NURS 370: GI Updated Final Exam Study Guide

Constipation

Less than 3 bowel movements per week, plus 2+ of:

• Straining during bowel movements

• Hard, dry stools

• Feeling of incomplete evacuation

• Bloating

• Abdominal pain/discomfort

Constipation Complications

Fecal Impaction

Intestinal Obstruction

Hemorrhoids

Fissures

Vagal Nerve Stimulation w/ Bradycardia/Syncope

Perforation (Rare)

Constipation Nursing Assessment

• Determine normal bowel pattern and recent changes

• Assess diet, fluid intake, activity level, and medications

• Inspect abdomen for distention, bowel sounds, and tenderness

• Review laboratory or imaging results if obstruction suspected

Constipation: Causes

• Dietary/fluid intake

• Sedentary lifestyle

• Medications/anesthesia

• Pain or fear

• Neurologic causes

Constipation: Clinical Manifestations

• Hard, dry stool

• Straining

• Sense of incomplete evacuation

• Abdominal distention/discomfort

• Decreased appetite, nausea

• Small amounts of liquid stool (possible impaction overflow)

Constipation Treatments: Non-Pharmacological (1st line)

• High fiber diet

• 2–3 L/day fluids (unless contraindicated)

• Early ambulation/activity

• Regular toileting

Constipation Treatments: Pharmacological (if needed):

• Stool softeners (docusate)

• Bulk forming agents (psyllium)

• Osmotic/stimulant laxatives (avoid chronic use)

• Prevent Laxative Dependence and Lazy Bowel.

Constipation: Patient Education

• Explain normal bowel patterns vary between individuals.

• Avoid excessive straining or delaying defecation.

• Incorporate fiber gradually to prevent bloating.

• Encourage stress management—stress affects gut motility.

Acute Abdominal Emergency Recognition: 3rd spacing

• ascites, abd distention, pain 

• Treatment - pericentesis, albumin, correct underlying issue. 

Acute Abdominal Emergency Recognition: Bowel Ischemia

• Reduced BS, pain, N/V, can start as hyperactive then hypoactive, crampy pain. 

• Early recognition: Monitor for sepsis, fever, tachypnea, tachycardia, hypotension 

• Management - ABx, IV fluids, vasopressors, surgery 

Acute Abdominal Emergency Recognition: Paralytic Ileus

•  pain, N/V, ABD distention, tenderness, hiccups, hypoactive BS, no stool or flatus,  

• Management - bowel rest, wean from opioids, increase mobility/motility with meds or ambulation, apply heat only with order, NPO

Acute Abdominal Emergency Recognition: Gastric perforation

• sudden severe pain UQ, vomiting, extreme tenderness and rig ABD, hypotension, tachycardia, shock. 

Acute Abdominal Emergency Recognition: Acute Peritonitis

• Rebound tenderness + cough test, dehydration w/ hemoconcentration, , acidosis, elevated WBCs, fever/chills, positive peritoneal lavage (> 500 WBCs), ABD distention, 

• Minimize severe complications like hypoxia, shock, ARF, sepsis, acidosis, 

• Treatment - FEn / acid-base balance, O2, IV hydration (200mL/Hr), bowel rest, calorie supplementation (TPN, PPN), NPO, suction 

Acute Abdominal Emergency Recognition: Perforation of Ulcers (anywhere)

• Sharp abdominal pain, ABD tenderness and N/V, bleeding (hematemesis, melena, hematochezia). bleeding can cause hypovolemia and shock so monitor for systemic conditions such as tachycardia, hypotension, pallor, cold/clammy skin, confusion)

Acute Abdominal Emergency Recognition: Acute Pancreatitis

• Hypovolemia, hypokalemia, hyperglycemia, 

• S/S of peritonitis, greys turner sign - bruising in flanks; accompanied by cullen sign - umbilical bruising.

• s/sx: LUQ pain, ABD tenderness, hypoactive, N/V, dehydration, tachycardia, low grade fever. Labs - elevated amylase, lipase, hypocalcemia, hypomagnesia, increase Hct, decrease albumin  

• Management - monitor for hypo/hyperglycemia, 3rd spacing, pain/anxiety., bowel rest, FEN, calcium replacement, O2, peritoneal lavage - evaluates bleeding in abd cavity. Transfusion, ERCP sphincterotomy, exploratory laparoscopy, T-insertion 

Acute Abdominal Emergency Recognition: GI bleeds

• Hematemesis, melena, hematochezia, occult bleeding (in stool), check stool consistency (color, shape, type) - bleeding can cause hypovolemia and shock so monitor for systemic conditions such as tachycardia, hypotension, pallor, cold/clammy skin, confusion)

• Maintain circulation with IV fluids and blood - 2 large-bore IVs, then isotonic crystalloids (NS, LR), blood transfusion if severe blood loss. O2

• If bleeding from varices - PPIs, H2Blockers, Ocreotide, NPO + prep for endoscopy, monitor labs - H&H, Bun/Cr, PT/INR/aPTT, liver enzymes 

Acute Abdominal Emergency Recognition: GI bleeds - Appendicitis

• RLQ pain - sharp, discrete; well localized, low grade fever, rebound tenderness, Rovsing’s Sign - palpate on LLQ but pain on right side, ( do not give laxatives as it may as straining = perforation) 

Acute Abdominal Emergency Recognition: Diverticulitis

• Microperforation & abscess formation.

• S/S - irritability, diarrhea, pain, tender, LLQ pain with BM, flatulence, rectal bleeding 10-30%, fever, chills 

• Complications - intra-abdominal abscess, fistulas, obstructions, perforation, adhesions, bleeding -> abdominal rigidity 

• Prevention - high-fiber diet, during flare up avoid high fiber, colloid laxatives (metamucil) anticholinergics (minimize opioids), ABx and bowel rest with flare ups. NPO, IV hydration, surgical - abscess drainage, resections, colostomy, fistulas repair, relieve obstruction. 

Acute Abdominal Emergency Recognition: Strangulated Hernias 

• Blood supply cut off due to strangulation or trapped tissue leading to ischemia or necrosis 

• S/S - sudden, severe pain, irreducible mass, tender, firm and tense hernia bulge, skin discoloration, absent BS, hypotension, tachycardia, fever, Abd distension, N/V. sudden pain + cannot reduce hernia, skin changes over hernia, tachycardia + vomiting - emergency 

• Management - NPO, surgery, pain control, NG tube, vitals ABx 

Acute Abdominal Emergency Recognition: Acute Cholecystitis

• Inflammation of the gallbladder. 

• S/S - pain after eating, epigastric pain. Mild jaundice, clay-colored stool, dark foamy urine, steatorrhea. Fever + RUQ pain + murphy sign = classic cholecystitis, Kehrs sign - R shoulder radiated pain w/ breathing. Elevated ALP, amylase + lipase. 

• Management - NPO, IV hydration, suctioning, T-tube, analgesic, anticholinergistics , antispasmodics 

chronic pancreatitis

• D/T alcoholism (calcification of the ducts) - pancreatic acinar damage 

• Exocrine functions - malabsorption, steatorrhea

• Endocrine functions - can cause DM

chronic pancreatitis s/sx

• Pain radiating to the back, worse after eating or drinking, weight loss, Hx of alcohol, possible jaundice with duct obstruction, tenderness, polyuria or polydipsia, malabsorption of vitamins, 

• S/S - pain, diarrhea, diabetes

chronic pancreatitis Treatment

• pain meds, alcohol cessation, pancreatic enzyme replacement w/ meals (vitamins), small frequent low fat meals, high calories insulin, PPIs or H2 blockers , anti-emetics, stop ETOH

chronic liver disease/cirrhosis

• Scarring + stagnation due to previous damage.

• Damage to the liver means improper glycogen storage, Vits/Mins, clotting factors, detoxification, metabolic functions, emulsification of fats.

chronic liver disease/cirrhosis s/sx

• Jaundice (eyes, sclera, urine, stool), generalized weakness, weight loss, A/N/V, flatulence, RUQ discomfort, malaise, ascites, coagulopathy, bruising, esophageal varices, anemic, edema, peripheral neuropathy, spontaneous bacterial peritonitis, portal hypertension, hepatorenal syndrome, 

chronic liver disease/cirrhosis Treatment

• Monitor bleeding, ascites, encephalopathy, maintain fluid balance, small, frequent meals; highcalorie;lowsodium;  moderate protein, skin care, daily weight, 

chronic peptic ulcer disease

• Caused by H.Pylori infection or NSAIDS, ulcer formation,  

• Assess pain type, location, onset, frequency, duration, associated activities w/ meals, this is to determine the location of ulcer (stomach, duodenal), 

chronic peptic ulcer disease s/sx

ABD tenderness, N/V, pain, check labs for CBC, electrolytes, H. pylori.

• Duodenal ulcers - pain 2-3hrs after meals, pain awakens at night, hypersecretion of HCL, referred shoulder pain

chronic peptic ulcer disease Treatmemt

Antibiotics, cessation of alcohol, caffeine, smoking, NSAIDs, avoid triggering foods; no high salt foods, H2blockers, antacids, PPIs, prostaglandins, stimulants. 

Peptic ulcer disease (PUD)

Is mucosal breakdown from acid–pepsin plus impaired mucosal defenses, often associated with H. pylori, NSAIDs, smoking, caffeine, alcohol, and stress.

Peptic Ulcer Disease: Gastric Ulcer

Age: > 50

Acid Production: Normal to Low

Pain Timing: 30-60 minutes after meals

Nocturnal Pain: Rare

Effect of Food: Worsens Pain (food = more acid)

Vomiting: Common

Bleeding: Hematemesis, Melena

Perforation: Less common

Peptic Ulcer Disease: Duodenal Ulcer

Age: 30-60

Acid Production: Hypersecretion

Pain Timing: 2-3 hours after meal

Nocturnal Pain: Common (awakens at night)

Effect of Food: Relieves pain (alkaline pancreatic secretions)

Vomiting: Uncommon

Bleeding: Melena, Hematemesis sometimes

Perforation: More common

Peptic Ulcer Bleeding Pathophysiology: Step 1

Acid and Pepsin Erode Mucosal Lining

• In peptic ulcer disease (PUD), gastric acid and pepsin digest and break down the protective mucosal lining of the stomach or duodenum.

Peptic Ulcer Bleeding Pathophysiology: Step 2

Ulcer Damages Blood Vessels → Bleeding

• As the ulcer deepens, it can erode into the submucosa and blood vessels. When a vessel is affected, bleeding can occur—ranging from slow oozing to brisk arterial hemorrhage.

Peptic Ulcer Bleeding Pathophysiology: Step 3

Blood Loss → ↓ Perfusion → Hypoxia

• Ongoing blood loss reduces circulatory blood volume.

• This impairs tissue perfusion, leading to cellular hypoxia (oxygen deprivation).

• Severe or untreated bleeding can lead to shock and multi-organ failure.

Peptic Ulcer Disease (PUD): Assessments

1. Pain pattern

2. Relation to meals

3. History of irritants (NSAIDs, ETOH, smoking, stress)

4. Exam for tenderness or peritonitis; labs (CBC for anemia, electrolytes), gastric fluid analysis (blood, HCL), and Esophagogastroduodenoscopy (EGD) with H. pylori testing confirm diagnosis.​

Peptic Ulcer Disease: Treatment

Conservative therapy aims to

1. Reduce Hyperacidity and Allow Ulcer Healing

2. Manage Symptoms and Support Healing

3. Prevent Complications

This also Includes Diet Modification:

1. Avoid Trigger Foods

2. Avoid Late Night Snacks

3. Reduce or Eliminate Caffeine

4. Avoid Alcohol

Peptic Ulcer Disease (PUD): Reduce Hyperacidity and Allow Ulcer Healing

Peptic ulcers develop when the balance between gastric acid secretion and mucosal protection is disrupted.
Therefore, therapy aims to decrease acid production and strengthen mucosal defenses.

Interventions Include:

• Antisecretory Drugs

• Antacids

• Cytoprotective Agents

• Eradicate H. pylori Infection

• Dietary Management

Nursing focus:

Administer medications on time (some before meals for best effect).

Educate about completing the full antibiotic course for H. pylori eradication.

Monitor for signs of GI bleeding (melena, coffee-ground emesis).

PUD Treatment: Antisecretory Drugs

Proton Pump Inhibitors (PPIs) (e.g., omeprazole, pantoprazole) — block acid secretion at the proton pump level.

H₂-receptor blockers (e.g., famotidine, ranitidine) — reduce acid production by blocking histamine in gastric cells.

PUD Treatment: Antacids

Neutralize existing acid to relieve pain and reduce irritation.

PUD Treatment: Cytoprotective Agents

Sucralfate coats the ulcer, forming a protective barrier against acid and pepsin.

Misoprostol enhances mucosal defense (especially if NSAID-induced ulcers).

PUD Treatment: Eradicate H. pylori Infection

PUD Treatment

Triple or quadruple antibiotic therapy (e.g., clarithromycin, amoxicillin, metronidazole + PPI).

Peptic Ulcer Disease (PUD): Manage Symptoms and Support Healing

Ulcer pain and nausea are common, often related to acid exposure and inflammation. Maintaining hydration and comfort promotes recovery.

Interventions:

Pain management:

• Administer prescribed PPIs or antacids to relieve epigastric burning or gnawing pain.

• Avoid NSAIDs, as they impair mucosal healing.

Hydration and nutrition:

• Replace fluid losses from vomiting or bleeding with IV fluids as needed.

• Begin with small, frequent, non-irritating meals when oral intake resumes.

Lifestyle management:

• Encourage smoking cessation, which improves mucosal blood flow and healing.

• Encourage stress reduction techniques — stress increases gastric acid secretion.

Nursing focus:

Assess pain patterns, hydration status, and intake tolerance.

Monitor urine output and vital signs for signs of dehydration or bleeding.

Peptic Ulcer Disease (PUD): Prevent Complications

Shock, Hypoxemia, Perforation, Bleeding

Uncontrolled ulcer disease can lead to:

• Hemorrhage: Ulcers can erode into blood vessels (e.g., left gastric or gastroduodenal artery), leading to GI bleeding and shock.

• Perforation: Ulcer can penetrate completely through the stomach or duodenum wall; GI contents leak into peritoneum, causing life-threatening peritonitis. Referred shoulder pain may occur if the diaphragm/phrenic nerve is irritated.​

• Pyloric (Gastric Outlet) Obstruction: Chronic duodenal ulcers may scar/edema, blocking food passage at gastric outlet, causing vomiting/bloating.

Peptic Ulcer Disease: Interventions to Prevent Complications

Monitor for signs of GI bleeding:

Hematemesis (vomiting blood) or melena (black tarry stools).

Drop in blood pressure, tachycardia, and pallor indicate hypovolemia or shock.

Maintain oxygenation:

Administer supplemental oxygen for hypoxemia caused by blood loss or anemia.

IV access and fluids:

Rapid IV replacement to restore circulating volume.

Prepare for emergency intervention:

Endoscopic therapy for bleeding ulcers or surgery if perforation occurs.

Nursing focus:

Recognize early warning signs: sudden sharp pain, rigid abdomen, vomiting blood, or syncope → possible perforation or hemorrhage.

Maintain NPO, position for comfort, and notify provider immediately.

Peptic Ulcer Disease: Avoid Trigger Foods

Certain foods can increase gastric acid secretion or irritate the stomach lining, worsening pain and delaying healing.

Common trigger foods include:

•Spicy foods (e.g., chili, hot sauce, pepper)

•High-fat or fried foods

•Tomato-based products (acidic)

•Citrus fruits or juices

•Chocolate, peppermint, and carbonated beverages

Nursing explanation:
Encourage patients to identify and avoid foods that cause discomfort or burning sensations. Trigger foods vary by individual, so keeping a food and symptom diary can help identify personal irritants.

Peptic Ulcer Disease: Avoid Late-Night (HS) Snacks

•Eating before bedtime increases acid secretion when the stomach is otherwise empty and not buffered by food.

•Lying down soon after eating can cause acid reflux, increasing mucosal irritation.

•Ulcer pain is often worse at night because gastric acid continues to be secreted during fasting.

Nursing explanation:
Advise patients to avoid eating 2–3 hours before bedtime and maintain regular meal times to reduce nighttime acid exposure.

Peptic Ulcer Disease: Reduce or Eliminate Caffeine

•Caffeine stimulates gastric acid production, even in decaffeinated coffee and tea.

•Caffeinated drinks (coffee, tea, cola, energy drinks) can worsen pain and delay ulcer healing.

Nursing explanation:
Encourage switching to non-caffeinated herbal teas or water. Emphasize that even decaf coffee still contains small amounts of caffeine and acids that may cause irritation.

Peptic Ulcer Disease: Avoid Alcohol (ETOH)

•Alcohol directly erodes and irritates the gastric mucosa, increases acid secretion, and interferes with the action of medications such as proton pump inhibitors (PPIs) or H₂ blockers.

•Chronic alcohol intake delays healing and raises the risk of GI bleeding.

Nursing explanation:
Encourage complete avoidance of alcohol during active ulcer treatment and moderation thereafter to prevent recurrence.

Ulcer Perforation & Penetration

Erosion through the gastric/duodenal wall into the peritoneal cavity (PERFORATION) or adjacent organs (PENETRATION) such as: Pancreases, Biliary Tract, Gastrohepatic Momentum.

S/SX

• Sudden, severe upper abdominal pain; may radiate to shoulder.

• Rigid “board-like” abdomen, marked tenderness.

• Nausea/vomiting, signs of shock: tachycardia, hypotension, pallor.​

• High risk for peritonitis and sepsis.

Ulcer Perforation & Penetration: Immediate Priorities

NPO, ABCs, large-bore IVs and fluids, oxygen, NG tube for decompression, urgent surgical consult and likely emergency laparotomy, and broad-spectrum antibiotics.

Peritonitis

• Acute, generalized inflammation of the lining of the abdominal cavity

• Most often secondary to a Perforation (appendix, PUD, diverticulum, ischemic bowel, trauma, PD catheter infection)

• May be suppurative (pus forming)

• May be contained to a local area (abscess)

• Can become systemic (leads to sepsis)

Peritonitis – Pathophysiology: Step 1 Contamination → massive inflammatory response.

• Inflammation/infection increases capillary permeability in the peritoneal lining, so WBCs, proteins, and fluids move into the peritoneal cavity.

• Lavage fluid withdrawn contains high WBCs, demonstrating the intense immune response to peritonitis.

• Infection initiates the process, introducing bacteria or toxins into the sterile peritoneal cavity.

• Contamination of the peritoneal cavity

  • Most commonly from GI perforation, but can also result from surgery, trauma, or bloodstream infection in immunosuppressed patients.​

• Activation of Immune Cells Release Pro-Inflammatory Cytokines

• Hyperemia (increased blood flow) occurs as part of the inflammatory response.

Peritonitis – Pathophysiology: Step 2 Capillary leak and third spacing into peritoneal cavity → hypovolemia, ileus.

• Inflammatory response and third spacing

  • Activated immune cells release pro-inflammatory cytokines (e.g., TNF-α, IL-1, IL-6) and mediators (e.g., prostaglandins, eicosanoids), causing massive fluid shifts out of vessels into the peritoneal space.​

• Huge fluid shifts (third spacing) occur to dilute toxins, resulting in loss of fluid into the peritoneal cavity.

  • This leads to a reduced extracellular volume (ECV) and can rapidly cause hypovolemia (low blood volume).

• Hypovolemia and ileus

  • Loss of fluid volume causes hypovolemic shock; local irritation reduces bowel movement leading to paralytic ileus (intestinal paralysis).​

  • Decreased peristalsis and lack of forward flow of intestinal contents occur due to irritation and inflammation.

Peritonitis – Pathophysiology: Step 3 Impaired ventilation from distention and pain; risk of sepsis and shock.

• Edema, capillary leak, and abdominal distention result from inflammatory mediators and vascular permeability.

• Impaired ventilation and impaired oxygenation can result if abdominal distention elevates the diaphragm.

• Systemic infection and sepsis if untreated

  • Spread of infection can lead to generalized peritonitis, septic shock, multiple organ dysfunction, and death without rapid treatment.

• Systemic infection develops if local infection spreads, leading to sepsis and potential multi-organ failure.

Types of Peritonitis

Primary Peritonitis:

• Acute bacterial infection (NOT due to a ruptured organ)

Secondary Peritonitis:

• Bacteria enter via perforated intestine or organ

S & Sx of Peritonitis: Early Stage

• Vague, diffuse abdominal pain

  • May begin as a dull ache and is often difficult to localize.

• May become sharp; can radiate to the shoulder

  • (especially with diaphragmatic irritation from free peritoneal air/fluid)

• Pain progresses in intensity and worsens with movement

  • Patients may lie still to minimize pain (lying motionless, "guarding").

• Rebound tenderness

  • Pain increases when pressure is quickly released after palpation.

• Positive cough test

  • Pain is worsened by coughing or sudden movements.

• At first, peritonitis presents with vague and diffuse symptoms because the inflammatory process is just beginning and localized.

S & Sx of Peritonitis: Later Stage

• Abdominal distention

• A/N/V (Anorexia, Nausea, Vomiting)

• Decreased or absent bowel sounds (ileus)

• May progress to systemic signs: fever, tachycardia, hypotension, rapid breathing, and signs of sepsis/shock.

• If untreated, may develop oliguria, confusion, or multi-organ dysfunction due to sepsis.

Signs & Symptoms of Peritonitis – LATE/Progressive

• Dehydration

  • Increased heart rate (HR↑), decreased blood pressure (BP↓)

  • Hemoconcentration: ↑ hematocrit (HCT), ↑ sodium (Na+), ↑ blood urea nitrogen (BUN) due to fluid loss

• Metabolic Disturbances

  • Acidosis (lactic/metabolic), elevated WBC (Leukocytosis) indicating severe infection

• Fever (≥39.4°C / 103°F), chills

• Abdominal X-ray: Free air indicates bowel perforation (critical/emergent finding)

• Peritoneal Lavage: >500 WBCs in peritoneal fluid, confirming peritoneal inflammation

• Life-threatening without intervention

  • Progression to systemic infection (sepsis), shock, and multi-organ failure

Progressive systemic signs (if untreated) or Peritonitis

• Fever, tachycardia, hypotension (possible sepsis)

• Cool, clammy skin, confusion, restlessness (may signal developing shock)

Causes of Spontaneous Bacterial Peritonitis (Primary Peritonitis)

• Often a complication of advanced liver disease (cirrhosis) or kidney failure (especially in patients with ascites).

• No identifiable direct source—usually occurs without a ruptured organ or bowel.

• Bacteria translocate from the gut or via the bloodstream, infecting peritoneal fluid.

• Example organisms: E. coli, Klebsiella, Streptococcus species.

• Most common in patients with ascites due to portal hypertension.

Causes of Secondary Peritonitis

• Caused by direct contamination due to perforation, rupture, or injury:

  • Appendicitis, ruptured peptic ulcer

  • Diverticular disease (especially ruptured diverticula)

  • Gangrenous (necrotic) organs or intestine

  • Volvulus (bowel twisting/obstruction), ectopic pregnancy, inflammatory bowel disease (IBD)

  • Abdominal trauma (blunt or penetrating)

  • Post-surgical leak (e.g., bowel anastomosis breakdown)

  • Infected peritoneal dialysis (PD) catheter or surgical drain

S & Sx of Peritonitis: Nursing Priority

• Recognize early symptoms promptly and notify the provider.

• Timely intervention (antibiotics, IV fluids, surgery) can prevent progression to sepsis and shock.

Peritonitis Therapeutic Interventions: Minimize potential for complications

Prevent hypoxia, shock, acute renal failure (ARF), sepsis, and acidosis through early detection and intervention.

Peritonitis Therapeutic Interventions: Supplemental oxygen

Administer oxygen to correct hypoxemia arising from impaired ventilation or sepsis.

Peritonitis Therapeutic Interventions: Monitor & maintain fluid, electrolyte, and acid-base (FEN) balance

• IV hydration: Maintain adequate perfusion with IV fluids (e.g., 200 mL/hour; rate may be titrated to patient’s needs and comorbidities).

• Electrolyte additives: Replace as needed, particularly sodium (Na⁺), potassium (K⁺), chloride (Cl⁻), bicarbonate (HCO₃⁻) to correct losses or imbalances from third spacing and vomiting.

• Caloric supplementation: Provide nutrition through parenteral routes if NPO—use PPN (peripheral parenteral nutrition) or TPN (total parenteral nutrition) based on duration/severity.

Peritonitis Therapeutic Interventions: Bowel Rest

• NPO (nothing by mouth): Prevent additional GI distress or perforation.

• NGT (nasogastric tube) suction: Decompress stomach and bowel, prevent aspiration, and reduce GI secretions.

Surgical Intervention – Peritonitis

• Common Procedures:

  • Exploratory laparotomy (lap): Surgical exploration of the abdomen to locate source of infection or perforation.

  • Open peritoneal lavage: Repeated irrigation of the peritoneal cavity to remove contamination.

  • Incision & drainage (I&D) of abscesses: Draining any localized pus collections.

  • Lysis of adhesions: Cutting/removal of fibrous bands causing obstruction.

  • Resections: Removal of necrotic bowel segments or tumors as needed.

  • Temporary ostomy: Creating a temporary opening for fecal diversion if colon/rectum cannot be immediately repaired.

GI Bleed

• Blood loss from anywhere in the gastrointestinal (GI) tract, extending from the mouth to the rectum (includes esophagus, stomach, intestines, colon, rectum).

• Even small, slow, or unrecognized bleeds can be clinically significant over time.

• Classification: Overt, Occult, Acute, Chronic.

• Types Small Bowel, Upper, Lower GI Bleeds.

Upper GI Bleeds

These bleeds originate in your:

• Stomach

• Esophagus

• Duodenum (first section of small intestine).

• Anatomic extent: From the esophagus to the duodenum (above the ligament of Treitz)

• Hematemesis (bright red or coffee-ground), melena (black tarry stool).

Upper GI Bleeds: Common Causes

• Peptic ulcer disease (gastric or duodenal ulcers)

• Erosive esophagitis

• Esophageal varices

• Arteriovenous malformations (AVMs)

• Mallory-Weiss syndrome (mucosal tear from forceful vomiting/retching)

• Cancers of the upper GI tract

• Gastritis

Lower GI Bleeds

These originate in your:

• Anus

• Rectum

• Colon

• Anatomic extent: From the jejunum (small intestine below the ligament of Treitz) to the rectum

• Hematochezia (bright red blood per rectum) or maroon stool.

Lower GI Bleed (LGIB) Common Causes

• Diverticulosis

• Colorectal cancer

• Inflammatory bowel disease (IBD—Crohn’s disease, ulcerative colitis)

• Hemorrhoids

• Polyps

• Vascular ectasias (angiodysplasia)

• Infectious or ischemic colitis

Acute GI Bleed

• Rapid blood loss with risk for hypovolemia and shock.

  • Signs: Tachycardia, hypotension, pallor, cool/clammy skin, confusion.

  • Common causes: Peptic ulcers, varices, Mallory-Weiss tears, or trauma.

Chronic GI Bleed

• Ongoing, slow loss over time results in iron-deficiency anemia.

  • Symptoms: Fatigue, weakness, pale appearance, shortness of breath (dyspnea) on exertion.

Physiologic Risk of a GI Bleed

Hypovolemic Shock

• If bleeding is not recognized or controlled, ongoing blood loss leads to:

  • ↓ Venous return → ↓ Cardiac output

  • Tissue hypoxia and organ dysfunction

  • Shock and potential death without intervention

• Nursing priority:

  • Assess hemodynamic stability—vital signs (heart rate, blood pressure), mental status, urine output.

  • Detect and report any early changes; prepare for fluid resuscitation, possible blood transfusion, and endoscopic (or surgical) intervention as indicated.

Nursing Focus GI Bleed

• Stabilize the patient first (airway, breathing, circulation) before focusing on diagnostic workup.

• Continuous monitoring of vital signs (VS), bleeding, and lab trends is essential to determine the urgency of intervention and monitor treatment efficacy.

Complications to Monitor in GI Bleed

• Hypovolemic shock: Acute blood loss lowers intravascular volume, leading to decreased venous return, reduced cardiac output, and shock.

• Acute kidney injury: Hypoperfusion from blood loss impairs renal function.

• Re-bleeding: Risk for recurrence of hemorrhage after initial hemostasis.

• Perforation: Ulcer erosion or procedural complication causing GI tract rupture.

• Sepsis or multi-organ failure: If bleeding is associated with infection or prolonged hypotension.

GI Bleed Assessment Steps

• Assess ABCs: Airway, breathing, and circulation—ensure stability.

• Check for overt bleeding:

  • Hematemesis (vomiting blood)

  • Melena (black, tarry stool)

  • Hematochezia (bright red blood per rectum)

• Monitor vital signs and urine output: Look for signs of shock or ongoing blood loss.

• Establish IV access: Prepare for rapid fluids, medications, and blood draws.

  • Draw labs for complete blood count (CBC) and coagulation studies (PT/INR).

Nursing Priorities and Actions GI Bleed: Maintain Hemodynamic Stability

• Goal: Preserve perfusion and prevent shock.

• Actions:

  • Assess vitals (HR, BP, orthostatics) frequently.

  • Maintain IV access for rapid fluid and transfusion therapy.

  • Position with legs elevated if hypotensive.

  • Monitor for early deterioration: tachycardia, hypotension, altered mental status, cool skin.

Nursing Priorities and Actions GI Bleed: Provide Oxygen if Hypoxemic

• Goal: Support oxygen delivery to vital organs.

• Actions:

  • Administer O₂ (nasal cannula/mask) if SpO₂ < 94%.

  • Monitor respiratory rate, work of breathing, pulse oximetry.

  • Arrange for ABG if severe anemia or distress present.

Nursing Priorities and Actions GI Bleed: Monitor Intake/Output and Labs

• Goal: Evaluate blood volume, kidney perfusion, and ongoing losses.

• Actions:

  • Measure urine output hourly (should be ≥ 30 mL/hr).

  • Monitor H/H, BUN/creatinine, electrolytes.

  • Track input/output, balance fluid resuscitation, watch for signs of fluid overload after transfusion.

GI Bleed Management: Monitoring Vital Signs and Labs

Vital Signs: Monitor heart rate, blood pressure, and watch for orthostatic changes frequently for early deterioration.
Labs to Monitor:

• CBC (Complete Blood Count): Look for low hemoglobin (Hgb) and hematocrit (Hct) as indicators of blood loss.

• Hemoglobin/Hematocrit (H/H): Assess ongoing blood loss and transfusion requirements.

• BUN/Creatinine: May rise with upper GI bleeding from blood protein absorption.

• Coagulation studies (PT/INR, aPTT): Identify risk for or presence of coagulopathy. Bleeding Disorder and Medications.

• Liver enzymes: If varices or hepatic disease is suspected.
  Ongoing Assessment:

• Watch for blood in stool (melena, hematochezia) and emesis (hematemesis).

• Track input/output for fluid balance.

• Monitor for recurrence of bleeding after initial stabilization.

 GI Bleed Diagnostic Studies

• CBC (Complete Blood Count): Look for low hemoglobin (Hgb) and hematocrit (Hct) as indicators of blood loss.

• Coagulation studies: Evaluate for bleeding disorders or medication effects.

• Type & crossmatch: Prepare for possible blood transfusion.

• Endoscopy/colonoscopy: Direct visualization and potential intervention for source of bleeding.

• Guaiac-based fecal occult blood test (gFOBT): Detects occult (hidden) blood in stool.

GI Bleed Management: Circulation with IV Fluids and Blood as Needed

Priority: Maintain hemodynamic stability and adequate tissue perfusion.

Interventions:

• Insert two large-bore IVs for rapid administration of fluids and blood products.

• Begin isotonic crystalloids (normal saline or lactated Ringer’s).

• If blood loss is significant or hemoglobin <7–8 g/dL, transfuse packed RBCs.

• Monitor for hypovolemic shock (tachycardia, hypotension, cool/clammy skin, confusion, decreased urine output).

• Provide supplemental oxygen as needed.

GI Bleed Management: NPO and Preparation for Endoscopy

Purpose: Identify and treat the bleeding source (cautery, clipping, banding).

Interventions: 

• Keep patient NPO (nothing by mouth) to prevent aspiration and allow for sedation.

• Obtain informed consent if able.

• Verify and maintain IV access and labs (CBC, coagulation panel, type and crossmatch for transfusion).

• Prepare suction equipment for possible active bleeding/emesis.

GI Bleed Management: Medications: PPIs, H₂ Blockers, Octreotide for Varices

• PPIs (Proton Pump Inhibitors): Decrease gastric acid secretion, stabilize clots, and prevent recurrent upper GI bleeding (e.g., IV pantoprazole).

• H₂ Blockers: Also reduce gastric acid—less potent than PPIs (e.g., famotidine).

• Octreotide: Used for esophageal or gastric varices; reduces portal hypertension and blood flow to GI tract.

• Nursing note: Initiate IV medication before endoscopy where possible. Monitor for drug side effects and evidence of response (improving H/H, decreased bleeding).

Gastric Outlet Obstruction

(often a late PUD complication) is a blockage that prevents food and liquids from passing normally from the stomach into the first part of the small intestine, the duodenum.

presents with epigastric fullness, early satiety, projectile or persistent vomiting of undigested food, weight loss, and metabolic alkalosis from repeated vomiting.

Gastric Outlet Obstruction: Cause

This condition is caused by either a mechanical obstruction, such as a tumor, scar tissue from ulcers, or inflammation, or a motility disorder that impairs stomach emptying

• Peptic Ulcer Disease (PUD) – scarring, inflammation, edema
  
  

• Malignancy (gastric or pancreatic cancer)
  
  

• Chronic gastritis
  
  

• Crohn’s disease
  
  

• Post-surgical strictures
  
  

• Benign gastric polyps

Gastric Outlet Obstruction: Presentation

presents with epigastric fullness, early satiety, projectile or persistent vomiting of undigested food, weight loss, and metabolic alkalosis from repeated vomiting.

Gastric Outlet Obstruction Management

includes NPO, NG decompression, correction of fluids/electrolytes, PUD treatment, and possible surgery if unrelieved.

Intestinal Obstruction

• An intestinal obstruction occurs when intestinal contents are prevented from moving normally through the gastrointestinal tract.

• Can involve either the small or large intestine, and may be partial (some passage of contents) or complete (total blockage).Intestinal Obstruction Pathophysiology

Intestinal Obstruction Pathophysiology

• Obstruction leads to accumulation of contents and bacterial overgrowth at the site, generating gas and causing distension.

• Bowel distension compresses blood vessels, causing venous compression and reduced oxygen supply (bowel ischemia).

• Cell death from lack of oxygen further decreases peristalsis and aggravates distension.

• Perforation can occur if distension becomes severe.

• Anaerobic bacteria and toxins may enter circulation, leading to sepsis.

• Fluid shift into the bowel leads to hypovolemia, loss of electrolytes, and shock.

• Vomiting is a compensatory response, worsening fluid/electrolyte loss and hypovolemic shock.

• Complications: bowel ischemia, perforation, sepsis.

Intestinal Obstruction Classification

• Partial or complete

• Vascular (Ischemic obstruction): emboli, atherosclerosis, strangulated hernias

• Non-mechanical (Adynamic): anesthetics, opioids, surgical manipulation, immobility, hypokalemia, peritonitis, spinal cord injury

• Non-Mechanical: is divided into:

  • Pan-intestinal: Paralytic ileus

  • Colonic: Acute colonic pseudo-obstruction

• Mechanical:

  • Intraluminal: foreign bodies, gallstones, fecal impactions, strictures, polyps, diverticulitis

  • Extraluminal: hernias, adhesions, tumors, abscesses, intussusception, volvulus.​

  • is divided into:

    • Small Bowel (80%): Causes include adhesions, hernia, malignancy, intussusception, and others.

    • Large Bowel (20%): Causes include colorectal cancer (60%), volvulus (5%), and diverticular stricture (20%).

Intestinal Obstruction: Pathophysiology (All Types)

Regardless of the cause, obstruction initiates the following process:

1. Lack of forward flow: Peristaltic waves increase above the blockage to try to push contents forward.​

2. Accumulation: Gas, fluid, and intestinal secretions accumulate proximal (before) to the obstruction.​

3. Distention and increased peristalsis: The bowel becomes distended, leading to increased peristalsis and pain, and the bowel wall may become edematous.​

4. Increased pressure impairs blood flow: Distention and pressure compress blood vessels, leading to ischemia and potential infarction of the bowel wall.​

5. Increased permeability and third spacing: Bowel wall permeability increases, allowing fluids and electrolytes to shift into the intestinal lumen and peritoneal cavity, causing hypovolemia, electrolyte imbalance, and loss of effective circulating volume (ECV).​

6. Serious complications: If prolonged, obstruction can cause ischemia, necrosis, perforation, and peritonitis.​

• Additional details: Vomiting may occur as a compensatory mechanism, worsening fluid and electrolyte losses and risk of hypovolemic shock. Over time, edema, necrosis, perforation, and sepsis may ensue.​

Small Intestine Obstruction Findings: Pain

Cramping & intermittent (spasms)

Mid to upper abdomen, epigastric

If severe & constant: suspect strangulation

Abdomen non-tender

Small Intestine Obstruction Findings: N/V and Distention

Early & profuse

Mild, upper abd/epigastric

Small Intestine Obstruction Findings: Bowel Sounds 

• Early in obstruction: Bowel sounds may be hyperactive, high-pitched, and borborygmi, often associated with cramping, especially as the intestines attempt to propel contents past the obstruction.

• Late or prolonged obstruction: Bowel sounds may become absent as intestinal motility fails or peristalsis fatigues.

Small Intestine Obstruction Findings: Stool Findings 

• Complete small bowel obstruction: Leads to obstipation—which means absence of both stool and flatus (“unable to pass gas due to severe obstruction”). This is a hallmark sign when the obstruction is total.​

• Partial obstruction: May show diarrhea or passage of small amounts of liquid stool—this is overflow around the blockage.​

• Progression: Early on, patients may still experience constipation (decreased frequency and hard, dry stools), but as the blockage becomes severe or complete, there is passage of neither stool nor gas (obstipation), with abdominal distention and pain.​

• Overflow: If impaction occurs proximal to the obstruction, occasionally small amounts of liquid stool may be seen “leaking” around the impacted mass.

Small Intestine Obstruction Findings: Fluids and Electrolyte Issues

Dehydration: vomiting/NGT, bowel edema

Loss Na+, K+, Cl-, H+ via vomiting/NGT

Loss hydrochloric acid → metabolic alkalosis