Hepatic Dysfunction

Liver Functions

-storage (fat soluble vitamins, minerals)

-synthesis (serum proteins, clotting factors, phospholipids and cholesterol)

-secretory (bile, bilirubin conjugation, cholesterol removal)

-metabolic (gluconeogenesis, amino acid conversion, ketone formation, ammonia conversion to urea)

-detoxification (hormones, drugs)

-filter (blood filter via Kupffer cells)

-vascular reservoir (1L volume expansion/compression)

AST (Asparatate Aminotransferase)

-Found in liver, heart, and muscle cells

-elevated due to Hepatocellular injury releases AST into bloodstream

-low specificity

ALT (Alanine Aminotransferase)

-More specific to the liver

-Indicates direct liver cell damage (e.g., hepatitis, cirrhosis)

LDH (Lactate Dehydrogenase)

-Found in many tissues

-Rises with tissue necrosis, including liver and muscle

Alkaline Phosphatase (ALP)

-Found in liver and bile ducts

-Increases with cholestasis or bile duct obstruction

Total Bilirubin

-Sum of direct + indirect bilirubin

-Indicates overall liver excretory dysfunction

-jaundice, dark urine, pale stool, and pruritus

Indirect (Unconjugated)

-Fat-soluble; before liver conjugation

-↑ with pre-hepatic causes (RBC breakdown) or impaired uptake by liver

Direct (Conjugated)

-Water-soluble; after liver conjugation

-↑ with intrahepatic damage or post-hepatic obstruction

Urine Bilirubin

-Normally none present

-Appears when conjugated bilirubin leaks into blood and urine (dark, tea-colored urine)

Total protein

-Albumin + Globulins

-Decreases with liver disease

-decreases due to Impaired synthesis

Albumin

-Maintains oncotic pressure, transports substances

-Decreases with liver disease

-Reduced liver synthesis → leads to edema, ascites

-good indicator for chronic liver disease

Globulins

-Immune proteins (antibodies)

-increases with liver disease

-increases due to compensatory immune response or chronic inflammation

abnormal labs in liver dysfunction

-enzyme elevations: AST, ALT, LDH, alkaline phosphatase

-bilirubin elevations: serum total, direct, indirect, urine bilirubin

-serum proteins: reduced serum total protein, serum albumin serum globulins

-elevated serum ammonia: brain affected

-prolonged PT/INR: best indicator of liver function severity

Abnormal Labs in Liver Dysfunction and their effects

-increase ammonia= neuro changes

-decrease albumin=edema/acites

-increase INR= bleeding risk

-increase ALP= obstruction

Common causes of liver injury

-Alcohol induced liver disease

-Non alcoholic fatty liver disease

Cirrhosis

•Diffuse, fibrotic (scarring) changes

•Less compliance; no longer a sponge

•Destruction of hepatocytes

•Congested/obstructed flow

‐ blood, lymph, bile

- Blood flow -> hitting "a stiff wall"

•Stagnation of blood and bile → toxin buildup and liver failure

•Chronic & progressive

Cirrhosis causes

•Laennec's (alcohol‐induced)

•Postnecrotic (hepatitis, toxic exposure)

•Non-Alcoholic Fatty Liver disease

•Biliary (obstruction, bile stasis, inflammation)

•Cardiac (right‐sided heart failure, vascular congestion)

Cirrhosis Early Signs (compensated stage)

•Often asymptomatic

•Fatigue, weight loss, abdominal discomfort

•Enlarged liver (hepatomegaly)

Cirrhosis Late signs (Decompensated Stage)

•Jaundice - from bilirubin buildup

•Ascites - fluid accumulation in abdomen

•Peripheral edema - from ↓ albumin

•Spider angiomas, palmar erythema - from ↑ estrogen

•Esophageal varices - from portal hypertension

•Hepatic encephalopathy - from ↑ ammonia → confusion, asterixis

•Coagulopathy - due to ↓ clotting factor synthesis

Complications of Cirrhosis

•Infection, Spontaneous bacterial peritonitis

•Edema

•Anemia, bleeding

•Mental deterioration (hepatic encephalopathy)

•Portal hypertension

•Ascites

•Hepatic encephalopathy

•Hepatorenal syndrome

•Esophageal/Gastric Varices Rupture -> GI bleed!

Jaundice

•Hyperbilirubinemia

•Causes:

•Hemolytic destruction of RBCs transfusion reaction, anemia, Gilbert syndrome, meds

•Hepatocellular (impairment conjugation, excretion ‐ hepatitis, cirrhosis)

•Obstructive (cholestasis within/outside liver)

Portal HTN

-Backflow problem

-Blood can't pass liver → pressure builds → blood finds alternate pathways → fragile veins form → BLEEDING RISK

-If you see portal hypertension, think: Variceal bleeding = EMERGENCY

Esophageal Varices Pathophysiology

•Cirrhosis → portal hypertension → distended, fragile blood vessels within the esophagus

•Over time → increased pressure and distension → vessel rupture → life-threatening upper gastrointestinal (GI) bleeding

Ruptured Esophageal Varices manifestations

•Asymptomatic without rupture

•Diagnosed during endoscopy

•Manifestations of hemorrhage:

>Vomiting bright red blood or clots (ie, frank hematemesis)

>Risk for aspiration

>Coffee-ground emesis (ie, digested blood) or melena

>Hypotension

>Tachycardia

>Pale or cyanotic skin

Variceal bleeding nursing priorities

•NPO, Elevate HOB, Intubation

•Fluids/PRBCs

•Octreotide infusion

•Proton pump inhibitor (eg, pantoprazole)

•beta blockers (propranolol)

•Prepare for emergency esophagogastroduodenoscopy (EGD)

>Sclerotherapy (injects agent to scar/close vessels)

>Band ligation (strangulates varices)

>Insertion of Sengstaken-Blakemore tube

Variceal Bleeding: prevent aspiration

-NPO prevents aspiration and prepares pt for urgent endoscopt

-elevate HOB

-suction if massive bleeding, decreased LOC, unable to protect airway

Variceal Bleeding: medications

-2 large bore IVs

-Rapid IV bolus to maintain perfusion

-Packed RBCs to replace blood loss

-May need platelets or FFP

-Octerotide Infusion causes splanchnic vasoconstriction

>decreases portal pressure

>decreases bleeding from varices

-PPI (pantoprazole) to reduce gastric acids and stabilize clots

-antibiotics (ceftriaxone) prevents SBP and infections

Clinical priorities of Variceal bleeding

•Airway first (risk of aspiration)

•Volume resuscitation (shock)

•Lower portal pressure (octreotide)

•Endoscopy ASAP

Portal Pressure Pops Veins

-Esophagus → varices

-Umbilicus → caput medusae

-Rectum → hemorrhoids

Sengstaken-Blakemore Tube

-If bleeding NOT controlled

-Balloon tamponade → compresses varices

-Temporary, high-risk (aspiration, rupture)

Ascites

•Almost all blood from GI tract is collected in the portal veins and carried to the liver

•Cirrhosis: blood back up to the GI, accumulation of protein into the peritoneal space

•Effective Circulating Volume (ECV)-> renin angiotensin response -> Na+ & H2O retention -> ↑ hydrostatic pressure & lymph formation -> worsening ascites

S&Sx of Acites

•Bulging flanks, protruding umbilicus

•Fluid wave ( palpate) , shifting dullness ( percussion)

Ascites Treatment

•Conservative unless ventilation/mobility impairment

•Na+ restrictions, diuretics, paracentesis

•IV colloids (albumin)

•Shunting or TIPS procedures

•salt first, then meds, then needle, then shunt

•restore comfort and breathing while protecting circulation and electrolytes

Paracentesis

•removal of fluid with a needle

•Caution: Look out for fluid redistribution post-paracentesis -> HYPOvolemia symptoms!

•Document how much fluid was "tapped" (removed) by MD

Hepatic Encephalopathy

•Impaired ammonia metabolism protein breakdown -> ammonia

NORMALLY liver converts to less toxic urea -> excreted in urine

•Alterations:

>consciousness, behavior, neuromuscular

•common triggers:

>Increased protein intake

>overuse diuretics

>CNS depressants

>Hypoxia increases toxicity of ammonia

>Acute infections

Hepatic Encephalopathy Treatment

•Safety: protect airway (aspiration risk); minimize injury, falls

•Lactulose: P.O. / NGT / enema

>gradient ammonia migration: serum to colon sugar content... osmotic diarrhea

•Neomycin sulfate & Xifaxin (rifaximin)

>Abx to destroy normal colon flora -> diminishes protein breakdown/absorption -> minimizes ammonia production

Hepatic Encephalopathy Nursing Interventions

•Monitor mental status, hand tremors, LOC

•Administer lactulose (traps ammonia in stool)

•Avoid high-protein diets during acute episodes

•Prevent constipation (reduces ammonia absorption)

Hepatitis Pathophysiology

•Widespread inflammation of the liver

•Causes by Viruses (hepatitis ABC), Alcohol, Medications

>medications: Acetaminophen, Statins, Isoniazid (INH)

Hepatitis A

-Fecal-oral route (contaminated food/water, poor hygiene)

-Acute, short-term only — no chronic infection

-Vaccine available; hand hygiene

Hepatitis B (HBV)

-Blood, sexual contact, perinatal (mother→baby)

-Can be acute or chronic; risk for cirrhosis and liver cancer

-Vaccine available; safe sex, avoid needle sharing

-need routine screening for HCC (ultrasound + AFP)

Hepatitis C (HCV)

-Bloodborne (needles, transfusions, IV drug use)

-Often becomes chronic; leading cause of liver transplants

-No vaccine; screen blood donors, needle safety

-Need routine screening for HCC (ultrasound + AFP)

Hepatitis D (HDV)

-Requires Hepatitis B virus to replicate

-Co-infection makes HBV more severe

-HBV vaccination prevents HDV

Hepatitis E (HEV)

-Fecal-oral route (contaminated water; rare in U.S.)

-Acute, self-limiting; dangerous in pregnant women

-Avoid contaminated food/water in endemic areas

Acute hepatitis Clinical Features

◦Fever

◦Anorexia, nausea, malaise

◦Pain - usually right upper quadrant

◦Jaundice

◦Pruritus (ammonia build up)

◦Dark urine and pale stools

◦Hepatomegaly

Diagnosis of hepatitis

◦Blood testing for antigens and antibodies

◦Elevated liver function tests (LFTs)

>AST

>ALT

Nursing Interventions of Hepatitis

•Antivirals (for Hepatitis B and C)

•Standard precautions

>Hand hygiene - Hepatitis A

>Appropriate needle disposal

•Monitor LFTs

•Adequate fluids (2 to 3 L/day) and rest

Hepatitis: Foci of Care

•Monitor/manage progression through labs, jaundice, stool/urine, A/N/V

•Monitor for destabilization

>encephalopathy, ascites, hemorrhage

>fluid retention, hypoglycemia

•Monitor/manage fatigue, skin integrity

•Monitor labs for wellness

•Knowledge deficit: self-care, transmission, prevention

Complications of Hepatitis

◦Changes in neurological status

◦Bleeding

◦Fluid retention

Hepatitis Recovery

•Convalescence lasts weeks

•Gradual decrease in symptoms

•Liver function tests slow return to normal (2‐6 months)

•Serum antibody levels rise

•95 percent of patients will recover completely

•rest, nutrition, and avoidance of alcohol remain essential

Hepatitis Teaching

•Usually treated as outpatient unless severe liver failure occurs

•Avoid high fat diet

•Eat small and frequent meals

•Avoid liver toxins: acetaminophen, alcohol

•Hepatitis A

>Refrain from sharing utensils or drinking glasses

>Proper hand hygiene and food handling

>Vaccination

•Hepatitis B and C

>Refrain from sharing razors, needles, and syringes

>Use condoms during sexual intercourse

>Receive Hepatitis B vaccination

Transjugular intrahepatic portosystemic shunt (TIPS)

-procedure that may be used to reduce portal hypertension and its complications especially variceal bleeding

Criteria for Transplantation

•End‐stage organ failure

•Short life‐expectancy

•Severe functional disability

•No other serious health problems

•Psychological readiness

•No Malignancies

•Candidates must have end-stage disease, no major comorbidities, and strong psychological and social readiness

NOT Considered for Liver Transplant

•If the patient's organs, infection status, or psychosocial readiness are unstable, transplant outcomes are poor

•Advanced sequelae of liver disease

•varices, hepatorenal syndrome

•Systemic conditions

•sepsis, CVS, DM, severe HTN

•Intellectual limitations/psychosocial instability

•Active alcoholism

•Advanced catabolic state

Portal vein thrombosis

Liver Transplant

•Deceased donors

•Living donors give partial organ

•Orthotopic organ placement

•Large organ, rich blood supply

>Hemorrhage risk

>Monitor liver & coagulation function tests

•Life‐long immunosuppressive medications

>Daily labs in hospital (discharge 7‐10 days)

•Rejection risk

Liver Transplant After-Care

•Bleeding, rejection, infection

•Organ shut‐down (primary nonfunction)

•Hepatic artery stenosis, thrombosis

•Portal vein stenosis, thrombosis

•Hepatic outflow obstruction

•Biliary complications (15‐20%; leaks, strictures, obstructions)

•Renal dysfunction (17‐95%; drug‐induced, diabetes, pre‐existing hepatorenal syndrome)

•Malignancy

Intentional Rounding Hepatic Dysfunction

•Patient's LOC, spontaneous activity

•Safety risks

•mentation (daily signatures)

•symptoms & management success

•Skin color, invasive devices entry sites

•Risk for bleeding

•Urine & stool color, consistency, volume

•Review medications/labs for toxicity

Clinical Priority Hepatic Dysfunction

-Brain → LOC changes = encephalopathy

-Bleeding → skin, stool, INR

-Fluid → ascites, edema, urine

-Infection → SBP risk, lines, fever

Cholelithiasis

•Inflammation of gallbladder

•bacterial, chemical irritation w/stone

•obstruction w/o stone d/t trauma, surgery, burns, sepsis, SLE

•Supersaturated bile, stasis, precipitates

•Cholesterol, pigmented

•Associations:

>more women than men, obesity, rapid weight loss, use of estrogens

Cholecystitis Risk factors

•Gallstones (most common cause)

•Female clients over the age of 40

•Multiparous women

•Oral contraceptive use

•Elevated serum cholesterol levels

•High-fat diet, obesity, sedentary lifestyle

•Diabetes mellitus

•Rapid weight loss (changes bile composition)

Cholelithiasis S&SX

•food stimulation moves stone to block duct

•pruritus

•pain after meal (especially high‐fat)

•persists rather than resolving

•nausea; belching, flatulence, indigestion

•epigastric pain, decreased or absent BS

•mild jaundice (obstruction of bile flow from liver)

>clay‐colored stools, dark foamy urine, steatorrhea

•bacterial, chemical irritation w/stone

•obstruction w/o stone d/t trauma, surgery, burns, sepsis, SLE

•Duration: Prolonged (>6 hours) and does not subside with rest

-Fever + RUQ pain + Murphy's sign

-Add jaundice or clay-colored stool, and bile flow is clearly obstructed

Diagnosis of cholelithiasis

ultrasound, oral cholecystogram, endoscopy, (ERCP)

What to watch for after ERCP

-Pain, Pancreatitis, and Perforation

-monitor for sudden abdominal pain, fever, or bleeding

Cholelithiasis: Collaborative Management

•Pain management

•Stone retrieval by:

>ERCP

>laparoscopic (90%)

>open cholecystectomy

•Oral dissolution therapy, lithotripsy

Cholecystitis Labs

•Kehr's sign

>right shoulder radiated pain w/breathing

•Murphy's sign

>pain on deep inspiration w/palpation RUQ

•Elevated: WBC, serum bilirubin, alkaline phosphatase, amylase/lipas

Endoscopic Retrograde Cholangio Pancreatography

-retrieves, lap chole removes, and lithotripsy breaks — all to get bile flowing freely again

-Procedure in which an endoscope is used to visualize the common bile duct and the pancreatic and hepatic ducts

-procedural sedation

-topical anesthetic spray to posterior oropharynx (to reduce

cholecystectomy Nursing Interventions

◦Pain management

>NSAIDs, opioids

◦IV fluids and electrolytes

◦IV antiemetics

◦IV antibiotics

◦Keep client NPO to rest the gallbladder

-Postoperative

◦Ambulation and hydration

◦Low-fat diet initially → regular diet after a few weeks

Cholecystectomy (laparoscopic)

•Ambulatory (outpatient, not hospital) surgery

•Multiple "stab" wounds, insufflation with CO2, cameras, laser, "bagged" & removed

•Fewer pulmonary complications (still a focus)

•Less painful

Cholecystectomy (laparotomy)

•Hospitalized (acute care setting)

•Prevent/minimize pulmonary complications!

>Proactive pain management: PCA opioids, splinting

>Incentive spirometry, TCDB & ambulate/mobilize

•NPO, NGT, antiemetics

•T‐tube/C‐tube, wound drain, incision care

•Patient discharge education

>pain, wound, tubes, diet, activity restrictions

Cholecystectomy Patient discharge education

-pain, wound, tubes, diet, activity resumption

-monitor for bile leak, infection, and gas-related shoulder pain after surgery

Cholecystitis Complications

•GB perforation (10%)

•Peritonitis (bile spill)

•Pericholecystic abscess (15% mortality)

•Empyema of gallbladder

Suppurative cholecystitis...->sepsis/shock

Self-Care Management Education

•Reportable conditions (obstruction, infection)

•Medications

•Wound/dressing/drain care

•Avoidance of ETOH 2 months

•No lifting >20 lbs. for 10 days

•Low‐fat diet

•teach patients to protect the incision, monitor for infection, rest the liver, and eat light

Foods to Avoid Cholecystitis or Cholelithiasis

-Foods high in cholesterol

-Dairy Products

-Fried Foods

-Gas forming foods

-Nuts, chocolate

-low-fat, small-meal pattern

Cholangitis

•Bacterial inflammation of bile ducts

•associated with stone obstruction (80%)

•predisposition: stagnant bile flow

•pancreatic cancer

•procedures (ERCP, T‐tube contrast injections)

•T‐tube infections (90% colonized within week)

Cholangitis: S/Sx

•Charcot's triad:

1. Fever with chills - from infection and bacteremia

2.RUQ abdominal pain due to bile duct inflammation

3.jaundice

•Elevated WBC, serum bilirubin, AST, ALT

•If sepsis develops, the triad progresses to "Reynolds Pentad":

>Charcot's Triad + Hypotension + Altered mental status

Cholangitis: Collaborative Management

•IV ABX

•Emergency GB decompression

•ERCP

•PTC (percutaneous transhepatic cholangiography)

•Surgery NOT done (20‐60% mortality)

•Major complication: hepatic abscess (15%)

Substance intoxication vs substance abuse

-Substance intoxication

>Changes in behavior caused by effect on central nervous system

-Substance abuse

>Unable to discontinue use

>Necessary for daily functioning

▪Sedatives

▪Amphetamines

▪Opiates

▪Cannabis

▪Alcohol

▪Nicotine

▪Cocaine

AUDIT screening

○Alcohol

○Use

○Disorders

○Identification

○Test

CAGE questionnaire

○Cut down

○Annoyed

○Guilty

○Eye-opener

TWEAK questionnaire

○Tolerance

○Worry

○Eye-opener

○Amnesia

○Kut down

Subjective Assessment

•Current level of intoxication

•Amount of substance consumed over a specific period of time

•Average amount of alcoholic beverages per day, per week

•History of substance use

Objective Assessment

•Vital sign changes

•Unsteady gait

•Altered level of consciousness

•Slurred speech

•Impaired judgment

•Facial flushing

•Pupillary changes

•Behavioral changes

Laboratory findings

•Serum protein gamma-glutamyl transferase (GGT)

○Indicator of chronic alcohol use

•Carbohydrate-deficient transferrin (CDT)

•Serum aspartate aminotransferase (AST)

•Blood alcohol concentration (BAC)

Mechanism of Action Opioids

-morphine, hydromorphone, methadone, CODeine, hydroCODone, oxyCODone, fentanyl, meperidine

-Opioids act on multiple receptor types (mu, kappa, delta) located throughout the brain, spinal cord, and GI tract

-Treat moderate to severe pain

-Release dopamine → pleasure and euphoria

Opioid Overdose - Risk Factors for Death

•Older age

•Concurrent COPD or asthma

•Use of opioids with other CNS depressants

Opioid Intoxication clinical features

•CNS depression

•Respiratory depression

•Pinpoint pupils

•Bradycardia

•Hypotension

•Decreased bowel sounds

•Cold and clammy skin

Opioid Intoxication Diagnostics

•ABGs - respiratory acidosis

Management of Opioid Intoxication

•Administer naloxone

>Opioid antagonist

>Reverses respiratory depression

>Acts quickly but short duration

>No response → repeat in 2-3 minutes

>May reenter intoxication due to short duration of action

>Monitor for symptoms of withdrawal

•Maintain airway

>Aspiration precautions

•IV fluids for hypotension

•Cardiac monitoring

•Fall precautions

•Emotional support

•Resources for addiction counseling

ETOH Withdrawal Syndrome

•Signs & symptoms of intoxication, withdrawal and overdose

•Alcohol withdrawal symptoms

•Sample "CIWA" scale for objective, consistent assessment of alcohol withdrawal and intervention

Clinical Institute Withdrawal Assessment (CIWA)

•Vital signs

•Orientation

•Nausea and vomiting

•Tremors

•Diaphoresis

•Seizures

•Paresthesias

•Auditory disturbances

•Visual disturbances

•Headaches

•Anxiety

•Irritability

Alcohol Withdrawal Syndrome Stages

1. anxiety, insomnia, nausea, abdominal pain

2. high blood pressure, increased body temp

3. hallucinations, fever, seizures, and agitation

Alcohol Withdrawal Syndrome Treatment

Benzodiazepines - still gold-standard for moderate to severe withdraw