Adult Health II Exam 2

Minimum Urine Output

30mL / hr

• Low urine output is a sign of hypovolemia or kindney injury

Isotonic

No net fluid shift into or out of RBCs

• Fluid = blood

• 250-375 mOsm/L

Hypertonic

Pulls fluid out of RBCs and into ECF

• >375 mOsm/L → High osmolality (fluid enters ECF)

Hypotonic

Fluid moves into RBCs from ECF

• <250 mOsm/L → Low osmolality ( Less fluid in ECF)

Isotonic Solutions

TYPES

• Normal Saline (0.9% NaCl)

• Lactated Ringer’s

• Dextrose 5% in Water (D5W)

  • D5W is isotonic in the bag but hypotonic in body after dextrose is metabolized (contraindicated in fluid resuscitation; hypotonic solution will worsen shock)

INDICATION

• Used for fluid resuscitation. Expands ECF w/o causing 3rd spacing

RISKS

• Fluid overload in elderly or pts with Heart Failure or Kidney Disease

Hypertonic Solution

TYPES

• 3 or 5% NaCl

• Dextrose 10% in Water (D10W)

• Dextrose 5% in NS

• Dextrose 5% in LR

• Parenteral Nutrition (TPN/PPN)

INDICATIONS

• HYPOnatermia

• Cerebral edema (due to increased ICP)

• Nutritional Support

RISKS

• Fluid overload & pulmonary edema

NURSING INTERVENTIONS

• Infuse slowly & monitor serum Na closely

Hypotonic Solutions

TYPES

• 0.45% NaCl

• 0.33% NaCl

• D5W (hypotonic in body)

• D2.5W

INDICATIONS

• Hypertonic dehydration

• Hypernatermia

• Gastric fluid loss

• Maintenance fluids

RISKS

• Avoid in patients at risk for increased intracranial pressure (stroke, head injury) or in third-spacing (ascites, burns, trauma)

  • Hypotonic causes cells to swell worsening edema that is already present.

Peripheral IV therapy

Assess site regularly and before use

• Assess for pain, infiltration, burning, swelling, or redness

• Label & document date, gauge, & site

• Change continuous sets q96h & intermittent sets q24hrs

Saline Lock

A PIV that is capped & flushed between intermittent doses

• Must keep insertion site visible under transparent dressing

• Dressing should be clean, dry , & intact

Flushing

Used before and after PIV use to keep IV patent & push all medications into the body.

• Uses 3-5 ml NS and up to 10ml

• Never push flush against resistenance (may indicate occlusion, or infiltration)

• Use slow-push method

Can CNAs flush IVs?

No, at least for most states. Answer is no on NCLEX

Phlebitis

Inflammation of vein wall

TYPES

• Mechanical via catheter movement or size

• Chemical via irritating drug/solutions

• Bacterial

SIGNS

• Red streak

• Palpable venous cord

• Warmth

• Pain & tenderness

• Wwelling

GRADING

• Use INS Phlebitis scale

TREATMENT

• Stop infusion & remove catheter (if grade 2 and +)

• Apply warm compress & elevate extremity

• Give analgesics

• Restart IV in opposite extremity

• Culture purulent drainage

INS Phlebitis Scale

Grade 0: no symptoms

Grade 1: Erythema at site, with or w/o pain

Grade 2: Pain at site with erythema and edema

Grade 3: Pain, erythema, edema, streak formation, & palpable venous cord

Grade 4: Grade 3 + palpable venous cord >1 inch & purulent drainage

Infiltration

Non-vesicant solution (is not necrotic) leaks into surrounding tissue

SIGNS (Compare effected extremity with opposite extremity)

• Swelling

• Coolness

• Blanching or taut skin (tight skin)

• Slowed or stopped infusion

• Leaking at site

• Apply light pressure above site, if infusion keeps running, infiltration is likely (means that it is not in the vein)

NURSING ACTIONS

• Stop infusion & remove catheter

• Elevate & apply warm or cold compress (depending on solution)

• Restart IV on opposite extremity

• Grade with INS infiltration scale

Obstruction

Partial or complete blockage of catheter

CAUSES

• Mechanical : Closed clamp, kinked tubing, extremity position, tight dressing

• Thrombotic: Blood clot

• Non-thrombotic: Drug or mineral precipitate

NURSING ACTIONS

• Trace line from patient to the bag

• Reposition extremity

• Flush gently w/10mL diameter syringe

  • NEVER force the flush. If occlusion continues, remove & restart

Extravasion

Vesicant solution leaks into surrounding tissue

• Most dangerous complication; causes tissue necrosis, compartment syndrome, & loss of function

• May need surgery if complications lead to nerve damage

NURSING ACTIONS

1. Stop the infusion & disconnect tubing

2. Aspirate flush to pull out the med

3. Notify provider

4. Give antidote per protocol

5. Elevate extremity

Types of Irritants

• Potassium Chloride at low concentrations

• Many IV antibiotics

Vesicants

• Chemotherapy agents

• Vasopressors

• Promethazine, vancomycin

• Concentrated solutions (ex: dextrose >12.5%, NaCl >3%)

Central Lines

Enters the lower part of SVC, near the cavoatrial junction.

• IS STILL A VENOUS LINE (The SVC is a large vein)

ADVANTAGES

• Lasts longer and more reliable than PIV

• Draws blood samples w/o need for 2 IVs

• Able to give vesicants, TPN, chemo, and hyperosmolar solutions

• Can give KCl (potassium chloride) at faster rates (up to 20mEq/hr)

• Can measure Central Venous Pressure (CVP) → Gives info on fluid status

• Long-term venous access

DISADVANTAGES

• CLABSI → Monitor for fever, chills, redness, drainage at site

• Sepsis

  • Due to direct connection of catheter to the heart

  • Only use central lines when necessary. Use PIV if possible to prevent increased CLABSI risk.

• Thrombosis (DVT) → Monitor for arm, neck, or face swelling, and pain

Ways to Prevent CLASBI

• Hand Hygiene

• Scrubbing the hub

• Dressing change

• Skin wipes

Types of Central Line

• Non-tunneled

• Tunneled

• Implanted ports

• Open Tips

• Valve Tips

Tunneled Central Line

Travels under the skin before reaching the SVC.

• Makes it safer to prevent CLASBI in long term use.

EX: Hickman

Non-tunneled Central Line

Enters directly into SVC

EX: central venous catheter, PICC lines

Implanted ports

“Port-a-cath”. Placed completely under the skin

• Uses a special type of needle to inject meds

WHEN ACCESSING

• Clean site using sterility

• Assess site for redness, pain, etc

• Put needles in & flush w/NS

WHEN DE-ACCESSING

• Flush w/ Heparin to maintain patency

• Should be routinely flushed & locked once per month even without use.

EJ Line

Is a peripheral line in the neck, NOT a central line

• PIV enter small veins

Peripherally Inserted Central Catheter (PICC)

Placed in a large vein of arm and then enters SVC, has two access ports to provide connection for fluids and meds.

• Can used same arm w/PICC to take blood pressure

Central vs Peripheral IVs

Central → Inserted into large veins and into SVC

Peripheral → Inserted into small veins

PICC lines vs Midlines

PICC lines are inserted at the arm and the cather extends into the SVC. Midlines is also inserted at the arm, but the catether stops at the armpit and does not enter the SVC

• Can also give TPN in PICC but not midlines

Power Injectable Devices

Power PICC/ Power Port → Used for contrast dye for CT test & etc

What needs to be done when IVs are placed?

• Must confirm tip position via chest X-ray

• Document the date, catheter type, number of lumens, length, site, tip confirmation, and sign with initials.

Complications of Central Line Insertion

• Arterial puncture, bleeding, or hematoma

• Pneumothorax (especially with subclavian & jugular lines due to proximity to lungs)

• Air embolism (Pt will have sudden SOB, chest pain, and hypotension. Make sure catheter is clamped, turn pt to the left, place Pt in Tredelanburg, and give O2)

• Catheter malposition

• Catheter shears off, causing catheter embolism

What does a correct PICC dressing look like?

• Clean, dry, & intact

• Labeled w/ date & times

• Visible insertion site

How to Remove Central Lines

Implanted Ports → Surgically removed

PICC & non-tunneled CVC → Removed by trained RNs per policy

• Place pt supine or in Trendelenburg

• Have patient perform Valsalva → Hold breath or hum as catheter is removed. Helps raise chest pressure to prevent air from being pulled in, reducing the risk of air embolisms.

• Apply pressure until bleeding stops, then apply an air-occlusive dressing for 24hrs

• Keep patient supine for 30 mins

• Make sure the removed catheter tip is intact and matches documented length.

Parenteral Nutrition (PN)

Nutrients give via IV that bypasses the GI tract

• Contains dextrose, amino acids, lipids, electrolytes, vitamins, & water

TYPES

• Total Parenteral Nutrition (TPN)

• Peripheral Parenteral Nutrition (PPN)

TPN

Meets full nutritional needs. Highly concentrated, so it is requires a central line (where blood flow is higher and dilutes TPN faster)

• Access: Central Line

• Osmolarity: HYPERtonic, 900 mOsm/L and above

• Dextrose Concentration: 15-25% or higher

• Duration: Long-term use

• Nutrition: Can meet full nutritional needs in a small volume

• Main Risks: CLASBI (due to central line use), metabolic complications, refeeding (due to Hx of malabsorption)

PPN

Lower-concentration formula through a peripheral vein. Used short-term or supplementally

• Access: Peripheral IV in a large vein

• Osmolarity: 900 mOsm/L or less

• Dextrose: Less than 10%

• Duration: Short-term (less than 2 weeks)

• Nutrition: Often partial, requires large volumes

• Main Risks: Phlebitis, infiltration, fluid overload

When is parenteral nutrition used?

It is used only when the GI tract cannot be safely used. If the gut is working, use it. Enteral nutrition (feeding tube into GI tract) is safer and better for the GI system. Save PN for those who really need it

When is PN most commonly used?

• Bowel obstructions → Mechanical blockage of GI tract

• Prolonged ileus → Decreased GI motility

• Short Bowel Syndrome → Not enough absorptive bowel to meet nutritional needs

• High-output fistula → Not receiving nutrients via food; just increases output

• Severe pancreatitis → Given when enteral feeding is not tolerated

• Severe Malabsorption → Intractable vomiting or diarrhea; severe GI toxicity

What is the main energy source in parenteral nutrients?

Dextrose. It contains glucose which is the biggest driver of energy

• 3.4 kcal per gram

2 in 1 Formulations

Includes Dextrose & Amino Acids. Hung for MAX 24 hrs; needs tubing changed every 24 hours.

• Should be a clear to slightly yellow color

• Lipids are given separately from bag

3 in 1 Formulations (TNA)

Contains Dextrose, Amino acids, & Lipids. Hung for MAX 24 hours; tubing is changed every 24 hours

• Discard any PN that is still hanging if time limit is reached, even if volume remains, to prevent bacterial growth.

• Should be a uniform milky white

• Discard if there is separation or oil droplets

Hanging PN (like med admin)

1. Verify → Check bag with MAR, double-check pt allergies

2. Inspect → 2-in-1 should be clear, 3-in-1 should be white

3. Warm PN

4. Prepare → Use aseptic technique, new tubing & filter, scrub hub before connection.

5. Connect to correct lumen

Why is a filter used in PN?

It traps particles and large fat droplets before it reaches the patient.

• If filter is clogged, DO NOT remove clogs. Replace it and notify pharmacy

Lipid Emulsion

Hung for max 12 hours, tubing is changed every 12 hours

• Has risk of growing bacteria faster than in a mixed bag.

Hypoglycemia Risk in PNs

1. Assess Blood sugar in the first 24-48 hours of PN

2. If the bag is interrupted/delayed, hang 10% dextrose at the same rate to prevent hypoglycemic risk (NEVER speed up PN rate to “catch up”

3. When stopping PN, taper off. Check glucose 30-60 mins after stopping

Monitoring Patients on PN

1. Blood glucose (q4-6h when starting)

2. Weight (same scale & time)

3. Record I&Os

4. Vitals & temp q4h

5. Monitors electrolytes, BUN, creatinine, Mg, & P

6. Monitor triglycerides & LFTs

7. Monitor Line site & dressing every shift

What is the most common metabolic complication?

Hyperglycemia.

• Is caused by dextrose load stress, infection, steroid use, and diabetes

• Treated with insulin and reduced dextrose

How does hypoglycemia occur in PN use

Caused by sudden interruption or delay to PN.

• Signs → Shakiness, sweating, tachycardia, confusion

• Prevention → Hang DW10 if PN is interrupted and taper instead of abruptly stopping PN.

Refeeding Syndrom

Occurs when feeding restarts after starvation. Insulin drives phosphorus, potassium, and magnesium into cells, so serum levels drop

NURSING ACTION

• Monitor for drops in phosphorus, potassium, or magnesium q12h within first 5 days; fluid retention, arrhythmias, resp failure, and confusion

PREVENTION

• start low with PN (only 10-20 kcal/kg/day) and slowly advance.

• Give thiamine 100 mg before feeding everyday for 5-7 days

• Correct electrolytes

MOST AT RISK

• Low MBI

• Significant weight loss

• Little to no intake fro 5-7 days

• Alc use disorder

• Eating disorders

Signs of CLABSI

• Fever

• Chills

• Rise in WBC

• Glucose is harder to manage

• Redness or drainage at site

Does TPN or PPN have a higher risk for phlebitis and infiltration?

PPN because it is peripherally administered.

• Should assess the site often and restart at the first sign of problems.

Complications to PPN

• Fluid overload (weight gain of more than 1kg per day)

• Electrolyte imbalance

• Hypertriglyceridemia

• PN-associated liver disease (elevated liver enzymes & cholestasis from long-term PN)

RBC storage

up to 42 days refrigerated at 1-6c

• Unused blood must be returned to blood bank

Platelet storage

Lasts 5 days at room temp. IS NEVER REFRIDGERATED

Rule of 3

HCT is about 3 times hemoglobin (HgB)

• One unit of RBC increases HgB by 1 and HCT by 3%

Normal HgB

Women: 12-16

Men: 14-18

Normal Hematocrit

Women: 37-47%

Men: 42-52%

Normal Platelets

150k-400k

Normal PT (prothrombin time)

11-13.5 sec

Normal INR

1.0

• Therapeutic range (with warfarin): 2-3

Normal aPTT

25-35 seconds

Packed RBCs

Purpose: Increase O2-carrying capacity or to replace blood loss

Indication: HgB <7 g/dL , after surgery, or after active bleeding

Expected Response: HgB increase by 1 g/dL, HCT increase by 3%

Key Points: Must complete tranfusion within 4 hours

Platelet Transfusion

Purpose: Control or prevent bleeding

Indication: <10K (for prophylaxis) or <50K with bleeding or surgery

Expected Response: Increase by 5K-10K

Key Points: Never refrigerate

Fresh Frozen Plasma (FFP)

Purpose: Replace clotting factors

Indication: INR >1.5 w/ bleeding or before a procedure

Expected Response: INR, PT, and aPTT decrease to normal

Key Points: Must be ABO-compatible; use within 24 hours of thawing

Which blood product has the highest risk for bacterial contamination?

Platelets due to being at room temperature. Has the highest risk for bacterial contamination and sepsis.

Blood Transfusion Verification & Administeration

1. Must obtain consent for each new situation

2. Must verify type & cross match (ABO & Rh factor), want a negative result

3. Must use Y-tubing that is 18-20 gauge, prime only with 0.9% NaCl, never run blood with meds or other fluids at the same time.

4. Must start blood infusion with 30 mins of receiving from blood bank

5. Must complete infusion within 4 hours of spiking the bag

6. Must assess baseline vital signs before administering blood

7. Stay with the patient for the first 15 mins and reassess vitals signs and ask about symptoms after 15 mins.

8. Then reassess vital signs every hour

9. After transfusion is complete, reassess vitals again and flush with normal saline.

What should a nurse do if a patient needs a blood transfusion but has only one IV that is running IV antibiotics and pain meds?

Call for a 2nd IV, give time sensitive pain meds and antibiotics first before transfusion.

What should a nurse do if a patient is called for an MRI but needs a transfusion?

Start the transfusion after the MRI because it is time sensitive or if the transfusion is already running, finish the transfusion before doing MRI.

Transfusion Reactions

Occurs when blood is not ABO and Rh compatible

SIGNS

• Febrile (rise of >1.8F)

  • Give antipyretics (acetaminophen)

• Allergy (urticaria (hives)pruritis, flushing, anaphylaxis)

  • Give antihistamines. Give fluids, epinephrine, & airway support if anaphylaxis

• Feeling of impending doom

  • Sign of ABO mismatch, give fluids to protect kidneys; monitor I&O and for DIC

• TACO (fluid overload) → will see dyspnea, HTN, crackles, JVD

  • Elevated HOB, give O2 & diuretics (furosemide)

• TRALI (lung injury) → will see sudden hypoxemia, pul edema within 6 hrs not caused by fluid overload

  • Give O2 & resp support

• Sepsis (high fever, rigors, hypotension)

Direct COOMBS

Looks for antibodies stuck onto RBCs after a transfusion

Indirect COOMBS

Looks for antibodies in plasma inside the bloodstream before a transfusion

Nursing Actions for Blood Tranfusion Reactions

1. STOP the transfusion → Disconnect line, pull back to remove as much blood as possible

2. Keep vein open by hanging NS on NEW tubing

3. Assess patient → VS, symptoms, & recheck pt ID & blood label

4. Notify Provider & blood bank

5. Send blood back to blood bank

6. Treat and document

Liver Function

Helps to breakdown hormones & drugs, filters waste (converts ammonia to urea), and makes bile.

• IF damage to liver → Will have jaundice (due to inability to remove bilirubin from bloodstream), have increased ammonia leading to confusion and change in LOC, and causes decrease clotting factors, increasing risk for bleeding

Liver Function Tests (LFTs)

ALT & AST

ALT

Measures amount of alanine aminotransferase (a type of liver enzyme) inside liver cells

• Normal range: 7-55 u/L

• Increases in liver damage

AST

Measures amount of aspartate aminotransferase (a type of liver enzyme) in liver cells.

• Normal range: 10-40 u/L

• Increases in liver injury, indicates damage due to alcohol

Bilirubin

Normal: 0.1-1.2

• Jaundice occurs when >2-3mg/dL

Ammonia

Normal range: 15-45 u/dL

• Increases in advanced liver disease, indicates encephalopathy

Hepatitis

Inflammation of the liver caused by viral infections (Type A,B, C, & D), alcohol, drugs, and autoimmune disease

• Acute = <6months , Chronic = >6 months

• Pathophysiology

  • Virus damages hepatocytes, causing impaired bile flow, clotting, glucose regulation, protein metabolism, & detoxification

    • If acute, hepatic cells will regenerate and usually make a full recovery

    • If chronic, will have ongoing hepatocyte destruction leading to fibrosis, then cirrhosis, then liver failure.

SYMPTOMS

• Will have systemic immune complexes → Rashes, arthritis, fever, vasculitis (inflammation of blood vessels), glomerulonephritis

Acute Hepatitis Symptoms

Pts are usually asymptomatic

• TRIAD → Jaundice, dark (cola-colored) urine, clay-colored stool

• Pruritis

• RUQ tenderness

• Hepatomegaly

Chronic Hepatitis Symptoms

• Anemia

• Easy bruising or bleeding

• Spider angiomas (spider-like dilations of blood vessels)

  • Caused by excess estrogen that is not broken down by live due to damage

• palmar erythema

• !! Chronic can progress to cirrhosis, portal hypertension, and liver failure

Hepatitis A

Transmission: Fecal-oral (via contaminated food or water). IS ONLY ACUTE

S&S: Can be asymptomatic, flu-like symptoms, may have Triad symptoms (jaundice, dark colored urine, and clay colored stool)

Treatment: Supportive care only, usually resolves on its own

Prevention: 2 dose vaccine series

Prophylaxis: Hep A vaccine or immunoglobulin after 2 weeks if exposure

Outcomes: usually a full recovery, no carrier state or chronic hepatitis

Hepatitis B

Transmission: Blood & body fluids (sexual, perinatal, shared needles). Can be acute or chronic

S&S: Can be asymptomatic. May have rashes or arthralgia (joint pain)

Treatment: If acute: supportive care, if chronic: oral antivirals (-vir meds)

Prevention: 2- or 3-dose vaccine series

Prophylaxis: HBIG & hep B vaccine within 24 hours of exposure

Outcomes: May be severe; carrier state possible. Increased risk for chronic hepatitis, cirrhosis, and liver cancer.

Hepatitis C

Transmission: Blood-borne (usually via injection drug use/sharing needles).

S&S: Usually asymptomatic or mild

Treatment: Oral direct-acting antivirals for 8-12 weeks

Prevention: No vaccine (only screenings in all adults at least once)

Prophylaxis: No post-exposure prophylaxis, only follow-up testing and treatment is infected

Outcomes: Chronic infection, increased risk of cirrohsis & liver cancer. Is curable with antivirals

• Hep C = Chronic

Cirrhosis

End-stage chronic liver disease develops over years to decades. Is non-reversible but has treatment

• Disorganized regeneration of liver cells causes fibrosis & nodules

  • Causes distorted vessels that impede blood flow, causing portal hypertension.

  • HTN leads to hypoxia & poor cell nutrition, leading to decreased liver function

  • NURSING ACTION: Give PPI’s, electrolyte replacement, & vit K (for clotting factors)

CAUSES

• Chronic hepatitis (B & C)

• Alcohol-associated liver disease

• MASLD (metabolic dysfunction-associated steatotic liver disease)

• Hemochromatosis

MANIFESTATIONS

• If early, very few symptoms → Fatigue, enlarged liver (hepatomegaly)

  • Other body systems will compensate for liver, so labs seem normal

• If late, other systems can no longer compensate for the liver (decompensated) → will see liver failure & portal hypertension

• Jaundice

• Ascites

• Peripheral edema

• Liver becomes small & nodular

• Skin → spider angiomas, palmar erythema, pruritus

• Blood → anemia, leukopenia, increased bleeding risk

• Neuro → encephalopathy, peripheral neuropathy

DIAGNOSTICS

• Elevated LFTs in early stage (AST & ALT may be normal at end stage due to smaller liver and less cells)

• US, CT, & MRI to visual liver size, nodules, & ascities

• Liver biopsy: Gives a definitive diagnosis

• Endoscopy: Screens for varices

COMPLICATIONS

• Portal hypertension → increased venous pressure in portal vein

• Esophageal & gastric varices (vessel dilations)

• Periperal edema

• Abdominal ascites → can become infected & lead to bacterial gastritis

• Hepatic encephalopathy

Nursing Interventions for Varices & Bleeding

1. Prevent bleeding → Do screening endoscopy, give non-selective beta-blockers (-lols), avoid alc & NSAIDs

2. Do Balloon tamponade to stop bleeding; do TIPS if bleeding persists

3. Do Band ligation for varices (pinches dilated vessel with band)

4. Give vit K & platelets as ordered to decrease bleeding risk

5. Monitor INR, platelets, H&H, hematemesis, & melena

Ascities

A complication of cirrohosis that occurs when portal hypertension causes protein to shift into lymph space, changing the osmotic pressure, and causes fluid to leak into peritonial cavity (3rd spacing)

• Hypoalbuminemia (low albumin): Decreases colloid oncotic pressure, causing fluid to shift out of vessels

• Hyperaldosteronism (high albumin): Increased Na reabsorption leads to water retention

TREATMENT

• Paracentesis (uses needle to remove fluid)

  • Give IV albumin if >5 L of fluid is removed

• TIPS (transjugular intraheptaic portosystemic shunt)

  • Procedure that shunts blood from portal vein directly to hepatic vein to lower portal blood pressure.

  • Allows albumin to bypass liver

  • Used for recurrent variceal bleeding or ascites

  • RISK: Increases risk for infection and worsening encephalopathy.

NURSING INTERVENTIONS

• Restrict sodium to <2g/day

• Give diuretics → Spironolactone (K+ sparing) & Furosemide

• Fluid restriction if Na is <125mEq/L

Hepatic Encepthalopathy

Complication of cirrhosis where ammonia cannot be converted to urea due to hepatocyte damage, and crosses over BBB changing LOC.

• If left untreated, will lead to cerebral edema, coma, or death

• Is usually reversible with treatment

MANIFESTATIONS

• Changes in LOC, Confusion, Poor concentration, Sleep changes

• Apraxia (distorted coordination between hands)

• Asterixis (flapping tremor of outstretched hands)

• Fetor Hepaticus (musty, sweet breath)

TREATMENT

• Lactulose → Jello-like. Needs to be titrated (adjusted) so that pt has 2-3 soft stools a day.

  • Traps ammonia and expels it in stool

  • Can cause bright colored urine

• Rifaximin → Added to lactulose to prevent recurrence of encephalopathy and to reduce ammonia-producing bacteria

NURSING INTERVENTIONS

• Promote protein → 1.2-1.5 g/kg/day. Give vegs & dairy if pt is protein intolerant

• Small, frequent meals & bedtime snacks.

• Replace B vitamins (thiamine, b12, etc)

• No alcohol

Liver Transplant

Definitive treatment fot decompensated, end-stage cirrhosis.

• Pt qualifies if they remain alc free for at least 5 years

Nursing Interventions for Cirrhosis

INTERVENTIONS

1. Reduce risk factors (alc, hepatotxic drugs, malnutrition)

2. Give frequent oral care & snacks

3. Cut nails short (to prevent deep scratches due to pruritus)

4. Give cool baths

5. Put pt in semi-Folwers in ascites to promote breathing. Ensure patient voids before paracentesis

MONITOR

1. Neuro → LOC, mental status, asterixis, & ammonia levels

2. Fluids → daily weight, I&O, abdominal girth, & electrolytes

3. Jaundice

4. Bleeding → INR, platelets, H&H, melena

Gallbladder Function

Stores and releases bile for lipid digestion

Cholelithiasis

Gallstones are caused by bile components (cholesterol, bilirubin, calcium)

• usually asymptomatic until stone movement

SYMPTOMS

• Biliary colic (severe upper GI pain) when stone moves or lodges a duct

• Severe RUQ/Epigastric pain, often after fatty meals

• Tachycardia, diaphoresis, nausea, prostration (like bending forward)

If complete obstruction of biliary duct, will see….

• Jaundice

• Dark urine

• Clay-colored stool

• Bile stasis (will lead to cholecystits) → When bile cannot enter duodenum, bile backs up back into gallbladder causing inflammation.

Cholecystitis

Inflammation of the gallbladder, usually from stone blocking a cystic duct.

• Acalculous: Cholecystitis that occurs without gallstones. Occurs in critically ill & elderly (caused by dehydration, fasting, opioids)

RISK FACTORS → the 4 F’s

• Female

• Fat

• Fertile

• Forty

SYMPTOMS

Acute

• RUQ pain & tenderness that radiates to R shoulder/scapula

• N&V

• Fever

• Leukocytosis

Chronic

• Fat intolerance

• Dyspepsia (indigestion)

• Heartburn

• Fatulence (gas)

DIAGNOSTIC STUDIES

• Ultrasound → FIRST-LINE TEST

• HIDA scan → assesses gallbladder function & cystic duct patency

• ERCP → Visualizes bile ducts & removes stones

• Percutaneous transhepatic cholangiography: Uses contrast dye to evaluate for dut blockage

LABS

• CBC → Will see leukocytosis

• Elevated LFTs (ALT, AST)

• Indirect, direct, and urine bilirubin

• Serum amylase if pancreas is involved.

Complications of Gallbladder Disease

• Gangrenous Cholecystitis (necrotic tissue)

• Abscess

• Pancreatitis

• Cholangitis

• Biliary cirrhosis

• Fistulas

• Rupture of gallbladder

Nursing Management of Gallbladder Diseases

Cholecystitis

• Pain control

• Antibiotics

• IV fluid & electrolytes

• NPO & NGT if vomiting

Stones

• Urodisol used to dissolve small stones

• ERCP used to remove bile duct stones

• Percutaneous transhepatic biliary drainage (PTBD)

Diet

• Small frequent, low fat meals

• Avoid rapid weight loss

Percutaneous Transhepatic Biliary Drainage (PTBD)

A procedure where a catheter is entered through the skin & liver into the bile ducts under imaging to drain bile into an external bag or into duodenum.

• Used when ERCP fails or is not possible.

NURSING CARE

• Secure catheter

• Monitor output

• Bleeding

• Bile leak

• Infection

• Flush only as ordered

Endoscopic Retrograde Cholangiopancreatography (ERCP)

Procedure where scope enters the mouth and into the duodenum, injecting contrast dye into the bile & pancreatic ducts to remove duct stones, place stents, or to perform sphincterotomy.

• Must be NPO for 6-8hr before

• Must be NPO until gag reflex returns

• Monitor for pancreatitis, bleeding, perforation, or infection

Laparoscopic Cholecystectomy

Removal of the gallbladder. Treatment of choice for gallbladder disease.

• Pt may have abdominal pain due to incision & trapped gas due to gallbladder inflation. Gas can cause pain in upper abdomen that radiates to upper shoulders.

  • Walking helps to expel gas.

MAIN RISKS

• Bile duct injury

CONTRAINDICATIONS

• Peritonitis

• Cholangitis (infection/inflammation of bile ducts)

• Gangrene/perforation

• Portal hypertension

• Bleeding disorder

Pancreas Function

• Exocrine function for digestion → Produces enzymes

• Produces islet cells that create & release insulin & glucagon

Acute Pancreatitis

Acute inflammation of pancreas. Can range from mild edema to hemorrhage to necrosis

CAUSES

• Gallstones & chronic alc use (most common)

• Hypertriglyceridemia (>1000mg/dL)

• Hypercalcemia

• Drugs

• Post-ERCP

• Tumors

PATHOPHYSIOLOGY

• Digestive enzymes active inside the pancreas, causing autodigestion (causes inflammation, vascular injury, & necrosis)

MANIFESTATIONS

• Sudden LUQ abdominal pain that radiates to back. (must be treated with IV opioids)

• N&V

• Vital Signs: Hypotension, tachycardia, fever, & tachypnea

• Monitor hypocalcemia (tetany, Chvostek’s sign, & Trousseau’s Sign)

• Hyperglycemia

• Abd tenderness & guarding

• Jaundice

• Tachycardia

• Crackles (Risk of ARDS)

• IF SEVERE: Flank & periumbilical ecchymosis (Grey Turner & Cullen’s sign)

DIAGNOSTIC TESTING

• Serum lipase or amylase 3x elevated

• Leukocytosis

• Other labs: liver enzymes, blood glucose & triglycerides

IMAGING

• Ultrasound to find gallstones (first line)

• CT if diagnosis is unclear

COMPLICATIONS

• Pancreatic pseudocysts

• Pancreatic abscess

• Systemic effects → hypocalcemia, hyperglycemia, ARDS, AKI, shock, paralytic ileus, change in mental status.

  • Pancreatitis is deadly due to its systemic effects

NURSING INTERVENTIONS

• Fluids → Early moderate IV Lactated Ringer’s, reassess often to avoid fluid overload

• Rest the pancreas → NPO and use NGT for low suction, Give PPIs to reduce acid secretion

• Pain → IV opioids (morphine, hydromorphone)

• Nutrition

  • If mild: low-fat solid diet within 24- 48 h as tolerated

  • If severe: enteral feeding, parenteral if not tolerated

• Teaching → Avoid alc & smoking; small low-fat meals; limit caffeine & spicy foods