Med Surg Test 4 CH 49 & 50

Chapter 49
Assessment and Management of Patients With Hepatic Disorders

A&P of hepatic system

 LIVER is the largest gland of the body
 LIVER is very VASCULAR
 Receives nutrient rich blood from GI tract via the PORTAL VEIN & from the HEPATIC
ARTERY
 Stores the nutrients or converts them into chemicals
 Filters waste products and secrets bile
 The majority of blood supply to the liver, which is rich in nutrients from the
gastrointestinal tract, comes from the portal vein.

Liver and biliary system

 Has 4 lobes
 Each lobe has thousands of lobules
 Blood Supply comes from PORTAL vein & HEPATIC artery and come together to mix
into the SINOSOID
  Hepatic duct leads the liver & combines w/ cystic duct from GB & together they form
COMMON BILE DUCT

Liver Functions
 Glucose metabolism
 Ammonia conversion
 Protein metabolism
 Fat metabolism
 Vitamin and iron storage
 Bile formation (creates bile)
 Bilirubin excretion (rids of bilirubin)
 Drug metabolism

Gero considerations
 Size change but not the function changes
 Decrease clearance of hepatitis B surface antigen
 Decrease drug metabolism and clearance
 Decrease intestinal and portal vein blood flow
 Decrease GB contraction after a meal
 Decrease rate of replacement and/or repair of liver cells after injury
 Decrease size & weight of liver
 Increased prevalence of gallstones (due to increase in cholesterol secretion in bile)
 Rapid progression of Hep C and lower response rate
 More severe complications of biliary tract disease

Assessment for liver dysfunction

 Health history
o Ask exposure to toxic substances or infectious agents
 o Occupational hazards
o Recreation activities and travel history
 Medication history
o OTC, acetaminophen, valproic acid
o Ask about Alcohol and drug consumption (Men 4 drinks a day, women 3 drinks a
day will lead to chronic liver disease)
 Ask about s/s:
o Jaundice, puritis
o Malaise, weakness, fatigue
o Abdominal pain
o Fever
o Anorexia
o Weight gain, edema
o Easy bruising, melena, hematemesis
o Changes in mental acuity, personality or libido

Physical exam od pt w/ liver dysfunction

 Pallor
 Jaundice
 Muscular dystrophy
 Edema
 Excoriation from scratching
 Petechial or ecchymosis
 Cognitive changes
 Gynecomastia and testicular atrophy in men
 Tremors or Sterixis
 Liver enlargement (by deep palpation or percuss right margin down abdomen and hear
change from dullness over liver to tympani over bowel and mark how far down in cm)
 Spider angiomas (increase in estrogen)

Liver Function Studies

 Serum aminotransferase: (indicators of injury to liver, detect acute hepatic, elevate in
shock)
o AST (10-40) (increases w/ tissue damage like liver, kidneys, heart, skeletal
muscle)
o ALT (8-40) (increase w/ primary liver disorders, cirrhosis, hepatitis)
o GGT (0-30) (for evaluating cholestasis)
o GGTP (0-30)
o LDH (100-200 units)
 Serum protein studies
o Serum albumin (3.5-5.5)
o *Albumin (4-6) can tell us about nutrition and overall protein, has half-life of 20
days, check pre-albumin 204 day half life
  Direct and indirect serum bilirubin (0.1-0.4) (yellow/orange substance that is produced
as we break down hemoglobin, processed by liver, excessive amounts of bilirubin will
cause jaundice, two types such as direct attached to liver by glycemic acid and elevated it
likely means viral hep or med damaged, alcohol disease and indirect (unconjugated, not
attached, formed from break down of hemoglobin, trauma, bleeding, ecchymosis, blood
transfusions)
 Urine bilirubin (<0.25mg/24hr)
 Urine bilirubin and urobilinogen (0.05-2.5mg)
 Prothrombin time (PT) (12-16 seconds) vitamin k is required to synthesize pt, to tell
how bad vitamin k deficiency is
 Serum Alkaline Phosphate (30-120) can increase by 30% after meals, type o blood run
higher, enzyme lives with in liver kidneys gi, bone disease, bile duct obstruction (with
biliary obstruction)
 Serum ammonia (15-45) liver converts ammonia into urea, levels rise and mental
confusion
 Cholesterol
 70% of liver parenchyma is likely damaged before LFT become elevated

Additional Diagnostic Studies

 Liver biopsy (To make definitive dx) check on PT and INR prior and monitor for risk of
bleeding after
 Ultrasound
 CT (usually start here)
 MRI
 Others:
 Chart 49-2

Hepatic Dysfunction
 Acute or chronic CIRRHOSIS of the liver (caused by damage of prmkinale cells, primary
liver disease, obstruction of bile flow, or hepatic circulation) 80% with cirrhosis
compensate for 10 years until dx
 Most common cause is MALNUTRTION r/t alcoholism (respond by replacing glycogen
with lipids leaves scar tissue)
 Infection (bacterial or viral)
 Anoxia
 Metabolic disorders
 Nutritional deficiencies
 Hypersensitivity states
 Medications

Manifestations of Liver Disease

 Jaundice
 Portal hypertension, acities, and varices
 Hepatic encephalopathy or coma
 Nutritional deficiencies
Jaundice
 Yellow or greenish yellow tinged sclera and skin, mucous membranes caused by increase
serum bilirubin levels
 Types:
o Hemolytic- caused by increase destruction of RBC
o Hepatocellular (most common cause) - problem w/in liver cells, caused by
viruses, meds, alchol use
s/s
 Mild to severe ill
 Lack of appetite, n/v, wt loss
 Malaise, fatigue, weakness
 HA, chills, fever, infection
o Obstructive (most common cause) - r/t occlusion of bowel duct from gall stone,
tumor, inflammation
s/s
 Dark orange brown urine
 Clay colored stools
 Dyspepsia and intolerance of fats, impaired digestion
 Pruritus
o Hereditary hyperbilirubinemia- genetic chart 42-9 most common Gilbert
Syndrome
 Hepatocellular and obstructive jaundice are most associated with LIVER DISEASE

Portal Hypertension
 Obstructed blood flow through the liver results in increased pressure throughout the
portal venous system
 Results in:
o Ascites (50% mortality rate)
o Esophageal varices

Notes:
-Liver is damaged and can’t metabolize aldosterone
-which leads body to retain sodium and water, increased intravascular fluid and
lymphatic flow will cause liver to not be able to synthesis albumin,
-Can cause severe intravascular dehydration or depletion

Ascites: Fluid in peritoneal cavity- causes

 Portal hypertension resulting in increased capillary pressure and obstruction of venous
blood flow
 Vasodilation of splanchnic circulation (blood flow to the major abdominal organs)
 Changes in the ability to metabolize aldosterone, increasing fluid retention
 Decreased synthesis of albumin, decreasing serum osmotic pressure
 Movement of albumin into the peritoneal cavity
Once noticed in pt their mortality increases to 50%
Assessment of Ascites:
 Record abdominal girth and wt daily (ask if its normal for them)
 Patient may have striae, distended veins, and umbilical hernia
 Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave
(should have dullness where there is fluid and tympani where there is no fluid)
 Monitor for potential fluid and electrolyte imbalances (hypokalemia, hyponatremia)

Assessing for abdominal fluid wave

 1st stabilize skin tissue with either pt doing it or another nurse
 Take both hands, one side press firmly, other hand feel for sensation of fluid wave

Treatment of Ascites
 Low sodium diet
 Diuretics
o Spironolactone: (used for ascites) blocks aldosterone, potassium sparing, can be
used with other diuretics
 Bed rest (short term)
 Paracentesis (needle through abdomen and ultrasound to look, pull off 5-6 liters of fluid,
may need transfusion of albumin after
 Administration of salt poor albumin
 Transjugular intrahepatic portosystemic shunt (TIPS)
 Always need IV accesses and fluids hanging

Transjugular intrahepatic portosystemic shunt TIPS:

 Goes through the liver to the jugular vein into the portal vein
 Stent is deployed to divert blood flow to relieve pressure off portal vein
 Often referred for these because of high mortality rate
 Can end up casing hepatic encephalopathy
 High risk 30 mortality day risk
 Use if paracentesis is contraindicated

Bleeding of Esophageal Varices

**Varices: (dilated torturous veins found in the submucosal of lower esophagus and can
distend into stomach)
 Occurs in about 1/3 of patients with cirrhosis and varices
 First bleeding episodes has a mortality rate of 30% to 50%
 Manifestation include hematemesis, melena, general deterioration, and shock
 Patients with cirrhosis should undergo screening endoscopy every 2 years
Treatment of Bleeding Varices
 1st establish large bore IV access, preferable proximal in the arm, 14g or 16g
 Endoscopy is needed to identify the source
 Treat for shock, administer oxygen
 IV fluids, electrolytes, volume expanders, blood and blood products
 Vasopressin (constricts the splenetic artirial bed), somatostatin, 1st line medication is
Octreotide (synthetic hormone) to decrease bleeding (watch glucose levels)
 Nitroglycerin in combination with vasopressin to reduce coronary vasoconstriction
 BB: Propranolol and nadolol to decrease portal pressure, used in combination with other
treatment **cant be given with acute bleed, on prior or after bleed resolves
 May need to intubate

*Bleeding esophageal varies result in a DECREASE in RENAL PERFUSION!

IV Catheter Flow Rates

 *SHORT & FAT is where it’s at!!
*Want 2 large bore IV
*14g liter of volume in patient at 1min and 30 seconds

Endoscopic Sclerotherapy
*Fine needle injects vasoconstriction meds like epinephrine

Esophageal Banding
  Done with endoscopy
 Suction and then pull forward to band it

Portal Systemic Shunts

 A: Normal system: lay closely to inferior vena cava

 B: End to side portacaval shunt: portal vein separated with ends into the inferior
vena cava, requires hepatic system to gets it blood supply from hepatic artery
alone, bypasses all the nutrient rich blood and puts directly into the inferior vena
cava, causes severe encephalopathy procedure is avoided
 C and d: are selective, only drain portions of the blood flow into the inferior vena
cava, more beneficial to the patient
Nursing Management
 All require form of conscious sedation or general anesthesia
 Monitor frequently for aspiration, changes in vital signs, emotional responses, and
cognitive status
 Monitor for associated complications: hepatic encephalopathy resulting from
blood breakdown in the GI tract and delirium related to alcohol withdrawal
 Oral care, tube, and GI suctioning through NG tube
 Implement measures to reduce anxiety and agitation
 Education and support of patient and family

Complication of Hepatic Encephalopathy and Coma

Assessment:
 EEG (look for seizures)
 Changes in LOC (fowl smelling breath)
 Potential seizures
 Fector hepaticus
 Monitor fluid, electrolytes, and ammonia levels
 Life threatening complications: accumulation of ammonia and other toxic
metabolites in the blood RESPIRATORY DEPRESSION with increase of
ammonia
 Stages: refer to table 49-3

Asterixis: involuntary flapping of the wrists

Apraxia: when you ask to pick up key, touch nose, and they CANNOT

Medical Management with hepatic encephalopathy or coma:

 Eliminate precipitating cause
 Lactulose to reduce serum ammonia levels (goal is to have 2-3 BM a day)
 IV glucose to minimize protein catabolism
 Put on Protein restriction
 Reduction of ammonia from GI tract by gastric suction, enemas (lactulose enemas), oral
ABX
 Discontinue sedatives analgesics and tranquilizers (avoid Benzodiazepines)
 Monitor or treat complications and infections
 Talk to pts next kin to make plan for goals of care, life support for patient

Hepatitis
 Viral hepatitis: a systemic viral infection that causes necrosis and inflammation of liver
cells with characteristics symptoms and cellular and biochemical changes within the
liver.
o A & E: fecal oral route (excreted in ones feces and picked up by another person
orally) 25% of cases
o B & C: blood borne (high risk for health care workers)
o D: only people with hepatitis B are at risk
o Hepatitis G & GB virus-C
  Nonviral hepatitis: toxic and drug induced
 Refer to table 49-4

Hepatitis A
 Spread by poor hand hygiene, fecal-oral
 There is a vaccine to prevent
 Incubation: 2-6 wks
 Illness may last 4-8 wks
 Mortality rate is .5% for those younger than age 40 years and 1-2% for those older than
age 40 years
 Manifestation s/s:
o Mild flulike symptoms
o Low grade fever
o Anorexia
o Later jaundice and dark urine
o Indigestion and epigastric distress
o Enlargement of liver and spleen

Hepatitis B
 Transmitted through blood, saliva, semen, and vaginal secretions, sexually transmitted to
infant at the time of birth
 A major worldwide cause of cirrhosis and liver cancer (healthcare workers get
vaccinated)
 Risk factors: refer to chart 49-8
o Close contact with carrier of hep b virus
o Frequent exposure to blood products
o Health care workers
o Hemodialysis
o IV injection drug use
o Male homosexual and bisexual activity
o Mother to child transmission
o Multiple sex partners
o Recipient of blood or blood products
o recent STI
o tattooing
o travel with unsanitary conditions
 Long incubation and variable, similar to hep A

Management of Hepatitis B
 Medications for chronic hepatitis type B: alpha interferon and antiviral agents, entecavir,
tenofovir
 Bed rest and nutritional support
 Vaccine: for persons at high risk, routine vaccination of infants
o Passive immunization for those exposed
 o Standard precautions and infection control measures to keep from spreading
o Screening of blood and blood products prior to being transfused
o Treatment for 16-24 weeks

Hepatitis C
 Transmitted by blood and sexual contact, including needle sticks and sharing of needles
 The most common bloodborne infection
 A cause of 1/3rd of cases of liver cancer and the most common reason for liver transplant
 Risk factors: refer to chart 49-9
o Children born to women infected with hep c
o Health care workers/ needle stick
o Multiple sex partners
o Past or current IV drug use
o Recipient of blood or blood products
 Incubation period is a variable
 Symptoms are usually mild or absent (goes undiagnosed for awhile)
 Chronic carrier state frequently occurs

Management of Hepatitis C
 Antiviral medications: interferon, ribavirin vs simprevir + ledipasiver-sofobuvir and
ombitasvir-paritaprevir-ritonavir packaged with dasabuvir is more commonly tolerated
 Have to be on meds for a long time
 Measures to reduce spread of infection as with hepatitis B
 (get pt to avoid alcohol) Alcohol potentiate disease, medications that effect the lvier
should be avoided
 Prevention: public health programs to decrease needle sharing among drug users
 Screening of blood supply
 Safety needles for health care workers

Hepatitis D and E
Hepatitis D
 Only persons with hepatitis B are at risk
 Blood and sexual contact transmission
 Likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis
 **Treatment for D is interferon for a year
 **Only persons with HEP B are at risk for HEP D
Hepatitis E
 Transmitted by fecal-oral route
 Incubation period, 15 to 65 days
 Resembles hepatitis A, self-limiting, abrupt onset, not chronic

G and GB-C
 5% from virus
 50% have had transfusions in the past
  not understood well

Other Liver Disorders:

 Nonviral Hepatitis
o Toxic hepatitis
o Drug induced hepatitis
*Recovery can be rapid if find the causative agent
*Meds hepato toxic like isoside (tb), halophane (not in US), acetaminophen,
raphampine, antimetoblotlites (chemo drugs)
 Fulminant hepatic failure
*Sudden and severe
*Develops within first 8 weeks of first onset of jaundice
o Survival rates 20-50% (high mortality rate)
o Reverse all reversible causes
o Assess for the possibility of transplant
o Newer technology includes ELAD (extracorpol liver assist device) exposes whole
blood to cartridges contain hepatoblastoma cells they filter the blood and do liver
functions and BAL (Bioartifical liver) exposes separated plasma to pig
hepatocytes, temporary liver dialysis

*MARS or ELAD device: those patients need to have plan to get off the machine and
only for weeks at a time

Hepatic Cirrhosis
 Types
o Alcoholic (develops scar tissue around portal area) MOST COMMON
o Post necrotic (broad bands of scar tissue are intertwined within the liver, late
result of viral hepatitis)
o Biliary (scaring around the bile ducts results from chronic biliary obstruction and
infection (cholangitis) Less Common
*Imaging MRI, CT, dx with liver biopsy
 Manifestations s/s:
o Liver enlargement
o Portal obstruction
o Ascites
o Infection
o Peritonitis
o GI varices
o Edema
o Vitamin deficiency
o Anemia
o Mental deterioration
o Refer to chart 49-10

Care of patient with Cirrhosis of the liver/ Assessment

  Focus on onset s/s, hx of precipitating factors
 Alcohol use or abuse (ask about them)
 Dietary intake and nutritional status via labs
*Patients without ascites, edema, or impending hepatic coma can have large amounts of
protein but should be restricted if they have those
*Vitamins supplements, B, A, C and K may be warranted
*For Ascites small frequent meal
 Exposure to toxic agents and drugs
 Assess changes in mental status, ADL, IADLS, job and relationships
 Monitor s/s related to bleeding, changes in fluid volume and lab data

Child Pugh Score for survivability within 1 year for Cirrhosis

*look at survival for 1 year

* scores calculated into 3 classes
*Class A 100%, 80% B, class C 45% chance for 1 year survival

Care of Pt with Cirrhosis of the Liver

 Promote rest
 Improve nutritional status
 Provide skin care
 Reduce risk of injury (r/t pressure)

 Monitor for and prevent bleeding and hemorrhage

 Monitor for and prevent hepatic encephalopathy
 Monitor for and prevent Fluid volume excess
Activity intolerance
 Rest and supportive measures (cluster care, walk shorter distance more frequently)
 Positioning for respiratory efficiency (elevated hob)
 Supplemental oxygen
 Planned mild exercises and rest periods
 Address nutritional status to improve strength
 Measures to prevent hazards of immobility

Imbalanced nutrition
 I&O
 Encourage small frequent meals
 High calorie diet/ sodium restriction
 Protein modified or restricted if patient is at risk for encephalopathy
 Supplemental vitamins, minerals, B complex, provide water soluble forms of fat soluble
vitamins if patient has steatorrhea
 Consider patient preferences for nutrition

Other interventions
 Impaired skin integrity
o Frequent position changes
o Gentle skin care
o Reduce scratching related to pruritus
 Risk for injury
o Prevent falls, trauma related to risk for bleeding

Cancer of liver of the Liver

 Primary liver tumors
o Associated with hepatitis B and C and Cirrhosis
o Hepatocellular carcinoma (HCC) (Most common liver cancer 75% of them, non
receptable)
 Liver metastasis (brain, lung, and testicular)
o Few cancers originate in the liver
o Frequent site of metastatic cancer
 Manifestations
o Dull persistent pain, RUQ, back or epigastrium
o Weight loss, anemia, anorexia, weakness
o Enlarged liver
o Jaundice, bile ducts occluded, ascites or obstructed portal veins
Nonsurgical management of Liver Cancer
 Underlying cirrhosis, which is prevalent in patients with liver cancer, increases risk of
surgery (because they just don’t heal, if they have ascites it wont heal)
 Major effect of nonsurgical therapy may be palliative
 Radiation therapy
 Chemotherapy
  Percutaneous biliary drainage (offloads the biliary tract by

inserting the drainage tube)

 Other nonsurgical treatments

Surgical management of Liver Cancer

 Treatment of choice of HCC if confirmed to one lobe and liver function is adequate
 Liver has ability to do regenerative capacity
 Types of surgery
o Lobectomy
o Local ablation
o Liver transplant

Liver Transplant

*shows where common bile duct is cut

*requires placing portal and hepatic back
*will have drainage tubes T tube duodenal and multiple around the liver resected

Nursing care of the patient undergoing a liver transplantation

 Preop
o Support, education, encouragement
*lots of screening to go to before
 Postop:
o Monitor for complication: metabolic abnormality & blood loss
  Complications: bleeding, infection, rejection
 Ethical dilemma: refer to chart 49-12
 Caregiver stress: refer to chart 49-14

MELD Score

*being assessed for candidacy for liver transplant

*based on projected 3-month mortality
*looks at all same as other
*lower score is low risk
*greater than 40 then100% chance of death in next 3 months

Liver Abscess
 Amebic (result of visiting developing countries, tropics, entaneaba histolytic) or pyogenic
(common in developed counties, polymycrobial substances, E.coli)
 S/s: sepsis, dull pain, enlarged liver, ect
 Seen with ultrasound or CT scan
 Blood cultures and aspirate
 IV antibiotics, open surgery if needed, supportive care (IV and ABX)

Chapter 50
Assessment and Management of Patients With Biliary Disorders

Review of A&P
 Gallbladder (hollow organ liver underneath the liver)
o Bile
 Pancreas
o Insulin
o Glucagon
o Somatostatin
Notes she said:
Gallbladder:
- is a hollow organ underneath the liver
-About 7 and a half to 10 centimeters long and holds 30-50 milliliters of bile
-Connected to the common bile duct by the cystic duct.
-When the sphincter of Oddi is closed bile enters the gallbladder
-Water in bile made from the hepatocytes is absorbed through the walls of the gallbladder so it is
5-10x more concentrated than it’s original form. 
-Food enters the duodenum the gallbladder contracts and the sphincter of Oddi opens allowing
bile to enter into the intestines (response occurs d/t cholecystokinin CCK released from the
intestinal walls)
-Bile is made up of water electrolytes (sodium, potassium, calcium, chloride and bicarbonate),
lecithin, fatty acids, cholesterol, bilirubin and bile salts
-Bile salts and cholesterol emulsify fats in the distal ileum
-Half of the body’s bilirubin ends up in the bile.  It is converted in the intestine to urobilirubin
where it is excreted in feces or urine
If bile flow is impeded and it can’t get to the intestines it in serum levels may rise

Pancreas
Exocrine function – secretion of pancreatic enzymes into the GI tract through the pancreatic duct
-Amylase (breaks down carbs) 
-trypsin (digestion of proteins)
-Lipase (breaks down fats)
Endocrine function – Insulin, glucagon and somatostatin into the blood stream, somatostatin
inhibits insulin and glucagon secretion leading to hypoglycemia

Cholecystitis (inflammation of the gallbladder)

 Inflammation of the gallbladder
 Pain, tenderness, and rigidity
 Most often caused by stones (stone gets logged and causes edema in cystic area)

Notes:
 -Calculous cholecystitis = 90% of all cases the gallbladder can develop edema which
compressed blood vessels which compromises vascular supply.
-Can get Gangrene and perforation may occur
-50% of pts will get secondary infections from organisms  that live in the GI tract like
ecoli, kleb and strep
-Acalculous cholecystitis = the other 10% and it comes after major surgical procedures,
severe trauma and burns, cyctis duct obstruction, primary bacterial infections and after
blood transfusion 

Cholelithiasis (calculi in the gallbladder)

 Formed from solid particles in bile
o Pigment stones
o Cholesterol stones
o Refer to chart 50-2
 Risk factors: refer to chart 50-1
Notes:
-5-20% in women 20-55 by age 70 over 50% have them
-Pigment stones are from unconjugated pigment in the bile forming stones 10-25% while
cholesterol stone are 75% of all cases

-Chart 50-1 Cystic fibrosis, DM, frequent change in weight obesity or rapid weight loss, women
-2-3x more prevalent in women than men, they are typically over 40 and obese “3 F’s Female,
Fat and Fourty”

Cholesterol Gallstones and Pigment Gallstones

*Cholesterol Gallstones on left
*Pigment Gallstones on right

Clinical Manifestations of Cholelithiasis

 None or minimal s/s, acute or chronic
 Pain and biliary colic
 Jaundice (if common bile duct is occluded)
 Changes in urine (dark) or stool color (grey, putty)
 Vitamin deficiency, fat soluble (vitamins A, D, E and K)
 Diagnostic tests: refer to Table 50-1
Notes
-Jaundice occurs with common bile duct occlusion 
-Urine becomes dark, stool no longer has bile therefor it is grey like putty
-Obstruction interferes with absorption of fat soluble vitamins
-Dx testing = Ultrasound – 90% accuracy, radionuclide imaing can show the uptake of the IV
radioactive agent and once can see it excreted through the biliary tract. 
-MRCP Magnetic resonance cholangio-pancreatography, cholangiogram Xray/Fluro with
contrast injected into the bile duct (usually done intraoperatively)
-ERCP can be done – discuss later

Medical Management of Cholelithiasis

 ERCP, PCT
 Nutritional and supportive therapies
 Medication:
o Ursodeoxyxholic acid
o Chenodeoxucholic acid
 Laparoscopic cholecystectomy
 Nonsurgical removal
o By instrumentation
o Intracorporeal or extracorporeal lithotripsy
Notes:
-Endoscopic Retrograde cholangio-pancreatography
-NURSING INTERVENTIONS: Monitor CNS and Respiratory systems as sedation is required,
monitor patient positioning
-Percutaneous Transhepatic Cholangiograpy – Dye is directly injected into the biliary tract,
typically reserved for those who can’t undergo -----ERCP d/t prior surgery
-80% of pts with an acute gallbladder attack can be treated with rest, IVF and NGT sx, analgesia
and abx – surgical intervention should be delayed until symptoms subside
Initially diet should include low fat liquids avoid eggs, cream, pork, fried foods, cheese, rich
dressings, gas forming vegies and alcohol 
-Extracorporeal was really replaced by lap chole

Nonsurgical Removal of Gallstones

Laparoscopic Cholecystectomy
Care of a patient with Cholelithiasis
 Knowledge and education needs
 Respiratory status and risk factors for respiratory complications postop
 Nutritional status
 Monitor for potential bleeding
 GI s/s: after laparoscopic surgery, assess for loss of appetite, vomiting, pain, distention,
fever, potential infection or disruption of GI tract
Notes:
-Pain may cause splinting (worse with open surgery)
-Big risk with lap chole is a bile duct injury it not noticed at the time of the injury presentation
is delayed by several days

Potential complications for Cholelithiasis

 Bleeding
 GI symptoms
 Complications related to surgery in general: atelectasis, thrombophlebitis
Notes:
-Large blood vessels are present in the area, if damaged will likely have to convert to open
-Typically lap choles lead to decreased risk of paralytic ileus but it can happen
***can see pneumoperitoneum after lap surgery from the CO2 they use to insufflate the abd,
typically resolves in hours

Care of the patient with Cholelithiasis

 Goals may include:
o Relief of pain
o Adequate ventilation
o Intact skin
o Improved biliary drainage
 Optimal nutritional intake
 Absence of complications
 Understands self-care routines

Interventions for Cholelithiasis

 Low fowlers
 NG or NPO until return of bowel function, then soft, low fat, high carb diet
 Care of biliary drainage system
  Analgesics, pain management
 Turn, cough, deep breathe, splinting to reduce pain
 Ambulation
 Self-care education refer to chart 50-2

Notes:
-Watch for ROBF – flatus and lack of nausea are more important the BS
-ERAS protocol eliminates NGT unless the patient has N/V
-Emptying an flushing perc chole tubes or post op drains if left

Pancreatitis
 Acute: pancreatic duct becomes obstructed, and enzyme back up, causing autodigestion
and inflammation of the pancreas
 Chronic: progressive inflammatory disorder with destruction of the pnacrea, cells are
replaced by fibours tissie, pressure within the pancreas increases, obstructing the
pancreatic and common bile ducts
Question: s/s of Chronic Pancreatitis: Recurrent attacks of severe upper abdominal and
back pain accompanied by vomiting
 Refer to chart 50-3
Notes:
-Acute can be life threatening
-Chronic can have acute flair ups and by the time it is noticed 90% of the exocrine function has
been lost. 
-80% of acute cases are related to cholelithiasis or sustained alcohol use
-Can be mild or severe; mild is typically interstitial edematous pancreatitis vs necrotizing
pancreatitis
-Mild can still be very ill, hypovolemic, can have electrolyte disturbances and develop sepsis
-Severe has the presence of necrotizing pancreases, can be sterile or infected, can involve the
tissue around the pancreas or the parenchyma which is worse
-Spillage of enzymes are toxic and can cause erosion of blood vessels causing thrombosis or
hemorrhage

Clinical manifestations of Pancreatitis

 Severe abdominal pain
  24 to 48 hours after heavy meal or alcohol
 unrelieved by antacids
 abdominal distention, mass decrease peristalsis, vomiting
 ominous signs: ridged abdomen, ecchymosis, hypotension, respiratory distress

Management of Pancreatitis
 Relieve symptoms and prevent complication
 NPO, Enteral feeds distally, NG
 H2 antagonist, PPI, Pain medication
 IV fluids
 Antibiotics only if infection is suspected
 Insulin therapy
Notes:
-DHT for feedings past the duodenum into the jejunum is ideal but can be very hard to place (if
surgery is done may get J tube or have DHT placed in OR) NGT to LIWS
-Decrease acid production with PPI
-Opioids for pain, consider PCA
-IVF – think of necrotizing pancreatitis as an internal chemical burns which requires a
tremendous amount of volume replacement
-Antibiotics are often prescribed and rarely needed
-Surgery should be last ditch effort – drains will be placed to irrigate and drain, J tube placement
for distal feeds – necrosectomy can be done via endoscopy, laparoscopically or open ideally you
wait until it is walled off otherwise surgery is difficult
-Management of chronic pancreatitis – monitor nutrition as they are often malnourished

Collaborate Problems and Potential Complications

 Fluid and electrolyte disturbances
 Necrosis of the pancreas
 Shock
 Multiple organ dysfunction syndrome
 Pancreatic cysts (walled off cysts on amylase containing fluid, they occur 4-6 weeks after
the acute pancreatitis)

Cancer of the Pancreas

  Pain, jaundice, weight loss are the common symptoms
 CT scans can confirm mass presence, EUS and ERCP can be used for fine needle biopsy
for diagnosis
 Chemotherapy, radiation (limited)
 Surgery, percutaneous cholecystostomy tube placement for jaundice
 Treatment may be palliative
Notes:
-4th leading cause of cancer related death in men and 5th in women, most people are in or beyond
their 60’s when dx 
-Risk factors include smoking and chronic pancreatitis, chemical and toxin exposure and high
fat/meat based diet
-Tumors can occur in the head, body or tail
-70% are in the head.  80-85% of people have advanced unresectable tumors leading to only a
7% 5 year survival rate over all d/t the delay in dx d/t lack of symptoms

Pancreatoduodenectomy (Whipple’s Procedure)

Notes:
-Removal of the gallbladder, a portion of the stomach, duodenum, proximal jejunum, head of the
pancreas, and distal common bile duct.
anastomosis of the remaining pancreas and stomach to the jejunum
-At Carilion all are admitted to the ICU post op, that is not the case at major centers but PCUs
are highly trained to recognize when pt’s are struggling Our pts get epidurals to decrease narcotic
use

Care
 Promote comfort
 Prevent complications
 Maximize QOL
 Choose a center close to home vs farther away

Multiple Sumps After Pancreatic Surgery

Pancreatic Islet Tumors
 Two types include secreting and non-insulin secreting
o They typically cause hypoglycemia
o Surgery is recommended
o Monitor serum glucose levels

Ulcerogenic Tumors
 Tumors involving the islets of Langerhans
 Zollinger Ellison Syndrome
o Causes gastric acid production leading to ulcers in the GI tract
o Tumors may be benign or malignant
o Surgical resection is reccomnneded but often not possible because they extend
beyond the pancreas
Notes:
-Causes gastric acid that produces ulcers in the stomach, duodenum and jejunum. 
-Can’t even be managed with partial gastric resection
Genetic