Prepared By: A pear ar-sha haped ped sac c lying ing on the e - - PowerPoint PPT Presentation

University of THi-Qar College of Nursing

Prepared By:

 A pear ar-sha haped ped sac c lying ing on the e under dersu surfa rface ce of the liver er.  It has s a capacity acity of 30 30 to to 50 50 ml and d stores tores bile, e, which ich it concen ncentr trates ates by absor

• rbi

bing ng water. er.  The e gall llbla bladder der is divided vided into to the fundus ndus, , body, dy, and d neck ck. .

• The fundus is rounded and projects

below the inferior margin of the liver, where it comes in contact with the anterior abdominal wall at the level of the tip of the ninth right costal cartilage.

• The body lies in contact with the visceral

surface of the liver and is directed upward, backward, and to the left.

• The neck becomes continuous with the

cystic duct, which turns into the lesser

• mentum, joins the common hepatic

duct, to form the bile duct

2

 The e perit ritoneum

• neum completel
• mpletely

y surrounds rrounds th the e fundus ndus of

• f th

the gallb llbladd ladder er and binds inds th the body y and d neck ck to to th the viscer ceral al surface rface

• f th

the liver ver.

Functio nction of

• f the Gallbl

lbladd adder er

• When

When di dige gesti stion is is not

• t ta

takin king place, place, the the sph phincter incter of

• f Odd

ddi rema remains ns cl close

• sed an

and bil bile accu accumul mulate ates in in the the gall gallbl bladde

• dder. The

The gal gallb lbla ladder dder co conc ncen entrate trates bile bile; sto stores res bile bile; sele selectively ctively abs absorbs

• rbs bil

bile sal salts, keeps keeps the the bil bile acid acid; excrete xcretes chole cholester sterol

• l; and

nd secrete ecretes mucu

• mucus. To

To aid aid in in the these se functi unction

• ns,

s, the the muco ucous us me membra mbrane ne is is th throw rown int nto per permane manent nt folds lds that at unite ite with th each ch other her, givin ing the surfa rface ce a honeyco

• neycombed

mbed appeara pearance nce. Relations

• Anteri

Anteriorly

• rly: The

he an anter terio ior abd abdom

• mina

inal wall wall an and the he inf inferi rior

• r su

surf rface ace of

• f the

the liver er

• Poste

Posteri riorly

• rly: Th

The tran transver sverse se col

• lon
• n an

and the the fi first st an and seco second nd part parts of

• f the

he duoden uodenum um

3

Blo lood Sup uppl ply

 The he cystic stic arte tery ry is is a branch nch of

• f the

the right ht he hepati atic artery tery.  The cyst stic ic vein drains ins directly ectly into to the the portal tal vein.  Se Several eral ve very ry small mall arteries arteries and and ve veins ins also also run un bet betwee ween the the liver liver and and gallbladd lbladder er.

Nerve Supply

• Sympath

Sympathetic etic and and parasy parasympath pathetic etic vaga vagal fibe fibers form form the the ce celiac liac plexu

• plexus. Th

The gallbladd gallbladder er contr contracts acts in in respon response to to the the ho hormo mone ne cholec cholecystoki ystokinin in, whi which ch is is produce produced by by the the mu mucous cous membrane membrane of

• f the

the du duodenum denum on

• n

the the arri arrival val of

• f fatt

atty foo food from from the the sto tomach mach.

Lymph Drainage

• The

he lymph lymph drains drains int into a cys cystic tic lymph lymph no node de sit situat uated ed near near the the neck neck

• f
• f

the the gallbladd gallbladder

• er. Fr

From

• m here,

here, the the lymph lymph vess vessels els pass pass to to the the hepati hepatic nod nodes es along along the the course course of

• f the

he hepati hepatic artery artery and th then to to the the celiac iac nodes es.

4

 The he cys cystic tic duct uct is is abo about ut 1.5 in in. (3.8 cm) cm) lon long and and connects connects the the neck neck of

• f the

the gallbladd gallbladder er to to the the comm common hepat hepatic ic du duct ct to to form form the the bile duct.  It It usu usually ally is is somewhat somewhat S-shaped shaped and and desc descend nds for for a variable variable distance distance in in the the right right fre free mar margi gin

• f
• f the

the lesseromentum sseromentum.

5

 The he mu mucous cous membr membrane ane of

• f the

the cys cystic tic duct uct is is rais raised ed to to form form a spir spiral al fold fold th that at is is cont continu nuou

• us with

with a si similar milar fold fold in in the the neck neck of

• f the

the gallbladd gallbladder

• er. The

he fold fold is is com common monly ly known nown as as the the “spir spiral al valve valve.” The he functi function

• n of
• f the

the spir spiral al valve valve is is to to kee keep the the lum umen en constan constantly tly

• pen.

What is it?

 By definition, cholecystitis is an inflammation of the gallbladder wall and nearby abdominal lining.

Abdominal wall Gallbladder

Can be caused by an obstruction, gallstone or a tumor.

 90% of all cases caused by gallstones.  The exact cause of gallstone formation is unknown.

When there is an obstruction, gallstone or tumor it prevents bile from leaving the gallbladder.

 Bile gets trapped and acts as an irritant which causes cellular infiltration within 3 – 4 days.

 This infiltration causes an

inflammatory process – the gallbladder becomes enlarged and edematous.  Eventually this

• cclusion along with

bile stasis causes the mucosal lining of the gallbladder to become necrotic.  Bacterial growth

• ccurs due to

ischemia.

Necrotic Gallbladder

 Rupture of the gallbladder becomes a danger, along with spread

• f infection of the hepatic duct and liver.

 If the disease is severe and interferes with the blood supply it can cause the gallbladder to become gangrenous.

Gangrenous gallbladder Gallstones

Gallstones Gallstones . .

 Th The presence nce of gallsto stones nes in the gallbla bladd dder er is ca called d

cholel

elithi ithiasis asis.

Co Composi

• sitio

tion n of bil f bile:

Bilirubin (by-product of haem degradation) Cholesterol (kept soluble by bile salts and lecithin) Bile salts/acids (cholic acid/chenodeoxycholic acid): mostly reabsorbed in terminal ileum(entero-hepatic circulation). Lecithin (increases solubility of cholesterol) Inorganic salts (sodium bicarbonate to keep bile alkaline to neutralise gastric acid in duodenum) Water (makes up 97% of bile)

Path athogenes

• genesis

is

Types of gallstone

Cho holesterol lesterol sto tones nes (20 20%) %) Pigment ment sto tones nes (5%) %) Mixed ed (75 75%) %)

Approx roxim imately ately 12 12% % of men and d 24 24% % of women n of all ages hav ave e gal allstones tones 80 80% % are asympto ptomatic matic 2-3% % of patients ents progress ress per year to sympto tomatic matic di disease 1% of % of pat atients ents with gal allston stones es de develop elop ac acute te co complica cation tions Approx roxim imately ately 12 12% % of patients ents unde dergo rgoing ing ch cholecys cystectomy tectomy found d to have e CBD stone nes

Epi pidemiology demiology

 Cholestero sterol l

Imbalance between bile salts/lecithin and cholesterol allows cholesterol to precipitate out of solution and form stones

 Pigment ment

Occur due to excess of circulating bile pigment (e.g. Heamolytic anaemia)

 Mi Mixe xed

Same pathophysiology as cholesterol stones

Path athogenes

• genesis

is

Ag Age

Risk isk is is x4 between between the the ages ages of

• f 40

40-69 69 co compa mpared red with with younger ger subjects jects Due to to incr creased eased ch cholestero sterol co content ent in in bile

Sex

Hig Highe her prevalance revalance in in wo women men, up up to to x3 between between age ages of

• f

30 30-39 39

Pregn egnanci ancies es / ho hormones nes

Re Related ated to to fre requ quen ency cy an and number er of

• f pre

regna gnancies ncies New biliary ary sludg dge may form in in up up to to 30 30% of

• f women

Oest Oestrogens rogens prom romote

• te ch

cholestero

• lesterol hype

hypersecreti secretion

• n in

in bi bile le an and re redu duce ce bile ac acid syn ynthes thesis is

Ri Risk sk fa factor ctors s fo for gal alls lstone tone fo forma mation tion

Proges gesteron terones es promote te stasis and impair co contracti actility ity

Oral al cont ntraceptives raceptives an and H HRT

As As above ve Al Also so found

• und to

to apply apply to to men men rec receiving iving oestrog

• estrogen

en the therapy rapy fo for prostate rostate ca cancer ncer, compa compared red to to thos those who who elec lecte ted for

• r
• rch

chiectomy ectomy (s (small study) dy)

Obesi sity ty

Enhanced anced ch cholestero esterol l syn ynthe thesis sis an and se d secr cretion etion

Ri Risk sk fa factor ctors s fo for gal alls lstone tone fo forma mation tion

Ga Gallblad bladder der sta tasis sis

Fasti ting ng states tes Ra Rapid d weight ght loss Major r trauma ma So Somato tostatin statin Due to exc xcess ssive ive reabsorp

• rption of water

er with h resultan ltant t ch cholesterol sterol supersatu rsaturation ation  Rapid d weigh ght t loss In Incr creases ases bile e ca calci cium um co concentration centration In Incr creases ases bile e muci cin co concen centrati tration

• n

Ri Risk sk fa factor ctors s fo for gal alls lstone tone fo forma mation tion

 Cirrhos rhosis is

Overall rall prev evalance alance appro roach aches es 30 30% Hi Higher gher inci cide dence nce with th Ch Childs ilds B and d C d C disea isease se High gh unconj conjuga ugated ted bilir lirubin ubin level vels High gh circulat irculating ing oestr trog

• gen

en level vels s (aromata romatase se)

 Impai aired red en enterohe erohepa patic tic circulati ulation

• n

Small all bowel wel resect section ion Crohn’s disease sease Reduce duced d levels vels of bile ile acid id content tent in bile, ile, lead ading ing to to poor r cholester

• lesterol
• l solub

lubility ity

Ri Risk sk fa factor ctors s fo for gal alls lstone tone fo forma mation tion

Drug ugs

Ce Ceftri triaxo axone ne (biliar ary exc xcre retion tion, , form rms a a co complex lex with h ca calci cium um and d preci cipitates) pitates) Clofibr brate ate (i (impairs s bile aci cid d formation tion, leadi ding g to supersatu rsaturation ation)

Phy hysi sical al in inac activi ivity ty / sede

dentar ntary y lifestyle style

Ri Risk sk fa factor ctors s fo for gal alls lstone tone fo forma mation tion

In Increased eased cir ircu cula lating ting un unconjugated njugated bil ilir irubin ubin

Haemol molytic ytic sta tates tes Ci Cirr rrho hosi sis Hyperspleni ersplenism sm Hi High gh-tu turnover nover haematolog ematological cal disease sease

Gene netic tic fa factors tors / et / ethn hnic icity ity

Pima ma Native tive Ameri ericans cans have e incid cidence ence of up to to 75 75% Ch Chilean ilean Mexi xican can

Ri Risk sk fa factor ctors s fo for gal alls lstone tone fo forma mation tion

Imbalance of bile content

Ch Chole lester terol

• l supersat

ersatur uration ation Too much h unconj conjug ugated ated bilir ilirubin ubin Inadeq adequate uate bile ile salt lt content tent

Gall bladder stasis Gal alls lstone

• ne fo

format atio ion n – in in su summar ary

St Statin atins Aspirin rin Vitamin in C (b (but only for women!) !) Coffee Coffee (> (>3 cups cups pe per day day), ), but but dec decaffeinate affeinated co coffe ffee not

• t

protective ective Diet rich ch in in unsatur turated ated fats (m (mono- and poly-)

Those who are most at risk.

 These are all adjectives to describe the person most at risk of developing symptomatic gallstones.

FAIR FAT FORTY FEMALE

Signs and Symptoms.

 Complaints of indigestion after eating high fat foods.  Localized pain in the right- upper quadrant epigastric region.  Anorexia, nausea, vomiting and flatulence.  Increased heart and respiratory rate – causing patient to become diaphoretic which in turn makes them think they are having a heart attack.

 Low grade fever.  Elevated leukocyte count.  Mild jaundice.  Stools that contain fat – steatorrhea.  Clay colored stools caused by a lack of bile in the intestinal tract.  Urine may be dark amber- to tea-colored.

Signs and Symptoms.

physical ysical ex exam

.

 Fecal studies.  Serum bilirubin tests.  Ultrasound of the gallbladder.

USS SS: first irst line line inves estig tigatio ation in in gall llsto tone ne disea isease se □Confi

• nfirm

rms presen esence ce of

• f gall

llsto tones nes □ Ga Gall ll bla bladd dder er wall wall thick hicknes ness (if (if thic thicke kened ned sug uggests gests cho holec lecystiti ystitis) s) □ Bil ilia iary ry tree tree cal calibr ibre (CBD (CBD/extrah extrahep epatic atic/intra intrahepat epatic ic) □ if if dil dilated ated sug sugge gests sts st ston

• ne in

in CBD CBD (n (nor

• rmal

mal CBD CBD <8mm) mm). Som

• metim

etimes es CBD BD ston

• ne can be

be seen en

 HIDA scan - imaging test used to

examine the gallbladder and the ducts leading into and out of the gallbladder - also referred to as cholescintigraphy.

 Oral cholecystogram - the patient

takes iodine-containing tablets by mouth - iodine is absorbed from the intestine into the bloodstream - removed from the blood by the liver and excreted by the liver into the bile – it is concentrated in the gallbladder -

• utlines the gallstones that are radiolucent

(x-rays pass through them).

 Operative cholangiography –

common bile duct is directly injected with radiopaque dye.

• Gallbl

bladd adder er has a grayis ish appear earance e & is edematou tous. .

• There is an obstr

truction

• n of the

cystic tic duct and the gallbla bladde der r begins ins to swell. l.

• It no longer

r has the "robin in egg blue" appeara arance e of a normal gallbla bladde der. r.

• As acute

te cholecyst ecystitis itis progre resses, es, the gallbl bladd adder er begin ins to become me necrotic

• tic

and gets ts a speckl ckled ed appear earance e as the wall begin ins to die.

• Gallbla

bladde der r undergoes es gangren renous change and the wall becomes mes very y dark green or black. .

• This is the stage

age when perfo foratio ration occurs rs.

Reca cap.

• p. St

Stages ages of Acu cute te Cholecys cysti titis tis

.

 Lithotrips

• tripsy

 for patients with only a FEW stones.

 If If the attack ack of ch choleli lithia thiasi sis is mild d –

 bed rest is prescribed.  patient is placed on NPO to allow GI tract and gallbladder to rest.  an NG tube is placed on low suction.  fluids are given IV in order to replace lost fluids from NG tube suction.

Med Medical ical Man Manage gemen ment. t.

Su Surgica rgical l Management. nagement.

Cholecystectomy lecystectomy

• r
• r

Lapar paros

• scopic

copic Cholecystectomy lecystectomy

– remo

moval al of the gall llbla ladder der. This is is the e trea eatm tmen ent t of choice.

• ice.

The e gall llbla bladder der along

• ng with

th the cysti tic c duct, ct, vein n and arter ery are ligated gated.

Medical Management.

 If stones are present in the common bile duct, an endoscopic sphincterotomy must be performed to remove them BEFORE a cholecystectomy is done.

 A number of various instruments are inserted through the endoscope in

• rder to "cut" or stretch the

sphincter.  Once this is done, additional instruments are passed that enable the removal of stones and the stretching of narrowed regions of the ducts.  Drains (stents) can also be used to prevent a narrowed area from rapidly returning to its previously narrowed state.

Nursing Interventions Post Op - Cholesystectomy

• 1. Administer oral analgesics to facilitate movement

and deep breathing – and to stay ahead of pts pain.

• 2. Observe dressings frequently for exudate and hemorrhage.
• 3. Vitals are routinely checked.
• 4. Patient teaching:
• Must understand how to splint the abd. before

coughing.

• Report any abnormalities such as,

severe pain, tenderness in RUQ, increase in pulse, etc . .

• Instructed that they usually can return to work in 3

days & can resume full activity in 1 week.

• 5. Fluid balance is maintained IV –

potassium added to compensate for loss from surgery.

Nursing Interventions

• 1. Urine and stool should be observed for alterations

in the presence of bilirubin.

• 2. NG tube must be monitored for amount, color & consistency
• f output.

Also, tube must be on LOW suction and nasal area should be monitored for irritation and necrosis.

• 3. Anti-emetics may be administered if nausea persists.
• 4. I & O are measured and described carefully.
• 5. Pt. must understand how to splint the abdomen

for post op coughing, turning and deep breathing. Interventions center on keeping patient comfortable by carefully administering meds and watching for reactions.

Eww!

Com

• mpl

plicatio ications ns of

• f Ga

Galls llston tones es

Obstructive Jaundice Pathogenesis: thogenesis:

Sto tone ne obstr tructing ucting CBD (bea ear r in mind th there re are oth ther er causes ses for

• bstr

tructiv uctive jaundice dice) ) – danger ger is progression gression to to asce cending nding cholangitis langitis.

USS SS

Will l confirm firm gallstones lstones in th the gallbladd lbladder er CBD BD dilatation atation i.e.

• e. >8mm

mm (no not t always!) ways!) May visu sualise alise sto tone ne in CBD (most st often ten does es not) t)

MRCP RCP

In In cases ses where re suspec pect sto tone ne in in CBD but USS indeterminate eterminate E.g.1 obstructive

• bstructive LFTs

LFTs but but USS USS show shows no no biliary biliary dil dilatat tation ion and no no sto tone ne in in CBD

Obstructive Jaundice ERCP RCP

If If confirmed nfirmed sto tone ne in n CBD BD on n US USS or MRC RCP P proce ceed d to to ERC RCP P which ch will l confi nfirm rm th this (diagnost agnostic) ic) and allow

• w extra

tract ction

• n of

sto tones nes and sphincterot ncterotomy

• my (th

there erepeut peutic ic)

Tr

Trea eatmen tmen

Must Must unobst nobstruct uct bili biliary ary tr tree ee wit with ERCP ERCP to to preve prevent nt progr progression ession to to asc ascendin ending chola cholangi ngitis tis Whil Whilst awaiti awaiting ng ERCP ERCP mo monit nitor

• r for

for sign signs of

• f sep

sepsis sis suggestive gestive of

• f cholangi

langitis tis

Pathogenesis:  Ston

• ne obst

struc ructing ing CBD CBD with with infection ction/pu /pus proximal ximal to to the the blockag

• ckage

Treatment  ABC  Fluid Fluid resusc uscitation itation (clear ear fuids and and IVF, cath thete eter) r)  Antibioti ibiotics cs (Augmentin mentin)  HDU/ITU /ITU if if unwel ell/se l/septic ptic shock

• ck

 Pus Pus must be be drained* ined* - this this is is done done by by decom compressing pressing the the biliary iary tree tree

Urgent gent ERCP CP Urge gent nt PTC C – if ERCP CP unavai vailable lable or

• r unsucce

uccesful sful

Ascen cendi ding ng Cholang ngitis tis

Acute Pancreatitis

Pathogenesis  Obstruction of pancreatic outflow Pancreatic enzymes activated within pancreas Pancreatic auto-digestion USS: to confirm gallstones as cause of pancreatitis  USS not good for visualising pancreas CT: gold standard for assessing pancreas.  Performed if failing to settle with conservative management to look for complications such as pancreatic necrosis

Treatment Analgesia Fluid resuscitation Pancreatic rest – clear fluids initially Identify underlying cause of pancreatitis 95% settle with above conservative management 5% who do no settle or deteriorate need CT scan to look for pancreatic necrosis

Pathogenesis:  Gallstone causing small bowel obstruction (usually obstructs in terminal ileum)  Gallstone enters small bowel via cholecysto-duodenal fistula (not via CBD) AXR – dilated small bowel loops  May see stone if radio-opaque Treatment  NBM  Fluid resuscitation + catheter  NG tube  Analgesia  Surgery (will not settle with conservative management) – enterotomy + removal of stone Diagnosis of gallstone ileus usually made at the time of surgery.

Ga Gallstone llstone il ileus eus