distension

Difficult word : Tenesmus : term used to describe the experience of straining to empty an already empty

bowel (rectal tenesmus) or bladder (bladder or vesical tenesmus). Tenesmus is an ongoing feeling of a need to empty, and sufferers can experience cramps, pain and feelings of urgency and/or incomplete evacuation. Efforts to continue emptying result in minimal passage of urine or stool.

Bloody Diarrhea : Bloody diarrhea is a potentially critical condition in which there is blood mixed in with loose, watery stools. The blood can arise from anywhere along your digestive tract, from the mouth to the anus. Bloody diarrhea is often a sign of gastrointestinal bleeding due to injury or disease. Diarrhea that contains bright red or maroon-colored blood may be referred to as hematochezia, while melena is used to describe black, tarry, and smelly diarrhea. Bloody diarrhea may also be referred to as dysentery, which is usually caused by a bacterial infection

Question :1. Anatomy and physiology digestive system2. Histology of digestive system 3. Pathomechanism of bloody diarrhea4. Relationship between all bloody diarrhea and tenesmus5. Relationship between all symptom6. Differential Diagnose :

i. Amoeba dysentryii. Basiller dysentry

iii. Meckel’s diverticle.

Answer :

1. Anatomy and physiology digestive system

Introduction to the gastrointestinal system

The gastrointestinal tract (GIT) consists of a hollow muscular tube starting from the oral

cavity, where food enters the mouth, continuing through the pharynx, oesophagus, stomach and

intestines to the rectum and anus, where food is expelled. There are various accessory

organs that assist the tract by secreting enzymes to help break down food into its component

nutrients. Thus the salivary glands, liver, pancreas and gall bladder have important functions in

the digestive system. Food is propelled along the length of the GIT by peristaltic movements of

the muscular walls.

 The primary purpose of the gastrointestinal tract is to break food down into nutrients, which

can be absorbed into the body to provide energy. First food must be ingested into the mouth to

be mechanically processed and moistened. Secondly, digestion occurs mainly in the stomach

and small intestine where proteins, fats and carbohydrates are chemically broken down into

their basic building blocks. Smaller molecules are then absorbed across the epithelium of the

small intestine and subsequently enter the circulation. The large intestine plays a key role in

reabsorbing excess water. Finally, undigested material and secreted waste products are

excreted from the body via defecation (passing of faeces).

In the case of gastrointestinal disease or disorders, these functions of the gastrointestinal tract

are not achieved successfully. Patients may develop symptoms of nausea, vomiting, diarrhoea,

malabsorption, constipation or obstruction. Gastrointestinal problems are very common and

most people will have experienced some of the above symptoms several times throughout their

lives.  

Individual components of the gastrointestinal system

Oral cavity

The oral cavity or mouth is responsible for the intake of food. It is lined by a stratified squamous

oral mucosa with keratin covering those areas subject to significant abrasion, such as the

tongue, hard palate and roof of the mouth. Mastication refers to the mechanical breakdown of

food by chewing and chopping actions of the teeth. The tongue, a strong muscular organ,

manipulates the food bolus to come in contact with the teeth. It is also the sensing organ of the

mouth for touch, temperature and taste using its specialised sensors known as papillae.

Insalivation refers to the mixing of the oral cavity contents with salivary gland secretions. The

mucin (a glycoprotein) in saliva acts as a lubricant. The oral cavity also plays a limited role in

the digestion of carbohydrates. The enzyme serum amylase, a component of saliva, starts the

process of digestion of complex carbohydrates. The final function of the oral cavity is absorption

of small molecules such as glucose and water, across the mucosa. From the mouth, food passes

through the pharynx and oesophagus via the action of swallowing.

Salivary glands

Three pairs of salivary glands communicate with the oral cavity. Each is a complex gland with

numerous acini lined by secretory epithelium. The acini secrete their contents into specialised

ducts. Each gland is divided into smaller segments called lobes. Salivation occurs in response to

the taste, smell or even appearance of food. This occurs due to nerve signals that tell the salivary

glands to secrete saliva to prepare and moisten the mouth. Each pair of salivary glands secretes

saliva with slightly different compositions.

 

Parotids

The parotid glands are large, irregular shaped glands located under the skin on the side of the

face. They secrete 25% of saliva. They are situated below the zygomatic arch (cheekbone) and

cover part of the mandible (lower jaw bone). An enlarged parotid gland can be easier felt when

one clenches their teeth. The parotids produce a watery secretion which is also rich in proteins.

Immunoglobins are secreted help to fight microorganisms and a-amylase proteins start to break

down complex carbohydrates.

Submandibular

The submandibular glands secrete 70% of the saliva in the mouth. They are found in the floor of

the mouth, in a groove along the inner surface of the mandible. These glands produce a more

viscid (thick) secretion, rich in mucin and with a smaller amount of protein. Mucin is a

glycoprotein that acts as a lubricant.

Sublingual

The sublinguals are the smallest salivary glands, covered by a thin layer of tissue at the floor of

the mouth. They produce approximately 5% of the saliva and their secretions are very sticky

due to the large concentration of mucin. The main functions are to provide buffers and

lubrication.

Oesophagus

The oesophagus is a muscular tube of approximately 25cm in length and 2cm in diameter. It

extends from the pharynx to the stomach after passing through an opening in the diaphragm.

The wall of the oesophagus is made up of inner circular and outer longitudinal layers of muscle

that are supplied by the oesophageal nerve plexus. This nerve plexus surrounds the lower

portion of the oesophagus. The oesophagus functions primarily as a transport medium between

compartments.

Stomach

The stomach is a J shaped expanded bag, located just left of the midline between the oesophagus

and small intestine. It is divided into four main regions and has two borders called the greater

and lesser curvatures. The first section is the cardia which surrounds the cardial orifice where

the oesophagus enters the stomach. The fundus is the superior, dilated portion of the stomach

that has contact with the left dome of the diaphragm. The body is the largest section between

the fundus and the curved portion of the J.

This is where most gastric glands are located and where most mixing of the food occurs. Finally

the pylorus is the curved base of the stomach. Gastric contents are expelled into the proximal

duodenum via the pyloric sphincter. The inner surface of the stomach is contracted into

numerous longitudinal folds called rugae. These allow the stomach to stretch and expand when

food enters. The stomach can hold up to 1.5 litres of material. The functions of the stomach

include:

1. The short-term storage of ingested food.

2. Mechanical breakdown of food by churning and mixing motions.

3. Chemical digestion of proteins by acids and enzymes.

4. Stomach acid kills bugs and germs.

5. Some absorption of substances such as alcohol.

Most of these functions are achieved by the secretion of stomach juices by gastric glands in the

body and fundus. Some cells are responsible for secreting acid and others secrete enzymes to

break down proteins.

Small intestine

The small intestine is composed of the duodenum, jejunum, and ileum. It averages

approximately 6m in length, extending from the pyloric sphincter of the stomach to the ileo-

caecal valve separating the ileum from the caecum. The small intestine is compressed into

numerous folds and occupies a large proportion of the abdominal cavity.

The duodenum is the proximal C-shaped section that curves around the head of the pancreas.

The duodenum serves a mixing function as it combines digestive secretions from the pancreas

and liver with the contents expelled from the stomach. The start of the jejunum is marked by a

sharp bend, the duodenojejunal flexure. It is in the jejunum where the majority of digestion and

absorption occurs. The final portion, the ileum, is the longest segment and empties into the

caecum at the ileocaecal junction.

The small intestine performs the majority of digestion and absorption of nutrients. Partly

digested food from the stomach is further broken down by enzymes from the pancreas and bile

salts from the liver and gallbladder. These secretions enter the duodenum at the Ampulla of

Vater. After further digestion, food constituents such as proteins, fats, and carbohydrates are

broken down to small building blocks and absorbed into the body's blood stream.

The lining of the small intestine is made up of numerous permanent folds called plicae

circulares. Each plica has numerous villi (folds of mucosa) and each villus is covered by

epithelium with projecting microvilli (brush border). This increases the surface area for

absorption by a factor of several hundred. The mucosa of the small intestine contains several

specialised cells. Some are responsible for absorption, whilst others secrete digestive enzymes

and mucous to protect the intestinal lining from digestive actions.

Large intestine

The large intestine is horse-shoe shaped and extends around the small intestine like a frame. It

consists of the appendix, caecum, ascending, transverse, descending and sigmoid colon, and the

rectum. It has a length of approximately 1.5m and a width of 7.5cm.

The caecum is the expanded pouch that receives material from the ileum and starts to compress

food products into faecal material. Food then travels along the colon. The wall of the colon is

made up of several pouches (haustra) that are held under tension by three thick bands of

muscle (taenia coli).

The rectum is the final 15cm of the large intestine. It expands to hold faecal matter before it

passes through the anorectal canal to the anus. Thick bands of muscle, known as sphincters,

control the passage of faeces.

 

The mucosa of the large intestine lacks villi seen in the small intestine. The mucosal surface is

flat with several deep intestinal glands. Numerous goblet cells line the glands that secrete

mucous to lubricate faecal matter as it solidifies. The functions of the large intestine can be

summarised as:

1. The accumulation of unabsorbed material to form faeces.

2. Some digestion by bacteria. The bacteria are responsible for the formation of intestinal gas.

3. Reabsorption of water, salts, sugar and vitamins.

Liver

The liver is a large, reddish-brown organ situated in the right upper quadrant of the abdomen. It

is surrounded by a strong capsule and divided into four lobes namely the right, left, caudate and

quadrate lobes. The liver has several important functions. It acts as a mechanical filter by

filtering blood that travels from the intestinal system. It detoxifies several metabolites including

the breakdown of bilirubin and oestrogen. In addition, the liver has synthetic functions,

producing albumin and blood clotting factors. However, its main roles in digestion are in the

production of bile and metabolism of nutrients. All nutrients absorbed by the intestines pass

through the liver and are processed before traveling to the rest of the body. The bile produced

by cells of the liver, enters the intestines at the duodenum. Here, bile salts break down lipids

into smaller particles so there is a greater surface area for digestive enzymes to act.

Gall bladder

The gallbladder is a hollow, pear shaped organ that sits in a depression on the posterior surface

of the liver's right lobe. It consists of a fundus, body and neck. It empties via the cystic duct into

the biliary duct system. The main functions of the gall bladder are storage and concentration of

bile. Bile is a thick fluid that contains enzymes to help dissolve fat in the intestines. Bile is

produced by the liver but stored in the gallbladder until it is needed. Bile is released from the

gall bladder by contraction of its muscular walls in response to hormone signals from the

duodenum in the presence of food.

Pancreas

Finally, the pancreas is a lobular, pinkish-grey organ that lies behind the stomach. Its head

communicates with the duodenum and its tail extends to the spleen. The organ is approximately

15cm in length with a long, slender body connecting the head and tail segments. The pancreas

has both exocrine and endocrine functions. Endocrine refers to production of hormones which

occurs in the Islets of Langerhans. The Islets produce insulin, glucagon and other substances

and these are the areas damaged in diabetes mellitus. The exocrine (secretrory) portion makes

up 80-85% of the pancreas and is the area relevant to the gastrointestinal tract.

It is made up of numerous acini (small glands) that secrete contents into ducts which eventually

lead to the duodenum. The pancreas secretes fluid rich in carbohydrates and inactive enzymes.

Secretion is triggered by the hormones released by the duodenum in the presence of food.

Pancreatic enzymes include carbohydrases, lipases, nucleases and proteolytic enzymes that can

break down different components of food. These are secreted in an inactive form to prevent

digestion of the pancreas itself. The enzymes become active once they reach the duodenum.

2. Histology of digestive system

The gastrointestinal tract is a muscular tube lined by a special layer of cells, called epithelium.

The contents of the tube are considered external to the body and are in continuity with the

outside world at the mouth and the anus. Although each section of the tract has specialised

functions, the entire tract has a similar basic structure with regional variations.

The wall is divided into four layers as follows:

Mucosa

The innermost layer of the digestive tract has specialised epithelial cells supported by an

underlying connective tissue layer called the lamina propria. The lamina propria contains blood

vessels, nerves, lymphoid tissue and glands that support the mucosa. Depending on its function,

the epithelium may be simple (a single layer) or stratified (multiple layers).

Areas such as the mouth and oesophagus are covered by a stratified squamous (flat) epithelium

so they can survive the wear and tear of passing food. Simple columnar (tall) or glandular

epithelium lines the stomach and intestines to aid secretion and absorption. The inner lining is

constantly shed and replaced, making it one of the most rapidly dividing areas of the body!

Beneath the lamina propria is the muscularis mucosa. This comprises layers of smooth muscle

which can contract to change the shape of the lumen.

Submucosa

The submucosa surrounds the muscularis mucosa and consists of fat, fibrous connective tissue

and larger vessels and nerves. At its outer margin there is a specialized nerve plexus called the

submucosal plexus or Meissner plexus. This supplies the mucosa and submucosa.

Muscularis externa

This smooth muscle layer has inner circular and outer longitudinal layers of muscle fibres

separated by the myenteric plexus or Auerbach plexus. Neural innervations control the

contraction of these muscles and hence the mechanical breakdown and peristalsis of the food

within the lumen.

Serosa/mesentery

The outer layer of the GIT is formed by fat and another layer of epithelial cells called

mesothelium.

3. Pathomechanism of bloody diarrhea

Inflammatory and Infectious Diarrhea

The epithelium of the digestive tube is protected from insult by a number of mechanisms constituting the gastrointestinal barrier, but like many barriers, it can be breached. Disruption of the epithelium of the intestine due to microbial or viral pathogens is a very common cause of diarrhea in all species. Destruction of the epithelium results not only in exudation of serum and blood into the lumen but often is associated with widespread destruction of absorptive epithelium. In such cases, absorption of water occurs very inefficiently and diarrhea results. Examples of pathogens frequently associated with infectious diarrhea include:

Bacteria: Salmonella, E. coli, Campylobacter Viruses: rotaviruses, coronaviruses, parvoviruses (canine and feline), norovirus Protozoa: coccidia species, Cryptosporium, Giardia

The immune response to inflammatory conditions in the bowel contributes substantively to development of diarrhea. Activation of white blood cells leads them to secrete inflammatory mediators and cytokines which can stimulate secretion, in effect imposing a secretory component on top of an inflammatory diarrhea. Reactive oxygen species from leukocytes can damage or kill intestinal epithelial cells, which are replaced with immature cells that typically are deficient in the brush border enyzmes and transporters necessary for absorption of nutrients and water. In this way, components of an osmotic (malabsorption) diarrhea are added to the problem.

PATHOMECHANISM VOMITING

Vomiting

Receptors on the floor of the fourth ventricle of the brain represent a chemoreceptor trigger zone, known as the area postrema, stimulation of which can lead to vomiting. The area postrema is a circumventricular organ and as such lies outside the blood-brain barrier; it can therefore be stimulated by blood-borne drugs that can stimulate vomiting or inhibit it.

There are various sources of input to the vomiting center:

The chemoreceptor trigger zone at the base of the fourth ventricle has numerous dopamine D2 receptors, serotonin 5-HT3 receptors, opioid receptors, acetylcholine receptors, and receptors for substance P. Stimulation of different receptors are involved

in different pathways leading to emesis, in the final common pathway substance P appears to be involved.

The vestibular system which sends information to the brain via cranial nerve VIII (vestibulocochlear nerve). It plays a major role in motion sickness and is rich in muscarinic receptors and histamine H1 receptors.

Cranial nerve X (vagus nerve), which is activated when the pharynx is irritated, leading to a gag reflex.

Vagal and enteric nervous system inputs that transmit information regarding the state of the gastrointestinal system. Irritation of the GI mucosa by chemotherapy, radiation, distention, or acute infectious gastroenteritis activates the 5-HT3 receptors of these inputs.

The CNS mediates vomiting arising from psychiatric disorders and stress from higher brain centers.

Act

The vomiting act encompasses three types of outputs initiated by the chemoreceptor trigger zone: Motor, parasympathetic nervous system (PNS), and sympathetic nervous system (SNS). They are as follows:

Increased salivation to protect the enamel of teeth from stomach acids (excessive vomiting leads to dental erosion). This is part of the PNS output.

A deep breath is taken to avoid aspiration of vomit. Retroperistalsis, starting from the middle of the small intestine, sweeping up the

contents of the digestive tract into the stomach, through the relaxed pyloric sphincter. A lowering of intrathoracic pressure (by inspiration against a closed glottis), coupled

with an increase in abdominal pressure as the abdominal muscles contract, propels stomach contents into the esophagus as the lower esophageal sphincter relaxes. The stomach itself does not contract in the process of vomiting except for at the angular notch, nor is there any retroperistalsis in the esophagus.

Vomiting is ordinarily preceded by retching. Vomiting also initiates an SNS response causing both sweating and increased heart rate.

The neurotransmitters that regulate vomiting are poorly understood, but inhibitors of dopamine, histamine, and serotonin are all used to suppress vomiting, suggesting that these play a role in the initiation or maintenance of a vomiting cycle. Vasopressin and neurokinin may also participate.

Phases

The vomiting act has two phases. In the retching phase, the abdominal muscles undergo a few rounds of coordinated contractions together with the diaphragm and the muscles used in respiratory inspiration. For this reason, an individual may confuse this phase with an episode of violent hiccups. In this retching phase nothing has yet been expelled. In the next phase, also termed the expulsive phase, intense pressure is formed in the stomach brought about by enormous shifts in both the diaphragm and the abdomen. These shifts are, in essence, vigorous contractions of these muscles that last for extended periods of time - much longer than a normal period of muscular contraction. The pressure is then suddenly released when the upper esophageal sphincter relaxes resulting in the expulsion of gastric contents. For people not in the habit of exercising the abdominal muscles, they may be painful for the next few days. The relief of pressure and the release of endorphins into the bloodstream after the expulsion causes the vomiter to feel better.

PATHOMECHANISM OF ABDOMINAL DISTENSION

The pathophysiology of gas and bloating is complicated. Understanding gut microflora, gas production, intestinal transit, intestinal propulsion of gas, and sensory function within the GI tract are essential for understanding symptom generation.

Gut Microflora

The term gut microflora (also called gut microbiome) refers to bacteria (and their byproducts) that inhabit the intestinal tract and their effects on both GI tract function and the body as a whole. Approximately 500 different species of bacteria reside within the colon, and nearly all of these species are anaerobes. Colonic microflora varies from individual to individual and refects multiple factors, including diet, antibiotic use, and method of feeding as an infant. The number of bacteria in the GI tract is thought to exceed 1014, which is more than the total number of cells in the human body.17 Because less than 10% of these bacteria can be cultured, our understanding of them is limited. Research over the past decade has shown that these bacteria play a vital role in gut immune function, mucosal barrier function, metabolism of drugs, and production of short-chain fatty acids and vitamins. Even minor disturbances in gut microflora can lead to significant changes in gut function, including gas production. Although the overall volume of gas production may not significantly change from individual to individual, the content (methane [CH4], hydrogen [H2], or carbon dioxide [CO2]) may vary greatly, potentially leading to changes in intestinal transit and visceral sensation.

PATHOMECHANISM OF FEVER

During a 24-h period, temperature varies from lowest levels in the early morning to highest in late afternoon. Maximum variation is about 0.6° C.

Body temperature is determined by the balance between heat production by tissues, particularly the liver and muscles, and heat loss from the periphery. Normally, the hypothalamic thermoregulatory center maintains the internal temperature between 37° and 38° C. Fever results when something raises the hypothalamic set point, triggering vasoconstriction and shunting of blood from the periphery to decrease heat loss; sometimes shivering, which increases heat production, is induced. These processes continue until the temperature of the blood bathing the hypothalamus reaches the new set point. Resetting the hypothalamic set point downward (eg, with antipyretic drugs) initiates heat loss through sweating and vasodilation. The capacity to generate a fever is reduced in certain patients (eg, alcoholics, the very old, the very young).

Pyrogens are substances that cause fever. Exogenous pyrogens are usually microbes or their products. The best studied are the lipopolysaccharides of gram-negative bacteria (commonly called endotoxins) and Staphylococcus aureus toxin, which causes toxic shock syndrome. Exogenous pyrogens usually cause fever by inducing release of endogenous pyrogens (eg, IL-1, tumor necrosis factor [TNF], interferon-γ, IL-6), which raise the hypothalamic set point. Prostaglandin E2 synthesis appears to play a critical role.

4.Relationship between all bloody diarrhea and tenesmus :

Bloody stools

Bloody stools often are a sign of an injury or disorder in the digestive tract. Your doctor may use the term "melena" to describe black, tarry, and foul-smelling stools or "hematochezia" to describe red- or maroon-colored stools.

Considerations

Blood in the stool may come from anywhere along your digestive tract, from mouth to anus. It may be present in such small amounts that you cannot actually see it, and it is only detectable by a fecal occult blood test.

When there is enough blood to change the appearance of your stools, the doctor will want to know the exact color to help find the site of bleeding. To make a diagnosis, your doctor may use endoscopy or special x-ray studies.

Black stool usually means that the blood is coming from the upper part of the gastrointestinal (GI) tract. This includes the esophagus, stomach, and the first part of the small intestine. Blood will typically look like tar after it has been exposed to the body's digestive juices as it passes through the intestines.

Maroon-colored stools or bright red blood usually suggests that the blood is coming from the lower part of the GI tract (large bowel, rectum, or anus). However, sometimes massive or rapid bleeding in the stomach causes bright red stools.

Eating black licorice, lead, iron pills, bismuth medicines like Pepto-Bismol, or blueberries can also cause black stools. Beets and tomatoes can sometimes make stools appear reddish. In these cases, your doctor can test the stool with a chemical to rule out the presence of blood.

Bleeding in the esophagus or stomach (such as with peptic ulcer disease) can also cause you to vomit blood.

Causes

The upper part of the GI tract will usually cause black stools due to:

Abnormal blood vessels (vascular malformation) A tear in the esophagus from violent vomiting (Mallory-Weiss tear) Bleeding stomach or duodenal ulcer Inflammation of the stomach lining (gastritis) Lack of proper blood flow to the intestines (bowel ischemia) Trauma or foreign body Widened, overgrown veins (called varices) in the esophagus and stomach

The lower part of the GI tract will usually cause maroon or bright red, bloody stools due to:

Anal fissures Bowel ischemia  (when blood supply is cut off to part of the intestines) Colon polyps or colon cancer Diverticulosis  (abnormal pouches in the colon) Hemorrhoids  (common cause) Inflammatory bowel disease (such as Crohn's disease or ulcerative colitis) Intestinal infection  (such as bacterial enterocolitis) Small bowel tumor Trauma or foreign body Vascular malformation (abnormal collections of blood vessels called arteriovenous

malformations or AVMs)

When to Contact a Medical Professional

Call your doctor immediately if you notice blood or changes in the color of your stool. Even if you think that hemorrhoids are causing the blood in your stool, your doctor should examine you to make sure that there is no other, more serious cause present.

In children, a small amount of blood in the stool is usually not serious. The most common causes are constipation and milk allergies. However, it is still worth reporting to your doctor, even if no evaluation is needed.

What to Expect at Your Office Visit

Your doctor will take a medical history and perform a physical examination, focusing on your abdomen and rectum.

The following questions may be included in the history to better understand the possible causes of your bloody or dark stools:

Are you taking blood thinners (aspirin, warfarin, clopidogrel, Aggrenox) or NSAIDs (ibuprofen, naproxen)?

Have you had any trauma to the abdomen or rectum, or have you swallowed a foreign object accidentally?

Have you eaten black licorice, lead, Pepto-Bismol, or blueberries? Have you had more than one episode of blood in your stool? Is every stool this way? Have you lost any weight recently?

Is there blood on the toilet paper only? What color is the stool? When did it develop? What other symptoms are present -- abdominal pain, vomiting blood, bloating, excessive

gas, diarrhea, or fever?

Treatment depends on the cause and severity of the bleeding. For serious bleeding, you may be admitted to a hospital for monitoring and evaluation. If there is massive bleeding, you will be monitored in an intensive care unit. Emergency treatment may include a blood transfusion.

The following diagnostic tests may be performed:

Angiography Barium studies Bleeding scan (nuclear medicine) Blood studies, including a complete blood count ( CBC) and differential, serum

chemistries, clotting studies Colonoscopy Esophagogastroduodenoscopy  or EGD Stool culture Tests for the presence of Helicobacter pylori infection X-rays of the abdomen

TREATMENT

If you have passed a lot of blood, you may need emergency treatment, which can include:

Blood transfusions Fluids through a vein Interventional radiography embolization (a procedure to block the blood vessels that

may be bleeding) Medications to decrease stomach acid Possible surgery if bleeding does not stop

TENESMUS

Normal Urge to Defecate

The need to have a bowel movement is first marked by an urging. This sensation compels a person to find suitable toilet facilities so that defecation can occur. There are a number of reasons why this sensation occurs including :

Stretching of the wall of the colon as waste and water accumulates in it. Increased pressure within the abdomen (intra-abdominal pressure). Defecation reflexes which are stimulation of the bowels by nerve signals. Filling of the rectum with feces.

These triggers for the defecation urge is considered normal. It occurs on daily basis for most people and facilitates the process of stool evacuation. The rectum fills with stool and the

external and internal anal sphincters relax allowing stool to pass out into the environment. Once all of the stool in the rectum has been passed out, the defecation urge sensation subsides completely.

Stimulation of Urge

For most people, the urging and subsequent defecation occurs at certain times of the day particularly in the early morning. This is more likely to occur in a person with good bowel training from childhood. Other factors that may trigger the defecation urge :

Physical activity like brisk walking. Pressure on the abdomen. After a large meal. Certain emotions.

All of these instances are considered normal yet it does not occur on most occasions. This is due to the fact that good bowel habit evacuates the sufficient waste material and water on a regular basis and the colon and rectum are therefore not as sensitive to additional factors.

Abnormal Defecation Urge (TENESMUS)

Sometimes the urging to defecate can be considered to be abnormal. In these cases the defecation urge persists and becomes annoying or even uncomfortable, and sometimes even painful yet it does not precede a bowel movement or subside after a bowel movement. This condition is known as tenesmus. The sensation may be considered abnormal when there is an urging in the following circumstances :

After a bowel movement. Inability to have a bowel movement even with sitting or straining. Small volume stool is passed out – feeling of incomplete evacuation. Tenderness, pain or itching in the rectum.

The urge in these cases is either persistent or intermittent (recurring every now and then). It is more likely to be triggered or intensified by the stimulatory factors discussed above.

Reasons for constant urging

The wall of the bowels are able to perform many functions that facilitate movement of food and waste through the gut, release enzymes for digestion and allow for nutrients to be absorbed into the bloodstream. Water is absorbed and the waste material is held in the lower parts of the bowel until it is ready to be expelled. These functions are mainly controlled by two types of signals – hormones (chemical) and nerve impulses (electrical). The bowel walls are constantly relaying signals through nerves and hormones to other parts of the gut and even other organs. It is also receiving signals from other parts of the body through the hormones and nerves. In this way its activities can be well coordinated for efficiency.

The defecation urge, as previously discussed, is caused by stretching of the colon wall as waste and water accumulates. It may also be triggered by pressure on the colon wall from within the abdomen. This causes nerve impulses to be sent to the spinal cord and back which can the initiate the defecation process. These pathways are referred to as defecation reflexes. It involves the colon and rectum and there are two types of such reflexes – inhibitory myenteric and parasympathetic defecation reflexes.

There are other defecation reflexes which are linked with other parts of the gut or even other organs in the abdomen. This means that stimulation or irritation of these organs will trigger the defecation urge and eventually lead to a bowel movement. The main such reflexes involve the stomach  and small intestine. To a lesser degree, other reflexes linked to the kidney, bladder and the abdominal lining known as the peritoneum may play a role in initiating defecation.

Therefore irritation or disease of these structures may lead to the urge to defecate :

colon or rectum (most likely) stomach or small intestine kidney, bladder or peritoneum

Causes of Abnormal Urging

The most common cause of abnormal defecation urging is constipation.  However, constipation on its own is a symptom and not a disease. Persistent or intermittent defecation urging is common with constipation and usually temporary. The cause of constipation in most cases is not known. Urging is more likely to arise with hemorrhoids, a common complication of constipation.

Colon and Rectum

Inflammatory bowel disease (IBD) is chronic inflammation of the wall of the bowel. There are two types – ulcerative colitis and Crohn’s disease. Sometimes other parts of the gut, right up to the mouth, can be affected with Crohn’s disease.

Irritable bowel syndrome (IBS) is a functional disorder of the bowels marked by episodes of diarrhea or constipation, bloating and abdominal pain or cramping. The cause of IBS is unknown.

Infectious colitis is an infection of the colon that may be caused by bacteria, viruses, parasites or with an overgrowth of certain natural bacteria in the bowels.

Colorectal growths, including polyps, benign tumors and cancer. Proctitis is inflammation of the rectum often caused by injury to the rectum or

infections. Hemorrhoids are inflamed veins of the rectum and anus often associated with

constipation, diarrhea and sitting on the toilet for excessively long periods of time. Tenesmus is more likely with thrombosed hemorrhoids.

Other colon and rectal problems include obstipation, fecal impaction, ischemic proctocolitis, rectal prolapse, foreign body in the rectum, rectal  perforation or perirectal abscess.

Anal problems may include anal fissures, fistulas, abscess (perianal), cryptitis and cancer.

5. Relationship between all symptom

6. Differential diagnose :i.Amoebic dysentry

Definition

is a type of dysentery caused primarily by the amoeba Entamoeba histolytica which is a normal flora in the human stomach

Etiology

Five species of Entamoeba:

E. histolytica (Pathogenic), E. dispar E. coli, E. hartmanni, E. gingivalis

Life cycle :

cyst postcyst

precyst large trophozoite

Epidemiology

This condition occurs worldwide, but it is most common in tropical areas with crowded living conditions and poor sanitation. Africa, Mexico, parts of South America, and India have significant health problems associated with this disease.

Pathogenesis

Caused by ingestion of tetra-nucleated cysts which can remain viable for weeks to months. After ingestion (faecal-oral transmission), the cysts undergo further nuclear division, and eight trophozoites are released in the terminal ileum. The trophozoites are carried to the large intestine where they produce the characteristic 'flask-shaped' amoebic ulcerations. Incubation period is 2-6 weeks.

Sign and symptoms

Abdominal cramps

Diarrhea

o Passage of 3 - 8 semiformed stools per day

o Passage of soft stools with mucus and occasional blood

Fatigue

Excessive gas

Rectal pain while having a bowel movement (tenesmus)

Unintentional weight loss

vomitting

Laboratory findings

Blood test for amebiasis

Examination of the inside of the lower large bowel (sigmoidoscopy)

Microscope examination of stool samples

Treatment

metronidazole 400mg tid for 10 days, for adults

tinidazole 2.0 qd 5 days

furamide 500mg tid for 10 days

Prophylaxis

To control the sources of infection

To interrupt the routes of transmission

Prevention

Control the source of infection

Interrupt the route of transmission

Protect susceptible persons

ii.Basiller dysentry Definition

Bacillary dysentery is a type of dysentery caused by Shigellosis. Bacillary dysentery is associated with species of bacteria from the Enterobacteriaceae family. Shigellosis is caused by one of several types of Shigella bacteria. Three species are associated with bacillary dysentery : Shigella sonnei, Shigella flexneri and Shigella dysenteriae.

Morphological Description of Biologic Agent

Shigella is a genus of gram-negative, non-spore forming rod-shaped bacteria closely related to Escherichia Coli and Salmonella. The causative agent of human shigellosis, Shigella cause disease in primates, but not in other mammals. It is only naturally found in humans and apes. During infection, it typically causes dysentery.

Mode of Transmission

Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host as few as ten bacterial cells can be enough to cause an infection.

Pathogenesis

Shigella bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively.

Signs and Symptoms Diarrhea: Diarrhea is bloody 25-50 percent of the time and most often contains mucus. Fever abdominal cramps. Rectal spasms.  illness starts 12 hours to 6 days, usually 1-2 days, after exposure.  Dehydration Nausea or vomiting may also be experienced Muscle aches also occur.

Treatment

Fluids and electrolyte replacement if excessive fluid loss through diarrhea or vomiting.

Agents are not recommended as they may prolong the course of disease.

Treatment is recommended for most symptomatic patients. Use of antibiotics will shorten the period of fecal excretion of the infecting strain and will shorten the clinical course of disease often to a few days.

Antibiotics

for adults and children, if the strain is susceptible, are ciprofloxacin or TMP/SMX or azithromycin.

Antibiotic resistance frequently develops after treatment.

Control Measures

Good personal hygiene

Toilet hygiene

Wash soiled clothing and bed linen

Handling food

While you are suffering from diarrhea you should not go to work/school.

Sanitation of food utensils

iii.Meckel’s diverticle Definition :

Meckel diverticulum (also referred to as Meckel's Diverticulum) is the most common congenital abnormality of the small intestine; it is caused by an incomplete obliteration of the vitelline duct (ie, omphalomesenteric duct). Although originally described by Fabricius Hildanus in 1598, it is named after Johann Friedrich Meckel, who established its embryonic origin in 1809.[1]

Despite the availability of modern imaging techniques, diagnosis is challenging. Although Meckel diverticulum is usually of no medical significance, two types of complications can require clinical attention. One type involves ectopic mucosal tissue and most often leading to GI bleeding in younger children. In the second type, the sequelae of the diverticulum involve an aberrant intra-abdominal structure.

Pathophysiology

Early in embryonic life, the fetal midgut receives its nutrition from the yolk sac via the vitelline duct. The duct then undergoes progressive narrowing and usually disappears by 7 weeks' gestation. When the duct fails to fully obliterate, different types of vitelline duct anomalies appear. Examples of such anomalies include (1) a persistent vitelline duct (appearing as a draining fistula at the umbilicus); (2) a fibrous band that connects the ileum to the inner surface of the umbilicus; (3) a patent vitelline sinus beneath the umbilicus; (4) an obliterated bowel portion; (5) a vitelline duct cyst; and, most commonly (97%) Meckel diverticulum, which is a blind-ending true diverticulum that contains all of the layers normally found in the ileum.[2] The tip of the diverticulum is free in 75% of cases and is attached to the anterior abdominal wall or another structure in the remainder of cases.

Enterocystomas, umbilical sinuses, and omphaloileal fistulas are among the other congenital anomalies associated with Meckel diverticulum.

The diverticulum is usually supplied by the omphalomesenteric artery (a remnant of the vitelline artery), which arises from the ileal branch of the superior mesenteric artery. Usually, the artery terminates in the diverticulum; however, it has been reported to continue up to the abdominal wall in some cases. Rarely, these blood vessels persist in the form of fibrous remnants that run between the Meckel diverticulum and the abdominal wall or small bowel mesentery.

Meckel diverticulum occurs on the antimesenteric border of the ileum, usually 40-60 cm proximal to the ileocecal valve. On average, the diverticulum is 3 cm long and 2 cm wide. Slightly more than one half contain ectopic mucosa. Meckel diverticulum is typically lined by ileal mucosa, but other tissue types are also found with varying frequency.

The heterotopic mucosa is most commonly gastric. This is important because peptic ulceration of this or adjacent mucosa can lead to painless bleeding, perforation, or both. In one study, heterotropic gastric mucosa was found in 62% of cases, pancreatic tissue was found in 6%, both pancreatic tissue and gastric mucosa were found in 5%, jejunal mucosa was found in 2%, Brunner tissue was found in 2% and both gastric and duodenal mucosa were found in 2%.[2] Rarely, colonic, rectal, endometrial, and hepatobiliary tissues have been noted.

Epidemiology United States

The prevalence of Meckel diverticulum is usually noted to be approximately 2% of the population,[3] but published series range from 0.2-4%.[4] Complications are only seen in about

5% of those with the anomaly. In a comprehensive survey of 43 children's hospitals in the United States, 815 children had a Meckel diverticulectomy during a 2-year span. Slightly more than half (60%) were symptomatic and the remainder were incidental in children who had laporotomy for a different reason.[50]

InternationalPrevalence figures similar to those found in the United States have been reported in Europe and Asia.

Sex

Although no sex-based difference was reported in studies that evaluated this condition as an incidental finding during operations or autopsies, males are as much as 3-4 times more prone to complications than females. In a large series of cases from 2007-2008, Meckel diverticulectomy was 2.3 times more common in boys and boys accounted for 74% of the primary cases.[50]

Age

The classic presentation in children is considered to be painless rectal bleeding in a toddler younger than 2 years. One large series found that 53% had surgery before their fourth birthday. However, the largest group (slightly more than 30%) were younger than one year.[50] Although most other pediatric cases occur in patients aged 2-8 years, many continue to present with hematochezia.

Although children usually present with hematochezia and adults usually present with obstruction, the same recent series of 815 children found that a primary diverticulectomy was performed in 30% of the children (< 18 y) for obstruction while 27% presented with bleeding and 19% had intussusception.[50] About one quarter did not have a clear cut diagnosis. Although neonatal presentation of Meckel is rare, case reports have described perforation, intussusception, segmental ileal dilation, and ileal volvulus in newborns. In one neonate, massive hematochezia was reported on day 6.[5]

In adults, obstruction and inflammation are more common presentations than lower GI bleeding. Several population-based studies have reported a decreased incidence of complications with increasing age, although other studies have not. Therefore, the issue of incidental diverticulectomy in older patients remains controversial.

Symptomatic Meckel diverticulum is virtually synonymous with a complication. This is estimated to occur in as many as 4-16% of patients.[2]Complications are the result of obstruction, ectopic tissue, or inflammation. In one study of 830 patients of all ages, complications included bowel obstruction (35%), hemorrhage (32%), diverticulitis (22%), umbilical fistula (10%), and other umbilical lesions (1%).

In children, hematochezia is the most common presenting sign.[6] Bleeding in adults is much less common.[7, 8]

o Acute lower GI bleeding is secondary to hemorrhage from peptic ulceration. Such ulceration occurs when acid secreted by heterotopic gastric mucosa damages contiguous vulnerable tissue, often times resulting in direct erosion of a vessel. Clinically, hemorrhage is usually noted to be substantial painless rectal bleeding. However, some patients may present only with pain preceding the onset of hematochezia. The pain can be quite significant and often delays the correct diagnosis.

o Not all patients have abdominal pain; however, when present, it can be significant. A rare cause of abdominal pain from the Meckel diverticulum is inversion without intussusception.[9]

Although intestinal obstruction in pediatrics is not considered very prevalent, some series report it in 25-40% of pediatric complications. It is the most common complication in adults. Obstruction can be the result of various mechanisms.[2]

o Omphalomesenteric band (most frequent cause)o Internal hernia through vitelline duct remnantso Volvulus  occurring around vitelline duct remnantso T-shaped prolapse of both efferent and afferent loops of intestine through a persistent

vitelline duct fistula at the umbilicus in a neonateo Intussusception  (when Meckel diverticulum itself acts as a lead point for an ileocolic or

ileoileal intussusception) None of these mechanisms have clinical features that are pathognomonic, and the precise

etiology is rarely known preoperatively. Like other diverticula in the body, Meckel diverticulum can become inflamed. Diverticulitis is

usually seen in older patients. Meckel diverticulum is less prone to inflammation than the appendix because most diverticula have a wide mouth, have very little lymphoid tissue, and are self-emptying.

o The clinical presentation includes abdominal pain in the periumbilical area that radiates to the right lower quadrant.

o Persistence of periumbilical pain or a history of bleeding per rectum may be helpful in distinguishing this entity from appendicitis.

o Subacute or chronic inflammation of Meckel diverticulum is rare, but a few cases of tuberculosis and Crohn disease within the diverticulum have been reported.

Less frequently, the Meckel diverticulum may develop benign tumors (eg, leiomyomas, angiomas, neuromas, lipomas). About three quarters of the malignant tumors are carcinoids[51] but others include sarcoma,[10]   carcinoid tumor ,[11] adenocarcinomas[12] and Burkitt lymphoma[13] , as well as additional rare lesions.[51] Rarely, the diverticulum may perforate from a swallowed fish bone or sewing needle.

Physical

Although most patients are asymptomatic, patients can present with various clinical signs, including peritonitis or hypovolemic shock. The 3 most common symptomatic presentations are GI bleeding, intestinal obstruction, and acute inflammation of the diverticulum.

Most often, painless rectal bleeding (hematochezia) occurs suddenly and tends to be massive in younger patients.[14] Bleeding occurs without prior warning and usually spontaneously subsides.

o When a severe bleeding episode occurs, the patient can present in hemorrhagic shock. Tachycardia is an early clinical sign of hemorrhagic shock, but orthostatic hypotension may actually precede this.

o The color of the stool often provides physicians with a clue to determine the site of bleeding. This has been well addressed in a classic description of the types of rectal bleeding associated with Meckel diverticulum.[15]

o Prevalence of different types of bleeding has been described as follows: Dark red (maroon) - 40% Bright red - 35% Bright red or dark red - 12% Da rk red or tarry - 6% Tarry - 7%

o When bleeding is rapid, stools are bright red or have an appearance like currant jelly. When slow bleeding occurs, the stools are black and tarry.

o Most patients with intestinal obstruction present with abdominal pain, bilious vomiting, abdominal tenderness, distension, and hyperactive bowel sounds upon examination.

o Patients may develop a palpable abdominal mass.o Occasionally, when patients do not present early or if the diagnosis is missed, the obstruction

can progress to intestinal ischemia or infarction. The latter manifests with acute peritoneal signs and lower GI bleeding.

Patients with diverticulitis present with either focal or diffuse abdominal tenderness. Usually, abdominal tenderness is more marked in the periumbilical region than the pain of appendicitis.

o Children may present with abdominal guarding and rebound tenderness, in addition to abdominal tenderness.

o Abdominal distention and hypoactive bowel sounds are late findings. Rarely, Meckel diverticulum has been reported to become incarcerated (Littre hernia) in the

inguinal,[16] femoral, or obturator hernial sacs or even incisional defects.Causes

Meckel diverticulum is caused by the failure of the omphalomesenteric duct to completely obliterate at 5-7 weeks' gestation, followed by one of the various complications listed above.

Laboratory Studies

Routine laboratory findings, including CBC count, electrolyte levels, glucose test results, BUN levels, creatinine levels, and coagulation screen results, are not helpful in establishing the diagnosis of Meckel diverticulum but are necessary to manage a patient with GI bleeding along with a type and cross.

Hemoglobin and hematocrit levels are low in the setting of anemia or bleeding. Patients with significant bleeding develop anemia. In one series, 58% of children had average

hemoglobin levels of less than 8.8 g/dL. Ongoing bleeding from a Meckel diverticulum can cause iron deficiency anemia. However,

megaloblastic anemia can also be seen due to vitamin B12 or folate deficiency. These can occur secondary to small bowel overgrowth if dilation and/or stasis related to the diverticulum is present. Low albumin and low ferritin levels may lead to a diagnosis of inflammatory bowel disease.

Imaging Studies

According to Mayo, "Meckel's Diverticulum is frequently suspected, often looked for, and seldom found." Preoperative diagnosis is difficult, especially if the presenting symptom is not GI bleeding. In one series, patients often had a correct preoperative diagnosis if the presenting symptom was GI bleeding, but only 11% of preoperative diagnoses were correct if other symptoms predominated.[17]

History and physical examination are of paramount importance for establishing a clinical diagnosis. Imaging studies are performed to confirm a clinical suspicion of Meckel diverticulum.

Plain radiography of the abdomen is of limited value. It may reveal evidence of nonbleeding complications, including enteroliths and signs of intestinal obstruction or perforation, such as

air or air-fluid levels (see the image below). Anteroposterior view of abdominal radiograph showing multiple dilated loops of a small bowel with air-fluid levels.

When a patient has GI bleeding suggestive of Meckel diverticulum, the diagnostic evaluation should focus on Meckel scanning, a technetium-99m pertechnetate scintiscan (0.2mCi/kg in children and 10-20mCi in adults). The pertechnetate is taken up by gastric mucosa. Because bleeding from the Meckel diverticulum is related to acid induced damage of mucosa adjacent to the parietal cell containing tissue, it is always included early in the work-up.[18]

After intravenous injection of the isotope, the gamma camera is used to scan the abdomen. This procedure usually lasts approximately 30 minutes. Gastric mucosa secretes the radioactive isotope; thus, if the diverticulum contains this ectopic tissue, it is recognized as a hot spot. The Meckel scan is the preferred procedure because it is noninvasive, involves less radiation exposure, and is more accurate than an upper GI and small-bowel follow-through study. In children the Meckel scan has a reported sensitivity of 80-90%, a specificity of 95% and an accuracy of 90%. However, in adults where GI bleeding is a much less common presentation, the scan has a lower sensitivity (62.5%), a much lower specificity (9%), and a lower accuracy (46%).[19]

Because the Meckel scan is specific for gastric mucosa (ie, in the stomach or ectopic) and not specifically diagnostic of Meckel diverticulum, false positive results occur whenever ectopic gastric mucosa is present. Duodenal ulcer, small intestinal obstruction, some intestinal duplications, ureteric obstruction, aneurysm, and angiomas of the small intestine have yielded positive results. False negative results can occur when gastric mucosa is very slight or absent in the diverticulum, if necrosis of the diverticulum has occurred, or if the Meckel is superimposed on the bladder.[20]

Accuracy of the scan may be enhanced with administration of cimetidine, glucagon, and pentagastrin. Cimetidine enhances the uptake and blocks the secretion of technetium-99m pertechnetate from ectopic gastric mucosa.[21]This helps to improve the lesion to background ratio in enhancing a Meckel scan. Pentagastrin also enhances uptake of the isotope but also increases peristalsis, attenuating its value. Glucagon is used to decrease peristalsis, thus allowing the signal to be taken up during a longer exposure time. One strategy uses both pentagastrin and glucagon. With newer imaging technology, false-positive and false-negative rates have declined. Barium studies have largely been replaced by other imaging techniques; however, if a barium study is indicated, it should never precede the technetium-99m scan because barium may obscure the hot spot. A bleeding scan can be performed to identify the source if the patient is bleeding at 0.1ml/min or more. This scan involves removing and labeling some of the patient's own RBCs with technetium-99m, reinjecting them into the patient, and then scanning the abdomen for hot spots.[22, 23]

Selective arteriography may be helpful in patients in whom the results from scintigraphy and barium studies are negative. Usually, this occurs if the bleeding is either intermittent or has completely resolved.

When the rate of bleeding is greater than 1 mL/min, a superior mesenteric arteriogram can be helpful, but interpretation may be difficult due to overlying blood vessels. In these cases, selective catheterization of the distal ileal arteries may be needed.

Demonstration of abnormal arterial branches, dense capillary staining, or extravasation of the contrast medium confirms the presence of a Meckel diverticulum. However, a well-developed arterial supply may not always be present in the Meckel diverticulum; thus, these arteriographic signs are not very reliable.

Traditional small-bowel series using barium have been unreliable in the detection of Meckel diverticulum. However, in patients who require barium study to primarily look for other conditions, enteroclysis is more sensitive in detecting Meckel diverticulum.

Enteroclysis involves using a continuous infusion of barium with adequate compression of the ileal loops and intermittent fluoroscopy to detect Meckel diverticulum.

If the barium mixture is too dense and the fold pattern cannot be visualized, carboxymethylcellulose sodium can be used as the contrast medium.

On barium studies, Meckel diverticulum may appear as a blind-ending pouch on the antimesenteric side of the distal ileum. If filling defects are visualized, the diverticulum may contain a tumor.

Characteristic radiologic signs for Meckel diverticulum include demonstration of a triradiate fold pattern or a mucosal triangular plateau. Occasionally, a gastric rugal pattern may also be found within the Meckel diverticulum.

A barium enema can be performed if intussusception is suspected. Some people have tried hydrostatic therapy to reduce intussusception, but this has not been found to be useful.

Abdominal CT scanning is usually not helpful because differentiating Meckel diverticulum from the small-bowel loops is difficult; however, a blind-ending fluid-filled and/or gas-filled structure in continuity with small bowel may be visualized. CT scanning may also reveal an enterolith, intussusception, or diverticulitis. CT enterography advancements have increased the sensitivity in the diagnosis of Meckel diverticulum.[18]

Ultrasonography has been used in some cases of Meckel diverticulum. Ultrasonography tends to be helpful if the patient presents with anatomic rather than mucosal complications.

Wireless capsule endoscopy has been successfully used to identify Meckel diverticulum in young children.[24] In adults, this same technique has been used to identify an inverted Meckel diverticulum that presented as GI bleeding.[52]

Histologic Findings

In one study, heterotropic gastric mucosa was found in 62% of cases, pancreatic tissue was found in 6%, both pancreatic tissue and gastric mucosa were found in 5%, jejunal mucosa was found in 2%, Brunner tissue was found in 2%, and both gastric and duodenal mucosa were found in 2%.[2]

Although some reports have associated Helicobacter pylori with ectopic gastric mucosa in Meckel diverticulum, a small series of 21 consecutive patients from Turkey using polymerase chain reaction (PCR) failed to identify 23S ribosomal RNA sequences from the organism even in the 12 surgical specimens with heterotopic gastric mucosa.[53]

Medical Care

The emergency department evaluation and treatment of patients depends on the clinical presentation of Meckel diverticulum.

Because most symptomatic patients are acutely ill, establish an intravenous line immediately, start crystalloid fluids, and keep the patient on nothing by mouth (NPO) status. Obtain the blood investigations suggested above with a type and cross match.

If significant bleeding occurs, perform a transfusion of packed red cells. A patient who presents with intestinal obstruction usually requires nasogastric

decompression; also perform plain radiography of the abdomen. When a child presents with bleeding, specifically a dark tarry stool, perform a gastric lavage to

rule out upper GI bleeding. If the gastric lavage is negative for bleeding, consider an upper endoscopy and flexible sigmoidoscopy.

Meckel scan results may be negative despite a high clinical suspicion of Meckel diverticulum. The surgery team should be consulted to discuss the possible need for laparoscopy and/or laparotomy.

Surgical Care

If the patient is bleeding but is hemodynamically stable, a Meckel scan is warranted. On the other hand, the presence of peritoneal signs or hemodynamic instability demands urgent surgical intervention. Signs of small bowel obstruction also require surgical intervention.[25]

Definitive treatment of a complication, such as a bleeding Meckel diverticulum, is the excision of the diverticulum along with the adjacent ileal segment.

o Excision is carried out by performing a wedge resection of adjacent ileum and anastomosis, with the use of a stapling device. Adjacent ileum is included in the resection because ulcers frequently develop in the adjacent part of the ileum.[26]

o Successful resection of a Meckel diverticulum, even in children and infants, can also be accomplished through laparoscopy, using an endoscopically designed autostapling device.[27,

28, 29] A large series of national trends in the surgical management of Meckel diverticulum found that one fourth of cases are now treated laparoscopically. This group was older (6.4 y ± 5.1 y vs 5.1 y ± 5.3 y) and had shorter length of stay and trended toward lower total hospital charges.[50]

o In some cases of Meckel diverticulum, a primitive persistent right vitelline artery originating from the mesentery has been found during operation. When present, the artery is found to supply the Meckel diverticulum; therefore, it must be identified and ligated during the operation.

Management of Meckel diverticulum in asymptomatic patients is controversial.o In the past, if a Meckel diverticulum was encountered in a patient undergoing abdominal

surgery for some other intra-abdominal condition, many surgeons recommended its removal.

o This practice was questioned when a large series described an overall 4.2% likelihood of complications in Meckel diverticulum and a decreasing risk with increasing age. These authors concluded that assuming a 6% mortality rate from Meckel diverticulum complications, 400 asymptomatic diverticula would have to be excised to save one patient.[30]

o Another faction favors prophylactic removal of a diverticulum, which is a simple operation. This view is supported by data that demonstrate that managing a complication of Meckel diverticulum is associated with high morbidity and mortality rates. Others feel the only exception to universal excision is if the diverticulum is so broad based or so short that stapled excision cannot be performed technically. Fortunately, patients are less likely to develop complications in both of these situations.

o One recent small series suggested that only patients younger than 50 years clearly benefitted from removal if discovered unintentionally.[31]

Consultations

Radiologist Surgeon Gastroenterologist

Medication Summary

In addition to the definitive therapy, urgently administer a regimen of antibiotics (eg, ampicillin, gentamicin, and clindamycin or cefotetan) whenever acute Meckel diverticulitis, strangulation, perforation, or signs of small bowel obstruction or sepsis are present.

Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the clinical setting.

Ampicillin (Omnipen, Marcillin)

 Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms.

Clindamycin (Cleocin)

 Useful treatment for serious skin and soft tissue infections caused by most staphylococci strains. Also effective against entericaerobic and anaerobic flora, except enterococci. Inhibits bacterial protein synthesis by inhibiting peptide chain initiation at the bacterial ribosome, where it preferentially binds to the 50S ribosomal subunit, causing bacterial replication inhibition.

Gentamicin (Gentacidin, Garamycin)

 If used in combination with an antianaerobic agent, such as clindamycin or metronidazole, provides broad gram-negative and anaerobic coverage. Dosing regimens are numerous and adjusted on the basis of creatinine clearance and changes in distribution volume.

Cefotetan (Cefotan)

 Second-generation cephalosporin used as single-drug therapy to provide broad gram-negative coverage and anaerobic coverage. Half-life is 3.5 h. Inhibits bacterial cell wall synthesis by binding to ≥ 1 of the penicillin-binding proteins; inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death.

Antibiotics have proven effective in decreasing rate of postoperative wound infection and improving outcome in patients with intraperitoneal infection and septicemia.