Refarat intestinal Obstruction

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THE SMALL INTESTINE

The small intestine is a convoluted tube, extending from the pylorus to the colic valve, where it ends in

the large intestine. It is about 7 meters long,168

and gradually diminishes in size from its commencement

to its termination. It is contained in the central and lower part of the abdominal cavity, and is

surrounded above and at the sides by the large intestine; a portion of it extends below the superior

aperture of the pelvis and lies in front of the rectum. It is in relation, in front, with the greater omentum

and abdominal parietes, and is connected to the vertebral column by a fold of peritoneum,

the mesentery. The small intestine is divisible into three portions: the duodenum, the jejunum, and

the ileum.

The duodenum and pancreas.

Duodenum has received its name from being about equal in length to the breadth of twelve fingers (25

cm.). It is the shortest, the widest, and the most fixed part of the small intestine, and has no mesentery,

being only partially covered by peritoneum. Its course presents a remarkable curve, somewhat of the

shape of an imperfect circle, so that its termination is not far removed from its starting-point.

In the adult the course of the duodenum is as follows: commencing at the pylorus it passes backward,

upward, and to the right, beneath the quadrate lobe of the liver to the neck of the gall-bladder, varying

slightly in direction according to the degree of distension of the stomach: it then takes a sharp curve and

descends along the right margin of the head of the pancreas, for a variable distance, generally to the

level of the upper border of the body of the fourth lumbar vertebra. It now takes a second bend, and

passes from right to left across the vertebral column, having a slight inclination upward; and on the leftside of the vertebral column it ascends for about 2.5 cm., and then ends opposite the second lumbar

vertebra in the jejunum. As it unites with the jejunum it turns abruptly forward, forming

the duodendojejunal flexure. From the above description it will be seen that the duodenum may be

divided into four portions: superior, descending, horizontal, and ascending.
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Interior of the descending portion of the duodenum, showing bile papilla.

Jejunum

The jejunum is wider. Its diameter is about four centimeters. It is thicker, more vascular, and of a deeper

color than the ileum. The circular folds of its mucous membrane are large and thickly set. Its villi arelarger than in the ileum. The aggregated lymph nodules are almost absent in the upper part of the

jejunum. In the lower part, the lymph nodules are less frequently found than in the ileum and are

smaller and tend to assume a circular form. The circular folds are absent in the lower part of the ileum.

The jejunum mostly occupies the umbilical and left iliac regions. The jejunum and ileum are attach to

the posterior abdominal wall by mesentery. The mesentery allows the freest motion so that each coil

can accommodate itself to changes in form and position.

Ileum

The ileum is narrow; its diameter is about 3.75 centimeters. Its coats are thinner and less vascular than

those of the jejunum. It possesses few circular folds and they are small and disappear entirely toward it

lower end. Peyers patches are larger and more numerous. The ileum chiefly occupies the umbilical,

hypogastric, right iliac, and pelvic regions. The terminal part of the ileum usually lies in the pelvis, from

which it ascends over the right psoas and right iliac vessels. It ends in the right iliac fossa by opening into

the medial side of the commencement of the large intestine. The jejunum and ileum are attach to the

posterior abdominal wall by mesentery. The mesentery allows the freest motion so that each coil can

accommodate itself to changes in form and position. Between the two layers of mesentery are blood

vessels, nerves, lacteals, lymph glands, and a variable amount of fat
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Vessels and Nerves

The jejunum and ileum are supplied by the superior mesenteric artery (SMA). SMA arises from the

abdominal aorta at lever L1 vertebrae, approximately 1 cm inferior to the celiac trunk, and runs

between layers of the mesentery sending 12 to 18 branches to the jejunum and ileum. The arteries unite

to form loops f arches, arterial arcades, which give rise to straight arteries, the vasa recta.

The superior mesenteric vein drains the jejunum and ileum. It lies anterior and to the right of SMA in

the root of the mesentery and unites with splenic vein to form portal vein.

The lymphatics of the small intestine (lacteals) are arranged in two sets:-

- The lymphatics of the villi commence in these structures in the manner described above. Theyform an intricate plexus in the mucous and submucous tissue, being joined by the lymphatics

from the lymph spaces at the bases of the solitary nodules, and from this pass to larger vessels

at the mesenteric border of the gut.

- The lymphatics of the muscular coat are situated to a great extent between the two layers ofmuscular fibers, where they form a close plexus; throughout their course they communicate

freely with the lymphatics from the mucous membrane, and empty themselves in the same

manner as these into the origins of the lacteal vessels at the attached border of the gut.

Solitary lymphatic nodules (noduli lymphatici solitarii; solitary glands) are found scattered throughout

the mucous membrane of the small intestine, but are most numerous in the lower part of the ileum.

Their free surfaces are covered with rudimentary villi, except at the summits, and each gland is

surrounded by the openings of the intestinal glands. Each consists of a dense interlacing retiform tissue

closely packed with lymph-corpuscles, and permeated with an abundant capillary network. The

interspaces of the retiform tissue are continuous with larger lymph spaces which surround the gland,


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through which they communicate with the lacteal system. They are situated partly in the submucous

tissue, partly in the mucous membrane, where they form slight projections of its epithelial layer

Aggregated lymphatic nodules(noduli lymphatici aggregati; Peyers patches; Peyers glands; agminated

follicles; tonsill intestinales) form circular or oval patches, from twenty to thirty in number, and

varying in length from 2 to 10 cm. They are largest and most numerous in the ileum. In the lower part ofthe jejunum they are small, circular, and few in number. They are occasionally seen in the duodenum.

They are placed lengthwise in the intestine, and are situated in the portion of the tube most distant

from the attachment of the mesentery. Each patch is formed of a group of solitary lymphatic nodules

covered with mucous membrane, but the patches do not, as a rule, possess villi on their free surfaces.

They are best marked in the young subject, become indistinct in middle age, and sometimes disappear

altogether in advanced life. They are freely supplied with bloodvessels which form an abundant plexus

around each follicle and give off fine branches permeating the lymphoid tissue in the interior of the

follicle. The lymphatic plexuses are especially abundant around these patches.

Nerves of the small intestines are derived from the plexuses ofsympathetic nerves around the superior

mesenteric artery. From this source they run to the myenteric plexus (Auerbachs plexus) of nerves and

ganglia situated between the circular and longitudinal muscular fibers from which the nervous branches

are distributed to the muscular coats of the intestine. From this a secondary plexus, the plexus of the

submucosa (Meissners plexus) is derived, and is formed by branches which have perforated the

circular muscular fibers. This plexus lies in the submucous coat of the intestine; it also contains ganglia

from which nerve fibers pass to the muscularis mucos and to the mucous membrane. The nerve

bundles of the submucous plexus are finer than those of the myenteric plexus.

The functions of the small intestine include the following:

1. Mechanical digestion. Segmentation mixes the chyme with enzymes from the small intestineand pancreas. Bile from the liver separates fat into smaller fat globules. Peristalsis moves the

chyme through the small intestine.

2. Chemical digestion. Enzymes from the small intestine and pancreas break down all four groupsof molecules found in food (polysaccharides, proteins, fats, and nucleic acids) into their

component molecules.

3. Absorption. The small intestine is the primary location in the GI tract for absorption of nutrients.- The components of carbohydrates, proteins, nucleic acids, and water-soluble vitamins are

absorbed by facilitated diffusion or active transport. They are then passed to bloodcapillaries.

- Vitamin B12: Vitamin B12combines with intrinsic factor (produced in the stomach) and isabsorbed by receptor-mediated endocytosis. It is then passed to the blood capillaries.

- Lipids and fat-soluble vitamins: Because fat-soluble vitamins and the components of lipidsare insoluble in water, they are packaged and delivered to cells within water-soluble clusters

of bile salts called micelles. They are then absorbed by simple diffusion and, once inside the


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cells, mix with cholesterol and protein to form chylomicrons. The chylomicrons are then

passed to the lymphatic capillaries. When the lymph eventually empties into the blood, the

chylomicrons are broken down by lipoprotein lipase, and the breakdown products, fatty

acids and glycerol, pass through blood capillary walls to be absorbed by various cells.

- Water and electrolytes: About 90 percent of the water in chyme is absorbed, as well asvarious electrolytes (ions), including Na+, K+, Cl, nitrates, calcium, and iron.

Modifications of the mucosa for its various specialized functions in the small intestine include the

following:

- The plicae circulares (circular folds) are permanent ridges in the mucosa that encircle the insideof the small intestine. The ridges force the food to spiral forward. The spiral motion helps mix

the chyme with the digestive juices.

- Villi (singular, villus) are fingerlike projections that cover the surface of the mucosa, giving it avelvety appearance. They increase the surface area over which absorption and digestion occur.

The spaces between adjacent villi lead to deep cavities at the bases of the villi called intestinal

crypts ( crypts of Lieberkhn). Glands that empty into the cavities are called intestinal glands,

and the secretions are collectively called intestinal juice.

- Microvilli are microscopic extensions of the outer surface of the absorptive cells that line eachvillus. Because of their brushlike appearance (microscopically), the microvilli facing the lumen

form the brush border of the small intestine. Like the villi; the microvilli increase the surface

area over which digestion and absorption take place.

The villi of the mucosa have the following characteristics:

- An outer epithelial layer (facing the lumen) consists of the following cell types:- Absorptive cells, the primary cell type of the epithelial layer, synthesize digestive enzymes called

brush border enzymes that become embedded in the plasma membranes around the microvilli.

Various nutrients in the chyme that move over the microvilli are broken down by these brush

border enzymes and subsequently absorbed. Refer to Table , earlier in this chapter, for a list of

these enzymes.

- Goblet cells, located throughout the epithelial layer, secrete mucus that helps protect theepithelial layer from digestion.

- Enteroendocrine cells secrete hormones into blood vessels that penetrate each villus.- Paneth cells, located in the epithelial layer facing the intestinal crypts, secrete lysozyme, an

enzyme that destroys bacteria.

- An inner core of lamina propria (connective tissues) contains blood capillaries and smalllymphatic capillaries called lacteals.

The submucosa that underlies the mucosa of the small intestine bears the following modifications:

- Brunner's (duodenal) glands, found only in the submucosa of the duodenum, secrete an alkalinemucus that neutralizes the gastric acid in the incoming chyme.


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- Peyer's patches (aggregated lymphatic nodules), found mostly in the submucosa of the ileum,are clusters of lymphatic nodules that provide a defensive barrier against bacteria.

LARGE INTESTINE

The large intestine consists of the cecum and colon. It starts in the right iliac region of the pelvis, just at

or below the right waist, where it is joined to the bottom end of the small intestine. From here it

continues up the abdomen, then across the width of the abdominal cavity, and then it turns down,

continuing to its endpoint at the anus.

The large intestine is about 1.5 metres (4.9 ft) long, which is about one-fifth of the whole length of

the intestinal canal.

Parts of the large intestine are:

- Cecum the first part of the large intestine- Taeniae coli three bands of smooth muscle- Haustra bulges caused by contraction of taeniae coli- Epiploic appendages small fat accumulations on the viscera

Locations along the colon are:

- The ascending colon- The right colic flexure (hepatic)- The transverse colon- The transverse mesocolon- The left colic flexure (splenic)- The descending colon- The sigmoid colon the v-shaped region of the large intestine

Blood supply and lymphatics

Arterial supply to the colon comes from branches of the superior mesenteric artery(SMA) and inferior

mesenteric artery (IMA). Flow between these two systems communicates via a "marginal artery" that

runs parallel to the colon for its entire length. Historically, it has been believed that the arc of Riolan, or

the meandering mesenteric artery (of Moskowitz), is a variable vessel connecting the proximal SMA to

the proximal IMA that can be extremely important if either vessel is occluded. However, recent studiesconducted with improved imaging technology have questioned the actual existence of this vessel, with

some experts calling for the abolition of the terms from future medical literature.
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Venous drainage usually mirrors colonic arterial supply, with the inferior mesenteric veindraining into

the splenic vein, and the superior mesenteric veinjoining the splenic vein to form the hepatic portal

vein that then enters the liver.

Lymphatic drainage from the entire colon and proximal two-thirds of the rectum is to the paraaortic

lymph nodes that then drain into the cisterna chyli. The lymph from the remaining rectum and anus can

either follow the same route, or drain to the internal iliac and superficial inguinal nodes. The pectinate

line only roughly marks this transition.

Physiology

There are differences in the large intestine between differentorganisms. The large intestine is mainly

responsible for storing waste, reclaiming water, maintaining the water balance, absorbing

some vitamins, such as vitamin K, and providing a location for flora-aided fermentation.

By the time the chyme has reached this tube, most nutrients and 90% of the water has been absorbed

by the body. At this point some electrolytes like sodium, magnesium, and chloride are left as well as

indigestible parts of ingested food (e.g., a large part of ingested amylose, protein which has been

shielded from digestion heretofore, and dietary fiber, which is largely indigestible carbohydrate in either

soluble or insoluble form). As the chyme moves through the large, most of the remaining water is

removed, while the chyme is mixed with mucus and bacteria (known as gut), and becomes feces.

The ascending colon receives fecal material as a liquid. The muscles of the colon then move the waterywaste material forward and slowly absorb all the excess water. The stools get to become semi solid as

they move along into the descending colon. The bacteria break down some of the fiber for their own

nourishment and create acetate, propionate, and butyrate as waste products, which in turn are used by

the cell lining of the colon for nourishment. No protein is made available. In humans, perhaps 10% of the

undigested carbohydrate thus becomes available; in other animals, including other apes and primates,

who have proportionally larger colons, more is made available, thus permitting a higher portion of plant
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material in the diet. This is an example of a symbiotic relationship and provides about one

hundred calories a day to the body. The large intestine produces no digestive enzymes - chemical

digestion is completed in the small intestine before the chyme reaches the large intestine. The pH in the

colon varies between 5.5 and 7 (slightly acidic to neutral).

INTESTINAL OBSTRUCTION

Mechanical or functional obstruction of the intestines, preventing the normal transit of the products of

digestion. It can occur at any level distal to the duodenum of the small intestine and is a medical

emergency. Although many cases are not treated surgically, it is a surgical problem.

Pathophysiology

Small-bowel obstruction (SBO) leads to proximal dilatation of the intestine due to accumulation of GI

secretions and swallowed air. This bowel dilatation stimulates cell secretory activity, resulting in more

fluid accumulation. This leads to increased peristalsis above and below the obstruction, with frequent

loose stools and flatus early in its course.

Vomiting occurs if the level of obstruction is proximal. Increasing small-bowel distention leads to

increased intraluminal pressures. This can cause compression of mucosal lymphatics, leading to bowel

wall lymphedema. With even higher intraluminal hydrostatic pressures, increased hydrostatic pressure

in the capillary beds results in massive third spacing of fluid, electrolytes, and proteins into the intestinal

lumen. The fluid loss and dehydration that ensue may be severe and contribute to increased morbidity

and mortality.

SBOs can be partial or complete, simple (ie, nonstrangulated) or strangulated. Strangulated obstructions

are surgical emergencies. If not diagnosed and properly treated, vascular compromise leads to bowel

ischemia and further morbidity and mortality. Because as many as 40% of patients have strangulated

obstructions, differentiating the characteristics and etiologies of obstruction is critical to proper patient

treatment.

Strangulated SBOs are most commonly associated with adhesions and occur when a loop of distended

bowel twists on its mesenteric pedicle. The arterial occlusion leads to bowel ischemia and necrosis. If

left untreated, this progresses to perforation, peritonitis, and death.
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Mechanical causes:

Obstructive Structural

Neoplasm Ileus

Hernia Acute anorectal conditions

Volvulus Rectal prolapse

Adhesive Endometriosis

Postsurgical abnormalities Rectocele

Inflammatory bowel disease Aganglionosis

Enteroliths Irritable bowel syndrome

Diverticular disease Chagas' disease

Stricture Neurofibromatosis

Small-bowel obstruction Inadequate fiber

Abscess

Ogilvie's syndrome

MOST FREQUENT CAUSES OF INTESTINAL OBSTRUCTION

Small bowel

1. Small bowel obstruction secondary to postoperative adhesions 60 to 80% intestinalobstruction.

2. Hernias 15 to 20%3. Malignant tumors, intramural (which are rare) and extramural (which are far more

common) 10 to 15%.

Colon

1. Cancer 60%.2. Diverticulitis 15%.3.

Volvulus 5%.

Causes ofsmall bowel obstruction include:

1. Adhesions from previous abdominal surgery2. Hernias containing bowel3. Crohn's disease causing adhesions or inflammatory strictures4. Neoplasms, benign or malignant
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5. Intussusception in children6. Volvulus7. Superior mesenteric artery syndrome, a compression of theduodenum by the superior

mesenteric artery and the abdominal aorta

8. Ischaemic strictures9. Foreign bodies (e.g. gallstones in gallstone ileus, swallowed objects)10. Intestinal atresia11.Carcinoid rare, preferred location: ileum

Metabolic Endocrine/Neurologic:

Drug Effects:

Narcotics Calcium-channel blockers

Aluminum (antacids) Barium sulfate

Psychotropic agents Diuretics

Ganglionic blockers Iron supplements

Calcium (antacids, supplements) Antihypertensives

Sucralfate Vinca alkaloids

Anticholinergics Metal intoxication (mercury, lead arsenic)

Antidepressants Antispasmodics

Hypothyroidism Amyloidosis

Hypercalcemia Scleroderma

Hypokalemia Multiple sclerosis

Porphyria Parkinson's disease

Glucagonoma Cauda equina tumor

Somatostatinoma Stroke

Pheochromocytoma Paraplegia

Pregnancy Collagen vascular disease

Uremia Psychologic

MEN IIa Psychiatric

Panhypopituitarism Anorexia nervosa
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CLASSIFICATION

1.MECHANICAL 2.DYNAMIC (ILEUS)

a. obturation a. spastic

b. strangulation b. adynamic

A. COMPLETE B. PARTIAL

CLASSIFICATION

1. Extraluminal (including adhesions and neoplastic disease)

2. Intraluminal (such as gallstone ileus or stricture)

3. Intramural (such as a Crohn's disease process).

The most obvious route of fluid and electrolyte loss.

- into the bowel lumen- into the edematous bowel wall- into the free peritoneal cavity- by vomiting or nasogastric suction

Volvulus.

Plain film of sigmoid volvulus. Note appearance

of bent inner tube\


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Knot formation.

Incarceration of the colon

Incarceration of the small bowel

Ileocecal invagination.

Barium enema, showing intussusception.

Physics of cecal rupture in colon obstruction


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SYMPTOMS

The four cardinal symptoms and signs of intestinal obstruction

1. crampy abdominal pain2. nausea and vomiting3. obstipation4. abdominal distention

Nausea and vomiting will occur in 100% of patients with a complete bowel obstructiono small bowel obstruction

mesis will develop early emesis large in volume emesis frequent - (shortly after po. intake)

o large bowel obstruction

emesis develops later often fecal in content

Abdominal/visceral pain - many patients will have this symptomo pain is colicky or crampingo pain is often near site of obstruction

Abdominal distention is more common in obstruction of large bowel Bowel sounds- complete obstruction

o absent bowel soundso absent flatuso partial obstruction- bowel sounds can be high pitched or tympanic

History of infrequent bowel movementsWhat is pseudo- obstruction?

It is important to be aware that a patient can present with some of the symptoms of a bowel

obstruction - i.e. nausea, vomiting, abdominal pain, distention etc. but the obstruction is secondary to

fecal impaction/obstipation or to paralytic ileus. An abdominal x-ray (3 views) will help delineate if the

patient's problem is due to increased stool in the colon.

DIAGNOSIS

Physical examination findings include: abdominal distension (more prevalent in distal obstructions),

hyperactive bowel sounds (early), or hypoactive bowel sounds (late). Fever, tachycardia and peritoneal

signs may be associated with strangulation. It is also important to look for possible causes of obstruction

such as inguinal hernias so always include a genitourinary examination. Rectal examination is importantas well, because gross blood or hemoccult positive stool suggests strangulation or malignancy.


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Plain radiography

All patients suspected of having a small bowel obstruction should have plain radiographs obtained. It is

essential is to obtain an upright chest film (looking for free air/perforation), an upright abdominal film

(looking for air fluid levels), and a supine abdominal film (looking for distended loops of bowel). The

diagnosis is made when multiple air-fluid levels are seen along with distended loops of small bowel.

Absence of air in the colon or rectum suggests a complete obstruction while the presence of air in the

colon suggests a partial obstruction.

Visible mucosal folds in the distended small bowel.

Small Bowel Series

The diagnosis and degree of small bowel obstruction can be confirmed by a small bowel follow-through

or enteroclysis (the duodenum is instilled with air and contrast). These studies used to be considered the

gold standard for determining whether an obstruction was partial or complete. More recently, CT has

been replacing small bowel follow-through for definitive diagnosis.

Computerized Tomography

Computerized tomography has been replacing the small bowel series as the study of choice to

differentiate partial versus complete obstruction as well as to identify strangulation early. One small

series reported a sensitivity of 93%, specificity of 100%, and accuracy of 94% in detecting obstruction.

Obstruction is present if the small-bowel loop is greater than 2.5 cm in diameter dilated proximal to a

distinct transition zone of collapsed bowel less than 1 cm in diameter. A smooth beak indicates simple

obstruction without vascular compromise; a serrated beak may indicate strangulation. Bowel wall

thickening, pneumatosis, and portal venous gas all suggest strangulation.

CT can also differentiate between the etiologies of SBO, that is, extrinsic causes such as adhesions and

hernia from intrinsic causes such as neoplasms or Crohn's disease. Furthermore, it has the ability to

identify a myriad of other causes of acute abdominal pain such as abscess, hernia, tumor, or

inflammation. The CT should be obtained with both PO and IV contrast, unless the patient has renal

failure or IV contrast allergy.


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CT scan through the mid abdomen shows dilated small bowel loops filled with fluid and decompressed

ascending and descending colon. These are typical CT findings in small bowel obstruction.

Laboratory studies

Essential laboratory tests are needed; these include the following:

1. Serum chemistries - Results are usually normal or mildly elevated2. Blood urea nitrogen (BUN) level - If the BUN level is increased, this may indicate decreased

volume state (eg, dehydration)

3. Creatinine level - Creatinine level elevations may indicate dehydration4. Complete blood count (CBC) - The white blood cell (WBC) count may be elevated with a left shift

in simple or strangulated obstructions; increased hematocrit is an indicator of volume state (ie,

dehydration)

5. Lactate dehydrogenase tests6. Urinalysis7. Type and crossmatch - The patient may require surgical intervention

Laboratory tests to exclude biliary or hepatic disease are also needed; they include the following:

1. Phosphate level2. Creatine kinase level3. Liver panels

TREATMENT

Fluid replacement with aggressive intravenous (IV) resuscitation using isotonic saline or lactated Ringer

solution is indicated. Oxygen and appropriate monitoring are also required. Antibiotics are used to cover

gram-negative and anaerobic organisms. In addition, analgesia and antiemetic are administered as

indicated clinically. As previously mentioned, a nonoperative trial of as many as 3 days is warranted for

partial or simple obstruction. Resolution of obstruction occurs in virtually all patients with these lesions

within 72 hours.

Antibiotics

These agents are for prophylaxis in surgical intervention, if needed.

1. Cefazolin : Cefazolin is a first-generation semisynthetic cephalosporin that arrests bacterial cellwall synthesis, inhibiting bacterial growth.
http://reference.medscape.com/drug/kefzol-cefazolin-342492http://reference.medscape.com/drug/kefzol-cefazolin-342492


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2. Cefoxitin (Mefoxin) : Cefoxitin is a second-generation cephalosporin indicated for gram-positivecocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-

resistant gram-negative bacteria may respond to cefoxitin.

3. Cefotetan : Cefotetan is a second-generation cephalosporin indicated for infections caused bysusceptible gram-positive cocci and gram-negative rods. Dosage and route of administration

depend on the condition of patient, the severity of infection, and the susceptibility of the

causative organism.

4. Cefuroxime (Ceftin, Zinacef) : Cefuroxime is a second-generation cephalosporin that maintainsthe gram-positive activity of first-generation cephalosporins; it adds activity against Proteus

mirabilis, Haemophilus influenzae, E coli, Klebsiella pneumoniae, and Moraxella catarrhalis. The

condition of the patient, the severity of the infection, and the susceptibility of the

microorganism determine the proper dose and route of administration

5. Meropenem (Merrem) : Meropenem is a bactericidal, broad-spectrum carbapenem antibioticthat inhibits cell-wall synthesis. It is effective against most gram-positive and gram-negative

bacteria.

Antiemetic

These agents should be administered for symptomatic relief, usually in conjunction with GI

decompression via placement of an NG tube for suction.

1. Promethazine (Phenergan, Phenadoz, Promethegan) : Promethazine is for the symptomatictreatment of nausea and vomiting. It is an antidopaminergic agent that is effective in treating

emesis. Promethazine blocks postsynaptic mesolimbic dopaminergic receptors in the brain and

reduces stimuli to the brainstem reticular system.

2. Ondansetron (Zofran, Zuplenz) : Ondansetron is a selective 5-HT3-receptor antagonist thatblocks serotonin peripherally and centrally; it is used in the prevention of nausea and vomiting.

Ondansetron is metabolized in the liver through the P-450 pathway.

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary

toilet, and have sedating properties, which are beneficial for patients who experience pain.

o Morphine sulfate (Astramorph, MS Contin, Kadian, Oramorph) : This is the drug of choice foranalgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with

naloxone. Various IV doses are used; morphine sulfate is commonly titrated until the desired

effect is obtained.
http://reference.medscape.com/drug/cefoxitin-342497http://reference.medscape.com/drug/cefotetan-342496http://reference.medscape.com/drug/ceftin-zinacef-cefuroxime-342500http://reference.medscape.com/drug/merrem-iv-meropenem-342565http://reference.medscape.com/drug/merrem-iv-meropenem-342565http://reference.medscape.com/drug/ceftin-zinacef-cefuroxime-342500http://reference.medscape.com/drug/cefotetan-342496http://reference.medscape.com/drug/cefoxitin-342497


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Surgical procedures for the relief of intestinal obstruction are divided into five categories:

(1) Procedures not requiring opening of bowel lysis of adhesions, manipulation-reduction of

Intussusception, reduction of incarcerated hernia

(2) Enterotomy for removal of obturation obstruction gallstone, bezoars

(3) Resection of the obstructing lesion or strangulated bowel with primary anastomosis(4) Short-circuiting anastomosis around an obstruction

(5) Formation of a cutaneous stoma proximal to the obstruction cecostomy (rarely performed),

transverse colostomy

Prognosis

With proper diagnosis and treatment of the obstruction, prognosis in small-bowel obstruction (SBO) is

good. Complete obstructions treated successfully nonoperatively have a higher incidence of recurrence

than do those treated surgically.

Complications of SBO include the following:

- Sepsis- Intra-abdominal abscess- Wound dehiscence- Aspiration- Short-bowel syndrome (as a result of multiple surgeries)- Death (secondary to delayed treatment)


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LARGE INTESTINE OBSTRUCTION

Large-bowel obstruction (LBO) is an emergency condition that requires early identification and

intervention. The etiology of LBO is age dependent.

LBO can result from either mechanical interruption of the flow of intestinal contents or by the dilation of

the colon in the absence of an anatomic lesion (pseudo-obstruction).

Distinguishing between a true mechanical obstruction and a pseudo-obstruction is important, as the

treatment differs

PATHOPHYSIOLOGY

The prevalence of mechanical large-bowel obstruction (LBO) increases with age as does it main

causes, colon cancer and diverticulitis. Sigmoid volvulusand cecal volvulus are also potential causes of

this disorder.

Large-bowel obstruction. Abdominal (KUB) radiograph depicting massive dilation of the colon due to a

cecal volvulus.

Mechanical obstruction of the large bowel causes bowel dilation above the obstruction. This causes

mucosal edema and impaired venous and arterial blood flow to the bowel. Bowel edema and ischemia

increase the mucosal permeability of the bowel, which can lead to bacterial translocation, systemic

toxicity, dehydration, and electrolyte abnormalities. Bowel ischemia can lead to perforation and fecal

soilage of the peritoneal cavity.

The pathophysiology ofacute colonic pseudo-obstruction (ACPO) is not clear, but it is thought to result

from an autonomic imbalance, which results from decreased parasympathetic tone or excessive

sympathetic output.

ACPO usually occurs in the setting of a wide range of medical or surgical illnesses. If untreated, colonic

ischemia or perforation can occur. This syndrome is characterized by a loss of peristalsis and results in

the accumulation of gas and fluid in the colon.
http://emedicine.medscape.com/article/277496-overviewhttp://emedicine.medscape.com/article/173388-overviewhttp://emedicine.medscape.com/article/373585-overviewhttp://emedicine.medscape.com/article/364967-overviewhttp://emedicine.medscape.com/article/184579-overviewhttp://refimgshow%285%29/http://emedicine.medscape.com/article/184579-overviewhttp://emedicine.medscape.com/article/364967-overviewhttp://emedicine.medscape.com/article/373585-overviewhttp://emedicine.medscape.com/article/173388-overviewhttp://emedicine.medscape.com/article/277496-overview


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CAUSES

Approximately 60% of mechanical large-bowel obstructions (LBOs) are caused by malignancies, 20% are

caused by diverticular disease, and 5% are the result ofcolonic volvulus.

1. Obstructions caused by tumors tend to have a gradual onset and result from tumor growthnarrowing the colonic lumen.

Large-bowel obstruction. Contrast study demonstrates colonic obstruction at the level of the splenic

flexure, in this case due to carcinoma.

2. Diverticulitis is associated with muscular hypertrophy of the colonic wall. Repetitive episodes ofinflammation cause the colonic wall to become fibrotic and thickened, leading to luminal

narrowing.

3. Colonic volvulus results when the colon twists on its mesentery. This impairs the venousdrainage and arterial inflow. Symptoms are usually abrupt.

4. Sigmoid volvulus typically occurs in older, debilitated individuals with a history of chronicconstipation, or those living in an institutionalized setting.

Large-bowel obstruction. Massive dilation of the colon due to a sigmoid volvulus.
http://emedicine.medscape.com/article/173388-overviewhttp://emedicine.medscape.com/article/197322-overviewhttp://refimgshow%287%29/http://refimgshow%284%29/http://refimgshow%287%29/http://refimgshow%284%29/http://emedicine.medscape.com/article/197322-overviewhttp://emedicine.medscape.com/article/173388-overview


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5. Cecal volvulus is caused by a congenital defect in the peritoneum, which results in inadequatefixation of the cecum, and increased cecal mobility. Patients usually present with this disorder in

the sixth decade of life

6. Intussusception is primarily a pediatric disease. It is estimated that between 5% and 16% of allintussusceptions in the western world occur in adults. Approximately two thirds of adult

intussusception cases are caused by tumors. Two main types of intussusception affect the large

bowel.

o Enterocolic intussusceptions involve both the small bowel and the large bowel. Theseare composed of either ileocolic intussusceptions or ileocecal intussusceptions,

depending on where the lead point is located.

o Colocolic intussusceptions involve only the colon. They are classified as either colocolicor sigmoidorectal intussusceptions.

Acute colonic pseudo-obstruction (ACPO), or Ogilvie syndrome, has many etiologies. This disorder is

typically seen in elderly patients who are hospitalized with a severe illness. In a retrospective review of

more than 1400 cases of ACPO, the most common predisposing conditions were operative andnonoperative trauma (11%), infections (10%), and cardiac disease (10-18%)

DIAGNOSIS

Physical

1. Abdominal distention may be significant in patients with a large-bowel obstruction.2. Bowel sounds may be normal early on but usually become quiet.3.

Abdomen is hyperresonant to percussion.

4. Palpation of the abdomen reveals tenderness. Fever, severe tenderness, and abdominal rigidityare ominous signs that suggest peritonitis secondary to perforation.

5. The cecum is the area most likely to perforate (following the Laplace law). Sigmoid diverticulitisand a perforated sigmoid secondary to carcinoma are clinically difficult to differentiate.

6. Guaiac-positive stool may be seen with carcinoma or diverticulitis.7. Rectal or lower sigmoidal mass may be palpated on rectal examination. An abdominal mass or

fullness may be palpated if a tumor is present in the cecum.

Laboratory Studies

Obtain a blood sample for a CBC, electrolyte levels, lactate level, prothrombin time (PT), and type andcrossmatch.

Imaging Studies

1. Obtain an upright chest radiograph and flat and upright abdominal radiographs. Chestradiographs demonstrate free air if perforation has occurred; abdominal radiographs may be

diagnostic of sigmoid or cecal volvulus (ie, kidney bean appearance on the radiograph).
http://emedicine.medscape.com/article/930708-overviewhttp://emedicine.medscape.com/article/184579-overviewhttp://emedicine.medscape.com/article/184579-overviewhttp://emedicine.medscape.com/article/930708-overview


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Large-bowel obstruction. This chest radiograph demonstrates free air under the diaphragm, indicating

bowel perforation

2. Intramural air is an ominous sign that suggests colonic ischemia.3. The absence of free air does not exclude perforation (this finding may be absent in half of all

perforations).4. Additional contrast studies include an enema with water-soluble contrast (ie, Gastrografin) or CT

with intravenous and oral or rectal contrast.

Large-bowel obstruction. Gastrografin study in a patient with obstipation reveals colonic

obstruction at the rectosigmoid level.

5. Contrast studies that reveal a column of contrast ending in a "bird's beak" are suggestive ofcolonic volvulus.
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Large-bowel obstruction. Contrast study of patient with cecal volvulus. The column of contrast

ends in a "bird's beak" at the level of the volvulus.

Procedures

Insert a nasogastric tube if the patient has been vomiting. Intravascular volume usually is depleted, and

early intravenous fluid resuscitation with isotonic saline or Ringer lactate solution is necessary.

TREATMENT

Antibiotics

Therapy must cover all likely pathogens in the context of this clinical setting.

1. Clindamycin (Cleocin) : A lincosamide useful to treat serious skin and soft-tissue infectionscaused by most staphylococcal strains. Also effective against aerobic and anaerobic

streptococci, except enterococci. Inhibits bacterial protein synthesis by inhibiting peptide chain

initiation at bacterial ribosome, where it preferentially binds to 50S ribosomal subunit, inhibiting

bacterial growth.

2. Metronidazole (Flagyl) : Imidazole ring-based antibiotic active against various anaerobic bacteriaand protozoa. Used in combination with other antimicrobial agents (used alone in Clostridium

difficile enterocolitis).

3. Aztreonam (Azactam) : Monobactam that inhibits cell wall synthesis during bacterial growth.Active against gram-negative bacilli. Effective against aerobic gram-negative organisms.

4. Cefoxitin (Mefoxin) : Second-generation cephalosporin indicated for management of infectionscaused by susceptible gram-positive cocci and gram-negative rods. Effective against aerobic and

anaerobic gram-negative organisms.

5. Cefotetan (Cefotan) : Second-generation cephalosporin indicated for management of infectionscaused by susceptible gram-positive cocci and gram-negative rods.

6. Imipenem and cilastatin (Primaxin) : Effective against aerobic and anaerobic gram-negativeorganisms.
http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/flagyl-metronidazole-342566http://reference.medscape.com/drug/azactam-aztreonam-342553http://reference.medscape.com/drug/cefoxitin-342497http://reference.medscape.com/drug/cefotetan-342496http://reference.medscape.com/drug/primaxin-imipenem-cilastatin-342562http://refimgshow%286%29/http://reference.medscape.com/drug/primaxin-imipenem-cilastatin-342562http://reference.medscape.com/drug/cefotetan-342496http://reference.medscape.com/drug/cefoxitin-342497http://reference.medscape.com/drug/azactam-aztreonam-342553http://reference.medscape.com/drug/flagyl-metronidazole-342566http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558


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7. Meropenem (Merrem) : Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria.

COMPLICATIONS

o Perforationo Sepsiso Intra-abdominal abscesso Death

DIFFERENTIALS

o Abdominal Pain in Elderly Personso Constipationo Diverticular Diseaseo Small Bowel Obstruction
http://reference.medscape.com/drug/merrem-iv-meropenem-342565http://emedicine.medscape.com/article/776663-overviewhttp://emedicine.medscape.com/article/774726-overviewhttp://emedicine.medscape.com/article/173388-overviewhttp://emedicine.medscape.com/article/774140-overviewhttp://emedicine.medscape.com/article/774140-overviewhttp://emedicine.medscape.com/article/173388-overviewhttp://emedicine.medscape.com/article/774726-overviewhttp://emedicine.medscape.com/article/776663-overviewhttp://reference.medscape.com/drug/merrem-iv-meropenem-342565


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ANATOMY

Peritoneum is a thin serous membrane that lines the abdominal wall and covers the organs within. It is

composed of a layer of mesothelium supported by a thin layer of connective tissue. The peritoneum

both supports the abdominal orages and serves as a conduit for their blood and lymph vessels and

nerves.

Layers

The abdominal cavity (the space bounded by the vertebrae, abdominal muscles, diaphragm and pelvic

floor) should not be confused with the intraperitoneal space (located within the abdominal cavity, but

wrapped in peritoneum). For example, a kidney is inside the abdominal cavity, but is retroperitoneal.

Although they ultimately form one continuous sheet, two types of layers of peritoneum and a potential

space between them are as follows:-

a. Outer layer: Parietal peritoneum; attached to the abdominal wall.b. Inner layer: Visceral peritoneum; wrapped around the internal organs that are located inside

the intraperitoneal cavity.c. The potential space between these two layers is the peritoneal cavity, it is filled with small

amount of serous fluid, about 50ml, that allows the two layers to slide freely over each other.

d. The term mesentery is often used to refer to a double layer of visceral peritoneum. There areoften blood vessels, nerves, and other structures between these layers. The space between

these two layers is technically outside of the peritoneal sac, and thus not in the peritoneal

cavity.

Subdivisions

There are two main reqions of the peritoneum, connected by

the epiploic foramen:

- The greater sac (red area in the diagram)- The lesser sac; or omental bursa (blue area in the

diagram). Further divided into:-

o Lesser omentum (or gastrohepatic) isattached to the lesser curvature of the

stomach and the liver.

o Greater omentum (or gastrocolic) hangs fromthe greater curve of the stomach and loops

down in front of the intestine before curving

back upwards to attach to the transverse

colon. In effect it is draped in front of the

intestine like an apron and may serve and an

insulating or protective layer.


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Left sagittal drawing of the compartments of the retroperitoneal space in

this area and its relationship to the contiguous viscera. Note that the

anterior and posterior layers of the renal fascia are fused superiorly but

open inferiorly, favoring the spread of infections inferiorly.

Physiology

The peritoneum is a bidirectional, semipermeable membrane that controls the amount of fluid within

the peritoneal cavity, promotes the sequestration and removal of bacteria from the peritoneal cavity,

and facilitates the migration of inflammatory cells from the microvasculature into the peritoneal cavity.

Normally, the peritoneal cavity contains less than 100 mL of sterile serous fluid. Microvilli on the apical

surface of the peritoneal mesothelium markedly increase the surface area and promote the rapid

absorption of fluid from the peritoneal cavity into the lymphatics and the portal and systemic

circulation. The amount of fluid within the peritoneal cavity may increase to many liters in various

diseases such as cirrhosis, nephrotic syndrome, and peritoneal carcinomatosis.

The circulation of fluid within the peritoneal cavity is driven in part by the movement of the diaphragm.

Intercellular pores in the peritoneum covering the inferior surface of the diaphragm (termed stomata)

communicate with lymphatic pools within the diaphragm. Lymph flows from these diaphragmatic

lymphatic channels through subpleural lymphatics to the regional lymph nodes and ultimately the

thoracic duct. Relaxation of the diaphragm during exhalation opens the stomata, and the negative

intrathoracic pressure draws fluid and particles, including bacteria, into the stomata.

Contraction of the diaphragm during inhalation propels the lymph through the mediastinal lymphatic

channels into the thoracic duct. It is postulated that this so-called diaphragmatic pump drives the

movement of peritoneal fluid in a cephalad direction toward the diaphragm and into the thoracic

lymphatic vessels. This circulatory pattern of peritoneal fluid toward the diaphragm and into the central

lymphatic channels is consistent with the rapid appearance of sepsis in patients with generalized intra-

abdominal infections as well as the perihepatitis of Fitz-HughCurtis syndrome in patients with acute

salpingitis.

The peritoneum and peritoneal cavity respond to infection in five ways:

1. Bacteria are rapidly removed from the peritoneal cavity through the diaphragmatic stomata

and lymphatics, as described in the preceding paragraph.


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2. Peritoneal macrophages release proinflammatory mediators that promote the migration of

leukocytes into the peritoneal cavity from the surrounding microvasculature.

3. Degranulation of peritoneal mast cells releases histamine and other vasoactive products,

causing local vasodilation and the extravasation of protein-rich fluid containing complement

and immunoglobulins into the peritoneal space.

4. Protein within the peritoneal fluid opsonizes bacteria, which, along with activation of the

complement cascade, promotes neutrophil- and macrophage-mediated bacterial phagocytosis

and destruction.

5. Bacteria become sequestered within fibrin matrices, thereby promoting abscess formation

and limiting the generalized spread of the infection.

PERITONITIS

Acute inflammation of peritoneal cavity, as usual, with exudative reaction of peritoneum.

AETIOLOGY

Primary peritonitis the source of infection is out of peritoneal cavity. Infection spreads by lymph

stream or through haematic system. For example tuberculous peritonitis.

- Spontaneous peritonitis in child- Spontaneous peritonitis in adult

Secondary peritonitis contact infection: acute purulent peritonitis after destructive appendicitis,

perforation of hollow organs of peritoneal cavity or posttraumatic (incl. surgery) infection

- Acute perforation peritonitis (from cholecystitis, appendicitis, PUD, pancreatitis etc)- Post-operative peritonitis- Post-traumatic peritonitis

PATHOGENESIS

Primary peritonitis is usually caused by liver disease. Fluid builds up in the abdomen, creating a prime

environment for the growth of bacteria.

Secondary peritonitis is caused by other conditions that allow bacteria, enzymes, or bile into theperitoneum from a hole or tear in the gastrointestinal or biliary tracts. Such tears can be caused by

pancreatitis, a ruptured appendix, stomach ulcer, Crohn's disease, or diverticulitis. Peritoneal dialysis,

which uses the blood vessels in the peritoneum to filter waste from your blood when your kidneys are

not able to do so, also may cause peritonitis.


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CLASSIFICATION

By the type of exudate:

1. Serous

2. Sero-fibrinous

3. Purulent

4. Fecal

5. Chemical

6. Haemorrhagic

7. Bile

By spreading:

1. Local

2. Spreading:

a. Diffuse (spreading out of inflammation zone on the neighbouring zones, but not on the all

peritoneal cavity),

b. Spilled (spreading to all peritoneal cavity)

By type:

1. Infected peritonitis

a. Perforation of part of the GIt, or, in women, of the reproductive system this could be due to

ingestion of a sharp object, e.g. a fishbone! Or could be due to trauma, or an ulcer etc. In these

cases you will most often find Gram negative bacteria and anaerobic bacteria in the peritoneum.A common example is E. Coli.

b. Disruption of the peritoneum e.g. by surgery or trauma. This can result in bacteria in the

peritoneum from the external environment. In this case, the most common causing agent is

staphylococcus aureus.

c. Spontaneous bacterial peritonitis (SBP)this can occur in children and in those with ascites

(i.e. in severe liver disease). It is treated differently to other types of peritonitis; usually only

requiring antibiotic treatment.

d. Systemic infectionse.g. such as TB can very rarely result in peritonitis.

2. Non infected peritonitis

a. Leakage of sterile bodily fluids into the peritoneume.g. such as blood, bile urine etc. It is

very important to note that although these fluids are sterile at first, they will usually become

infected once in the peritoneal cavity, causing full blown peritonitis within 24-48 hours.

b. Auto-immune diseasesuch as Lupus can cause peritonitis.


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Bacteria from gastrointestinal tract:

1. E. Coli2. Aerob and anaerob streptococci3. Closridum4. Bacteroides5. Klebsiella pneumonia

Bacteria from non GIT:

1. Chlamydia2. Pneumococcus3. B hemolytic streptococcus4. Mycobacteria tuberculosis5. Gonococcus

THE SYSTEMIC RESPONSE TO PERITONITIS

This includes the release of catecholamines, glucocorticoids, aldosterone, and vasopressin

(antidiuretic hormone). These responses, combined with hypovolemia from the copious

fluid sequestration within the peritoneum, can create hemodynamic instability with hypotension,

reduced cardiac index, increased peripheral resistance, and increased peripheral oxygen consumption.

The patient may manifest the hyperdynamic hemodynamic picture of septic (distributive)

shock, i.e., increased cardiac output, decreased peripheral resistance, and decreased arteriovenous

oxygen difference. Fluid resuscitation may change the patient's condition from a hypodynamic to ahyperdynamic state.

RISK FACTORS:

The following factors may increase the risk for primary peritonitis:

- Liver disease (cirrhosis)- Fluid in the abdomen- Weakened immune system- Pelvic inflammatory diseaseRisk factors for secondary peritonitis include:

Appendicitis (inflammation of the appendix) Stomach ulcers Torn or twisted intestine Pancreatitis Inflammatory bowel disease, such as Crohn's disease or ulcerative colitis Injury caused by an operation Peritoneal dialysis TraumaSIGNS AND SYMPTOMS:

The signs and symptoms of peritonitis include:

Swelling and tenderness in the abdomen with pain ranging from dull aches to severe, sharp pain Fever and chills Loss of appetite Thirst


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Nausea and vomiting Limited urine output Inability to pass gas or stoolCollateral manifestations

Diffuse abdominal rigidity ("washboard abdomen") is often present, especially in generalisedperitonitis;

Fever; Sinus tachycardia; Development of ileus paralyticus (i.e. intestinal paralysis), which also causes nausea and vomiting

DIAGNOSIS

Inspection and Auscultation of Abdomen

The abdomen should be inspected for distention and any scars noted. Auscultation is performed to

simply determine whether bowel sounds are diminished, normoactive (determined according to when

the patient last ate), or hyperactive.Hyperactive bowel sounds suggest an obstructive element either as a primary disease process or as part

of a localized inflammatory process.

Palpation of Abdomen

The parietal peritoneum is innervated by somatic and visceral afferent nerves and is quite sensitive. The

anterior parietal peritoneum is the most sensitive, and the pelvic peritoneum the least sensitive. The

ability to localize an inflammatory stimulus affecting the parietal peritoneum, particularly of the anterior

abdominal wall, underlies much of our ability to diagnose acute intraabdominal infection. Gentle

palpation of the abdomen, the last step in the examination, is intended to determine whether the pain-

producing intraabdominal process has resulted in parietal peritoneal inflammation.

Rectal and Vaginal ExaminationsRectal and vaginal examinations are essential to locate the extent of tenderness and whether a pelvic

mass or pouch of Douglas abscess is

present. Vaginal examination of the cervix may provide clues to the origin of the inflammatory process.

Peritonitis can be life threatening, so the doctor will first conduct a physical examination to determine

whether you need surgery to correct the underlying problem. The doctor will feel and press the

abdomen to detect any swelling and tenderness as well as signs that fluid has collected in the area. The

doctor may also listen to bowel sounds and check for difficulty breathing, low blood pressure, and signs

of dehydration.

The following procedures also may be performed:

Blood tests -- to see if there is bacteria present in your blood Samples of fluid from the abdomen -- identify the bacteria causing the infection CT scan -- identifies fluid in the abdomen, or an infected organ X-rays -- detect air in the abdomen, which indicates that an organ may be torn or perforated


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TREATMENT

Medications

Your doctor will prescribe antibiotics to kill bacteria and prevent the infection from spreading. The

antibiotics prescribed vary, depending on the type of peritonitis and the organism causing the condition.

Antimicrobial therapy

The goals of antibiotic therapy for intraabdominal infections that will be treated by either percutaneous

or operative intervention are to hasten the elimination of infecting microorganisms and thereby shorten

the clinical manifestations of infection and minimize the risk of recurrent intraabdominal infection.

Antibiotics used for intraabdominal infections should be active against enteric gram-negative facultative

and obligate anaerobic bacilli. The identity and density of microorganisms depend on the site of the

gastrointestinal tract perforation.

Appropriate Antibiotic Choices in Peritonitis

Monotherapy:

- Ampicillin/sulbactam- Cefotetan- Cefoxitin- Piperacillin- Piperacillin/tazobactam

Combination therapy:

- Aminoglycoside/metronidazole orclindamycin- Aztreonam/metronidazole orclindamycin

Nutrition and Dietary Supplements

Peritonitis is a medical emergency and should be treated by a medical doctor. Do not try to treat

peritonitis with herbs or supplements. However, a comprehensive treatment plan for recovering from

peritonitis may include a range of complementary and alternative therapies. Ask your team of health

care providers about the best ways to incorporate these therapies into your overall treatment plan.

Always tell your health care provider about the herbs and supplements you are using or considering

using.

When recovering from any serious illness, it is important to follow good nutrition habits:

Eat antioxidant foods, including fruits (such as blueberries, cherries, and tomatoes) and vegetables(such as squash and bell peppers).

Eat foods high in B-vitamins and calcium, such as almonds, beans, whole grains (if no allergy), darkleafy greens (such as spinach and kale), and sea vegetables.

Avoid refined foods, such as white breads, pastas, and especially sugar. Eat fewer red meats and more lean meats, cold-water fish, tofu (soy, if no allergy), or beans for

protein.

Use healthy oils in foods, such as olive oil or vegetable oil.


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Avoid caffeine and other stimulants, alcohol, and tobacco. Drink 6 - 8 glasses of filtered water daily. Ask your doctor about taking a multivitamin daily, containing the antioxidant vitamins A, C, E, the B-

complex vitamins, and trace minerals such as magnesium, calcium, zinc, and selenium.

Probiotic supplement (containing Lactobacillus acidophilus among other species), 5 - 10 billion CFUs(colony forming units) a day, for gastrointestinal and immune health. Probiotics can be especially

helpful when taking antibiotics, because probiotics can help restore the balance of "good" bacteria

in the intestines.

Preoperative preparation.

Preoperative preparation of patients with peritonitis involves fluid resuscitation, administration of

antibiotics and oxygen, nasogastric intubation, urinary catheterization, and monitoring of vital signs and

biochemical and hemodynamic data. Major metabolic derangements and fluid deficits should be

corrected before operation, and treated after it.

Peritonitis is a potentially life-threatening condition, and you should see immediate emergency medical

attention when symptoms occur. You will likely need to be hospitalized for treatment. You may needsurgery to remove the source of infection, such as an inflamed appendix, or to repair a tear in the walls

of the gastrointestinal or biliary tract. Antibiotics are used to control infection. Integrative therapies may

also be used for supportive care when recovering from peritonitis.

MANAGEMENT OF DIFFUSE PERITONITIS

Operative management of peritonitis involves immediate evacuation of all purulent collections, with

particular attention to subphrenic, subhepatic, interloop, and pelvic collections. The perforated organ

should be resected or wall defect should be closed or isolated.

Draining of the Abdominal Cavity.

The abdominal cavity has to be drained adequately in different places

Cleaning the Abdominal Cavity

Various approaches to cleaning the abdominal cavity include suction, swabbing, lavage, radical

debridement, and postoperative irrigation.

Continuous Postoperative Irrigation

Four to six catheters are placed in the abdominal cavity and irrigation fluid infused, and the cycle is

repeated.


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Prognosis and Complications

Complications from peritonitis can include:

Sepsis -- an infection throughout the blood and body that can cause shock and multiple organ failure Abnormal clotting of the blood (generally due to significant spread of infection) Formation of fibrous tissue in the peritoneum Adult respiratory distress syndrome -- a severe infection of the lungs

Abdominalo Acute intestinal obstruction due to peritoneal adhesiono Paralytic ileumo Residual abcesso Portal pyemia (liver abcess)

Systemico Endotoxic shocko Bronchopneumoniao Renal failure (by sepsis)o Bone marrow suppression

The prognosis for peritonitis depends on the type of the condition. For example, the outlook for people

with secondary peritonitis tends to be poor, especially among the elderly, people with compromised

immune systems, and those who have had symptoms for longer than 48 hours before treatment. The

long-term outlook for people with primary peritonitis due to liver disease also tends to be poor.

However, the prognosis for primary peritonitis among children is generally very good after treatment

with antibiotics.


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First Moscow State Medical University

MEDICAL FACULTY

Division of Foreign Students with Instruction Conducted in English

Department of Surgery

INTESTINAL OBSTRUCTION

By Mardiana Kamal

Medical Faculty, English Medium, Group 93

Supervisor: , MD PhD

MOSCOW 2011

Documents

Refarat intestinal Obstruction