ACCESSORY ORGAN DISORDERS

LIVER CIRRHOSIS
 A chronic, progressive disease of the liver characterized by
diffuse degeneration and destruction of hepatocytes. Portal hypertension causes
 Repeated destruction of hepatic cells causes formation of scar  Back up of blood in spleen → splenomegaly
tissue.  Increased breakdown of
 Many patients die within 5 years of onset. o WBC – prone to infection
o RBC - anemia
TYPES o platelets – prone to bleeding

 Laennec’s cirrhosis Albumin production

o the most common, and is due to alcoholism and poor
nutrition. Colloidal osmotic pressure
o Cellular necrosis causes eventual widespread scar tissue - abdomen (third spacing)
with fibrotic infiltration of the liver.
Aldosterone metabolism

Alcohol → transformed to acetaldehyde
( alter hepatocyte function)
Inhibits the removal of proteins from the liver & vitamins and mineral
metabolism altered
As large amounts of alcohol are
consumed, fat accumulates in the
liver known as“ fatty liver”
 Postnecrotic cirrhosis
o Cirrhosis occurs after massive liver necrosis.
o complication of viral hepatitis or exposure to hepatotoxins.
o Scar tissue
 Biliary cirrhosis
o Cirrhosis develops from chronic biliary obstruction, bile
stasis, and inflammation resulting in severe obstructive
jaundice.
 Primary – biliary obstruction (swelling)
- is a disease of the bile ducts inside the liver.It
interferes with the proper drainage of bile, so the
bile backs up into the liver and into the
bloodstream, causing various symptoms.
 Secondary – biliary obstruction ( gallstones)
 Cardiac cirrhosis
o follows severe, right sided congestive heart failure (CHF)
o Failure of the heart to pump blood to different areas of the
body
o Congestion causes anoxia to the liver, necrosis and
fibrosis
 Decrease nutritional intake → normal structure is lost
 Disorganized structure - SCAR
 Widespread scarring
 Pressure/obstruction - blood vessels and biliary ducts
 Inc.capillary pressure → ↑ fluid in the abdomen
 Collateral circulation
 ascites
 caput medussae – distended blood vessels
 Dilated and tortuous veins in the submucosa of the
esophagus – esophageal varices
o irritated by alcohol and food causing rupture and
excessive bleeding
o Not elastic
o Very fragile
o Easy to bleed
Results in sodium retention and increased fluid retention
DYSPNEA
ASCITES
 Accumulation of fluid in the peritoneal cavity
 Capillary congestion leads to plasma leaking directly from the
liver surface and portal vein
 Decreased liver function results in inability to inactivate
adrenocortical hormone, testosterone, estrogen, and aldosterone
 If the liver is not functioning
o ammonia is not broken down
o it accumulates in the blood stream
o crosses the blood brain- barrier
o goes in to the brain tissue
o leads to HEPATIC ENCEPHALOPATHY – brain tissue
damage
 Ammonia is produced by bacteria and enzymes, which
breakdown amino acids
 LIVER – ammonia converted to urea and eliminated
 Altered though process
DIAGNOSTIC TEST FINDINGS
 Abdominal x-rays show enlarge liver, cyst, or gas within the
biliary tract or liver;liver calcification; and massive fluid
accumulation (ascites)
 Liver biopsy reveals tissue destruction and fibrosis
 Computed tomography( CT) and liver scans show liver size,
abnormal masses, hepatic blood flow, and obstruction
 Esophagogastoduodenoscopy (EGD ) reveals bleeding
esophageal varices, stomach irritation or ulceration
 Urine studies shows increased bilirubin and urobilirubinogen
level
 Fecal studies show decreased fecal urobilirubinogen level
 Blood studies reveal various abnormalities
o Liver enzyme levels ↑
o Total serum bilirubin and indirect bilirubin ↑
o Total serum albumin and protein levels ↓
o Prothrombin time is prolonged
o Hemoglobin level, hematocrit , and serum electrolytes ↓
o Vitamins A, C, and K are deficient
LIVER BIOPSY
 Tiny incision is made between the ribs and a needle is inserted
in order to reach the area of the liver where a tissue sample is
taken
 Requires local anesthetic
 Post procedure – right lateral position

 Melena
o black tarry-colored feces as a result of secretions of
free blood from intestine

 Hematemesis
o aggravated by coughing, vomiting, lifting or straining.

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 ACCESSORY ORGAN DISORDERS

ASSESSMENT
 Renal Findings
 Neurological Findings o Hepatorenal syndrome
o Sensory disturbances - Altered level of consciousness, o Increased serum bilirubin
neurological symptoms, impaired thinking, and
neuromuscular disturbances  Endocrine Findings
o Asterixis o Increased aldosterone
o Paresthesias of feet o Increased ADH
o Peripheral nerve degeneration o Increased circulating estrogens
o Reversal of sleep-wake pattern o Increased glucocorticoids
o Gynecomastia
 Gastrointestinal Findings
o Abdominal pain - due to liver inflammation  Immune System Disturbances
o Anorexia - distaste for certain foods(early stage) and o Increased susceptibility to infection
gastric stasis(late stage) o Leukopenia
o Ascites
o Clay colored stools  Cardiovascular Findings
o Diarrhea - caused by malabsorption o Cardiac dysrhythmias
o Gallstones o Development of collateral circulation
o Gastritis o Fatigue
o Gastrointestinal bleeding o Peripheral edema
o Hemorrhoidal varices o Portal hypertension
o Hepatomegaly o Spider angiomas
o Malnutrition
o Nausea and vomiting - inflammatory response and  Pulmonary Findings
systemic effects of liver inflammation o Dyspnea
o Small nodular liver o Pleural effusion and limited thoracic expansion due to
abdominal ascites, leading to inefficient gas exchange
o Hyperventilation
SUSPECT ASCITES o Hypoxemia
1. Shifting dullness test
2. Fluid wave test  Hematologic Findings
o Anemia
+ SHIFTING DULLNESS TEST o Impaired coagulation
 Wait for 30-60 seconds o Splenomegaly
o Thrombocytopenia
o Disseminated intravascular coagulation (DIC)

Disseminated intravascular coagulation (DIC)

 a serious disruption in the body's clotting mechanism.
 Normally - the body forms a blood clot in reaction to an injury.
 With DIC, the body overproduces many small blood clots
throughout the body, depleting the body of clotting factors and
platelets.
 Small clots (dangerous) - interfere with the blood supply to
organs, causing dysfunction and failure.
FLUID WAVE TEST  Massive bleeding - body's lack of clotting factor and platelets.
 Client in supine.  Coagulation defects
 Ask client to help. o Decrease synthesis of bile fats in the liver prevents the
 Place the ulnar side of the hand and the lateral side of the absorption of fat soluble vitamins.
forearm firmly along the midline of the abdomen o Without vitamin K and clotting factors 11,V11,1X,and X,
 Place palmar surface( fingers and hands) against one side of the client is prone to bleeding
abdomen.
 Use other hand to tap opposite side.  Dermatologic Findings
 Abnormal: fluid wave is transmitted. o Axillary and pubic hair changes
o Caput medusa
Esophageal varices o Ecchymosis
o Increased skin pigmentation
o Jaundice
- unable to conjugate and excrete bilirubin
- structural changes prevents normal bile flow out of
the liver
o Palmar erythema
o Pruritus – deposition of bile salts in the skin
hemorrhoidal varices o Spider angiomas

 Fluid and Electrolyte Disturbances

o Ascites - due to portal hypertension and decreased
plasma proteins.
o Decreased effective blood volume

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 ACCESSORY ORGAN DISORDERS
o Dilutional Hyponatremia/Hypernatremia
o Hypokalemia
o Peripheral edema due to portal hypertension and
decreased plasma proteins.
o Water retention
*continuation next page
INTERVENTIONS
 Assess the patient for signs of impaired breathing related to
congestion and infection.
 Elevate the head of the bed to minimize shortness of breath.
 Encourage to have enough rest
Nutritional needs
o Initiate enteral feedings or parenteral nutrition as prescribed.
o Provide supplemental vitamins(B complex, vitamins A,C, and
K, folic acid, and thiamine)
o If ascites and edema are absent and the client does not exhibit
signs of impending coma, a high protein diet supplemented
with vitamins is prescribed.
 Administer diuretics as prescribed to treat ascites.
 Record intake and output and monitor electrolyte balance.
 Weigh client and measure abdominal girth daily.
 Inspect the ankles and sacrum for dependent edema
Observe closely for signs of behavioral or personality changes
 Assess for precoma state(tremors, delirium).
 Report increasing, stupor, lethargy, hallucinations, or
neuromuscular dysfunction
 Watch for asterixis, a sign of developing hepatic
encephalopathy
o Asterixis - a coarse tremor characterized by rapid non
rhythmic extensions and flexions in the wrist and fingers.
Simple tasks like handwriting becomes difficult
o Fetor hepaticus, the fruity, musty breath odor of severe
chronic liver disease
 Smells similar – freshly mowed grass, acetone, old
wine
Monitor the patient for bleeding
 Check skin, gums, stools, and vomitus regularly
 Apply pressure to injection site
 Warn the patient against taking nonsteroidal anti-inflammatory
drugs (NSAIDs ),straining at stool, and blowing his nose or
sneezing too vigorously
 Maintain gastric intubation to assess bleeding or
esophagogastric balloon tamponade to control bleeding varices if
prescribed
 Administer blood products as prescribed
 Monitor coagulation laboratory results; administer vitamin K as
prescribed
 Prevent skin breakdown
 Avoid using soap when you bathe the patient; use lubricating
lotion or moisturizing agents.
 Handle the patient gently
 Turn and reposition the patient often to keep his skin intact
 Administer low sodium antacid as prescribed
 Administer Lactulose (Chronulac) as prescribed, which
decreases the pH of the bowel, decreases production of
ammonia by bacteria in the bowel, & facilitates the excretion of
ammonia
 Administer neomycin (Mycifradin) or metronidazole (Flagyl)
as prescribed to inhibit protein synthesis in bacteria & decreases
production of ammonia
 Avoid medications such as opioids, sedatives, & barbiturates &
any hepatotoxic medications or substances
 Instruct the client about the restriction of alcohol intake.
 Refer the patient to Alcoholic Anonymous(AA), if necessary.
COMPLICATIONS
 Portal hypertension
 Esophageal Varices (Bleeding)
 Ascites
 Hepatic encephalopathy
 Hepatorenal syndrome
MEASURING PORTAL HYPERTENSION
 Insertion of a catheter with a balloon into the antecubital or
femoral vein and is advanced to the hepatic vein under
fluoroscopy.
 Fluid is infused once the catheter is in position to inflate the
balloon.
 During angiography, a catheter may be placed selectively via
either the transjugular or transfemoral route into the hepatic vein.
CONSEQUENCES OF PORTAL HYPERTENSION
 Hepatic venous pressure gradient (HVPG) is defined as the
difference in pressure between the portal vein and the inferior
vena cava.
 Thus, HVPG is equal to the WHVP value minus the FHVP
value (ie, HVPG=WHVP-FHVP).
 Normal HVPG is defined as 3-6 mm Hg.
 Portal hypertension is defined as a sustained elevation of portal
pressure above normal.
 An HVPG of 8 mm Hg is believed to be the threshold above
which ascites potentially can develop.
 An HVPG of 12 mm Hg is the threshold for the potential
formation of varices.
 High portal pressures may predispose patients to an increased
risk of variceal hemorrhage.
 Avoid activities that will initiate vasovagal responses.
 Endoscopic procedures or surgical procedures
BLEEDING ESOPHAGEAL VARICES
 Bleeding varices are life threatening (emergency)
 Hemorrhagic shock- produces decreased cerebral, hepatic and
renal perfusion.
 Hemorrhage  DEATH
 The goal - control bleeding and prevent the recurrence of
bleeding.
INTERVENTIONS
 Monitor vital signs
 Elevate the head of the bed
 Monitor for orthostatic hypotension
 Monitor lung sounds
 Administer oxygen as prescribed to prevent tissue hypoxia
 Level of consciousness -monitored
 NPO status
 IVF given - to restore fluid volume and electrolyte imbalances;
monitor intake and output
 Hgb and Hct values and coagulation factors - checked
 Administer blood transfusions or clotting factors as prescribed,
Vit. K
 NGT or a balloon tamponade
 Iced saline irrigations -vasoconstriction
 Vasopressin(Pitressin) by IV or intraarterial- to induce
vasoconstriction
 Avoid activities that will initiate vasovagal responses.
 Endoscopic procedures or surgical procedures
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 ACCESSORY ORGAN DISORDERS
VASOPRESSIN
(PITRESSIN)
 Monitor fluid I and O and electrolyte levels → hyponatremia,
antidiuretic effect of the drug
 Administer nitroglycerin with the vasopressin if prescribed to
prevent vasoconstriction of the coronary arteries.
 Contraindicated – C.A.D., S. E.coronary vasoconstriction may
precipitate M.I.
TREATMENT NON-SURGICAL MODALITIES
PHARMACOLOGIC AGENTS
 Propranolol (Inderal )/Nadolol (Corgard)
o reduces portal pressure by beta adrenergic blocking action
used in combination with variceal band ligation or
sclerotherapy
 Somatostatin /Octreotide (Sandostatin)
o reduces portal pressure by selective vasodilation of portal
system
MEDICAL TREATMENT
 Sclerotherapy
o is a procedure to treat bleeding esophageal varices and
prevent future variceal bleeding. The procedure involves
the passage of an esophagoscope and injection of a
sclerosing agent into or around esophageal varices
 Band ligation
o used to treat enlarged veins in the esophagus
o The doctor uses suction to pull the varices into a chamber
at the end of the scope and wraps them with an elastic
band, which essentially "strangles" the veins so they can't
bleed.
SENGSTAKEN BLAKEMORE TUBE
 A triple lumen gastric tube with an
 inflatable esophageal balloon
 inflatable gastric balloon
 a gastric aspiration lumen.
 Applies direct pressure to bleeding veins.
 Used if sclerotherapy and ligation fails
 Endotracheal intubation before insertion of the tube to protect the
airways and ↓ risk of aspiration
 Gastric balloon inflated with 100-200ml of air
 X-ray confirms that it is
 properly positioned
 Irrigation of the tubing is done to detect bleeding.
 If returns are clear, esophageal balloon, not used
 If bleeding - continues - esophageal balloon is inflated.
 stopped - esophageal balloon is deflated first and the
patient is monitored for recurrent bleeding.
 After several hours without bleeding, the gastric balloon can
be deflated safely
 Deflate esophageal balloon – DYSPNEA (SCISSORS Bedside)
 Bleeding does not stop – inflate 25-45 mm Hg
 Compress gastric varices directly and to decrease blood flow to
esophageal varices
 NGT inserted – opposite nares, suction secretions above the
esophageal balloon
 Gastric suctioning
 Minnesota tube (4 lumen gastric tube) - is a modified
Sengstaken- Blakemore tube with an additional lumen for
aspirating esophagopharyngeal secretions.
INTERVENTIONS
 Check patency and integrity of all balloons before insertion.
 Label each lumen.
 Place the client in the upright or Fowler’s position for insertion
 Immediately after insertion, prepare for radiography to verify
placement.
 Maintain head elevation
 Double clamp balloon ports to prevent air leaks.
 Maintain pressure of the esophageal balloon (20-25 mmHg )
 Monitor for loss of pressure /over inflation, which can cause
rupture of the esophagus.
o To prevent ulceration or
o necrosis of the esophagus, release esophageal pressure
as prescribed.
 Keep scissors at the bedside at all times to monitor for
respiratory distress, and if it occurs, cut the tubes to deflate the
balloons and remove the tube.
 Monitor for increased bloody drainage, which may indicate
persistent bleeding.
 Monitor for signs of esophageal rupture:
o Esophageal rupture is an emergency and signs of
esophageal rupture must be reported to the physician
immediately.
o Drop in blood pressure
o Increased heart rate
o Back and upper abdominal pain
 Esophageal gastric balloon
o Tube pulled gently (TRACTION) to exert a force against the
gastric cardia.
 Surgical treatment of bleeding varices
o portacaval shunt
o splenorenal shunt
o TIPS
SURGICAL TREATMENT
 Distal Splenorenal Shunt (DSRS)
o A surgical procedure that connects the splenic vein to the
left kidney vein in order to reduce pressure in the varices
and control bleeding.
 Portacaval shunt
o it involves anastomosis of the portal vein to the inferior
vena cava, diverting blood from the portal system to the
systemic circulation.
 Mesocaval shunt
o is an anastomosis between the superior end of the divided
IVC and the side of the superior mesenteric vein\
 Transjugular intrahepatic portosystemic shunting (TIPS)
o TIPS is placed by an interventional radiologist between the
hepatic vein and portal vein.
o a stent (a tubular device) is placed in the middle of the
liver.
o A catheter is placed through a vein in the neck to relieve
the high blood pressure that has built up in the liver.
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 ACCESSORY ORGAN DISORDERS
Devascularization  The blood which contains toxins is “shunted” or redirected,
back to the central circulation and into the brain without first
 Modified Sugiura procedure going through the liver for detoxification.
o (esophagogastric devascularization with esophageal  Ammonia cross the blood-brain barrier and enter brain cells
transection and splenectomy)  Interferes with brain metabolism, cell membrane pump
o Extensively devascularize the esophagogastric – interrupts mechanisms, and neurotransmission.
esophagogastric varices  EFFECTS - Disorientation, confusion ,personality changes,
memory loss, a flapping tremor called asterixis,
 sulphurous breath odor referred to as fetor hepaticus
(breath of the dead), and lethargy to deep coma

DIAGNOSTIC TEST
 Electroencephalogram (EEG)
o shows generalized slowing, an increase in amplitude of
brain waves and characteristic triphasic waves.

HEPATIC ENCEPHALOPATHY
 is a CNS manifestation of liver failure that often leads to coma
and death and w/c is related to an increase serum ammonia
level.
 A failing liver (advance cirrhosis ) can no longer break down
ammonia  accumulates in the blood
 Largest source of ammonia is the enzymatic and bacterial
digestion of dietary and blood proteins in the GI tract.
 ↑ Ammonia levels – GI bleeding, high protein diet, bacterial
infection, uremia

PATHOPHYSIOLOGY
 Ammonia forms in the intestine by bacterial action on ingested
proteins.

STAGES OF HEPATIC ENCEPHALOPATHY

STAGE SYMPTOMS SIGNS & EEG NURSING

CHANGES DIAGNOSIS
1 -Normal LOC -Asterixis; impaired -Self care deficit
with periods of writing and ability to -Activity
lethargy & draw line intolerance
euphoria; figures(constructiona -Disturbed sleep
-Reversal of l pattern
day-night apraxia)
sleep pattern -Normal EEG.

2 -Increased - Asterixis, fetor - Impaired social

drowsiness hepaticus - Interaction
-Disorientation -Abnormal EEG with - Risk for injury
-Agitation with generalized - Ineffective role
-Mood swings slowing performance
-Inappropriate
behavior

3 -Stuporous -Asterixis -Imbalance

-Difficult to -Increased deep nutrition
rouse tendon reflexes -Impaired mobility
Sleeps most of -Rigidity of -Impaired verbal
time extremities communication
-Incoherent -EEG markedly
speech abnormal
-Marked
confusion

4 -Comatose -Absence of asterixis -Risk for aspiration

-May not -Absence of deep -Impaired gas
respond to tendon reflexes exchange
painful stimuli -Flaccidity of -Impaired tissue
extremities integrity
-EEG markedly -Disturbed sensory
abnormal perception

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 ACCESSORY ORGAN DISORDERS

Mental Signs
 forgetfulness, mild confusion
 poor judgement
 being extra nervous or excited
 not knowing where they are or where they’re going
 inappropriate behavior or severe personality changes

Physical signs
 breathe with a musty or sweet odor
 change in sleep patterns
 worsening of handwriting or loss of other small hand movements
 shaking movements of hands or arms
 slurred speech
 Cirrhotic patients have protein intolerance. Too much protein will
result in an increased amount of ammonia in the blood
*continuation next page
HEPATORENAL SYNDROME
 progressive kidney failure in a person with cirrhosis of the liver
 a serious and often life-threatening complication of cirrhosis.
 Decrease in kidney
MEDICAL MANAGEMENT function
 Therapy is directed toward treating or removing the cause.
 Neurologic status assessment frequently- LOC
 Mental status assessment.
 Daily recording of handwriting and arithmetic performance
o Constructional apraxia – inability to reproduce a single
figure. Reflexes active→ FLACCID

 Fluid intake and output and body weight are recorded daily
 Vital signs monitoring and recording q 4 hours
 Potential sites of infection (peritoneum, lungs) assessment &
recording of abnormal changes
 Serum ammonia level is monitored daily.
 Lactulose (Cephulac ) - a laxative given to reduce serum
ammonia levels .
 It pulls water into the gut to soften stool and increase peristalsis
and helps to pull ammonia from the blood into the colon and
promotes excretion of ammonia in the stool.
 less urine is removed from the body, nitrogen-containing waste
 Protein intake moderately restricted on comatose patients and
who have encephalopathy
 Reduction in the absorption of ammonia from the GI tract with
the use of gastric suction, enemas, and oral antibiotics like
neomycin to reduce the amounts of ammonia producing
bacteria in the intestines.

o S.E. – NEPHROTOXICITY - patients with renal

problems

 Electrolyte status is monitored

 Sedatives, analgesics and tranquilizers are discontinued.
 Benzodiazepine antagonists like Flumazenil (Romazicon) may
be given to improve encephalopathy

products build up in the bloodstream (azotemia)

 An acute deterioration in kidney function associated with severe
renal vasoconstriction.

Schematic representation of the splanchnic circulation

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 ACCESSORY ORGAN DISORDERS

 splanchnic circulation' describes the blood flow to the abdominal

gastrointestinal organs including the stomach, liver, spleen,
pancreas, small intestine, and large intestine.

splanchnic vasodilation
 is a result of an important increase in local and systemic
vasodilators

MANAGEMENT
 Salt poor albumin
 Diuretics
 Na and water restriction
 no NSAID’s

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 ACCESSORY ORGAN DISORDERS
GALLBLADDER DISORDERS
PATHOPHYSIOLOGY
Acute or chronic inflammation causing painful distention of the
gallbladder.  Fatty chyme in the duodenum - intestinal mucosa secrete
cholecystokinin
CHLOCYSTITIS
 inflammation of the gallbladder  Stimulates the gallbladder to contract and empty.

CHOLELITHIASIS  If a stone lodges in the cystic duct, the gallbladder contracts but
 stone formation in the gallbladder cannot empty.

TYPES
 Cholesterol stone
o is usually solitary, oval and up to 2-3 cm in length.
o radiating glistening cholesterol crystals(pale yellow) and
often has a tiny dark central deposit is associated with
excessive cholesterol in the bile

 Bile pigment stones

o are always multiple and are usually due to chronic
hemolysis with excess bilirubin production.
o Rarely more than 1cm in diameter, black and irregular.

 Mixed stones
o Account for 80% of all gallstones and are always multiple
and faceted
o due to contact with one another.

CAUSES
 Gallstones (most common)
 Abnormal metabolism of cholesterol and bile salts
 Poor or absent blood flow to the gallbladder
 When intestinal bacteria infiltrate the gallbladder and ducts,
PREDISPOSING FACTORS:5 F’S an infection can
 Female, be established
 Fat (Obese),
 Fair(Caucasian), o A
 Forty, s
 Fertile(multigravida; use of Contraceptive pills) c
e
Rapid weight loss n
d
Gallstone formation results from when liquid stored in the gallbladder i
(bile) hardens into pieces of stone-like material. n
g cholangitis
PRINCIPAL CONSTITUENTS OF BILE ARE  when infection moves to the direction of the liver.
 Cholesterol o Suppurative cholangitis
 Phospholipids  if pus is produced in the biliary tract.
 bile salts.

o An abnormal metabolism of cholesterol and bile salts plays

an important role in gallstone formation.
o The ratio of cholesterol: bile salts is very important.

PATHOPHYSIOLOGY

Increased biliary cholesterol secretion

Increased cholesterol synthesis
Decreased bile acids

Ratio increased
Cholesterol ↑
Bile salts ↓
TEST FOR CHOLECYSTITIS
Nucleation(formation of tiny stones)  Press fingertips under liver margin and ask client to inhale
deeply.
Progressive accumulation of cholesterol & pigments  MURPHY’S SIGN: accentuated sharp pain when client hold his
or her breath
ENLARGING STONES
(most common gallstones are formed from cholesterol which is a major SIGNS AND SYMPTOMS
component of bile)  Decreased fat emulsification
o Fat intolerance
o Flatulence
o Anorexia
o N & V- triggered by the inflammatory response
o Steatorrhea

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 ACCESSORY ORGAN DISORDERS
 Decreased bile flow in colon
o Acholic stool – pale / clay color (gray)
o Poor absorption of fat soluble vitamin
 Increased serum bilirubin
o Jaundice from obstruction of the common bile duct by
calculi.
o Pruritus – bilirubin deposits in the skin
o Tea colored urine
 Infection - ANTIBIOTIC THERAPY
o Low grade fever secondary to infection
o Cholecystitis
o Pancreatitis
*continuation next page
DIAGNOSTIC TEST FINDINGS
 X-ray
o reveals gallstones(if they contain enough calcium to be
radiopaque)
 Ultrasonography
o detects gallstones as small as 2 mm and distinguishes
between obstructive and non obstructive jaundice
 Percutaneous transhepatic cholangiography
o supports the diagnosis of obstructive jaundice and reveals
calculi in the ducts.
 Levels of serum alkaline phosphate, lactate dehydrogenase,
aspartate aminotransferase (AST), and total bilirubin are high.
 Serum amylase level is slightly elevated.
 WBC counts are slightly elevated during a cholecystitis attack.
TREATMENT
 Cholecystectomy
o to surgically remove the inflamed gallbladder.
 Choledochostomy
o to surgically create an opening into the common bile duct
for drainage.
 Laparoscopic cholecystectomy
o the surgical procedure using laparoscopy to remove the
gallbladder
o A small incision is made at the umbilicus plus 3 other
puncture sites.= 4 incisions
o Carbon dioxide gas is pumped into the abdominal cavity to
help to separate the organs
o A laparoscope with video camera and laser technology is
introduced.
o Stones in the CBD – it cannot be performed, instead open
cholecystectomy with IOC, CBD exploration
(choledochotomy)
 T tube - prevents bile from spilling into the peritoneal cavity
TREATMENT
 Endoscopic retrograde cholangiopancreatography (ERCP)
o to remove gallstones
 Lithotripsy
o to break up gallstones and relieve gallstones.
 Oral Chenodeoxycholic acid (Chenodiol) or
Ursodeoxycholic acid(Actigail)
o to dissolve calculi.
 Low fat diet to prevent attacks.
 Vitamin K to relieve itching, jaundice, and bleeding tendencies
caused bt vitamin K deficiencies.
 Antibiotics to treat infection during an attack.
 Nasogastric tube insertion during an acute attack for abdominal
decompression.
NURSING CONSIDERATIONS
 Before surgery
o Teach the patient to deep breathe, cough, expectorate and
perform leg exercises that are necessary after surgery.
o Teach splinting, repositioning, and ambulation techniques
 After surgery
o Monitor the patient’s vital signs for signs of bleeding,
infection, or atelectasis.
o Evaluate the incision site for bleeding.
o Serosanguinous drainage is common during the first 24 to
48 hrs if the patient has a wound drain.
o If a T-tube drain is placed in the duct and attached to a
drainage bag,make sure that the drainage tube has no
kinks and is well secured.
o Measure and record the T-tube drainage daily (200-300 ml
is normal)
 If discharge with a T-tube teach - dressing changes and
routine skin care.
 Monitor intake and output
 Check for bladder distension.
 Encourage deep breathing and leg exercises
 Have the patient ambulate after surgery
 Provide elastic stockings to prevent stasis and clot
formation.
 Pain management
 Incentive spirometry
o operative incision is near the diapragm
 At discharge
o Advise the patient against heavy lifting or straining for 6
weeks.
o Urge him to walk daily.
 Post - laparoscopic cholecystectomy patient MGH the same
day or within 24 hours after surgery.
o have minimal pain
o able to tolerate a regular diet within 24 hours after surgery
o able to return to normal activity within 1 week
o Discharge instructions for a post-cholecystectomy client,
the nurse would include the importance of notifying the
physician of the development of jaundice or itching
 Care of a T- tube
o Used in common bile duct exploration.
o Preserves the patency of the duct and ensures drainage of
bile until edema resolves and bile is effectively draining
into the duodenum.
o Helps prevent bile from spilling into the peritoneal cavity. A
gravity drainage bag is attached to the T tube to collect the
drainage.
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 Pancreatic cyst or tumor

1. Semi-Fowlers position to facilitate drainage.  Ischemic vascular disease
2. Monitor the amount, color, consistency and odor of the drainage.  Abdominal trauma
(Brownish red for the first 24 hours;this is due to the combination  Medications
of bile and blood.)  Infections
3. Report sudden increases in bile output to the physician.  Tumors
 First 24 hrs - T-tube usually drains 300-500ml  Genetic/anatomical variants
 After 3-4 days - the amount decreases to less than  High triglyceride levels
200ml/24 hours
 High calcium levels
4. Monitor for inflammation and protect the skin from irritation.(Bile
is erosive and extremely irritating to the skin)
5. Keep the drainage system below the level of the gallbladder.
6. Monitor for foul odor and purulent drainage and report its
presence to the physician
7. Avoid irrigation, aspiration, or clamping of the T-tube without a
physicians order.
8. As prescribed
 clamp the tube before a meal and observe for abdominal
discomfort and distension, nausea, chills or fever
 unclamp the tube if nausea and vomiting occurs.
Primarily, the pancreas becomes inflamed when the organ’s own
PANCREATITIS enzymes – especially trypsin cause the pancreas to digest itself
 Acute or chronic inflammation of the pancreas, with associated (autodigestion)
escape of pancreatic enzymes into surrounding tissue
 may be the result of a bacterial infection, trauma, or chronic
disease such as cancer.

Autodigestion develops when:

Reflux of duodenal contents
 Acute pancreatitis with activated enzymes enters
o edema and inflammation of the pancreas. the pancreatic duct

Activates other enzymes setting up a cycle of more pancreatic damage

 Chronic pancreatitis
o is a continual inflammation & destruction of the pancreas, Swelling on the opening
with scar tissue replacing pancreatic tissue.  obstructs the release of bicarbonate - neutralizes chyme
 obstructs the release of the enzyme trypsin -digest proteins
 The end result - mechanical obstruction of the pancreatic  Amylase - digest carbohydrates
duct and CBD and the duodenum.  lipase for fat digestion
 There is atrophy of the epithelium of the ducts, inflammation, and  Autodigestion – impairment of endocrine functions – D.M.
destruction of the secreting cells of the pancreas.
ETIOLOGY
CAUSES  Gallstones (30-40%)
 exact mechanism UNKNOWN  Alcohol
 Hypertriglyceridemia
 Chronic Alcohol use  ERCP
o excess HCl causes spasm of the sphincter of Oddi ,  Smoking
ethanol is a direct toxic insult to the acinar cell, causing  Drugs
inflammation and membrane destruction.  Infections
 Trauma
 Biliary tract disease  Vascular disease
o gallstone lodges at the Ampulla of Vater (obstruction)

 Bacterial or viral disease

o complication of mumps virus

 Blunt or surgical trauma

 E.R.C.P.
 Drugs – corticosteroids, oral contraceptives, sulphonamides,
thiazide diuretics and NSAIDs.
 Penetrating peptic ulcers

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In severe attack
 Weight loss
o decrease dietary intake secondary to anorexia or fear -
precipitate the attack

 Muscle wasting

 Jaundice
o obstruction of biliary tract

 Signs & symptoms of DM

ASSESSMENT
COMPLICATIONS
Acute Pancreatitis
 Biliary and duodenal obstruction
 Abdominal pain - sudden onset at a midepigastric or LUQ
 Massive hemorrhage and shock
location with radiation to the back.
 Diabetes mellitus
 Pain aggravated by a fatty meal, alcohol, and is greater when
 Portal and splenic vein thrombosis
lying supine and improves when leaning forward, flexion of the
knee, or fetal positioning  Respiratory failure
 Nausea & vomiting  Pseudocyst
o a collection of pancreatic fluid in the peritoneal cavity
 Weight loss
enclosed in a layer of inflammatory tissue resulting from
 Cullen’s sign
autodigestion or liquefaction of pancreatic tissue.
o discoloration of the abdomen & periumbilical area
o connected to a pancreatic duct, so that it continues to
increase in mass.
 Turner’s sign
o develops near the head of the pancreas ,close to the
o bluish discoloration of the flanks w/c indicate that the
common duct jaundice may occur
injured pancreas is releasing blood.

 Tachycardia - dehydration
 Low grade fever - inflammation
 Cold, sweaty extremities - cardiovascular collapse
 Absent or decreased bowel sounds DIAGNOSTIC TEST FINDINGS
 Elevated WBC count, & glucose, bilirubin, alkaline phosphatise,  Elevated serum amylase and lipase confirm diagnosis
& urinary amylase levels  Blood and urine glucose test reveal transient glucose in urine
 Elevated serum lipase & amylase levels and hyperglycemia
 In chronic pancreatitis, serum glucose levels may be transiently
In severe attack elevated
 Persistent vomiting  WBC count is elevated
o hypermotility or paralytic ileus  Serum bilirubin levels are elevated in acute and chronic
pancreatitis
 Abdominal distention  Blood calcium levels may be decreased
o accumulation of fluids in the abdominal cavity.  Stool analysis reveals elevated lipid and trypsin levels in chronic
pancreatitis
 LUQ mass  Abdominal and chest x-rays
 CT scan and ultrasonography
 Steatorrhea & foul-smelling stools  Hemoglobin and hematocrit levels to monitor for bleeding
o impaired fat digestion  ERCP

 Extreme malaise related to malbsorption or diabetes

Chronic Pancreatitis

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TREATMENT
 IV replacement of fluids, protein, and electrolytes to treat shock
 Fluid volume replacement to help correct metabolic acidosis
 Blood transfusions to replace blood loss from hemorrhage
 NPO to rest the pancreas and reduce pancreatic enzyme
secretion

o Somatostatin, a treatment for acute pancreatitis, inhibits the SURGERY

release of pancreatic enzymes.
Pancreatico-jejunostomy(Roux-en –Y)
 NG tube suctioning to decrease stomach distention and  joining of the pancreatic duct to the jejunum to relieve ductal
suppress pancreatic secretions obstruction and to allow drainage of the pancreatic secretions
 Antiemetics to alleviate nausea and vomiting into the jejunum.
 Meperidine to relieve abdominal pain
 Antacids to neutralize gastric secretions Pancreaticoduodenectomy (Whipple Procedure)
 Histamine antagonist to decrease hydrochloric acid production  A pancreaticoduodenectomy also known as a Whipple
 Antibiotics to fight bacterial infection procedure, involves the removal of the pancreas head due to a
 Anticholinergics to reduce vagal stimulation, decrease GI tumor in the pancreas or bile duct, or pancreatitis
motility, and inhibit pancreatic enzyme secretion
 Insulin to correct hyperglycemia
 Surgical drainage to treat a pancreatic abscess or pseudocyst or
to re-establish drainage of the pancreas
 Laparotomy ( if biliary tract obstruction causes acute
pancreatitis) to remove obstruction

UNCOMPLICATED CYST
 bulge into stomach/ duodenum
 No solid tissue/ vessels (EUS)
 Wall thickness 0.5-1 cm (EUS)
 Technical expertise available

ENDOSCOPIC DRAINAGE

SEPSIS
 Infected pseudocyst (abscess) not amenable to image guided
drainage

EXTERNAL DRAINAGE
(Risk of pancreatic fistula morbidity: 10-15%)

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 Instruct the client to avoid heavy meals

 Instruct the client in the importance of avoiding alcohol
 Provide supplemental preparations & vitamins & minerals to
increase caloric intake
 Administer insulin or oral hypoglycaemic medications as
prescribed to control DM, if present
 Administer pancreatic enzymes as prescribed to aid in the
digestion & absorption of fat & protein
o Pancreatic enzyme replacement- ex. pancrelipase
(Lipancreatin) to help digest and absorb fats, proteins, and
carbohydrates.

Pancreatic enzyme replacement

 A blockage in the pancreatic duct, or removal of part of the
pancreas, can cause a change in the flow and amount of
pancreatic juice. 
 If your body cannot produce enough pancreatic juice, you will
have difficulty getting nourishment from foods and eventually you
will lose weight.
 Enzyme supplements contain Pancreatin – a mixture of
pancreatic enzymes lipase, amylase and protease.  These assist
the digestion of fat, carbohydrates and proteins.

Exocrine pancreatic insufficiency (EPI)

 is a condition characterized by deficiency of the exocrine
pancreatic enzymes
o inability to digest food properly, or maldigestion.

 Management - pancreatic enzyme replacement therapy

(PERT)
o should be taken with every meals and snacks

 Creon - commonest preparation

o CREON should not be crushed or chewed. 

Management approaches to exocrine pancreatic insufficiency

 Lifestyle modifications (eg, avoidance of fatty foods, limitation of
alcohol intake, cessation of smoking, and consumption of a well-
balanced diet)
 Vitamin supplementation (primarily the fat-soluble vitamins A, D,
E, and K)

INTERVENTIONS

Acute Pancreatitis
 Monitor vital signs and hemodynamic stability
 Give plasma or albumin, if ordered, to maintain blood pressure
 Record fluid intake and output
 Check urine output hourly, and monitor electrolyte levels
 Assess for crackles, rhonchi, or decreased breath sounds
 Maintain constant NG suctioning for bowel decompression, and
NPO
 Perform good mouth and nose care
 Watch for calcium deficiency
 Administer analgesics as needed to relieve the patient’s pain and
anxiety
 knee-chest position

Meperidine HCL (Demerol)

o for pain
o less incidence of smooth muscle spasm of the pancreatic duct &
sphincter of Oddi.
o Note: although Morphine SO4 or Codeine maybe prescribed,
they generally are avoided because they can cause spasm of the
sphincter of Oddi & increase pain. Focus is on the management
of pain.

Chronic Pancreatitis
 Instruct the client in the prescribed dietary measures ( fat &
protein maybe limited)

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