GI Disorders

GI Disorders Overview

• Focus on peritonitis, bowel obstructions, ostomy, pancreatitis, and biliary tract diseases.

Learning Objectives

• Describe the interprofessional and nursing management of peritonitis.

• Distinguish among small and large bowel obstructions, including causes, clinical manifestations, and interprofessional and nursing management

• Select nursing interventions to manage the care of the patient after bowel resection and ostomy surgery.

Key Terms

• Acute Pancreatitis, Bowel Obstruction, Cholecystitis, Cholelithiasis, Chronic Pancreatitis, ERCP, Fistula, Jaundice, Ostomy, Paralytic Ileus, Peritonitis.

Peritonitis

Etiology and Pathophysiology

• Inflammation of the peritoneum due to contamination of bacteria/infection or irritating chemicals (peritoneum lines abdominal cavity). Can kill someone within 6 hours if untreated.

  • Irritating Chemical: Blood, hydrochloric acid (should stay within GI tract/stomach acid), etc.

• Causes:

  • Primary: Blood-borne organisms (virus, bacteria, infection).

    • Ex. Ascites from cirrhosis/liver failure → accumulation of fluid in the abdominal cavity allows bacteria to grow → infection.

    • Kidney failure → accumulation of toxins and fluid imbalances → infection.

  • Secondary: Organ perforation (leakage into the peritoneum from organs/anything that ruptures).

    • Ex. Ruptured appendix, stab wound, peritoneal dialysis (bad catheter care), ulcer perforation, diverticulitis.

• Pathophysiology: Initial chemical irritation (peritonitis) can progress to bacterial peritonitis → fluid shifts and adhesions.

  • Contents (chemicals) irritate the peritoneum and activate the compliment system. WBCs and fluid move toward site of irritation from intravascular fluid → adhesions develop → peritonitis.

Clinical Manifestations Peritonitis

• Severe, continuous RUQ abdominal pain—most common symptom.

• Rebound tenderness, rigidity/board-like abdomen, guarding, and spasm - common.

• Other symptoms: Shallow breathing (fluid shift), tenderness over area, fever, tachycardia, shallow breathing, nausea, vomiting, altered bowel habits.

• Potential complications: Hypovolemic shock (fluid shift into peritoneum & decreased perfusion), sepsis (lactic acid buildup/system response), intra-abdominal abscess (pus) (adhesions), paralytic ileus (volume sitting on top → temporary blockage of food and gas in the digestive tract), ARDS (fluid in air sacs from fluid shift of ascites and immune response).

Diagnostic Studies

• Involves history & physical examination (H & P), CBC, CMP, imaging tests (US, x-ray, CT), BUN & creatinine, GFR, and peritoneoscopy.

  • H&P: Peritoneal dialysis? Normal process? At home or clinic? (H&P)

  • Hematocrit (fluid shift) may be falsely elevated → look at RBCs and hemoglobin to see if pt is bleeding.

Interprofessional Care

• Perforation requires immediate surgical intervention.

• Preoperative (mild cases or poor surgical risk): NPO, NG suction (intermittent), IV fluids, antibiotics, analgesics, antiemetics (Zofran).

  • Often used as early intervention methods.

• Postoperative: Similar to preoperative care with additional monitoring and parenteral nutrition.

Nursing Management

• Vital sign monitoring (I&Os, O₂ needs)

• IV access (18 G or sometimes a 20 G for blood if needed)

• Pain management

• NPO; NG tube to low & intermittent suction

• Monitor fluid and electrolyte balance.

• Assess for worsening symptoms (sepsis, peritonitis spread).

• Emotional support.

• Drain care (if one is placed)

Intestinal Obstruction

• Simple: Intact blood supply

• Strangulated: No bloody supply

• GI System Review:

  • Stomach: Digestion in two ways: mechanical (movement) and chemical (hydrochloric acid/stomach acid and pepsin digestive enzyme). Produces intrinsic factor (needed for absorption of B12).

  • Small Intestine:

    • Duodenum: Absorbs minerals (iron, calcium, magnesium) and is where stomach contents meet pancreatic and liver enzymes to neutralize acid.

    • Jejunum: Absorbs nutrients (water soluble vitamins like B complex and C), sugar, and fats.

    • Ileum: Absorbs amino acids, fat-soluble vitamins (ADEK), vitamin B12, and has patches apart of immune system to protect against pathogens.

  • Large Intestine: Water absorption and mucus secretion.

    • Pts with a colostomy will still pass mucus and it will feel like a bowel movement (option to have anus sewn shut if too much).

Types and Causes (mechanical vs nonmechanical)

• Small Bowel Obstruction (SBO):

  • Mechanical (physical obstruction blocking movement): Surgical adhesions aka scar tissue (most common), hernias, Crohn’s disease (strictures), cancer, intussusception (blockage from intestine telescoping into another).

    • Ask about prior abdominal surgeries.

  • Nonmechanical (reduced or absent peristalsis): Paralytic ileus (most common), vascular emboli.

• Large Bowel Obstruction (LBO):

  • Mechanical (physical obstruction blocking movement): Colorectal cancer/CRC and diverticular disease (most common), volvulus (intestine folds onto itself), adhesions (scar tissue), ischemia, Crohn’s disease.

    • Diverticular disease includes diverticulosis (diverticula/small pouches protruding in the colon) and diverticulitis (diverticula become inflamed or infected).

  • Nonmechanical (reduced or absent peristalsis): Pseudo-obstruction (impaired peristalsis w/out obstruction), paralytic ileus, vascular emboli.

• Most mechanical obstructions occur in the small intestine.

• Pathophysiology for SBO and LBO: Fluid, gas, and intestinal contents back up proximally (right before site) of the obstruction and reduces fluid absorption and stimulates intestinal secretions (hydrochloric acid, pancreatic enzymes, etc).

  • Results in proximal bowel distension → reduces fluid absorption and stimulates intestinal secretion → Distal bowel empties and collapses (determines partial/full)→ Pressure in bowel lumen → increased capillary permeability (fluid moving out) → fluid leaks into the peritoneal cavity (peritonitis risk) → decreased circulating BV → hypotension and hypovolemic shock→ Bowel becomes edematous and ischemic (lactic acid increased from tissue breakdown) → Gangrene and necrosis → Perforation of the bowel wall → peritonitis and severe systemic infection.

  • Perforation requires immediate surgical intervention.

    

Nonmechanical Obstruction Subtypes

• Paralytic ileus (most common): Lack of intestinal peristalsis and bowel sounds.

  • Causes: Abdominal surgery (bowel and bladder last two things to wake up after surgery); peritonitis; inflammatory disorders; electrolyte imbalances (potassium/hypokalemia; potassium moves smooth muscle → Lasix is a risk factor); thoracic or lumbar spinal fractures (those nerves go into GI system).

  • Antispasmodics/ Anticholinergics contraindicated.

  • Usually affects both intestines.

• Pseudo-obstruction (rare): Impaired peristalsis with no actual obstruction and mainly affects large intestine only.

  • Causes: Neurologic conditions, drugs, endocrine and metabolic problems, lung disease, trauma, or burns.

• Vascular obstruction: Emboli or thrombi alter blood supply to a part of the intestines.

Clinical Manifestations of Bowel Obstruction

• Hallmark Symptoms (Order depends on cause and obstruction):

  • 1. Abdominal pain

  • 2. N/V (may be projectile)

  • 3. Distention

  • 4. Constipation (may be nothing there)

• ** Bowel sounds may be high pitched (above obstruction), absent (paralytic ileus), or hypoactive (LBO).

Interprofessional and Nursing Management (least invasive → most invasive, unless emergency)

• Conservative Management (Preferred if paralytic ileus or early bowel obstruction):

  • NG Tube for Decompression (hallmark treatment)

    • Monitor I&Os (30mL/hr normal) / electrolytes / acid-base

    • Reduces bowel distention and risk of edema, necrosis, and perforation.

    • Measurement: Nares → earlobe → xiphoid process

  • IV Fluids (D10W or D5W & Electrolyte Replenishment.

    • Dehydration Sign: Dry mucous membranes, decreased skin turgor, BP, tachycardia, and low urine output.

  • NPO Status.

• Paralytic ileus and adhesion-related obstructions often resolve without surgical intervention.

• Acid-Base Imbalances:
  ◦ Metabolic alkalosis – high obstruction (from vomiting a lot).
  ◦ Metabolic acidosis – low obstruction.

• Surgical Management:

  • Strangulation/Perforation → Emergency Surgery.

  • Colonoscopy for tumor removal or stricture dilation.

  • Partial or total colostomy or ileostomy for obstruction, necrosis, or perforation.

  • Resection of obstructed segment with anastomosis (put pieces of bowel back together).

    • Anastomosis works = bowel rest

    • Anastomosis doesn’t work = ostomy

      

• Diagnostics:

  • Imaging

  • LBO: Sigmoidoscopy or colonoscopy (finds location of obstruction and fixes)

  • Blood tests (CBC, CMP)

    • Increased WBC = strangulation (necrotic tissue) or perforation

    • Increased Hct = Hemoconcentration (increased concentration of blood cells, falsely elevated from fluid shift)

    • Decreased Hct and Hgb = Bleeding

    • Serum electrolytes, BUN, creatinine, GFR = hydration

Bowel Resection and Ostomy Surgery

Indications

• Removes cancer, repair obstruction/fistula (connection that shouldn’t be there)/perforation/traumatic injury, and treat an abscess, hemorrhage, or inflammatory diseases.

  • Common Etiologies: Colorectal cancer (CRC), IBD (Crohn’s and ulcerative colitis), necrotic bowel, perforated ulcer, diverticulitis, trauma.

  • Fistulas might exist between small bowel and large, between rectum and bladder.

  • Pts with Crohn’s disease or ulcerative colitis may have bowel resections done.

Ostomy Types

• Traditional Ostomy

  • End Stoma: Distal bowel removed and permanent stoma.

  • Loop Stoma: (Usually temporary) anterior wall opened for fecal
    diversion and distal opening to drain mucus; plastic rod in place 7 to 10 days

  • Double-barrel Stoma (usually temporary, trying to put back together): Bowel divided and two stomas created; proximal for fecal diversion and distal for mucus drainage.

• Continent Ileostomy (pt manually drains stool by insertion of catheter and holds more)

  • Kock Pouch

  • Barnett Continent Ileal Reservoir

• Temporary or permanent “takedown” procedure to reverse.

• Stoma should appear red, moist, and painless.

• The more distal the ostomy, the more likely contents will
  resemble normal feces (because the stool has more time to pass through).

  

• Sigmoid colostomy may not require a stoma bag if the patient has regular bowel movements.

Preoperative Care

• Stoma site selection and considerations

  • Within rectus muscle (decreased risk of hernia)

  • Flat surface (no creases, seal less likely to leak)

  • Patient is able to see it but it’s under clothing

Nursing Interventions Post-Surgery

• Monitor for Postoperative Complications:

  • Delayed wound healing, infection, hemorrhage, fistulas.

    • Record bleeding (minimal bleeding normal → intestines are vascular)

    • Unusual/foul odor → infection.

    • Edema, redness, high WBCs, drainage → infection.

      • WBCs should decreased after surgery otherwise notify HCP.

  • Electrolyte imbalances and dehydration.

  • Abnormal output → notify HCP

• Ostomy Assessment:

  • Normal: Pink-red, moist, mild swelling.

  • Abnormal: Pale, dark, excessive bleeding, “dusky” (blueish).

  • Assess every 4 hours (especially if new)

• Ostomy Care:

  • Empty pouch when 1/3 full.

  • Prevent gas buildup with diet modifications.

• Ostomy Education:

  • Demonstrate and observe patient/caregiver practice the following:

    • Remove old skin barrier, clean skin, correctly apply new skin barrier

    • Irrigation for regulation (distal colon ostomy)

    • Apply, empty, clean, remove pouch.

    • Empty pouch when 1/3 full.

  • Males: 3-12 months erectile dysfunction

  • Females: Vaginal dryness and decreased sensations

  • “Burp bag” due to gassiness.

  • May experience rectal bowel movement up to 3 days after surgery if emergency surgery was performed

• Dietary Management:

  • Small, frequent meals, adequate fluid intake.

    

• Psychosocial Support:

  • Address body image concerns, depression, coping strategies.

  • Normal ADLs within 6-8 weeks and avoid heavy lifting.

• Colostomy Function:

  • Output after peristalsis returns or up to 2 days after resuming diet

  • Some mucus production likely.

  • Excess gas common for 2 weeks

• Ileostomy Function:

  • First 24-48 hours minimal drainage (liquid-semiliquid)

  • Peristalsis returns → 1500-1800 mL/day and will decrease about 500 mL/day

  • Water absorption increases and feces thickens while volume decreases → watch for dehydration.

  • Chew thoroughly any nuts, raisins, popcorn, coconut, mushroom, olive, stringy veggies, foods with skins, dried fruits, and meats with casings (otherwise lead to an obstruction).

  • Hypocalcemia: Confusion

• Anal Canal:

  • Kegel exercise recommended after 4 weeks

  • Incontinence of mucus

  • Phantom rectal pain (do not strain)

Acute Pancreatitis

Pathophysiology and Etiology

• Pancreatic enzyme activation that causes autodigestion of pancreas and severe pain by digesting normal organ tissue.

  • Autodigestion of pancreas → injury to pancreatic cells, activation of pancreatic enzymes → activation of trypsinogen to trypsin within pancreas (bleeding occurs).

  • Mild Pancreatitis:

    • Edematous or interstitial

  • Severe Pancreatitis:

    • Necrosis, organ failure, sepsis

    • 50% have long-lasting endocrine and exocrine dysfunction

    • Overall fatality rate 9%

  • Anatomy: Pancreas sits behind stomach.

    • Pain in pancreas → Happens in the upper abdomen and can radiate to the back.

    • Secretes 1000 mL of pancreatic juice per day.

    • Two functions:

      • Endocrine function: Related to diabetes and blood sugar function → produces hormones such as insulin and glucagon.

      • Exocrine Function: Cells secrete buffers (watery solution) and digestive enzymes (pancreatic amylase for breaking starches, lipase for breaking lipids, proteolytic for breaking proteins, and proenzymes).

    • 15 digestive enzymes → packaged into zymogens (proenzymes).

      • When meal is ingested → vagal nerves, polypeptides, and hormones stimulate release of proenzymes into pancreatic duct.

    • Digestion in Three Phases:

      • Cephalic: Think about, smell, and prepare food. Body starts producing liver enzymes, pancreatic enzymes, and hydrochloric acid (stomach acid) at that time.

      • Gastric: Food enters stomach.

      • Intestinal: Food enters into duodenum.

• Causes:

  • Gallstones / gallbladder disease (most common in women)

    • May cause blockage of pancreatic juices from getting into small intestine and backs up into pancreas (autodigestion → pancreatitis).

  • Chronic alcohol use (most common in men)

    • 10-11 drinks per day for 10 years.

  • Hypertriglyceridemia (>1000 mg/dL): High triglycerides

    • Increases chylomicrons (low-dense large particles that can obstruct capillaries).

  • Less common: Drug reactions or pancreatic cancer.

Clinical Manifestations of autodigestion

• Elevation of blood sugar (diabetes may develop)

• Sudden onset

• Abdominal pain: Severe, LUQ or mid-epigastric pain, radiating to the back.

• Eating worsens pain

• Starts when lying down (recumbent)

• Nausea/Vomiting (remains unrelieved) & Abdominal Guarding.

• Jaundice, Abdominal Distension.

• Cullen’s Sign (periumbilical ecchymosis/bruising around the navel) & Grey Turner’s Sign (flank ecchymosis/bruising on the flanks) = sign of bleeding/hemorrhage.

• Vital Signs:

  • Resp: Cyanosis, dyspnea, crackles (fluid builds up and decreases movement of diaphragm) → compliment system activation (pleural effusion)

  • GI: N/V, decreased/absent bowel sounds, distension (if ileus)

  • Low-grade fever and leukocytes

  • Cardiovascular: Tachycardia, hypotension, shock

  • Skin: Jaundice, abdominal skin discoloration

Complications

• Pancreatic Pseudocyst: Fluid, pancreatic enzymes, debris, and exudates surrounded by wall.

  • S/S: Abdominal pain, palpable mass, N/V, anorexia.

  • May perforate (secondary peritonitis)

  • Surgical intervention

• Pancreatic Abscess (more urgent because already infected with necrosis): Infected pseudocyst; results from extensive necrosis.

• S/S: Upper abdominal pain, leukocytosis, mass, high fever (necrosis).

• May rupture or perforate (secondary peritonitis) and needs prompt surgical intervention.

• Potential Systemic Complications:

  • Pleural effusion, atelectasis (partial or full collapsed lung), pneumonia, ARDS, hypotension or shock, thrombi, PE, DIC (multiple clots), tetany (hypocalcemia → Chvostek’s and Trousseu’’s), abdominal compartment syndrome (wet-dry and change dressing frequently, soaked saline gauze packed into abdomen).

Diagnostic Studies/Labs

• Amylase and lipase, abdominal x-ray or US (best option), contrast CT imaging (look at vasculature to see if hemorrhage).

• MRCP: Moves stones magnetically.

• Amylase and lipase → first line labs.

  • Amylase (sensitive but not specific):

    • Normal 60-120

    • Produced by salivary glands, skeletal muscles, ovaries, etc.

    • Elevates within 12 hours and normalizes in 48-72

    • Pseudo cyst or abscess = elevated (useful in early diagnostics)

    • May be elevated in a perforated bowel, penetrated peptic ulcer, duodenal obstruction.

  • Lipase (primary diagnostic marker):

    • Normal 0-60.

    • Elevates within 24-48 hours and normalizes after 5-7 days.

    • This lab is trended to monitor progress.

    • In pancreatitis elevations are 5-10x normal.

  • Elevated bilirubin and liver enzymes (AST and ALT) → common if obstructive

  • Triglyceride level

  • Elevated glucose and decreased calcium

Interprofessional Care

• Aggressive hydration (LR to convert lactate into bicarb or NS), usually start 250 mL/hr.

• Metabolic: Give oxygen if less than 95% (curve is moving to the right) and monitor blood glucose levels.

• Pain management (morphine unless pancreatitis caused by gallstone because it causes spasms)

  • Flex trunk

  • Elevate 45 degrees bed

  • Frequent oral and nasal care (NPO)

• NPO, NG suction, meds to decrease acid secretion (H2 blockers, antacids, “prazoles”)

• Enteral nutrition to avoid necrotizing pancreatitis.

• Check lipase labs to see if the care is working.

• Vital Signs:

  • Monitor for hypotension and tachycardia

    • Long-standing tachycardia can decrease perfusion overtime.

  • Magnesium should be given first for potassium to stick.

  • Hypocalcemia:

    • Tetany (jerking, irritability, twitching), Chvostek’s and Trousseau’s sign → treat with calcium gluconate

Acute Pancreatitis Recovery

• Nutrition Therapy:

  • Small, frequent feedings.

  • High carbs, low fat (fats require more pancreatic enzymes)

  • Supplemental fat-soluble vitamins (ADEK)

• Lookout for hyperglycemia signs (the 3 Ps → polydipsia, polyphagia, polyuria)

• Monitor for infection, diabetes, sta

Biliary Tract Disease

Overview

• Cholecystitis and cholelithiasis are the primary disorders.

  • Cholelithiasis (most common):

    • Stones in gallbladder (leads to pancreatitis because pancreatic duct cant empty)

    • Bile salts can become hyper concentrated leading to stone formation.

  • Cholecystitis:

    • Inflammation of the gallbladder.

    • Acute or chronic or “acute on chronic”

    • Associated often with gallstones or biliary sludge.

  • Causes decrease in digestion and abdominal pain.

Risk Factors

• Female, multiparity, estrogen therapy.

• Older than 40.

• Sedentary lifestyle or obesity

• Genetics

• Native Americans

Interprofessional Care

• Emphasis on infection management, fluid balance, and post-surgical recovery.

Gallbladder Disorders (Cholelithiasis & Cholecystitis)

Pathophysiology

• Cholelithiasis: Gallstones obstruct bile flow.

  • Formed from bile salts, cholesterol, protein, bilirubin, and calcium.

  • Contributing Factors:

    • Lithogenic bile (bile supersaturated with cholesterol)

    • Biliary sludge (stasis of bile)

      • Caused by immobility, pregnancy, inflammation.

  • Stones may stay or migrate → cause pain or obstruction → cholecystitis, pancreatitis, obstructive jaundice (yellow seen in eyes first), and increased LFTs (AST/ALT).

  • Choledocholithiasis = gallstone obstruction of the common bile duct

• Cholecystitis: Inflammation of the gallbladder due to obstruction or infection.

  • Either confined to mucus lining or involves entire wall.

  • Gallbladder is edematous and hyperemic

  • May be distended with bile or pus (may be infected)

  • Scarring and fibrosis after attack → chronic decreased function (more likely leading to stricture and decreased immobility of gallbladder → more likely to develop stones).

  • Cystic duct may become occluded

  • Acalculous cholecystitis occurs in:

    • Older adults and critically ill

    • Prolonged immobility, fasting, prolonged parenteral nutrition, diabetes

    • Adhesions, cancer, anesthesia, opioids

  • If inflammation or infection (acute cholecystitis):

    ◦ Leukocytosis

    ◦ Fever, chills

• If chronic cholecystitis develops:

  • fat intolerance,

  • dyspepsia,

  • heartburn,

  • flatulence

Clinical Manifestations

• Biliary Colic (stones moving or obstructing): Severe pain post-high-fat meal (within 3-6 hours) or when lying down because that’s when it hits the intestine and gallbladder needs to dump bile into the intestine.

  • tachycardia, diaphoresis, prostration.

  • Pain in RUQ and toward scapula as gas tries to move out.

  • Indigestion, N/V, abdominal pain/guarding, restlessness

• Jaundice, Dark Urine, Clay-colored Stools, pruitis, bleeding tendencies, pruritis, intolerance for fatty foods → total obstruction, backed up bile, hyperbilirubinemia → liver congested.

Complications

• Cholelithiasis leads to cholecystitis

• Gangrenous cholecystitis → gallbladder rupture leads to peritonitis

• Abscess and fistulas develop

• Cholangitis and choledocholithiasis. If obstructive:

  • Pancreatitis: Inflammation of the pancreas that can result from gallstones or chronic alcohol use.

  • Transaminitis: Elevation of liver enzymes, typically indicating liver inflammation or damage.

  • Biliary cirrhosis: A chronic disease that results in inflammation and destruction of the bile ducts in the liver, ultimately leading to liver failure.

Diagnostics:

• Abdominal US → checks for gallstones

• Lab changes:

  • Elevated WBCs

  • Elevated bilirubin (hyperbilirubinemia, jaundice)

  • Elevated urinary bilirubin level

  • Elevated liver enzymes (transaminitis)

  • Elevated amylase or lipase (pancreatitis)

Interprofessional Care

• Conservative Therapy:

  • Extracorporeal shock-wave lithotripsy (ESWL): Uses shock waves to break down gallstones (used if ECRP fails).

• Pain Management: Opioids, Anticholinergics (decrease GI secretions and counteract smooth muscle spasms).

• NPO, NG Suction if Severe Vomiting.

• Surgical Treatment:

  • Laparoscopic Cholecystectomy (LapChole) → Gold Standard.

    • Treatment for symptomatic gallstones

    • Removal of gallbladder through1-4 puncture holes.

    • Resume normal activities within 1 week.

    • Drain: Originates in gallbladder and allows pus, purulent fluid, and bile to drain.

  • Open Cholecystectomy (less common) → Requires T-Tube for Bile Drainage.

    • Removal of gallbladder through right subcostal incision.

    • Indicated if unable to perform LapChole

    • Drain: Originates in common bile duct and allows excess bile to drain after surgery

  • ERCP with sphincterotomy for Common Bile Duct Stones.

    • Direct visualization

    • Dilation of bile duct for placement of stents

    • Stones removed with basket or out with stool

    • Remain NPO until return of gag reflex

    • Drain (if ERCP fails): Transhepatic Biliary Catheter → a procedure that allows for drainage of bile directly from the liver due to obstruction → used in cases of transaminitis and jaundice.

Postoperative Nursing Management

• Monitor VS, Pain, & Infection Signs.

• Early Ambulation (day 0) & Deep Breathing.

• Dietary Modifications:

  • Low-fat, small frequent meals and intake of fiber and calcium.

  • Avoid high-fat, gas-producing foods.