jcmendiola_Achievers2013

Care of Clients with Problems In Oxygenation,

Fluids and Electrolytes, Metabolism and Endocrine
(NCM103)
Patients With Hepatic, Biliary and Pancreatic Disroders

Accessory Organs
Anatomy and Physiology of the
Liver

What are the Functions of the Liver
1. Bile secretion / production
(Choleresis Synthesis)
600 1200 mL/day
Bile emulsifies the fat!

Enterohepatic Circulation
Recycling of bile salts
90% total bile salts
o Absorbed at the
distal ileum
o 18 times recycled












2. Bilirubin Metabolism
















4. Vascular and Hematologic Function
Store Blood
Kuppfer Cells
Prothrombin, Fibrinogen, Factors I, II, VII, IX, and X Synthesis
Topics Discussed Here Are:
1. Anatomy and Physiology of:
a. Liver
b. Biliary Tract
c. Pancreas
2. Assessment of the Liver
3. Alterations in the Gall Bladder
a. Cholelithiasis
b. Cholecystitis
c. Choledocholithiasis
4. Alterations in the Pancreas
a. Pancreatitis
b. Chronic Pancreatitis
5. Alterations in the Liver
a. Hepatitis
b. Liver Cirrhosis
6. Complications of Liver Cirrhosis
a. Portal Hypertension
b. Esophageal Varices
c. Ascites
d. Hepatic Encephalopathy
7. Liver Transplantation
LOOKY
HERE
Hepatic Artery
o Amount of blood receives 300 500 mL/min
of O
2
blood from the heart
Hepatic Vein
o Excretes deoxygenated blood but is FULL of
nutrients (1,000 1500 mL/min)
o Kuppfer Cells Immunity, destroys
microorganisms
Bile Duct Pathway of bile
Portal Circulation All blood coming from
spleen and intestines and others drain to the liver
Hepatic
Secretions
Intestinal
absorption
Hepatic
resection



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Vitamin K Absorption
Synthesis of Vitamin K Stimulates production of clotting factors
Microorganisms make VITAMIN K
Vit. K is a FAT SOLUBLE vitamin

5.
Fat Metabolism



Protein Metabolism



Function:
- Protein Metabolism






NH4 GIVES BRAIN PROBLEMS

Liver Plasma Protein

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6. Protein Metabolism



7. Storage of Iron and Vitamin



8. Metabolism Detoxification



9. Metabolic Detoxification



BILIARY TRACT
1. Common Bile Duct (CBD)
+ Composed of cystic and hepatic duct, leads to duodenum
+ Function: Transports bile to duodenum when food is present in small intestine
2. Cystic Duct
+ From gallbladder to the Common Bile Duct
+ Function: Passageway for bile to the gall bladder
3. Gall Bladder
+ Sac like organ located under the right side of the liver
+ Function: Storage and concentration of bile
+ Stimulated to contract by cholecystokinin and motilin

PANCREAS
Exocrine:
o Gland located behind stomach on left side of abdomen
o Pancreatic Enzymes:
Amylase Breaks down Carbohydrates (N: 27 131 u/L)
Lipase Breaks down Fats (N: 20 180 u/L)
Trypsin Breaks down Protein
MAJOR PROTEOLYTIC ENZYME
Secretin:
o Secretin Secretes alkaline fluid
o Inhibits action of gastrin Gastric acid secretion and motility



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Cholecystokinin and Acetyl CoA
C and A Acinar Cells Enzyme Release
Feedback mechanism inhibits secretions of more pancreatic enzymes

Assessment of Liver Disease
Assess
Hepatotoxic Substances / Infectious Agents
Occupational, recreational and travel history
History of alcohol and drug use
Evaluation of the past medical history
Signs and symptoms that suggest liver disease

Technique for palpating the liver
Place one hand under the right lower rib cage and press downward

Abdominal Assessment:
Murphys Sign
o Painful deep breathing during liver palpation
o Client is unable to complete the inspiration; abruptly stops inspiration midway
o Sharp Pain caused by inflamed liver / gall bladder (Cholecystitis) onto examiners hand

Percussing the Liver
Identify upper border (Start at midclavicular line and lower border) Start at right lower
quadrant




Specific maneuver for assessing ASCITES
o FLUID WAVE TEST

Measuring Abdominal Girth
Consistent Landmark Umbilical Area
Consistent Position (Standing preferred)
Consistent Tape Measure
Consistent Time of Day
Post void and Before breakfast

Laboratory Test
Bile Formation and Secretion
Test Normal Value
1. Direct (Conjugated Bilirubin) 0 0.3 mg/dL
2. Indirect (Unconjugated Bilirubin) 0 1 mg/dL
3. Total Serum Bilirubin 0.1 1.2 mg/dL

Test Normal Value
1. Total Serum Protein 7.0 7.5 g/dL
2. Serum Albumin 3.5 5.5 g/dL
3. Serum Globulin 2.5 3.5 g/dL
RESONANT ABOVE
8 cm DULLNESS
RESONANT BELOW

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4. A/G Ratio 1.5:4 to 2.5:1
Coagulation Studies
Test Normal Value
1. Prothrombin Time 11.5 14 seconds
2. Partial Thromboplastin Time 25 40 seconds

Test Normal Value
1. AST (SGPT) 8 20 u/L
2. ALT (SGOT) 10 35 u/L
3. Alkaline Phosphatase 32 92 u/L
4. LDH LDH
5. Blood ammonium 150 250 mg/dL

Diagnostic Tests
1. Abdominal X-Ray To visualize solid / liquid part
2. Liver Scan
To outline the liver, location (tenderness/mass)
To detect a tumor
Detects possible scarring (Previous inflammation)
Put patient on NPO (4 6 hours)
Insertion of a dye
3. Splenoportogram
To detect pressure on spleen and portal pressure
To know if organs / structures compensate through collateral circulation
5. Endoscopic Retrograde
Cholangiopancreatography
PostOp!
Put patient on NPO (2 3 hours) after procedure
Assess gag reflex
Vital Signs Monitoring!
Alterations in BP?
Bleeding by irritation, dry mucosal lining
Endoscopic Retrograde is used to visualize the hepatobiliary tract
6. MRI
REMOVE magnetic objects!
Assess claustrophobia
Ultrasound:
CHEAPER
7. CT Scan
8. Percutaneous Liver Biopsy
To collect tissue of liver
To know if malignant / benign
Right hypochondriac

BEFORE DURING AFTER
1. Test 1. Expose Right Hypochondriac 1. Position
2. Consent 2. Inhale-exhale THEN HOLD BREATHE
AT THE END OF EXPIRATION!
2. NO COUGHING / STRAINING
3. NPO 3. Vital Signs
4. Vital Signs
Large bore needle
4. No heavy lifting

JAUNDICE
Yellow-Greenish Yellow discoloration of sclera, skin and degenerative tissue
PreOp!
Assess for allergies to iodine
Ask consent (Good for 24 hrs)

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Types
1. Hemolytic Jaundice (Pre-Hepatic)
o Causes:
Blood Transfusions, immune reactions, membrane defects
of erythrocytes, toxic substances in circulation
o Problem is in the BLOOD, not the liver!
2. Hepatocellular Jaundice (Intrahepatic)

3. Obstructive Jaundice (Posthepatic)


Clinical Manifestations
Yellow Sclera
Yellow-orange Skin
Clay colored feces
Tea-colored urine
Pruritus Bile salts in skin
Fatigue
Anorexia

Medical Management
1. Determine cause of jaundice
a. Health History
b. Physical Examination
c. Liver Function Test
d. Hematologic Test
2. Reduce pruritus and maintenance of skin integrity
a. Oral cholestyramine-resin
b. Antihistamine and phenobarbital

Nursing Management
1. Assess:
Assess for any signs of jaundice formation
2. Nursing Diagnosis
Impaired skin integrity
i. Tepid water / emollient bath
ii. Frequent application of lotion
iii. Loose and soft clothing
iv. Soft bed linen (e.g. Cotton)
v. Keep the room cool
Alteration in body image
i. Encourage verbalization of feelings
ii. Assist in perineal hygiene as needed


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iii. Promote activity as tolerated

SURGICAL MANAGEMENT:
- Cholechostomy: Exploration of the CBD

Alterations of the Liver
Biliary Tract and Exocrine Pancreas

CHOLETHIASIS
1) Formation of STONES on gallbladder
2) 10 20% of men are affected
3) 20 40% on women

4 Fs Of Gallbladder Disease~
F Female
F Fat
F Forty
F Fertile (Have children)

GALLSTONES
Are crystalline structures formed by concentrated (Hardening) or accretion (adherence) of
particles, accumulation of normal or abnormal bile constituents

Theories of Gallstone Formation:
1. Bile Change in composition
2. Gall Bladder Stasis Bile stasis
3. Infection predisposes a person to stone formation
4. Genetics and demography

There are Three Types of Gallstones!~
Cholesterol
1. Most common type
2. Usually smooth and whitish, yellow
Pigment
1. Bile contains excess unconjugated bilirubin.
2. Blade / earthly calcium bilirubinate
Mixed Combination Minor Constituents
1. Calcium Carbonate, bile salts and palmitate

GALLSTONE FORMATION
Causes:
1. Too much absorption of water from bile
2. Too much absorption of the bile ducts from bile
3. Too much cholesterol in bile
4. Inflammation of the epithelium
Course Followed by Bile:
1. During rest
2. During Digestion (3 4 hours after meal)


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Unconjugated
bile precipitate
Pathophysiology of Gall Stone Formation
Formation of
pigmented
stones
Malabsorption
disorder
Malabsorption
of bile salts
Bile synthesis
Estrogen
therapy
Pregnancy
Gallbladder
sludge
Obesity
increase with
age
Hepatic
secretion of
cholesterol
Supersaturation of Bile with Cholesterol
Rapid weight
loss
Liver excrete
extra cholesterol
Clofibrate
medications
Serum
cholesterol level
Cholesterol excretion into the bile
Cholesterol
saturate gallstone
CHOLECYSTITIS
Irritate
gallbladder lining
Ultrasound
Cholecystography
ERCP
Obstruction of the passage for Bile
Abdominal Guarding
Facial Grimacing
After meal
Contraction of
the gall bladder
RUQ pain,
referred to the
back shoulders
Vagal
stimulation
N/V
Gallbladder distention
and inflammation
Marked tenderness in
the RUQ on deep
inspiration
Prevents full
inspiration and
excursion
Bile in the
duodenum
Malabsorption of
Vitamins ADEK
Signs and
Symptoms
Bile retention
in the gall
bladder
Bile absorbed in
the circulation
JAUNDICE!
Bile salts in
the skin
Continuous bile retention in the gall bladder
Abscess, necrosis, perforation
Seeping into the peritoneal cavity
Peritonitis!
Pruritus
GIT
Kidney
Clay-colored
feces, very
dark urine,
tea colored

Assessment:
1. Biliary Colic Pain
Abrupt
In intensity for 30 minutes 1 hour
RUQ / Epigastric area, referred to the back, right shoulder and the right scapula / the
mid-scapular region
Pain occurs 3 6 hours AFTER HEAVY MEAL / when the client LIES down
2. Anorexia & N/V Stimulation of the VAGUS NERVE

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3. Intolerance to FATTY FOODS, sensation of FULLNESS
4. Jaundice, bleeding, tenderness and Steatorrhea, clay colored stool

Diagnostic Tests
1. Ultrasound
Most sensitive test to detect and visualize stone
I: Obstruction, jaundice, allergies to contrast media
2. ERCP (Endoscopic Retrograde Cholangiopancreatography)
Direct visualization of hepatobiliary system, performed via a flexible endoscope
Multiple positions are required during procedures to pass the endoscope
3. MRI
To detect neoplasms; diagnose cysts, abscesses and hematomas
4. PTC (Percutaneous Transhepatic Cholangiography)
Injection of a dye to the biliary tract
Hepatic duct within the liver, CBD (Common Bile Duct), cystic duct and gallbladder
are outlined clearly
5. Cholecystography
I: Detects gallstones and assess the ability of the gallbladder to fill, concentrate its
contents, contract and empty
E.g. Contrast agent: Iopanoic Acid

Nursing Diagnoses:
- Alteration in comfort: pain related to gallbladder spasms
- Alteration in fluid and electrolyte balance related to vomiting

Health Promotion
- Fat diet
- Ideal Body Weight (IBW)
- Limit number of pregnancies
- TPN for 1 month (Monitor closely!)
- Physical activity

Nursing Management
- Pain measures: Verbalization of feelings, Diversional activities
- Comfort measures
- Diet modifications
- Weight loss
- Intravenous fluid
- ** for signs of dehydration

Medical Management
1. Medications
Analgesics
Antacids, H
2
Blockers, Proton Pump Inhibitor (PPI)
Antiemetics
Antibodies
Nitroglycerin
2. Fluid & Electrolyte Balance
IV Fluid
NPO

Management
Gallstone Dissolution
Cholesterol Dissolving Agents (May have recurrence after 3 5 years)

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Chenodeoxycholic Acid (CDCA) / Chenodiol 7 mg/kg
Ursodeoxycholic Acid (UDCA) / Ursodiol 8 10 mg/kg [6 12 months]
Mechanism of Action: Cholesterol synthesis in the bile

NON-SURGICAL MANAGEMENT
1) Through Endoscopy


2) ESWL (Extracorporeal Shockwave Lithotripsy)
Symptomatic cholelithiasis with less than 4 stones
Stone < 3cm diameter
No history of liver / pancreatic disease Or bile duct disease
CI:
1. Recent acute cholecystitis
2. Cholangitis
3. Pancreatitis
Position:
Stones in Gall Bladder = PRONE
Stones in CBD = SUPINE

SURGICAL MANAGEMENT
PreOp!
1. Consent
2. NPO BEFORE MIDNIGHT
3. Skin preparation
4. Enema
5. Antibiotic

Laparoscopic Cholecystectomy
I: Symptomatic gallbladder disease, acute cholecystitis
Advantage: Minimal trauma to abdomen
CI: Choledocholitiasis

How is It DONE?
- Operational port; dissector**
- Laparoscope to visualize
- Dissecto**
- Retractor
- USES Pneumoperitoneum to dilate
- USES General Anesthesia!

Laparoscopic VS Open Cholecystography
Complications
Pneumonia / Atelactasis
Deep Vein Thrombosis (DVT)
Pulmonary Embolism
Biliary Tract Injury
Hemorrhage
PostOp!
- DBE
- Coughing
exercises

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Open Cholecystectomy
Consists of excising the gall bladder from the posterior liver wall and ligating the
cystic duct, vein and artery
Complications
Hemorrhage
Pneumonia
Thrombophlebitis
Urinary retention
Bile leakage to abdominal cavity

NURSING MANAGEMENT OF SURGICAL PATIENTS
PostOp!
1. Monitor respiratory status
2. Monitor drainage from biliary tubes and incision site
3. Analgesia
4. Maintain fluid balance and hydration
5. Prevent infection
6. Maintain NGT (Assess Bowel SOUNDS q4 hours)
7. Assess CVD Status and manifestations of Shock/Hemorrhage

Signs of Bile Leakage
- Pain and tenderness (P&T) in the RUQ
- Abdominal Girth
- Tachycardia
- Bile / Blood leaking from wound
- BP Drops!

T-Tube
- After Cholecystectomy
On level with the bed (Bile bag)
- ONE HOUR BEFORE and AFTER EATING (CLAMP)!
- Normal amount of bile after surgery
1
st
Day: 300 500 mL of bile
Maintenance: 1 2 weeks or 10 days
8
th
Day RETURN for CHOLANGIOGRAM to know if there is
presence of obstruction
- Nursing Responsibility for Patients with T-Tube
_ Semi-fowlers
_ Characteristics of drainage
_ Report sudden increase in bile output
_ Monitor for inflammation and protect skin from irritation
As prescribed, clamp tube BEFORE a meal
and observe for abdominal discomfort and
distention, nausea, chills / fever
Unclamp tube if N/V OCCURS!
Patient can go back to work after 4 6 weeks
Avoid lifting HEAVY OBJECTS

Cholecystitis
Inflammation of the gall bladder
Types:
Acute inflammation = Inflammation without the presence of a stone
Chronic Cholecystitis
- Instruct that client can go home after 3 4
days
- Client must gradually increase their FAT
intake
- After the procedure, client MUST void after
6 hours! (Assess BLADDER if not voided)
- Clay Colored Stool = NO BILE!
- Obstruction = Many**Removed
- If excess of more than 800 mL,
patient can DRINK the BILE with
JUICE / NGT
- Check for FOUL odor and purulent
drainage
- NO TENSION ON TUBINGS!

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Acalculous Cholecystitis

Pathophysiology
Acute Calculous Cholecystitis
Risk / Predisposing Factors:
- 4 Fs of Gall bladder disease
- Sedentary Lifestyle!
- Ethnic groups (Chinese, Jewish, Italian)

Complications:
- Perforation
- Pericholecystitis abscess
- Fistula Abnormal opening from an organ due to chronic inflammation

Acalculous Cholecystitis
Cause / Predisposing Factors:
- Multiple Blood transfusions
- Gram Negative bacterial sepsis
- Tissue damage after burns, trauma / surgery\
- Hyperalimentation
- Prolonged fasting
- Anesthesia and opioid analgesic
- Mechanical Ventilator with PEEP
- Patients with DM and systemic arthritis
_ Chance of perforation

Assessment
- Pain and tenderness in the RUQ radiating to scapula after eating fatty foods and may
persist4 6 hours
_ Acute:
Last several days
Pain located in Epigastric, subscapula RUQ region or at times at right
scapula
Pain starts suddenly, increase steady and peak in about 30 minutes
- + Murphys Sign
- N/V
- Fever
- Mild Jaundice
- Guarding rigidity and rebound tenderness
- Tachycardia
- Signs of dehydration
_ Chronic Cholecystitis :
Temperature is not as high
Leukocyte count is LOWER
Less severe pain
Temperature is not
Low Leukocyte count
Vague manifestations of indigestion, Epigastric pain, fat intolerance
and heart burn
Diagnostic Findings: Cholelithiasis, gallbladder wall thickening (3 cm)
and delayed visualization / non visualization of gall bladder

Nursing Diagnosis
Alteration in comfort: Pain related to disturbance of the gall bladder
Alteration in body temperature: Hyperthermia

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Medical Management
1. Antibiotics
2. Cholecystoctomy = Gall bladder must be decompressed
3. Cholecystostomy
a. Surgical drainage of gall bladder
b. FIRST PROCEDURE BEFORE CHOLECYSTOCTOMY

Nursing Management
Diet (Same with Cholelithiasis [ Calories, Protein])
Antibiotics, analgesics, and anti spasmodic as ordered
For chronic: Small, low fat meals
NPO Status during N/V status
Maintenance of Nasogastric decompression
Monitor for Complications

Choledocholithiasis
Stone formation on CBD
Etiology: Same with Cholelithiasis and narrowing of papilla
: Stone pass from gall bladder and lodges in the CBD

Assessment
- Frequency, mild / severe RUQ pain
- Intermittent / progressive jaundice (Clay colored feces, tea colored urine)
- Chills and Fever

Surgical Management
- Cholecystectomy
- PreOp!: ERCP with Endoscopic papillotomy and stone extraction followed by
laparoscopic Cholecystectomy
- Choledocholithotomy = Drainage of CBD
- Cholecystectomy = Drainage for stain

Alterations in the Pancreas
Pancreatitis
Inflammation of the pancreas
Associated with escape of pancreatic enzymes into surgical tissue
Classification:
Acute Pancreatitis
Chronic Pancreatitis

Acute Pancreatitis
- Acute inflammatory process of the pancreas resulting in autodigestion of the pancreas by its own
enzymes
- Etiology and Risk Factors
4 Alcohol ABUSE! (Men)
4 Biliary Tact Disease (Women) Theres a BACKFLOW
4 Gall bladder Disease (Cholelithiasis) Spasms
- Less Common Cause
4 Trauma (Post-surgical abdomen)
4 Viral infection
4 Penetration duodenal ulcers
NOTES:
If activated in the pancreas, causes
damage
ALCOHOL ACTIVATES PANREATIC
ENZYMES!
Amylase Drug or Lipase for therapy
Alcohol Physiochemical Change

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4 Cysts and abscesses
4 Metabolic disorders (Renal failure, hyperthyroidism, hyperlipidemia)
4 Vascular disease
4 Drugs













































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Leakage to
peritoneal cavity
Board-like abdomen
Cullens Sign
Turners Sign
Decreased Bowel Sounds
Exudate with
pancreatic enzymes
form peritoneal cavity
to pleural cavity via
transdiaphragmatic
lymphatic channels
Atelectasis, Pneumonia
Hypovolemia
Hypertension
Cyanosis
Cold Clammy Skin!
Destruction of
pancreatic islet
Hyperglycemia



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Assessment
1. Pain
a. Abdominal pain
b. Includes sudden onset of mid Epigastric / LUQ radiating at the back
c. Aggravated by a fatty meal, alcohol, or supine position
2. Abdominal tenderness and guarding
3. N/V
4. Weight loss
5. Cullens Signs = Discoloration of abdomen and Periumbilical area
6. Turners Sign = Bluish discoloration of the left flank
7. Bowel Sounds
8. WBC, Glucose, Bilirubin, Alkaline Phosphatase Bone Problems, either CVD
obstruction
9. Serum lipase and amylase, urine amylase

Diagnostic Tests
1. History and Physical Examination
2. ERCP
3. CT Scan
4. Abdominal X-Ray
5. Lab Work Up:
Serum Ca
Serum Amylase and Lipase
BUN
Glucose
Bilirubin
Alkaline Phosphatase

Nursing Diagnosis
- Alteration in comfort: Pain related to inflammation of the pancreas and surrounding
tissue
- Imbalance nutrition: less than body requirements related to inability to ***

Medical Management
- Pain medications
- Fluid volume status and electrolyte imbalance
- Nutritional status
- Exocrine functions
- Treat complication

Surgical Management
1. Laparotomy with support drainage
2. Debridement with surgical / retroperitoneal drainage
3. Subtotal pancreatectomy
4. Whipples Surgical procedure (Pancreaticoduodenectomy)

Nursing Management
- No Alcohol!
4 Bed rest
4 Position = Semi fowlers / High fowlers
- NPO and Hydration, NGT suction (To remove gastric contractions), TPN
- Supplemental preparations

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- Pain medications, antacids, H2 receptor antagonist, and anticholinergics

Chronic Pancreatitis
- Continuous prolonged inflammation and fibrosis process of the pancreas
- Fibrin of scar tissue

Etiology:
- Alcohol (70 80% of case)
- Idiopathic (25%)
- Hereditary
- Biliary obstruction of pancreatic duct and by stores)
4 Recurrent and chronic inflammation

Pathophysiology












Types:
1. Chronic Obstructive Pancreatitis
2. Chronic Calcification Pancreatitis

Calcium Induced Pancreatitis
- Most common form
- Inflammation and sclerosis maintaining at head of pancreas and pancreatic duct


Assessment
1. Abdominal Pancreatitis
Continuous intermittent / absent
Gnawing feeling / **** cramp like
Not relieved with food / antacids
Patient experience more pain in supine
Attack lasts a few days 2 weeks
2. Weight loss and malnutrition
3. Hyperglycemia, DM manifestations
4. Abdominal distention with flatus and cramps
5. Steatorrhea

Diagnostic Tests
- ERCP
- Imaging Studies: CT, MRCP, Transabdominal ultrasound


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- Secretin Stimulation Test
- Lab Study: Serum amylase, lipase bilirubin

Medical Management
1. Medications
Pancreatic enzymes rep (Pancreatic Cotazym)
Non-opioid to opioid analgesics
Antibiotics
Antacids
H
2
: Ranitidine (Zantac)
PPI
CAI: Acetazolamide
Antispasmodic Dicyclomine (Bentyl)
Antiemetic
Antipyretic
2. Diet
3. Control DM
4. Bile salts

Surgical Management
- Whipples
- Total pancreatectomy
- Chole**
- Total Pancreatectomy with S placing
- Biliary Stents (Cotton Leung Stent)
- Percussing celiac plexus nerve block




Hepatic Alterations
Hepatitis
Inflammation of the liver caused by a virus, bacteria or exposure to medications or hepatotoxins
Goal of Therapy: Rest the inflamed liver (3 4 months regeneration)

Types
1. Alcoholic Hepatitis
a. Male: SHOULD BE LESS THAN 80 mg to be SAFE
b. Female: SHOULD BE LESS THAN 40 mg to be SAFE


Clinical Manifestations
Anorexia, nausea
Abdominal pain
Splenomegaly Backing up of blood in the spleen
Hepatomegaly
Ascites (Accumulation of fluid in the peritoneal cavity)
Fever Inflamed liver
Encephalopathy
Jaundice

Nursing Management
- Medications
- Assessment
- NPO (3 7 days) cystic suction
- Physical movement and mental stimulation
- Position for comfort
- IV fluids replacement of electrolytes


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Diagnostic Tests
Labs: Anemia, Leukocytosis, Bilirubin
Biopsy: Fatty hepatic tissue (FATTY LIVER)

Nursing Management:
Vitamins, Carbohydrate diet
Administer folic acid ( metabolism), thiamine supplements
Steroids SAFEST DRUG OF CHOICE
Parenteral fluids
Liquid formula to increase caloric intake
NO ALCOHOL

2. Viral Hepatitis (P = Preventable, T = Treatable)
Hepatitis A Infectious hepatitis (P&T)
Hepatitis B Serum hepatitis (P)
Hepatitis C Non-A,B hepatitis, post transfusion (P&T)
Hepatitis D Delta agent hepatitis
Hepatitis E Enterically transmitted or epidemic Non-B hepatitis

Stages:
Pre-Icteric / Predominal Stage (No Jaundice Yet!)
2 weeks AFTER EXPOSURE and ENDS WITH APPEARANCE of
JAUNDICE
Manifestations:
Flu-like symptoms, fatigue, malaise, fever
Anorexia, N/V
Headache, muscle ache
Mildpain in the RUQ
in bilirubin and enzyme level
Icteric Stage (Illness Stage)
1 2 weekds after PRODROMAL PHASE
Lasts 2 6 WEEKS !
Manifestations :
Pre-icteric signs
Jaundice Liver is enlarged
Pruritus
Light colored stool = If conjugated bilirubin cannot flow on the liver
because of an obstruction
Brown-colored urine
Fever
Fatigue
Post-Icteric Stage (Recovery Phase)
Resolution of jaundice 6 8 weeks prior to exposure
Symptoms diminishes, but liver remains to be ENLARGED and TENDER
Liver function returns to normal 2 12 weeks prior onset of jaundice
Manifestations:
Energy levels
Pain subsides
Minimal to absent GI symptoms
Serum bilirubin and enzyme levels return to normal

Medical Management:
1. Reduce fatigue
2. Maintain nutritional fluid balance: Calorie / CHO, Fat, NO ALCOHOL [2,500 3000 kcal/day]

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3. Bile acid sequestrants (To DILUTE the cholesterol bile containing acid)
a. Cholestyramine Questran
b. Colestipol Colestid
4. Immunoglobulin prophylaxis (IM Injection)
5. Vaccine
6. Avoid Hepatotoxic drugs (Acetaminophen [Tylenol], Chlorpromazine [Tranquilizers])

Nursing Management
Assess for history of exposure to risk factors, manifestations, liver function studies

Nursing Diagnoses:
a. Fatigue related to decreased metabolic energy production secondary to liver dysfunction
Goal: Client will convey reduced fatigue and heightened energy level as
manifested by gradual increase of activity
Interventions:
4 Bed rest / rest periods
4 ADL
4 Personal hygiene
4 No alcohol
4 Vitamin supplements
4 Antiemetics
b. Alteration in nutrition less than body requirements related to anorexia, nausea, impaired
absorption and metabolism of nutrients
Interventions
4 Nutritious meal, NO FATTY FOODS (Low TO MODERATE
PROTEIN)
4 Small but frequent meals

Complications
Chronic Hepatitis
Autosomal recessive disease
Liver infection for greater 3 6 months
Fulminant Hepatitis
Severe impairment or necrosis of liver cells and potential liver failure
May occur as a complication of HBV, HCV, congenital metabolic disorder
Jaundice, coagulation defect, electrolyte disturbance, hypoglycemia, encephalopathy,
hepatitis

Liver Cirrhosis
A chronic progressive disease of the liver, characterized by Diffuse degeneration, fibrosis
(Scarring) and nodule formation

Clinical Manifestations
Spider angiomas

Types
1. Laennecs Cirrhosis
2. Post-Necrotic
3. Biliary Cirrhosis
4. Cardiac Cirrhosis
LAENNECS CIRRHOSIS
Types:
Portal Cirrhosis
Alcohol Cirrhosis
Micronodular Cirrhosis


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Pathophysiology
Prolonged
alcohol
ingestion
Enzyme induction
and activity of
medications
Produce end-products
ACETYLDEHYDE and
FREE RADICALS
Toxic
effects to
the liver
NAD (Nicotinic
Adenine Dinucleotide)
Availability
Mitochondrial
electrical transport
system
Protein
synthesis
Lipid synthesis
or ketogenesis
Fatty liver!
Collagen
synthesis
Fibrogenesis/
lesions
Liver
damage
Scarring
Inflammation
Pain
Anorexia
Nausea
Jaundice
Ascites
Liver,
yellow
and
enlarged
Nodules
Portal
Hypertension
Toxic Effects to the LIVER


















POST-NECROTIC
Occurs after massive liver necrosis
Etiology: Post acute viral (Hep B&C) exposure to toxins
Scar tissue cause destruction to liver lobules

Pathophysiology




jcmendiola_Achievers2013
Hepatitis B
Virus
Enters the vagina,
mucus membranes, skin
Health care workers
Immune system
Liver cell
(Inflammation)
Clinical Cirrhosis
Carrier
Acute
Icteric
Chronic
Hepatitis
Convalescent
Cirrhosis
Progressive liver cell /
Hepatodysfunction
Fibrosis / Scarring
Pressure in the
portal circulation
Portal HTN!!


BILIARY CIRRHOSIS
Characterized by: Prolonged state of bile duct inflammation and jaundice due to retention of bile
due to narrowing of ducts
Primary Inflammation: Destruction, fibrosis, and destruction of Intrahepatic bile salts
resulting in nodular regeneration and cirrhosis
Secondary Inflammation: Inflammation, scarring and obstruction of bile ducts outside
of the liver
Pathophysiology


CARDIAC CIRRHOSIS
Pathophysiology


Other Pathophysiology :\...

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1
Glycogenesis and Glycogenolysis and
Gluconeogenesis
Altered glucose metabolism
Energy
Weakness,
fatigue,
malaise
2
FA and TAG Synthesis
FA Oxidation and Triglyceride Release
Fatty liver
Hepatomegaly
Energy
production
Weakness,
fatigue,
malaise
Production of albumin
3
Colloidal osmotic pressure
Edema, Ascites
4
Production of clotting factors
Altered clotting studies
Bleeding tendencies
Blood loss
Anemia
CHON Synthesis (In general)
Altered immune function
and altered healing
Susceptibility to
infection
5




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Metabolism of steroid Hormone
6
Estrogen, Progesterone,
Testosterone
Male Female
Loss of muscular
characteristics
and development
of some feminine
characteristics
Loss of feminine
characteristics
and development
of some
masculine
characteristics
Aldosterone
Na and Water
Retention
K and H
Excretion
Edema,
Ascites
Hypokalemia,
Alkalosis
Metabolism of Ammonia
7
Ammonia Levels
Hepatic Encephalopathy Coma
Death
Changes in
coordination,
memory orientation
Asterixis
Fetor
Hepaticus
Metabolism of Drugs
Drug toxicity
8
Storage of Vitamins
and minerals
RBC
Production
Energy
Production
Anemia
9


Obstruction of bile flow Bile reabsorbed in the blood
Fat absorption
Vitamin K absorption
Clotting factors
Bleeding / Anemia
Bilirubin in GIT
Bilirubin in feces
Clay-colored Feces
10
Bile salts in skin
Pruritus
Jaundice Kidney
Dark urine
Bilirubin
Level



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Nursing Diagnoses
Ineffective tissue perfusion related to bleeding tendencies
Imbalanced nutrition: Less than body requirements related to anorexia, impaired liver function and
decreased absorption of soluble vitamins secondary to inflammation, obstruction and destruction
on the bile duct
Activity intolerance related to fatigue and lack of energy due to decreased nutrients

Nursing Interventions
- Assess for signs of bleeding (Gums, melena)
- Check VS: Signs of shock
- Provide sufficient rest and comfort
- Monitor / prevent bleeding
- Prevent infection
- Administer diuretics as ordered (Strict I&O!!) To decrease portal hypertension
- Sufficient rest and comfort Relieve pruritus
- Promote nutritional intake: TPN, NGT
- Health Education:
4 Vitamin supplements Vit B and FSV (ADE)
4 Vitamin K Injection To improve blood clotting
4 Collaborate with lab technicians, physician, SO

Complications of Liver Cirrhosis
Portal Hypertension
Abnormally high blood pressure in portal venous system / vena cava that results from obstruction
of blood flow through the damaged liver
pressure at least 12 mmHg
Normal venous BP at least 5 10 mmHg
Long term portal hypertension cause distended, twisted, collateral veins; transformed to
varicosities
Collateral channels: Lower esophagus, anterior abdominal wall, parietal peritoneum, rectum-
hemorrhoids
Pressure; Plasma volume
Lymphatic flow


Pathophysiology

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Clinical Manifestation
- Splenomegaly, hemorrhoids, esophageal varices

Diagnostic Evaluation
- Splenoportogram: Indirect measurement of portal venous blood flow
- Liver Scan

Complications
- Hemorrhage

Esophageal Varices
Complex tortuous collateral veins (from collateral channels) at the lower end of the esophagus due
to prolonged elevation of pressure
Life-threatening condition!

CARDINAL SIGN: ESOPHAGEAL BLEEDING (DARK COLORED BLOOD)

Assessment:
- History of alcohol abuse
- Hematemesis?
- Melena?
- Anorexia?
- Nausea?
- Splenomegaly?
- Caput medusae More prominent than
SPIDER ANGIOMA
- Splenic dullness


Clinical Manifestation:
- Hematemesis
- Anorexia
- Nausea
- Splenomegaly
- Caput medusae
- Splenic dullness

Diagnostic Evaluation
Barium Swallow
NPO After midnight, assess for allergies (Laxatives)
Fluids and laxatives AFTER the procedure
Stool: White-ish

Medical Management
Sclerotherapy

Transjugular Intrahepatic Portosystemic Shunt (TIPS)
More than successful 90%
Percutaneous placement of a Portosystemic shunt
Fluoroscopy, an expandable metal stent is inserted to the hepatic vein through angiogram
and then to the liver, a direct portocaval channel
Vasopressin
Given to stop variceal bleeding
MOA: Reduces portal venous blood flow by constricting different afferent arterioles
SE: Hypothermia, MI, GI ischemia, Acute renal failure
CI: Clients with recent MI (Causes VASOCONSTRICTION)
May be given with nitroglycerin (To vasodilate MI patients)
Balloon Tamponade
Puts pressure of the esophagus and gastric balloon to stop bleeding
A.k.a. Sengstaken Blakemore Tube / Minnesota Tube
Presence of 4 esophageal opening

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1. Gastric Balloon Inflation lumens
2. Esophageal Balloon Inflation lumens
Not always inflated for 24 hours
During deflation, esophagus balloon will comf 1
st
before gastric
balloon
3. Gastric aspiration lumen
Complications:
1. Esophageal rupture
2. Aspiration
3. Pneumonia
Care of Patients with SB Tube!~
1. Facilitate placement of tube
2. PLACE PATIENT ON A SEMI-FOWLER\S
3. Maintain traction by securing tube to a piece of sponge or foam placed on the
nose so the balloon wont be displaced
4. Keep scissors at bedside (emergency cut tubes)
5. Monitor respiratory rate
6. Label each lumen to avoid confusion
7. Maintain prescribed amount of pressure as ordered
25 40 mmHg for esophageal balloon
100 120 mmHg for gastric balloon
8. Provide oral/nasal care q 1-2 hrs
9. Suction gently if cannot expectorate secretions
10. Vitamin K therapy or BT
11. For severe thirst: Oral hygiene and moist sponges on the lips
12. Gastric lavage with cool saline

Surgical Management
1. Endoscopic Band Ligation
a. Device with a small rubber band (O ring) at the end of the endoscope Over the varix
b. MD places rubber band covered varix which sloughs off after days
c. Important for clients who are taking beta-blocker therapy
d. Stops bleeding from varices
2. Portosystemic Shunt
a. Anastomosing = the high pressure portal venous system to low pressure systemic venous
system
b. MOA: portal venous blood pressure, thus the risk of ruptured esophageal varices
c. Reserved to clients who do not respond to treatment
d. Types:
4 Portacaval End side/side-side anastomosis of portal vein to IVC
4 Splenorenal From Splenic vein to left vein (artery) hmm
4 Mesocaval End to side or use of graft to anastomose IVC to side of superior
mesenteric vein

Nursing Management
Assess patent airway
Nutrition and Neurologic status
Gastric lavage with cool saline
Quiet environment
Vasopressin
Signs and Symptoms of Bleeding and Shock!
Early: Tachycardia
Late: Bradycardia; BP
Health Education
Esophageal irritation
PeriOp! Nursing Management
PreOp! PostOp!
1. Explain 1. Assess
2. Tests 2. Nutrition
3. Consent 3. IVF
4. Dressing
5. Blood and urine
levels


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NO ALCOHOL
NO IRRITATING AGENTS
No in abdominal / thoracic / portal pressure

Ascites
Accumulation of fluid in the peritoneal cavity that results from several pathological changes
Due to damaged liver 15 mL/more srum albumin-rich fluid accumulating in the peritoneal cavity =
serum osmotic pressure = movement of fluid to peritoneal cavity = ASCITES
Inactivation of aldosterone = Na Retention
Portal HTN

Contributing Factors
- Portal HTN
- Plasma colloid osmotic pressure
- Flow of hepatic lymph
- Hyperaldosteronism
- Impaired water excretion

Pathophysiology
Liver damage, cirrhosis
Metabolism of
aldosterone
Na and water
retention
Hypovolemia
Splanchic arterial
vasodilation
Blood volume
Activation of
RAAS
Albumin
synthesis
Oncotic
pressure,
especially in the
peritoneal cavity
Fibrous tissue
and nodules
Capillary
pressure
Obstruction of
venous flow


Clinical Manifestations
1. Abdominal girth
2. Weight gain
3. Shortness of breath
4. Striae
5. Distended veins in the abdomen
6. Umbilical hernias
7. Fluid wave
8. Bulging flanks when lying supine

Assessment
Dull upon percussion
Fluid wave, detect
Paracentesis
Abdominal x-ray
Ultrasound

Medical Management
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Diuretics: Spironolactone (1
st
line of DRUG!)
Paracentesis
Nursing Diagnoses:
- Alteration in fluid volume balance: excess /
deficient related to fluid shifts secondary to
portal hypertension, hypoalbuminemia and
hyperaldosteronism
- Ineffective breathing pattern related to
increased intra-abdominal pressure on
diaphragm
Medical Management:
- Paracentesis
- Albumin IV
- Maintain fluid and electrolyte balance (1 L 1.5 L/day)
- Dietary modification
- Diuretics
- Maintain skin integrity
- TIPS

jcmendiola_Achievers2013
Transabdominal removal of fluid from the cavity through a puncture of small incisions
from the peritoneal cavity
Large volume Paracentesis
6 L yields immediate effect in combination with IV infusion of salt-poor
albumin (helps correct the ineffective arterial blood volume that lead to Na
retention)

Nursing Management
Before Procedure
1) Explain
2) Consent
3) VS, Abdominal Girth, Weight
4) Empty bladder
5) Position client (Semi fowlers / High fowlers
After Procedure
Assess for signs of hypovolemia due to aspiration
Assess comfort
Dressing
Patient education
No Na in diet
Bed rest
Upright position activates RAAS which promotes Na and water retention
Promoting skin integrity
Weight daily
Avoid NSAIDS and Aspirin: Inhibits prostaglandin which leads to Na retention

Surgical Management
LeVeen Shunt (Peritoneal Venous Shunt)

Hepatic Encephalopathy (Portal Systemic Encephalopathy)
Accumulation of ammonia (theres already a problem in the conversion of ammonia to urea) and
other toxic metabolites in the blood
Ammonia inhibits neurotransmission and synaptic regulators
Characterized by altered level of consciousness, neurologic symptoms

Stages of Encephalopathy
Prodromal
Changes may be subtle
Inability to concentrate
Forgetfulness, altered sleep habits
Agitation, restlessness, memory disturbances, impaired judgment, slurred speech
Impending
With increasingly obvious impairment, periods of confusion, asterixis
Lethargy, disorientation to time, deterioration in handwriting
Stuporous
Evident severe mental deficits
Difficult to arouse
Asterixis, incoherence, inability to follow commands, hyperreflexia, muscle twitching
Coma
FINAL STAGE is DEEP COMA
Theres a Babinski reflex (damaged brain), comatose, fetor hepaticus, unresponsive to
painful stimuli, possible decorticate / decerebrate

Diagnostic Tests
Electroencephalogram: Shows a generalized slowing, increased amplitude of brain waves
Surgical Management
- LeVeen Shunt
o Permits reinfusion of ascetic fluid into the venous
system through a silicone catheter with one way
pressure-sensitive valve
o One end of the catheter is implanted in to the
peritoneal cavity channeled to the SVC where the
other end of the catheter is inserted

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Serum ammonia and CSF glutamine levels
Electrolyte level
Blood gases
Hepatic function test results (e.g. bilirubin, prothrombin, albumin and enzymes)

Nursing Diagnosis
Ineffective therapeutic regimen related to reduction in protein in the diet in and pharmacologic
intervention
Increased risk for injury

Medical Management
1. Assess
2. Neomycin
a. Decreases the action of intestinal bacteria
b. CI: Renal insufficiency
3. Lactulose
a. Promotes excretion of ammonia in stool
b. Ammonia kept in ionized state in colon pH No passage from colon to blood
c. Bowel evacuation Ammonia not absorbed from colon
d. Fecal flora changed into organisms that do not convert ammonia to urea
4. Antibiotics
5. Oral MgSO
4
or Enemas after hemorrhage
6. IVF and Vitamin: To minimize CHON breakdown

Nursing Management
1. Assess
2. Restrict CHON to avoid presence of ammonia from amino acids, provide CHO intake and Vitamin
K supplements
3. Medications
4. Protection from injury
5. Bed rest

Liver Transplantation
For end-stage liver disease
6 18 hours procedure
Complications:
1. Cardio and pulmonary problems
2. Infection
3. Rejection
a. Which occurs on the 4
th
6
th
day
b. CM: TRIF!! Tachycardia, RUQ/flank pain, jaundice, fever (early sign)
4. Hemorrhage
5. Atelactasis
6. Failure of anastomosis
7. Acute renal failure
Nursing Management:
Post Operative
Monitor signs of rejection
Cyclosporine, corticosteroids, Azathioprine (Imuran) > 6 months (Drugs to
prevent rejection)


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Contraindications:
\ Life threatening systemic disease
\ Uncontrolled extrahepatic bacterial or fungal infection
\ Pre-existing advanced cardiovascular or pulmonary disease
\ Multiple, uncorrectable congenital anomalies
\ Metastatic making to ***
\ Active alcoholism / drug abuse
\ Cholangiogram
\ HIV
Discharge Instruction
\ Infection?
\ Rejection?
\ Medications?
\ Potential body changes?
\ Follow up care: 2 3 days AFTER

Pathophysiology
Pulmonary
HTN
Liver cell damaged
and necrosis
Failure to convert
ammonia
Serum NH3
Glial and nerve cell
affectation
Altered CNS metabolism
and function
Form of new
compound
octopamine
False
neurotransmitter