Management of Patients with

Hepatic/Biliary Dysfunction

Hepatitis
Cirrhosis
Gall Bladder Disease

N24-SP2010
Marjorie Miller MA
A&P
 Key Questions
What is the role of Glissons capsule around
the liver?

What clinical manifestations occur when the

patient has distention of the liver?
 Circulation of the liver
Dual Blood Supply
Portal system
Hepatic veins drain liver &
empty into IVC
1000-1200 ml/min
(rich in nutrients)

Hepatic artery
400-500 ml/min blood
flow
Oxygenated blood
Portal Vein
Receives 1050 mL/min from
Spleen
Intestines
Pancreas
Stomach
Incompletely saturated
Supplies 60-70% O2 needs
Empty into IVC
Stores 450 mL blood that
can be shifted in times of
stress
 Overview of liver
pathophysiology
Inflammation Obstruction
Edema internal pressure

pressure external pressure

Hepatocellular damage
breakdown of urea NH3 encephalopathy

absorption of fat soluble vitamins (Vit. K)

synthesis of clotting factors bleeding

synthesis of plasma proteins (albumin)

malnutrition & edema

 Diagnostic Tests non-invasive
Non invasive LFTs
Enzymes
Proteins ALP, LDH, GGT, AST, ALT
Prothrombin time serum & urinary bilirubin
CBC serum albumin & proteins
Prothrombin time
platelet count
 Diagnostic Tests - Invasive
Liver Bx Nursing role

Angiograms
Hepatitis
H e p a t it is A H e p a t it is B H e p a t it is C
HAV HBV HCV
n o n -A , n o n -B

o r a l-f e c a l b lo o d tr a n s f u s io n p r i m a r ily b lo o d
c o n ta m in a t e d IV d r u g a b u s e IV d r u g e x p o s u r e
fo o d o r w a te r * s e x u a l c o n ta c t s e x u a l c o n t a c t ( lo w )
h e m o d ia ly s is , H C W

1 5 -5 0 d a ys 4 8 -1 8 0 d a ys 1 4 -1 8 0 d a ys
(3 w e e k s ) (1 0 0 d a y s )
c o m m u n ic a b le
1 -2 w k s p s y m p to m s

f e v e r , f a tig u e , c h r o n ic c h r o n ic p r o g r e s s iv e
n a u s e a , d ia r r h e a , S j o g r e n 's
a n o r e x ia , ja u n d ic e c a r d io - r e n a l
R U Q p a in ly m p h o m a
 You are the home care nurse evaluating a
45 year-old RN after her discharge from
the hospital for acute liver failure.

Previous history includes:

working in a munitions factory;
OSHA compliance officer monitoring chemical regs;
auto accident (age 16) with multiple transfusions;
Frequent socializing with alcohol intake
Frequent intake of shell fish

What are her risk factors for Hep. A, B, C ?

 Case Situation (continued)
Clinical manifestations include:
Mild confusion
Jaundice
Pruritis
Chronic fatigue

What is the pathophysiological cause of each

of her clinical manifestations?
 Pathophysiology of Hepatitis
Liver damage
Inflammation
Cellular degeneration
Impaired function
Cellular necrosis
Interruption of bile flow
Stone development
 Clinical manifestations-similar

Preicteric
Non-
specific
Icteric
Altered
bilirubin
RUQ pain excretion Posticteric
Anemia Fatigue
Relapses
Jaundice
Bruising/bleeding
 Diagnosis of Hepatitis
Viral specific serological
markers (Surface antigens)
Current infection

Carrier state
Antibodies
Current or recent

infection
IgM = acute infection Carrier state

IgG = past exposure

probable
immunity
 Diagnosis of Hepatitis lab
findings
Laboratory tests
ALP, LDH, GGT, AST,
ALT
liver damage or
serum & urinary
altered function
bilirubin
serum albumin &
proteins
Prothrombin time
platelet count
 Prevention !
t in g
r ic as h
Eliminate exposure St w
n d
Fecal/oral routes h a
Contact with infected
blood or body fluids
Safer sexual contact
Vaccines
Mother/newborn
A
exposure B
C (unavailable)
D (protected by
Hep B vaccine)
 Nursing Diagnoses
Activity Intolerance Physical & emotional rest
Fatigue
Altered Nutrition fat w/ vit. Supp.
Protein may be restricted
Risk for infection r/t exposure
immune function
invasive procedures
Risk for transmission
Ineffective health
Patient & family
maintenance education
 Drug Therapy
Hepatotoxic drugs Alpha interferon

Ribavirin

Immune globulin

Vaccines
Flu-like symptoms for HCV patients on
interferon
Take medication at night
 Complications of Hepatitis
HAV & HBV Chronic active
(mild/mod./severe) hepatitis
Most acute cases may progress to cirrhosis
resolve without
complications Chronic persistent
(minimal/mild) hepatitis has a
delayed convalescent period

Fulminant hepatitis is a
complication of HBV that leads
to liver failure
 Cirrhosis

Diffuse fibrotic bands of

connective tissue in
response to
inflammation

Distorts normal
architecture and
function
 Cirrhosis of the Liver
Pathophysiology
Degeneration Regeneration attempts
Destruction Nodule (scar) formation
Necrosis

Compression of vascular Fibrous tissue

system & lymphatic proliferation in
bile duct channels a disorganized
pattern

Poor cellular
Altered flow
nutrition
Hepatocellular
hypoxia
 Cirrhosis - 4 Types
Alcoholic (Laennecs) Post necrotic - Massive
Long term ETOH hepatic cell necrosis
abuse Post viral hepatitis
Toxic exposure
Autoimmune process

Biliary Cardiac
Chronic biliary obstruction Severe RHF
Bile stasis Corpulmonale
Inflammation Constrictive pericarditis
Tricuspid insufficiency
 Clinical Manifestations
Early
GI disturbances
anorexia Altered metabolism of
Dyspepsia fats, CHO, proteins
Flatulence
Nausea & vomiting
bowel habits
Swelling/stretching
Abdominal pain
of liver capsule
Dull, heavy
RUQ or epigastrium
Spasm of biliary
ducts
Intermittent vascular
Additional CMs
Early
Fever
Lassitude
Slight weight loss
Hepatosplenomeg
aly
Palpable liver
 Clinical Manifestations
Later
Skin Lesions
Jaundice

Hematologic Problems Endocrine Disturbances

Peripheral Neuropathy
 Diagnosis
Liver function Invasive studies
studies liver biopsy
enzymes angiograms
proteins
cholesterol
prothrombin time
Liver may be
contracted or
enlarged
 Normal Bilirubin Excretion
Breakdown of hgb Lab tests:
bilirubin (non Indirect = unconjugated, BU
water-soluble). or pre-hepatic
Carried by albumin to Direct = conjugated, BC or
the liver for post-hepatic
conjugation where it Urobilinogen is the
is made water- breakdown of conjugated
soluble. bilirubin that is excreted in
the urine (small amount)
and feces (most).
 Bilirubin
Unconjugated Congugated
indirect bilirubin direct bilirubin-
Overproduction d/t impaired excretion of
Hemolysis bilirubin from liver d/t
Impaired hepatic hepatocellular disease
intake d/t certain Drugs
drugs Sepsis
Impaired Hereditary disorders
conjugation by Extra-hepatic biliary
glucoronide obstruction
 RBC bilirubin Unconjugated
Break Joins with
down albumin In blood
stream to
liver

To intestine Liver - bilirubin

in bile releases from
Intestine -
albumin, combines
bilirubin
with glucuronic acid
converted to
Excreted in (conjugation)
urobilinogen
stool
Small amount
Conjugated
Excreted
enters circulation
via kidneys
 Lab Test Abnormalities
Cirrhosis
ALP, LDH, GGT, AST, ALT
indicate liver damage or
altered function
serum bilirubin
urinary bilirubin

PT
platelet count

serum albumin & proteins

 Jaundice

Inability of liver to
conjugate bilirubin

Bilirubin- bile pigment from

breakdown of Hb from
RBCs by macrophages
Skin & sclera jaundice
Excreted in urine tea
colored urine
Blocked from flow into
intestines clay colored
stools
Hyperbilirubinemia
>1.2mg/dl
What changes do you see and
why?
Skin & Sclera

Jaundice Urine

Tea colored

Stool

Clay colored
 Skin Lesions
Spider angiomas
Small, dilated blood
vessels with red
center and spider In circulating
like branches estrogen d/t ability
of liver to metabolize
Palmar erythema steroids
Reddened palms
that blanch with
pressure
 Hematologic Problems
Thrombocytopenia d/t splenomegaly
back up of blood from
Leukopenia
portal vein into spleen
Anemia Overactivity of enlarged

spleen - removal of blood

cells from circulation
d/t livers inability to produce
Prothrombin and other clotting
Coagulation defects factors
d/t synthesis of bile fats
absorption of fat soluble vits
Without Vit. K, clotting factor
production
 Endocrine Problems
Gynecomastia
Loss of axillary/pubic hair
Testicular atrophy
libido/impotence

hyperaldosteronism Na
H20

K
 Peripheral Neuropathy
Mixed form
Sensory
predominant

Dietary of
Thiamine
Folic acid
Cobalamin Vit. B 12
Complications of Cirrhosis
Portal Hypertension Hepatic
Esophageal Varices Encephalopathy

Ascites Hepatorenal
Peripheral Edema Syndrome
 Portal Hypertension &
Esophageal Varices
Compression & destruction
Obstruction of normal
Portal veins
flow through portal
Hepatic veins
sinusoids
system portal
hypertension

Collateral circulation Collateral circulation

develops primarily in develops to
Portal pressure
Lower esophagus Plasma volume
Anterior abdominal wall Lymphatic flow
Rectum
Parietal peritoneum
 Varices

C o lla t e r a l C ir c u la t io n
d /t p o r ta l h y p e r te n s io n

Low er E sophagus A b d o m in a l W a ll R e c tu m

E s o p h a g e a l V a r ic e s C aput M edusae H e m o r r h o id s
 Esophageal Varices
risk for bleeding

Fragile, inelastic, thin- Chemical irritants

walled esophageal Alcohol
veins become Medications
distended or irritated Refluxed gastric acid
leading to rupture

Mechanical trauma
esophageal pressure Poorly chewed, coarse food
Vigorous exercise, heavy lifting Vomiting
Coughing, sneezing N/G insertion
Retching/vomiting
Straining at stool
Esophageal Varices
Medical Management
Prevent
initial Manage
hemorrhag acute
e hemorrha
ge

Prevent
recurrent
hemorrhag
e
 Prevent initial hemorrhage
Pharmacological Mgt.
-blockers
portal pressure by
splanchic blood flow
flow in collateral channels
Stool softeners Dietary Modifications
alcohol
H-2 blockers, PPIs
caffeine
spicy foods
coarse foods
 Manage acute hemorrhage
Pharmacological Mgt.
65-75% of cirrhotic Vasopressin/NTP
patients develop Octreotide
esophageal varices.
Ruptured varices have Endoscopic injection
a 30-60% mortality rate sclerotherapy

Supportive
Rx Balloon tamponade
FFP, RBCs Sengstaken-Blakemore
Vit. K Minnesota
H2 blockers Black-
Neomycin 1156
 Nursing Management
Impaired Gas Exchange r/t O2 exchange 2
Aspiration pneumonitis occurring after balloon Airway
obstruction tamponade with Sengstaken- Blakemore tube

Aspiration Pneumonia
Assure suction port
Suction frequently
Nares Erosion
Clean, lubricate external nares
Pad if necessary
Airway Obstruction
 Prevent recurrent hemorrhage
Shunts
portal pressure

divert flow away from

collateral channels
send portal venous
Complications
blood directly to IVC Hepatic
bypassing liver encephalopathy
Heart Failure

Bacteremia

Shunt Clotting
Shunts Black-
1158
 Shunts Post op Priority
Potential complication:
Shunt clotting

Assessment:
pain
distention
nausea
 Shunts Post op Priority
Fluid Volume r/t retention of fluids 2
Portal hypertension
Liver failure Outcomes: normovolemia:
Hemodilution r/t new shunt Stable or abd. Girth

Regular resp. rate/rhythm

Unlabored breathing
Interventions: Assess Output intake
Abd girth, Weight, I/O
Edema
Pulm. Ed.: dyspnea,
orthopnea
 Shunts post-op complications
Hepatic Post-op hemorrhage
encephalopathy Hb, Hct, Pro-times
NH3
Bilirubin Other labs
Liver enzymes Renal BUN
Heart failure Electrolytes
Shunt pre-load Serum Proteins

Transfusions
Vit. K
TPN
Albumin IV
 Ascites
Pathophysiology/Interventions
PRO leak through liver capsule to
peritoneal cavity oncotic pressure
of PRO pulls more fluid

albuminemia d/t livers inability to

synthesize PRO colloidal osmotic Fowlers Position
pressure
Pro, Na diet
aldosteronism d/t livers inability to mouth care/
metabolize aldosterone Na dehydration
reabsorption serum osmolarity
K-sparing diuretics
ADH secretion water retention
Paracentesis
Salt Poor Albumin
Ascites and Peripheral Edema
Portal hypertension
protein & plasma leak into the

peritoneum
osmotic pressure pulls more fluid in

Hypoalbuminemia
Hyperaldosteronism
 Therapeutic Goals & Outcomes
metabolic demand on the
liver
Treat complications

Balanced fluid volume

Absence of breathing
problems
Corrected coagulation defects
Absence of infection
Adequate nutritional intake
 Portal Systemic Encephalopathy
Hepatic Encephalopathy
Build up of NH3 in serum and
CSF neurotoxicity
Altered LOC
Impaired thinking
Neuromuscular disturbance
Early Sign: Change in hand
writing

Neomycin
Lactulose
 Hepatorenal Syndrome
CMs & Pathophysiology
Azotemia ( BUN, creatinine)
Sudden oliguria
Intractable ascites

Redistribution of blood flow from

kidneys to peripheral & splachnic
Hypovolemia d/t ascites
Intrarenal imbalance of
vasoconstriction & vasodilating
mechanisms d/t Liver disease
Hepatorenal Syndrome
Risks & management
Precipitants
Overly vigorous Diuretics
GI/Vericeal hemorrhage
Paracentesis
Hepatic encephalopathy
NSAIDs
Sepsis
Salt Poor Albumin
Na & H20 restriction
Diuretic therapy
 Alcohol Withdrawal Syndrome
(48-72 Hours after last Drink)
Facts Clinical
Hidden disease Manifestations
Potent CNS depressant
Tremor/shakiness
VS
Withdrawal awakens SNS Diaphoresis
Untreated or undertreated Agitation, Anxiety
ETOH withdrawal
mortality and morbidity GI
Delirium-Tremens (DTs) Confusion
can be a life-threatening Sleep disturbance
medical condition Hallucinations
Seizures
Alcohol Withdrawl - Goals
patient discomfort
dangerous cms
Prevent complications
Prepare patient for rehabilitation

Admission assessment
Frequent monitoring
Prompt & adequate
treatment
Benzodiazepines
The Biliary Tract

Gallbladder Hepatic Duct

Common
bile duct
Cystic duct
 Function of the Gallbladder
Concentration and
storage of bile
produced by the
liver
Bile release
stimulated by
presence of food in
GI tract
 Disorders of the Gallbladder

Cholelithiasis
cholesterol, bile and
calcium stone
formation

Cholecystitis
inflammation and/or
obstruction

stones
bacterial
 Clinical Manifestations
Indigestion & fat
intolerance
steatorrhea (fatty stools)
Moderate to severe
pain
referred to right shoulder
and scapula
temperature,
biliary colic, RUQ
WBCs
tenderness jaundice
Nausea and vomiting dark urine
clay-colored stools
pruritis
bleeding tendencies
 Diagnosis
History
Ultrasound
Oral cholecystograms
Percutaneous transhepatic cholangiography
Endoscopic retrograde
cholangiopancreatography (ERCP)
Lab studies
elevated direct and indirect bilirubin
elevated AST (aspartate aminotransferase) (SGOT)
Normal Bilirubin Excretion

Breakdown of hgb bilirubin (non water-

soluble). Carried by albumin to the liver for
conjugation where it is made water-soluble.

Lab tests:
Indirect = unconjugated, BU or pre-hepatic
Direct = conjugated, BC or post-hepatic
Urobilinogen is the breakdown of conjugated
bilirubin that is excreted in the urine (small
amount) and feces (most).
 Treatment
Cholecystitis (conservative)
pain control
anti-nausea meds
antibiotics
NG tube
Diet restrictions/ NPO
anticholinergics
Cholelithiasis
Fat soluble vitamins (A, D, E, K)
dissolve stones
endoscopic intervention
Extracorporeal
shockwave lithotripsy
(ESWL)
Surgical Intervention
Laparoscopic Surgery
preferred treatment
Open or incisional cholecystectomy
for more complicated cases
 Post-Operative Care
Laparoscopic Open or incisional
pain management pain management

meds mobility

Sims position C&DB
mobility wound care
C&DB T- tube monitoring
DC teaching DC teaching

activity & diet
activity & diet
 Care & Teaching: T-tube
Keep bag level w/abd
Prevent tension
Monitor output
Skin site care
Clamp 1-2 hr ac and
unclamp 1-2 hr pc
Unclamp if distress
Time: Approx. 10
days
References
Medical-Surgical Nursing, Clinical
Management for Positive Outcomes,
Black, J., Hawks, J., 8th Ed., 2009
Saunders
Pathophysiology, Copstead, L.,
Banasik, J., 3rd Ed., Elsevier
Mosbys Medical & Nursing
Dictionary 1983 Mosby Co., St. Louis