surgerysmallintestineandappendixtg-090603090515-phpapp02

8/7/2019 surgerysmallintestineandappendixtg-090603090515-phpapp02

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Surgery

Small intestine and appendix

Dr. Teresa Galdona PA-C


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Small intestine

Most common surgical emergencies, acute appendicitis, mechanical SBO,

paralytic ileus, Crohns Ds.

Functions: digestive, nutritional, immunological, and endocrine.

ANATOMY: 3 segments: duodenum, yeyunum and ileum.

Ligament of Treitz separates duodenum from yeyunum and ileum, also

separates upper GIT from Lower GI track. Duodenum is mostly

retroperitoneal and is encircling pancreas.

Duodenum is divided in 4 segments: one of most important segments is

descending there is located duodenal papilla or ampulla of Vater, also 2

small papillas, one small papilla for accesory pancreatic duct (Santorino

duct) and mayor papilla for main pancreatic duct (Wirsung duct)

40% is yeyunum and 60% is ileum.


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Small intestine

40% is jejunum and 60% is ileum.

Blood supply:

SMA for SB

Duodenum blood supply by gastroduodenal art.

Venous drainaje is parallel to arterial drainaje with majority of veins

draining at SM vein which joins splenic vein and Inf Mesenteric that

drains into Portal vein.

Terminal ileum has abundant lymphatic tissue (Peyer patches) and

ileum terminates at ileocecal valve.

Besides this lymphatic tissue there are other 2 lymphatic tissues.

One is called GALT (gut associated lymphoid tissue) located at the

lamina propia and mucosa of ileum.


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Small intestine

The other lymphatic tissue is called MALT (mucose associated

Lymphoid tissue) form by B cells from periphery of Peyers patches

that migrate to mesenteric nodes to bloodstream then these cells

return to mucosa adjacent to Peyers patches as B2 memory cells

forming MALT. Nerve supply:

Through CNS 2 systems: extrinsic and intrinsic neural plexus

Pain fibers activated by intestinal distension communicate primarily

by sympathetic visceral afferent fibers


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Small intestine

Appendix arises from cecum

Blood supply via appendiceal art. terminal branch of ileocolic art.

Rich in lymphatic tissue.

Variable positioned called atypical like retrocecal, retroperitoneal in

relation with cecum.

PHYSIOLOGY:

Main function is:

1) digestion of food through digestive enzimes, secretion of digestive

juices, absorption of water, electrolytes, and nutrientes. 2) Motility

3) propulsion

4) storage


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Small intestine

Nerve innervation is given by: Enteric nervous system

1) Intrinsic neural plexus ------ Submucosal (Meissner)

------ Auerbach or Myenteric (Mucosa +smooth muscle)

Ach ------ excitatory neurotransmitter at the Myenteric

VIP + Somatostatin ------- inhibitory neurotransmitter

These plexus determine pattern of contraction

2) Extrinsic neural plexus ------ Parasympathetic (Vagus)

(giving by CNS to ANS) and pelvic parasympathetic nerves

(excitatory)

------ Sympathetic (Splachnic nerves) (inhibitory)

These plexus determine contraction (no type ofcontract.

like fast or slow)


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Small intestine

Daily we produce about 5 to 10 Lt of digestive fluids by salivary

glands, stomach, biliary tree, pancreas, and intestine which is

handle by SB which absorbs about 80% of it.

Na is major ion b/c it regulates osmotic gradient promoting H2O

absorption. Cl ion regulates secretion of H2O.

SB absorbs: fat, carbs and proteins.

Triglycerides and cholesterol absorption:

Fats are broken down to ---- FFA + monoglicerides + Ca

Bile salt act as detergens allowing formation of micelles (smaller

substrates + fat soluble Vit)

micelles dissociate at the enterocyte apical membrane delivering

FA, Colesteroland and monoglycerides where they cross the

membrane into the cell


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Small intestine

Inside the enterocyte, triglycerides are reconstructed and form anew form or molecule called chylomicrons transported bylymphocytes to portal system

Fat absorption occur mostly at duodenum and upper jejunum

Bile salts are reabsorbed in terminal ileum Carbohydrates digestion start in the mouth by salivary amylasa and

it is complete in jejunum by pancreatic amylasa and converted intoglucosa, galactose and fructose

Proteins are absorbed like fats in duodenum and upper jejunum

Digestion of proteins star in stomach with gastric pepsin. CCK is

secreted by intestinal endocrine cells and stimulated bypolypeptides in intestinal lumen that in turn stimulates pancreaticsecretion of peptidases (like trypsin, chymotripsin, elastase andcarboxipeptidase) which breaks proteins to AA


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Small intestine

Certain substances are absorbed in specific segments of SB

For Vit B12 + IF absorbed at terminal ileum

Fat soluble Vit ADEK + bile salts are absorbed at terminal ileum

Ca, Fe are absorbed at duodenum.

Small intestine is rich in hormone production some of them arethese:

Secretin ---- produce by duodenal S cell in response to bile or acidthat stimulates pancreatic production of HCO3 and H2O

CCK ---- release by proximal SB mucosa in response to FA and AAand stimulates emptying of gallbladder and pancreatic enzymes


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Small intestine

Small intestine is rich in hormone production some ofthem are these:

Secretin ---- produce by duodenal S cell in response tobile or acid that stimulates pancreatic production of

HCO3 and H2O

CCK ---- release by proximal SB mucosa in response toFA and AA and stimulates emptying of gallbladderandpancreatic enzymes


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Small intestine

Motilin ---- produced in jejunum and it coordinates stomach and

esophageal function with SB activity during fasting.

Gastric Inhibitory peptide (GIP) ---- produced by jejunal K cells and

stimulates insulin release in response to carbohydrates and fat.

Neurotensin ----- secreted in response to fat, stimulates pancreaticexocrine secretion that facilitates fat absorption.

Glucagon like peptide 2 (GLP2) ------ potent SB trophic hormone

VIP (vasoactive intestinal peptide) ---- stimulates pancreatic and

intestinal secretion, inhibits gastric secretion.

Gastrin releasing peptide ----- stimulates release of all intestinalhormones except secretin, helps regulate gastric acid and gastrin

secretion.


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Small intestine

Somatostatin ----- acts as an on and off switch for intestinalhormones, gastric and pancreatic secretion and intestinal motility.

It stimulates parietal cells to decrease HCL acid production, inhibitsgastrin release, reduces Histamine released from ECL cells.

Peptide YY---- produce in distal SB and proximal colon, affectsgastric and pancreatic secretion.

Small Bowel Ds:

Meckels diverticulum

It is MC congenital abnormality of SB

Remnants of embryonic vitelline or omphalomesenteric duct

Present in 2% of population

2:1 / male:female


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Small intestine

2 types of mucosa: 1) gastric Most common)

2) pancreatic or colonic

Located 2 feet of ileocecal valve

S/S:

Symptoms are rare, and they tend appear as the patient increases

in age.

ANATOMY: Caused by incomplete obliteration of vitelline duct (from midgut)

Which should close between 8th and 10th weeks of gestation.

Blood supply is from the vitelline vessels.


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Small intestine

Pathophysiology:

Cells of vitelline duct are pluripotential ( they have multiplecapabilities) and it is not rare to find different types of mucosa inthere.

MC mucosa find is gastric (50%), less frequent pancreatic or colonicmucosa.

Because gastric mucosa can produce acid in the proximity of SBmucosa, it can cause ulceration and hemorrhage of adjacent SB.

Benigns tumors like lipomas, leiomyomas, neurofibromas, andangiomas have been describe also in the diverticula, and they can

act as lead point for intossusception and Bowel obstruction. Another consequence of the diverticula is that persistence of vitelline

duct can cause a sinus from umbilicus to ileum, presenting as anenteric fistula at the umbilicus


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Small intestine

2) hemorrhage: can present as BRBPR, mostly painless, in infants


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Small intestine

7) Umbilical fistula

8) Perforation

9) Miscellaneous (fistula, tumor)

Less common complications:

Deficiency anemia

Malabsorption

Foreign body

Perforation

Incarceration in an hernia (Littres hernia) including inguinal, femoraland umbilical hernia.


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Small intestine

D/D:

1) Acute appendicitis, SBO from other causes, Regional enteritis, allthese 3 present similarly to and are more common than Meckelsdiverticulum.

2) Lower GI bleeding, except in very young pts, is most commonlydue to diverticulitis or angiodysplasia

3) Think of Meckels in small children that develop lower abdominalpain, obstruction, lower GI bleeding or umbilical drainaje and shouldbe considered as a secondary diagnosis in older pts in whom otherpathologies are far more likely.

Dx of Meckels: particularly in older pts should include endoscopyand GIT series, other pts may have their Dx when in surgery andother pts with atypical presentation and negative work-up will getbenefits from Meckels scan, SB series, or even laparoscopy.


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Small intestine

Tx:

Resection of Diverticula is curative

Incidentalomas happened, it is when an asymptomatic diverticulum

is found at time of surgery for other purposes.

In younger pts --- low morbidity of resection is justified as apreventive measure.

in no that young pts ----- it is indicated when they have a narrow

base, or when a mesodiverticular band is present, or when there

evidence of a heterotopic tissue, also resection may be appropiated

in pts with hostile abdomen in whom would be difficult to re-explorefor example in presence of multiple adhesions, in recurring SBO

and in pending radiation.


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Small intestine

Crohn Ds

7 to 10 cases per 100,000 population

Underlying genetic, environmental factors and microflora acttogether inducing events

First degree relatives have increased risk of having Crohns than

regular population. Genetic relation: increased disease in monozygotic twins than indizygotic ones.

IBD 1 locus chromosome 16 has been associated with Crohns Ds.

Most common environment factors associated with Crohns are:

NSAIDs and smoking

The disease has a bimodal presentation:

1) late teens and early twenties

2) late in six or seven decades


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Small intestine

Crohn Ds

Distribution of disease goes from any part from the mouth to the

anus, although, SI and colon are most commonly involved.

Involvement by %:

1) ileocecal area 40% to 50%

2) Small intestine 30% to 40%

3) Colon 20%

Ds:

It is not curable

It can go on remission for long time

Flares and exacerbations occur


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Small intestine

Crohn Ds

Crohns involvement in SI and colon tend to be segmental withsparing areas between involved mucosa which is different than withUC, skip areas.

Also Crohns is a chronic, transmural inflammatory disease, becauseof that fistulas can happen and histological it is characterized by noncaseating granulomas

There are a few extraintestinal manifestations like in skin(pioderma), eyes (iritis, conjunctivitis,uveitis, iridocyclitis, episcleritis)mouth (ulcers), joints (arthritis), biliary tract (sclerosingcholangitis,pericholangitis, granulomatus hepatitis), vasculitis andaphtous stomatitis.

These pts have altered imune responses that stimulate continuoslythe mucosal epithelium explained by an increased surface adherentand intracellular bacteria (in the mucosal epithelium)


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Small intestine

Crohn Ds

Constant and continue inflammatory and immunological stimulation

induces release of cytokines,arachidonic acid (prostaglandines), and

nitric oxide that in turn destroys mucosa and causes damage.

Due to continue inflammation an remission these pts develop

strictures and obstruction on SI and colon Adherences is also another type of presentation it can happen to

adherence to another loops or to bladder that can lead to fistulas

formationand when that happen then abcesses develop. There are

few different types of fistulas: retroperotoneal, intraabdominal,

perianal (mostly seen in colorectal involvement)

S/S:

Triad of abdominal pain,diarrhea, and weight loss.

Progressive, waxing and wanning symptoms


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Small intestine

Crohn Ds

RLQ location most common due to ileocecal involvement

Bleeding is not as common.

Associated Signs and symptoms like anorexia, weight loss, fever,

malaise.

Perianal involvement with fistulas, fissures and abcesses iscommon.

Note: surgical intervention unaware of this disease in perianal

abcesses or an anal fistula can cause difficulty healing and that

should alert the clinician that something else is going on.

Nutritional malnourish due to decreased oral intake andmalabsorption when terminal ileum is involved, hypoalbuminemia

ADEK deficiency.

Course of Ds is urgent or slow (indolent)


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Small intestine

Crohn Ds

Dx:

No specific lab study

H/P can lead to suspect Crohns.

Endoscopy help with Dx.

Colonoscopy, Barium enema and SB contrast studies.

(visualization of terminal ileum) MC used to Dx ulceration, fistulas,

stricture.

CT scan for abscesses, masses, obstruction and fistulas.

Enteroclisis (air and contrast injection to see mucosa outline)

Bxs

Cystography / Cystoscopy/ vaginal exam (urinary, vaginal fistulae)


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Small intestine

Crohn Ds

Dd: dificcult ito differentiate between Crohns and colitis also when

Ds present in acute fashion.

Also difficult to differentiate from acute appendicitis, acute regional

ileitis, PID, or TB.

Tx: Medical

Analgesics, decrease motility of bowel, wound care for fistulae,

hydration, nutritional (parenteral) due to decreased oral intake and

malabsorption particularly at terminal ileum disease vitamins

(ADEK). For chronic diarrhea use of lactose, loperamide, diphenoxylate,

codeine, cholesteramine ( bile salt induce diarrhea) (induced

paralitus ileus, toxic magacolon, bacterial overgrowth.


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Small intestine

Crohn Ds

Serum phosphate and K levels in malnurish pts

Sulfasalazine two components 1) sulfonamide moiety ofsulfasalazine (Bacteriostatic)

2) 5-aminosalicylate

Anti-inflammatory action, by limiting production of prostaglandinsand leukotriens.

New product is mesalamine (no sulfonamide moiety part)

Corticosteroides:

Topical

Prednisone (60 mgs/day) oral

Hydrocortisone IV in pts with oral intolerance

Budenoside (luminal steroid) Keep in mind side effects of steroids.

(HTN, weight gain, striae, osteoporosis)


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Small intestine

Crohn Ds

Immunossupressive therapy: azathioprine, 6 mercaptopurine, MTX

cyclosporine, new ones are monoclonal antibodies like Infliximab.

Surgical Tx:

Mostly when pt has fistulae, obstruction, perforation, hemorrhage is

not treated surgically in Crohns, because there is a great recurrenceof Crohns after surgery.

Complications:

Malnutrition, electrolyte imbalance, fistulae, perforation, steroids side

effects (osteoporosis, cataract, weight gain, striae, HTN), wound

healing in pts taking immunossupressive medications (MTX,Infliximab)


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Small Bowel Tumors

Tumors of SB are not common.

They may present as SBO , GI bleeding, sometimes they show

metastasis S/S as a form of presentation, also intossusception can

be another presentation.

Dx:endoscopy, capsule endoscopy is another method based on a

capsule size device swallow by pt that produces some emissions

like a chip that transmits 2 images that later are read, this is a good

one b/c small tumors can be diagnosed.


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Small Bowel Tumors

These tumors are more common than malignants.

Asymptomatic.

1:1 / man/female, sixth decade.

MC one is leiomyoma, in jejunum.

Lipomas can also present as benign tumors in duodenum and ileum,

Hemangiomas, Hamartomas, Lymphangiomas, Schwanomas,

neurofibromas.

Peutz-Jeghers syndrome assotiated with multiple hamartomas and

mucocutaneous hyperpigmentation.


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Small Bowell

Malignant tumors

Malignant TUs of SB represent about 2% of all GIT.

More common in men than in females, sixth decade.

MC TUs are:

ADC:

Represent of SB TUs. MC location is duodenum. Obstruction

presentation in a pt without hernia or previous abdominal surgery withprobably adhesions should make the clinician to think of neoplasia. Alsoassociated S/S of anemia, occult GI bleeding and weight loss may indicatedmalignancy. When tumor is located in the ampullar area jaundice andpancreatitis may first S/S.

Tx:

Surgical with resection + lymphatic removal Carcinoid Tumors

Lymphoma

GI Stromal/ Leiomyosarcoma


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Small Bowell

Malignant tumors

Carcinoid Tumors:

Develop from Kulchistky cells in cryps of Lieberkuhn which are cells

that form part of the APUD(amine precursor uptake and

decarboxilation) system or argentaffin cells.

Size of tumor is proportional to malignancy, the bigger the tumor thebigger the possibility of malignancy.

1 cm tumors have only 2% possibilities of mets

>2 cm tumors have 90% possible mets. Almost 50% of all carcinoids

are located in appendix as in 1st place, SB carcinoids are in 2nd

place mostly in ileum. Presentation is usually SB obstruction.

Dx:

Laparoscopy


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Small Bowell

Malignant tumors

Tx:

Surgical with excition of bowell + hemicolectomy.

Carcinoid Syndrome is manifestation of metastatic intestinal

carcinoid. It is characterized by attacks of flushing (head, trunk),

bronchospasm, abdominal cramping and diarrhea, pellagra likesymptoms,(R ) side vavular HD.Alcohol, exertion, excitement,

anesthesia, can trigger these S/S.

Serotonin (5-hydroxitryptamine) produced by the tumor ---- in the

liver it becomes 5-HIAA, and with other susbstances like kallikrein,

histamine, ACTH, causes S/S.


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Small Bowell

Malignant tumors

Dx:

urinary 5-HIAA (5-hydroxiindole acetic acid)

TX:

resection

Lymphoma:

SI MC place for them. 10%-15% of all lymphomas are located in SB

5th and 6th decades.

Ileum MC place (Peyers patches). MALT lymphomas more common

in stomach associated to H.pyloris are also seen in SB. S/S:

vague abdominal pain, fatigue, weight loss

Perforation, GI bleeding, obstruction, intussusception.


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Small Bowell

Malignant tumors

Dx:

CTscan.

Tx:

Surgical resection.+ chemo and radiation.Poor prognosis.

GI Stromal (GIST)/ Leiomyosarcoma:

Mesenchimal TUs of GIT known as leiomyosarcomas are now

known as GIST tumors.

Benign show the c-kit protein, malignant ones dont have that

marker. Poor prognosis.

6th decade, presentation can be as any of the previous presentatons

like perforation, bleeding or obstruction.

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