Liver, Pancreas, and Biliary Tract Dx

Pancreas

The pancreas has an endocrine function because it releases juices directly into the bloodstream, and it has an exocrine function because it releases juices into ducts.

Exocrine - it helps with the digestion of food

Enzymes, or digestive juices, are secreted by the pancreas into the small intestine. There, it continues breaking down food that has left the stomach.

The pancreas also produces the hormone insulin and secretes it into the bloodstream, where it regulates the body’s glucose or sugar level. Problems with insulin control can lead to diabetes.

endocrine function of pancreas

helps with the regulation of sugar with insulin

exocrine function of the pancreas

it helps with the digestion of food - fats, CHO, protein

bile excretion & storage in GB

toxin metabolism—> alcohol

Blood coagulation→ metabolism of RBC into bilirubin

enzymatic function-→ trypsin, lipase, amylase

pancreatic disorders: pancreatitis

Inflammation of pancreas presenting in two forms (acute and chronic) that have different courses and must be considered as two different disorders. Disease can ranges from mild inflammation to hemorrhagic complications.

Major complications of pancreatitis is hemorrhage

If the patient has pancreatitis, the function is diminished

- Not able to regulate glucose

Issues with digestion/ excretion

Acute Pancreatitis + common causes

Inflammation of the pancreas

Present many times with life-threatening conditions

Causes—most common

Alcohol

Obstruction- Gallstones

Trauma/Biliary tract disease

Viral Infections

Drug hypersensitivity (BB)

gallstones causing pancreatitis

If bile contains too much cholesterol, too much bilirubin, or not enough bile salts, gallstone is formed.

Gallstones are a common cause of pancreatitis. Gallstones, produced in the gallbladder, can slip out of the gallbladder and block the bile duct, stopping pancreatic enzymes from traveling to the small intestine and forcing them back into the pancreas. The enzymes then begin to irritate the cells of the pancreas, causing the inflammation associated with pancreatitis.

Move through the common bile duct

- Enzymes in the pancreas is inactive but when the duct is blocked, the inactive enzymes become activated in the pancreas causing a lot of pain

- The enzymes are supposed to be activated in the small BI

- Stones moves through the common bile duct and blocks the duct, preventing the inactive enzymes in the pancreas from traveling through SI

- The enzymes become active in the pancreas eating it, causing pain and inflammation

→ Trypsin→ lipolysis, proteolysis

gallbladder + function

part of the digestive system.

Function= storage of bile

Bile helps the digestive system break down fats

Pathophysiology of Acute Pancreatitis & cx

loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes.

Pancreatitis occurs when digestive enzymes become activated while still in the pancreas, irritating the cells of the pancreas and causing inflammation. With repeated bouts of acute pancreatitis, damage to the pancreas can occur and lead to chronic pancreatitis.

Autodigestion of organ

ETOH and biliary disease

Infections such as mumps, scarlet fever and endocrine disorders

Enzyme activation

Major concern is hemorrhage

trypsin

enzyme that helps us digest protein

Trypsin is produced by the pancreas in an inactive form called trypsinogen. The trypsinogen enters the small intestine through the common bile duct and is converted to active trypsin.

lipase

amylase

pancreatic enzyme necessary to digest fats, turns fat into glycerol

pancreatic enzyme necessary to digest carbs

Acute Pancreatitis: Assessment/clinical manifestations

Sudden onset of epigastric pain—upper left quadrant or mid-abdomen

- Severe pain

- Pain can radiate to left flank/ back

- Deep and very sharp pain

N/V/anorexia

- Nursing intervention is to watch for dehydration

- Raise HOB

- admin isotonic IV, fluid replacement NPO

Abdominal fullness

- Too many things going on in the body

Cullen’s sign – indicates hemorrhage

- Redness within the umbilical region

- Sign of hemorrhage

Grey Turner’s sign- indicates hemorrhage

- Redness on the flank area

- Sign of hemorrhage

Steatorrhea, clay-colored stools

- Fatty stools

Islets of Langerhans are usually not impaired.

- Alpha (production of glucagon) and beta (production of insulin) cells

Respiratory distress due to accumulation of fluids in retroperitoneal.

- Fluid accumulation near the kidney→ Kidney disease

- Can have SOB and crackles, dyspnea

Labs: increased amylase, lipase, leukocytosis, WBC, glucose, C-reactive protein

If complications present

- Hypotensive, tachycardia

- Fever, abdominal rigidity, tenderness & guarding (peritonitis)

- Decreased bowel sounds

- Decreased lung sounds or adventitious breath sounds

Positive Trousseau’s or Chvostek’s sign

- Low calcium (fat necrosis)

Chvostek's sign

twitching of facial muscles in response to tapping over the area of the facial nerve

Tap near the cheek and see if the face twitches

Low calcium can be a sign of hypoparathyroidism

Trousseau's sign

carpopedal spasm (spasms that are extremely painful cramps or contractions that mostly occur in the hand and feet muscles) that results from ischemia, such as that induced by pressure applied to the upper arm from an inflated sphygmomanometer cuff

Inflate the BP cuff, start complaining of spasms in the arm

Low calcium can be a sign of hypoparathyroidism

Cullen sign

hemorrhagic discoloration of the umbilical area

Hemorrhage

Grey Turner sign

discoloration (Grey Color) of the left flank associated with acute hemorrhagic pancreatitis.

Hemorrhage

Acute Pancreatitis Diagnostic Assessment

Amylase

Lipase

Trypsin

Elastase

CBC

- WBC

BMP

- BUN/CR

-- Creatine may be high bc of kidney impairment

- Glucose—may be elevated

-- Pancreas infected, beta cells infected, insulin not produced, blood glucose is high

- Ca & Mg—may be decreased

LFT

- Associated with gallstones, liver involvement

- Gallbladder and liver work complementary to each other

CT scan- most accurate diagnostic test

MRI

Abdominal ultrasound

Acute Pancreatitis: Medical Management and Nursing Interventions - NPO

NPO

When you eat food, body releases enzymes, this causes more irritation to the pancreas→ PAIN

May require TPN if NPO for prolonged period or jejuna TEN

Daily weights & I&O- Document any changes

- If they are throwing up, want to see if they are becoming emaciated

If on TPN—monitor F&E status, blood glucose, monitor for infection

If on TEN—monitor for residuals

- Aspiration

- 150CC and above - put it back, notify doctor, and hold feeding for 2 hr

Once eating—small frequent meals

- Moderate to high carbs, high protein, low-fat meals

- Low fat cause high cholesterol leads to gallstones

- Do not want dumping syndrome

NPO patients, monitor their glucose q 6

- Want to make sure that sugar does not drop low

Acute Pancreatitis: Medical Management and Nursing Interventions - other interventions

IV Fluids

- Dehydration from throwing up

Replacement of Ca and Mg

- Usually low and need to be compensated

NGT—for severe pancreatitis

- Bc they are throwing up a lot, to decrease the stomach

- Intermittent suction to allow for rest

-- Continuous suction is drastic and can cause bleeding to the stomach

Acute Pancreatitis: Medical Management and Nursing Interventions: pain management

Side-lying with legs draw up to chest (fetal position) most comfortable to decrease abdominal tension

- Also decreases the secretions of those enzymes

- Not supine or prone, or raise HOB

Opioids- hydro/morphine

PPI-zoles’ &/or H2RA- famotidine

Acute Pancreatitis: Medical Management and Nursing Interventions: Sphincterotomy

(remove common bile duct/Stone)

If caused by gallstones

Opens sphincter of Oddi

Acute Pancreatitis: Medical Management and Nursing Interventions: Endoscopic retrograde cholangiopancreatography (ERCP)

ERCP used diagnosis and treatment

MRCP is only used for diagnosis (perfered bc it has a small mortality rate)

NPO

Consent is required

MRCP (magnetic resonance cholangiopancreatography)

non-invasive, useful for imaging the gallbladder, bile ducts and surrounding tissues but does not offer a way to treat the disease found

US is less expensive and easier test to perform for the diagnosis of cholecystitis

Acute Pancreatitis Complications

Necrotizing Hemorrhagic Pancreatitis

- Infection in the pancreatitis

→ Low grade fever,

Hypovolemic shock

Pancreatic hemorrhage and pancreatic pseudocyst

AKI

ARD’s

Acute Pancreatitis Summary of treatment

NPO

Fluids and Electrolyte replacement

- Calcium and magnesium

Pain control

Nutrition Support/TPN

NG/Bowel Rest

- Decompress the stomach

Surgery to Remove source

• cholysysectomy

Secondary Prevention

• avoid fatty foods, alc, caffeine

Chronic Pancreatitis

Most common cause is prolonged, heavy, alcohol use

Similar signs/symptoms of acute Pancreatitis

- Same symptoms but the difference with chronic is that it comes and goes (remission and exacerbation)

Acute pancreatitis once you have it, does not happen again

Complications:

• T2 DM. [c/b damage to panc cells]

• DEC bicarb.

• Pleural effusions [r/t

• Pancreatic ascites [r/t FVO]

Chronic Pancreatitis treatment

TX: Lifelong abstinence from alcohol

Pain management

Lifelong pancreatic enzyme replacement

CP SRG Tx

indicated: ongoing pain, reoccurring episodes, cx- pseudocyst or abscess

• Laparoscopy- drain abscess

• Laparoscopic cholecystectomy- incision made in CBD

• sphincterotomy- enlarge sphincter

Pathophysiology of Chronic Pancreatitis

Continuous, progressive, and irreversible destructions of cells, with replacement with fibrotic tissue.

Alternating periods of remission and exacerbation

Clinical Manifestations of chronic pancreatitis

Characterized by remissions and exacerbations

Intense, unrelenting pain is the hallmark

Hypocalcemia due to increased serum lipids, which bind with free calcium

Symptoms of malabsorption, especially of fats (steatorrhea, weight loss).

Diabetes mellitus develops later in disease due to malfunction of islets of Langerhans.

- Beta cells are damaged (BG regulatory issues)

Mean duration of the disease is 25 years after diagnosis; death is often not related to pancreatic failure.

- Usually bc they have necrotizing pancreatitis

Medical and Nursing interventions of chronic pancreatitis

Diet

• Initiate and maintain a low-fat, high-carbohydrate, low-protein diet to provide rest to organs.

Teach

• importance of taking enzyme supplements after every snack and meal. [PERFT]

→ Viokase, Cotazym (with meals)

- Will need this supplement for the rest of their life

Monitor stools for fat to help determine pancreatic enzymes

• enzyme for fat digestion

Explain to the patient the importance of avoiding ETOH [avoid alc pls] & unnecessary drugs

Medical and Nursing interventions of chronic pancreatitis: surgical interventions

may be performed to remove the source of problems (gallstones. Psuedocysts), removal of necrotic pancreatitis tissue, or repair problems with the biliary system

pancreatisis Continued Care and rehabilitations

Patient with acute pancreatitis may never experience another episode but should be counseled to exercise moderation in food and alcohol intake.

Patients with chronic pancreatitis will experience remissions and exacerbations of the problem.

- Pain management will be constant problem; counsel regarding excesses in alcohol, adherence to diet and medication regimen.

- Diabetes mellitus may develop several years after diagnosis- patient education. [consult w/ CDE, may need insulin due to beta cell damage tx]

Pancreatitis Evaluation

Patient remains complication free

Patient verbalizes medical treatment plan

Pain free or at acceptable levels of pain [3-4/10]

Maintains weight (or gains if necessary)

Abstains from alcohol

Cholecystitis

inflammation of the gallbladder, usually caused by the presence of gallstones (cholelithiasis)

Gallstones in the gallbladder causes inflammation (cholecystitis)

Key features of Cholecystitis

Upper ABD pain

N/V

dyspepsia

eructation [burping]

flatulence

fever (in some cases)

cholelithiasis [actual gallstone present]

Presence of the stone (cholelithiasis)

Patients with cholecystitis has cholelithiasis

Patients with cholelithiasis does not necessarily have cholecystitis

Cholecystitis Etiology and pathophysiology

Stone development usually occurs in individuals with consistently high blood cholesterol levels

Stasis of bile in gallbladder results in aggregation of particles leading to stones.

Lodging of stone in neck of gallbladder or common bile duct results in symptoms

Cholecystitis Clinical Manifestations

Pain: biliary colic or epigastric pain that may radiate to right shoulder; usually occurs after a heavy meal or lying-down position.

RUQ tenderness, rigidity.

Nausea, vomiting, indigestion especially after ingestion of fat.

Signs/symptoms of inflammation: fever, increased WBC.

Jaundice with bile duct obstruction.

May be asymptomatic.

Murphy’s Sign (Pain on palpation under the rib cage during inspiration) = cholecystitis

- Raise right arm up, take a deep breath and hold it, tap the abdomen, patient will complain of pain, sign of inflammation of the gallbladder

Cholecystitis: Diagnostic Assessment

- important test for gallbadder

Abdominal x-ray

- Trying to find stone and x ray in the gallbladder

Ultrasound

- Trying to find stone in the gallbladder

Hepatobiliary iminodiacetic acid scan (HIDA)

- Most important test for gallbladder

- Patient will be NPO for 4 hours

Endoscopic retrograde cholangiopancreatography (ERCP)

Cholecystography - allergic to iodine

Cholangiogram - allergic to iodine

CBC

- Elevated WBC

LFTs

- Elevated

- Anything that involves the bile duct - liver enzymes will be elevated

ACUTE Cholecystitis: FE balance & Pain mx

NPO

IV hydration

- Bc of N/V

Correct fluid and electrolyte imbalances

Pain & nausea management [analgesics & antiemetics]

NGT

• decompress from gastric secretions

Cholecystitis: Lithotripsy Extracorporeal shock wave lithotripsy (ESWL)

nonsurgical alternative to manage gallstone to relieve stones

Lithotripsy

• uses radiofrequency to break apart gallstone into pieces

Pre-Op

• Informed consent

Post-Op

• Monitor I&O for elimination of stone

• send stone to lab

Cx associated w Procedure

Cholecystitis: Laparoscopic Cholecystectomy [OPEN] **

Laparoscopic Cholecystectomy (too big of a stone, open cholecystectomy)

- Put CO2 in the stomach fill it up for more space

- Expected to find shoulder pain, CO2 that has migrated to shoulder

T-tube assessment

- Monitor T-tube output

- Protect the skin from bile drainage

- Anchor T-tube to prevent accidental dislodgement.

May include common bile duct exploration (CBDE or Cholechodotomy); this requires an open procedure

Big surgery

Transhepatic biliary catheter to relieve bile duct obstruction

- Catheter goes into the biliary to take out the stone

Cholecystitis: Diets and med Mx

Diet

-AVOID Fatty foods, red meats, heavy alcohol (will exacerbate the stones)

Medications

- Ursodiol, Actigal, chenodeoxycholic acid to dissolve stones

- Cholestyramine for pruritus

Itching because of an increase in Bile

- Fat soluble vitamins.

Cholecystitis: Patient Education

Conservative treatment includes low fat diet, weight loss program

- Most patients that have cholecystitis are overweight

Following cholecystectomy, fats are slowly introduced to diet

Once duodenum becomes accustomed to constant infusion of bile, dietary restrictions only based on individual intolerance.

Teach about pain medications: analgesics, NSAIDs, anticholinergics to reduce spasms.

- AVOID Aspirin/salicylates, patients with GERD/upper GI problem should not take aspirin because of risk for bleeding

Liver Disorders: Cirrhosis

Extensive, irreversible scarring of the liver

Post necrotic cirrhosis

Caused by viral hepatitis, certain drugs, or toxins

Laennec’s or alcoholic cirrhosis

caused by alcohol

Biliary cirrhosis or cholestatic

Caused by chronic biliary obstruction or autoimmune disease

S/S

• Ascites

• Jaundice

• itching c/b INC bilirubin.

Cirrhosis: Liver Functions - storage

minerals and vitamins

Iron, Magnesium, Fat Soluble Vitamins (DEAK)

Cirrhosis: Liver Functions - protective

Kupffer cells

- Engulf harmful bacteria and anemic red blood cells

- Destroys and engulfs any bacteria in the body

Detoxifies

- Any toxins in the body i.e alcohol & drugs

Cirrhosis: Liver Functions - metabolsim

1. Amino acids—broken down into urea and excreted by kidneys

//Cx= increased urea→ increase ammonia→ TOXIC to brain=Hepatic encephalopathy.

2. Synthesis of plasma proteins

- Albumin, prothrombin, and fibrinogen

//Cx = risk of bleeding

3. Storing and releasing of glycogen

- Liver stores glycogen, so when body needs more glucose, converts the fat into glucose

4. Synthesizes, breaks down, and temporarily stores fatty acids and triglycerides

5. Production of antibodies

- Antibodies help to fight in the immune system

Cirrhosis Complications

Portal hypertension

- The pressure in the hepatic vein gets high bc of the build up of metabolism in the body

Ascites and esophageal varices

- Swelling of the stomach

- Metabolites in the body

Coagulation defects

- No thrombin

Jaundice

Portal-systemic encephalopathy (PSE) with hepatic coma

Hepatorenal syndrome

- Liver affected, the kidney's can also be affected

Spontaneous bacterial peritonitis

Cirrhosis: early Compensated Cues

Slow onset

Fatigue

Change in weight

Anorexia and vomiting

Pain associated w [Abd., liver tenderness]

Abnormal LFT + thrombocytopenia (c/b hepatic cell destruction)

Advanced Cirrhosis Uncompensated Cues

End stage Liver failure

Skin:

• Jaundice and icterus

• Dry skin

• Rashes

• Petechia/ecchymosis

• Palmar erythema

• Spider angiomas

• Ascites

• Peripheral dependent edema

  • Both will cause Resp issues bc of fluid buildup.

Vitamin deficiency

Hepatomegaly

Splenomegaly

Caput medusa (a cluster of swollen veins in the abdomen).

Fetor hepaticus (Rotten egg smell)

- Bad smell from the mouth

Amenorrhea= blood in stools/vomit

- Hemorrhoids bc of impairment of the coagulation factors

Gynecomastia (overdevelopment or enlargement of breast in men or boys) C/b INC estrogen

Asterixis (Involuntary movement)

Change in mental status

Clay-colored stools

Dark urine

Hepatic encephalopathy

• c/b increased levels of NH4

hepatorenal syndrome characterized by

oliguria- sudden decrease in urinary output <500 ml

elevated BUN/Cr with low Na excretion

increased urine osmolality (urine specific gravity/concentrated)

Cirrhosis: Diagnostic labs

Elevated LFTs

- Anytime there is an issue of kidney, gallbladder, and liver

Total protein

- Elevated—acute liver disease

- Decreased—chronic liver disease

Decreased albumin

• advanced liver disease (hepatic destruction)

Elevated serum ammonia (10-20)

- Confusion, hepatic encephalopathy or ALD

Prolonged PT and INR

CBC

- Low platelet count

- Decreased H&H—with bleeding

- WBC—may be low

BMP

- Dilutional hyponatremia (ascites) or Hypernatremia

-- Low sodium because of lots of fluid in the patient stomach

- Elevated BUN/CR

→ kidney damage r/t hepatorenal syndrome

Cirrhosis: Diagnostic Tests

Plain abdominal x-rays

• hepatomegaly, splenomegaly, ascites

CT scan

MRI

- MR elastography

Ultrasound

• biliary stones, bile duct obstruction

EGD

• visualize upper GI tract (esophageal varices, stomach ulceration, duodenal ulceration)

Endoscopic retrograde cholangiopancreatography (ERCP)

Liver biopsy

- To see if there is carcinoma of the liver

risk for bleeding

Jaundice

c/b biliruben build up

• urine→ frothy, dark

• feces→ light, grey colored

• skin→ yellowing, itchy

Rx for itching

• Choleycystraine [helps excrete biliruben]

• benedryl

• bathe reg, lotion q8h

Portal hypertension

• obstruction of blood flow through liver

  • INC pressure in portal vein→ major vein that leads to liver

• pressure backs up→ causing scarring of liver lobules

• dilated veins→ esophageal varices [rectum too]

• splenomegaly→ bc of turbulent blood flow out of liver

• Periumbilical veins→ caput medusae

• Rectal veins→ hemoroids

Most common cause of the portal hypertension is the cirrhosis of the liver

Cirrhosis: Medical Management and Nursing Interventions - nutrition and fluid

FLUID BALANCE:

Nutritional therapy

- Low sodium diet (1-2g/day)

- Trying to decrease the BP & fluid retention

- Vitamin supplementation (thiamine, folate, MVI)

Cirrhosis: Medical Management and Nursing Interventions - drug therapy

Diuretics (Furosemide, Spironolactone)

→ goal is to dec edema

- Monitor daily weights

- Monitor electrolytes and I&O

• dehydration & f/e shift

Cirrhosis: Medical Management and Nursing Interventions - Ascites

→ Albumin and furosemide

Paracentesis (insertion of the catheter in the abdomen/liver to remove the fluid)

Patient needs to be NPO for 4 to 6 hours

Assess output

Monitor VS

Pre-procedure—assess coagulation studies, void prior to procedure.

- PPT and INR because liver makes coagulants

- If this is compromised, pt will require platelet or plasma replacement before the surgery is done

- Need to void prior to procedure so there is a decrease risk in puncturing the kidney

Educate the patient on what to expect

2x2 in the stomach, stay in bed for 2 hr

Cirrhosis: Medical Management and Nursing Interventions -

SBP

Spontaneous bacterial peritonitis (SBP) [kupner cell compromsied]

• Monitor for low-grade fever

• Loss of appetite

• Assess bowel sounds [hypoactive] & abdominal rigidity

TX: IV cefotaxime, third-generation cephalosporins, fluroquinolones

Cirrhosis: Medical Management and Nursing Interventions - dyspnea and F/E

Respiratory support

- Dyspnea from increased abdominal pressure

- Fluid build up in the stomach

- Auscultate lungs sounds every 4-8 hours for crackles

Monitor F&E status

- BUN/CR, serum protein, HCT

Trans jugular intrahepatic portal-systemic shunt (TIPS)

• cirrhosis

• preventing & managing hemorrhaging

Used to control long term ascites & reduce variceal bleeding

Helps to DEC pressure in the hepatic vein by putting a shunt in it

Bc there is too much pressure in the portal vein, connect shunt into the hepatic vein to decrease the pressure

Post OP

→ FU US to check patency of shunt

→ used to treat portal hypertension

CX of procedure & management

• Hepatic encephalopathy

  • lactulose

• INC in PAP

  • Diuretics

• Bleeding

  • NG tube to assess bleeding

  • PRBC, plasma, dextran, albumin, platelets through 2 large bore IV catheters

  • **Monitor VS Q1H→ PT+PTT, INR & platelet count.

Cirrhosis: Medical Management and Nursing Interventions - Esophageal varices

→ dilated distended esophagus & gastric veins c/b INC portal HTN

Preventing bleeding

• Beta-blocker (propranolol)

• Sandostatin (octreotide)

  • DEC blood flow to GI to reduce pressure

AVOID!!→ Cough, Valsalva maneuver bc it DEC abd pressure

IF Rupture or bleed occurs…

MONITOR→ hypovolemic shock, fluid resuscitation [2 large bore IV caths]

• Blood products: PRBC, plasma, albumin

---

SURGICAL MANAGEMENT

Endoscopic variceal ligation (banding)

• small o shape band placed around varices

Sclerotherapy→ Inject blood to varicose vein to shrink

TIPS→ portal vein stent to relieve pressure from portal vein & DEC PAP

Sengstaken-Blakemore tube (Emergency tube to stop bleeding)

- NG tube to evacuate the stomach and put a stomach to stop the bleeding

TIPS (Hepatic vein to portal vein shunt)

Hepatic encephalopathy

Medical Management and Nursing Interventions

Encephalopathy (craziness because of ammonia in their brain, build up of metabolites in the brain)

Nutrition therapy

Moderate protein and fat and simple carbohydrates

If you give them a lot of protein, the more ammonia they will build up

- Bc liver is not taking care of ammonia in the body

Monitor drug therapy

Opioid, sedatives, and barbiturates

Opioids are metabolized in the liver

Medication therapy

Lactulose (will cause patient diarrhea)

- Helps promote excretion of ammonia in stool

- Bowel movement is expected

- Potassium will drop

- Monitor for hypokalemia and dehydration

Antibiotics

- Neomycin, rifaximin, metronidazole

Monitor for changes in LOC, asterixis, fetor hepaticus

Thiamine and benzodiazepines if patient at risk for alcohol withdrawal.

- Benzodiazepines if the medication of choices for alcohol withdrawal

- Give them thiamine bc liver is the powerhouse of vitamins and they are not making them vitamins

Cirrhosis: Evaluation

Patient Verbalizes knowledge of disease process

States prevention of complications

Discuss common therapeutic modalities

Splenomegaly Mx [cirrhosis]

→ spleen enlarged due to portal HTN

Causes destruction of

• WBC, RBC & platelets→ thrombocytopenia

MONITOR: petechia, hemorrhage, bruising & bleeding

RISK 4: falls

Edema & ascites Mx [cirrhosis]

INC P HTN & DEC albumin→ decreases colloidal osm. pressure→ edema

• free fluid in peritoneal cavity [“third spacing”] → ASCITES

  • causes sodium & water retention

Managment

• Paracentesis

  • Monitor→ I&O, abd girth, VS, electrolytes, BS

  • CX→ SBP

• SPB s/s: low grade fever, loss of appetite, reduced UO, INC urine osm. & INC BUN/Cr, change in mental stat.

Drug Tx

• cephalosporins

• fluroquinolones

• Diuretics

  • 2 types: Furosemide & Aldactone

    • Monitor!! Hypotension, DEC B/p due to fluid loss

Diet

• low sodium diet!!

Paracentesis (NOT CURATIVE)

Pre-OP

→ check weight, VS, VOID! to avoid kidney damage

→ check PT,PTT → Give albumin tranfusion

• to avoid hypotension & renal dysfunction

Post-OP Teaching

• position→ sitting

• Drainage amount & specimen collection

  • VS, weight, hypovolemia s/s [dec b/p, inc HR, thready pulse]

HOME Mx

• plleurX

Hep enceph Cues

Etiology→ ammonia buildup

• c/b liver being unable to convert ammonia into urea after protein breakdown.

Cues

• changes in mood

• hyperflexia

• confusion

• hallucinations

Worsening s/s

• fetor hepaticus

• asterixis

HPE Mx- diet & drug

Goal: lower NH4 levels

Diet: mod protein, INC CHO & mod fat

Meds:

• Lactulose: excretes ammonia

• Neomycin: antibiotic: antiseptic

• Levodopa: mx for hyperflexia

Assess

• LOC

• Serum ammonia & dec/absent asterixis.

Hepatorenal syndrome

Redistribution of BF from kidneys to periphery

→ azotemia & oliguria

CUES:

• DEC UO

• INC BUN/Cr & dilutional hyponatremia

• UA: INC urine specific gravity

Nursing MX goals for cirrhosis

SAFETY!

• Mx/prevent hemorrhage

• Mx/prevent HPE

• Mx FVO

Hep A route of transmission

Fecal-oral

Contaminated water or food

Hep B+C route of transmission

Percutaneous or mucosal

Blood, body fluids, needles or sharp instruments

Same way you get HIV

HepB: HbsAg

Immunoglobulin

vaccines available

Hep A acute or chronic

acute

Hep B acute or chronic?

both

Hep C acute or chronic

chronic

Hepatitis vaccines?

Hep A and Hep B

no vaccine for C, but there is a cure

Hep treatment

A - Symptomatic

- treated on when symptomatic

B - Interferon and antivirals

Hepatitis - clinical manifestations

Symptoms intermittent or ongoing

- Low-grade fever

- Malaise

- Fatigue

- Myalgia/arthralgia

- Right upper quadrant tenderness

- Enlarged liver

- Nausea, vomiting

- Pruritus

- Dark urine

- jaundice

hepatitis acute phase

Sick and max infectivity

Hepatitis convalescent phase

Begins as jaundice is disappearing

Lasts weeks to months

Major complaints

Malaise

Easy fatigability

Hepatomegaly persists

Splenomegaly subsides

hepatitis recovery phase

most recover; some relapse

what causes jaundice?

when the liver is damage, it is not able to take the uncongugated billirubin in the blood stream and congugated it for it to be released by in bile

Hemolytic Jaundice

Caused by: Transfusion reactions, Sickle cell dz, Hemolytic anemia

Liver unable to handle increase load of unconjugated bilirubin in the blood

Hepatocellular jaundice

Caused by: hepatitis, cirrhosis, hepatocellular carcinoma

Liver unable to take up bilirubin from blood, to conjugate it, or excrete it. Also caused from damaged hepatocytes

Might be from liver cancer

Obstructive jaundice

Caused by: Hepatitis, cirrhosis, hepatocellular cancer, common bile duct obstruction, pancreatic cancer

Liver flow decreased or obstructed by intrahepatic or extrahepatic blockage

Hepatitis - Complications

- 5 complications

Acute liver failure: Acute liver failure is loss of liver function that occurs rapidly — in days or weeks — usually in a person who has no preexisting liver disease

Chronic hepatitis-inflammation of the liver that lasts at least 6 months

Cirrhosis: is a late-stage liver disease in which healthy liver tissue is replaced with scar tissue and the liver is permanently damaged

- Irreversible unless you get a liver transplant

Portal hypertension: Portal hypertension is elevated pressure in the portal venous system. The portal vein is a major vein that leads to the liver

Hepatocellular carcinoma: Primary liver cancer—cancer that starts in the liver—is called hepatocellular carcinoma (HCC)

Hepatitis: NSG Analysis / Diagnostics

Antigen vs. Antibody-

- What is the difference?

- Antigen is the disease

- Antibody is the immune system that copes with the disease

Liver biopsy

Diagnostic lab findings (liver panel)

Hepatitis: NSG Diagnosis/Planning

Imbalanced nutrition: less than body requirements

- Adequate calories

- Care with fat because of bile production decreased

- Vitamin supplement especially B complex and K

- Fluid and electrolyte balance

Activity intolerance

Risk for impaired liver function

- When the patient does not have liver problem

- Ex. they are heavy drinkers

Hepatitis: IP & NSG Care - acute and chronic

Rest

- Degree and strictness varies

Avoid alcohol intake and drugs detoxified by liver

Notification of possible contacts

- Maryland law requires they notify their person of contact without saying the patient name (case manager)

- Use a condem with Hep B

Drug Therapy

- Acute HAV infection: no specific

- Acute HBV infection: only if severe

- Acute HCV infection

- Direct-acting antivirals (DAAs)

Supportive drug therapy

- Antihistamines

- Antiemetics

Hepatitis: IP & NSG Care - nutrition and teaching

Nutrition Care

- Well-balanced diet; maybe low fat – why?

- Vitamins B-complex and K

-- If the patient has anemia the patient needs vitamin B 12

- IV glucose or enteral nutrition

Teaching – Ambulatory Care

Fatigue

Transmission

S&S to report

ID complications

No alcohol

No blood donation

Med admin (subcut) teaching

Chronic hepatitis B

Blood borne pathogen

Focus on decreasing viral load and slowing rate of dz progression

Drug Rx will not eradicate the virus but rather suppress vial replication

- Nucleoside and nucleotide analogues - Lower viral load by affecting viral DNA synthesis

- Interferon - Immune modulator

-- Will need liver function tests every 4-6 weeks

-- Need to be screened for depression and other mood disorders

Long term goals

- Preventing development of cirrhosis, Portal hypertension, liver failure, and hepatocellular cancer

Chronic Hepatitis C

Based on specific genotype

Care focused on preventing other concurrent health problems

Treatment primarily with direct active antivirals to block proteins necessary for HCV viral replication

- No vaccination

Hepatitis: Medical Management & Nursing Intervention drugs

Hep B

Tenofovir

- Monitor kidney function

- Can cause bone de-mineralization

Adefovir

- Monitor kidney function

Lamivudine

- Monitor kidney function

Entecavir

- Monitor kidney function

Hep C

Telaprevir

- Monitor CBC for anemia

Boceprevir

- Monitor kidney function

- Monitor liver function

- Monitor electrolytes

PegIFN/RBV

- Patient’s cannot miss a dose

Non-alcoholic fatty liver disease (NAFLD)

Non-alcoholic steatohepatitis (NASH)

People who have diabetes or overweight

Most important thing for them is to lose weight and not drink too much alcohol

Non-alcoholic fatty liver disease (NAFLD)

Non-alcoholic steatohepatitis (NASH)

causes

diagnosis

treatment

Causes:

- DM

- Obesity

- Elevated lipid profile

DX: Elevated AST and ALT

TX: Weight loss, glucose control, lipid-lowering agents

- Monitor LFTs