NURS 370 Final Exam Study Guide: GI

Constipation Treatments

Non-Pharmacological (1st line):

• High fiber diet

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

• Early ambulation/activity

• Regular toileting
  Pharmacological (if needed):

• Stool softeners (docusate)

• Bulk forming agents (psyllium)

• Osmotic/stimulant laxatives (avoid chronic use)

• Prevent Laxative Dependence and Lazy Bowel.

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: Causes

• Dietary/fluid intake

• Sedentary lifestyle

• Medications/anesthesia

• Pain or fear

• Neurologic causes

Constipation

Definition: 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

Nursing Assessment Constipation

• 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: 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.

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: anesthetics, opioids, surgical manipulation, immobility, hypokalemia, peritonitis, spinal cord injury

• Mechanical:

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

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

Mechanical (Dynamic) Obstruction

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%).

Non-Mechanical (Adynamic) Obstruction

is divided into:

• Pan-intestinal: Paralytic ileus

• Colonic: Acute colonic pseudo-obstruction

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

Large Intestine Obstruction Findings: Pain

Intermittent

Lower abdomen

Abdomen non-tender

Large Intestine Obstruction Findings: N/V and Distention

Less & follows constipation

Large Intestine Obstruction Findings: Bowel Sounds 

Early: borborygmi

Late: Absent

Large Intestine Obstruction Findings: Stool Findings 

Ribbon stools (partial obs.)

Constipation early; obstipation late

Large Intestine Obstruction Findings: Fluids and Electrolyte Issues

No Major Imbalance

Intestinal Obstruction - Labs & Diagnostics: Elevated BUN and Creatinine

• Reason: Hypovolemia leads to decreased renal perfusion and reduced glomerular filtration rate (GFR).

• BUN and creatinine rise as kidney filtration slows, reflecting prerenal azotemia.

• Nursing Implications:

  • Monitor BUN, creatinine, and urine output closely.

  • Maintain adequate IV fluid replacement.

  • Report oliguria (<30 mL/hr) promptly.

Intestinal Obstruction - Labs & Diagnostics: Elevated Sodium, BUN, and Hematocrit

• Reason: Fluid loss and third spacing cause hemoconcentration (increased blood solute concentration).

• Sodium (Na⁺) may be elevated due to fluid deficit.

• BUN rises proportionally with dehydration.

• Hematocrit increases as plasma volume decreases.

• Nursing Implications:

  • These findings confirm dehydration and volume deficit.

  • Rehydrate cautiously with IV fluids, monitoring for signs of overload as bowel function returns.

Intestinal Obstruction - Labs & Diagnostics: Elevated White Blood Cell Count (WBC)

• Reason: Rising WBCs indicate infection, inflammation, ischemia, or infarction of the bowel wall.

• Prolonged obstruction can lead to necrosis and bacterial translocation, triggering sepsis.

• Nursing Implications:

  • Monitor for fever, tachycardia, worsening abdominal pain.

  • Report significant WBC elevation or inflammatory signs immediately.

  • Prepare for possible antibiotic therapy or surgical intervention if infection or perforation is suspected.

Intestinal Obstruction: Diagnosis by 

• Symptoms: Colicky abdominal pain, distention, vomiting, absence of stool or flatus.

• Abdominal X-ray (“Flat Plate”): Shows dilated loops, air-fluid levels, absence of gas beyond obstruction. Non-invasive and usually first imaging test.

• CT scan: Further detail on location/cause; detects complications like strangulation, ischemia, perforation.

• Endoscopy: Direct visualization and sometimes relief (foreign body removal, decompression of volvulus).

• Barium Enema: May be used for large bowel obstruction (narrowing, volvulus, intussusception); contraindicated if perforation suspected, as barium leakage may cause peritonitis.

Unresolved Intestinal Obstruction 

• 3rd spacing leads to decreased effective circulating volume (ECV) and acute kidney injury.

• Bowel perforations can occur.

• Bowel ischemia/infarct may develop; toxins can enter the bloodstream, resulting in sepsis and potentially death.

Unresolved Intestinal Obstruction Nursing Focus

• Early recognition and rapid response are critical.

• Monitor for sepsis criteria: fever, tachypnea, tachycardia, and hypotension.

• Notify provider immediately; anticipate broad-spectrum antibiotics, IV fluids, vasopressors, and surgical intervention.

• Provide emotional support to the patient and family.

Intestinal (Bowel) Perforation: Background

• Definition: Rupture in the wall of the gastrointestinal tract, allowing enteric contents to leak into the peritoneal cavity.

• Also referred to as intestinal or bowel perforation.

• It is a life-threatening condition.

Intestinal (Bowel) Perforation: Causes

• Inflammation

• Infections

• Malignancy

• Trauma

• Bowel ischemia & obstruction

• Peptic ulcer disease

Intestinal (Bowel) Perforation: S/SX

• Sudden onset

• Acute abdominal pain or cramping

• Nausea

• Vomiting

• Chills

• Fever

• Shoulder pain

• Abdominal bloating

Priority Nursing Diagnoses: Intestinal Obstruction

• Altered elimination pattern due to intestinal obstruction with potential for ischemia, infarct, peritonitis, or perforation.

• Alteration in comfort/pain/anxiety due to bowel obstruction.

• Altered nutrition (deficit) due to inability to ingest food & fluids.

Nursing Assessment Intestinal Obstruction

• Cramping or colicky abdominal pain (mechanical) or constant pain (ischemia).

• Visible abdominal distention.

• Nausea and vomiting (may be fecal in complete obstruction).

• Absence of stool or flatus.

• High-pitched or absent bowel sounds.

• Signs of dehydration: tachycardia, hypotension, dry mucous membranes.

Therapeutic Interventions – Intestinal Obstruction

• Conservative approach if there is no strangulation

• Bowel rest (NPO, NGT suction)

• IV hydration

Intestinal Obstruction: Nursing Management

• Keep the patient NPO to rest the bowel.

• Insert and manage a nasogastric (NG) tube for decompression.

• Provide IV fluids and electrolyte replacement.

• Minimize or avoid opioids that decrease motility.

• Encourage early ambulation to promote peristalsis.

• Monitor for return of bowel function (flatus, bowel sounds, stool).

• Prepare for surgical intervention if obstruction does not resolve or if there are signs of ischemia or perforation.

Surgical Intervention – Intestinal Obstruction

• Approach: Laparotomy or laparoscopic approach may be used.

• Procedures: Reduction of obstructions, resection of infarcted tissue, and re-anastomosis.

• Postoperative Priorities: Minimize pulmonary compromise.

Surgical Interventions Intestinal Obstruction: Nursing Role Intra- and Postoperatively

• Ensure accurate documentation of bowel segments resected and whether an ostomy was created.

• Provide wound and ostomy care education if needed.

• Monitor for signs of infection, anastomotic leak, or return of bowel function.

• Post-op pulmonary complications are high risk after abdominal surgery!! TCDBM (Turn, Cough, Deep Breath, Mobilize)

Peritonitis

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

• May be suppurative (pus forming)

• May be contained to a local area (abscess)

• Can become systemic (leads to sepsis)

Types of Peritonitis

Primary Peritonitis:

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

Secondary Peritonitis:

• Bacteria enter via perforated intestine or organ

Peritonitis – Pathophysiology

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

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

• 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).

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

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

Peritonitis Pathophysiologic Cascade:

1. Contamination of the peritoneal cavity

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

2. 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.​

3. Hypovolemia and ileus

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

4. Systemic infection and sepsis if untreated

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

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: 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.

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.

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 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)

Peritonitis: Pathophysiology Connection

• 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.

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.

Postoperative Priorities (Care Pathway)

• ABCs:
  Maintain airway, breathing, and circulation; aggressively prevent pulmonary (respiratory) complications (e.g., atelectasis, pneumonia)—encourage deep breathing, coughing, and incentive spirometry.

• Hydration:
  Maintain extracellular volume (ECV) and prevent or correct hypovolemia with adequate IV fluids and monitoring.

• Positioning:
  Optimize positioning to promote abdominal drainage and adequate ventilation; prevent aspiration and respiratory compromise.

• Acid-base/FEN management:
  Monitor and correct fluid, electrolyte, and acid-base imbalances (FEN = fluids, electrolytes, nutrition).

• Wound/drain management:
  Inspect and care for surgical wounds; monitor drains for output, type, and signs of infection.

• Pain/anxiety management:
  Administer analgesics promptly, use additional comfort/support strategies to minimize anxiety.

• Maintain mobility:
  Encourage early, safe mobilization to reduce risk of venous thromboembolism, pulmonary complications, and to aid in GI recovery.

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.

GI Bleed Classification: Overt (Visible) Bleeding

• Blood is visible in vomitus (emesis) or stool.

  • Hematemesis: Vomiting bright red blood or "coffee ground" material.

  • Melena: Black, tarry stool from digested blood—classically from an upper GI source (e.g., esophagus, stomach, duodenum).

  • Hematochezia: Bright red blood per rectum, commonly from a lower GI source (e.g., colon, rectum).

• Nursing implication: Easily detectable; always demands immediate assessment and stabilization.

GI Bleed Classification: Occult (Hidden) Bleeding

• Blood loss is not visible to the naked eye—detected only by laboratory testing (e.g., stool guaiac, occult blood testing).

• Often stems from slow, small-volume bleeding (ulcers, malignancies, inflammation).

• Subtle clinical signs: Fatigue, pallor, iron-deficiency anemia, or a positive stool blood test.

• Nursing implication: Requires vigilance for subtle/anemic symptoms; often detected during routine labs or workup for anemia.

GI Bleed Classification: Acute (Sudden) vs. Chronic (Slow) Bleeding

• 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.

Small Bowel Bleeds

These bleeds originate in your:

• jejunum (middle section of your small intestine).

• Ileum (last section of your small intestine).

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)

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

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

Peptic Ulcer Disease

Upper GI Bleed Cause

• Most common cause; ulcers in stomach or duodenum may erode blood vessels.

Gastric/Duodenal ulcer & erosion

Upper GI Bleed Cause

Due to H. pylori, NSAIDs, drugs, stress

Esophageal Varices

Upper GI Bleed Cause

• Dilated veins in the esophagus, commonly from portal hypertension due to liver cirrhosis; often life-threatening when ruptured.

Neoplasms or Vascular Lesions (rare)

Upper GI Bleed Cause

Tumors or tangled blood vessels that rupture

Mallory-Weiss Tear

Upper GI Bleed Cause

• Linear mucosal laceration at the gastroesophageal junction; typically follows vomiting or retching.

• Laceration of distal esophagus from forceful vomiting/coughing

Gastritis/Erosive Esophagitis

Upper GI Bleed Cause

• Inflammation or erosion from infection (e.g., H. pylori), NSAIDs, alcohol, or severe GERD.

• Tissue inflammation from severe reflux or alcohol/irritants can erode and bleed

Diverticulosis/Diverticulitis

Lower GI Bleed Cause

• Outpouchings (diverticula) in the colon wall can bleed, or become inflamed/infected (diverticulitis).

Colorectal Cancer or Polyps

Lower GI Bleed Cause

• Benign or malignant growths in the colon or rectum; bleeding may be chronic and occult or brisk and visible.

Infectious Colitis

Lower GI Bleed Cause

Fever, tenesmus, abdominal pain, loose/bloody stools; often C. difficile post-antibiotics

Intestinal Ischemia (acute/chronic)

Lower GI Bleed Cause

Decreased blood flow to bowel → pain, nausea, bleeding

Diverticular Hemorrhage

Lower GI Bleed Cause

Top cause of brisk hematochezia (massive bright red bleeding); not always with diverticulitis

Inflammatory Bowel Disease (IBD)

Lower GI Bleed Cause

• Includes ulcerative colitis and Crohn’s disease; inflammation damages the intestinal lining, leading to bleeding.

• Especially ulcerative colitis—chronic mucosal inflammation, sunken ulcers, bleeding

Hemorrhoids or Anal Fissures

Lower GI Bleed Cause

• Hemorrhoids: swollen rectal veins causing painless bright red bleeding

• Anal fissures: tears in anal canal leading to painful, bright red blood per rectum

• Swollen rectal veins; painless bright red bleeding

Pathophysiology Example: Peptic Ulcer Bleeding

• 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.

• 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.

• 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.

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.

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).

 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 Medical & Nursing 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 Medical & Nursing 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:

• 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.

• 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 Medical & Nursing 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 Medical & Nursing 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).

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.

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.

Inflammatory Bowel Disease (IBD)

is an umbrella term for two chronic, relapsing inflammatory diseases:

• Ulcerative colitis (UC): Recurrent, inflammatory, ulcerative disorder affecting the colon and rectum.

• Crohn’s disease (regional enteritis): Acute or chronic inflammatory disorder that can affect any GI segment (mouth to anus), characterized by "skip lesions."

Takeaway

• IBD is chronic and relapsing.

• Nursing priorities: Manage inflammation, maintain nutrition and hydration, and provide psychosocial support for lifelong adaptation and coping.

IBD: Epidemiology & Risk Factors

• More common in industrialized countries.

• Incidence is higher among teenagers.

• May have a hereditary (genetic) tendency.

• Strong positive correlation: Smoking and oral contraceptive use increase risk.

Pathology & Colonoscopy Findings

• IBD = Inflammation + Damage: This means IBD causes visible, structural changes seen on colonoscopy.

• IBS = Irritation + Sensitivity: In contrast, IBS is functional, with normal-appearing tissue on colonoscopy.

Key Distinction:
Both IBD and IBS cause chronic bowel symptoms, but only IBD results in tissue injury and systemic effects (fever, weight loss, anemia).

Crohn’s Disease (CD) Location

Anywhere in GI tract (mouth to anus)

Can affect any part of the GI tract from mouth to anus, most commonly the terminal ileum and right/proximal colon.

Crohn’s Disease (CD) Pattern

"Skip lesions" (patchy, with normal tissue in between)

Characterized by segmental inflammation (“skip lesions”) with unaffected (normal) bowel between inflamed segments.

Crohn’s Disease (CD) Depth of Inflammation

Transmural (all layers of bowel wall)

Crohn’s Disease (CD) Appearance

Cobblestone

Deep ulcers

Thick walls

Fistulas

Strictures

Crohn’s Disease (CD) Symptoms 

Crampy abdominal pain

non-bloody diarrhea

weight loss

malabsorption

Crohn’s Disease (CD) Complications

Fistulas

Strictures

Abscesses

Malnutrition

Gallstones

Kidney stones

Crohn’s Disease (CD) Extraintestinal Manifestations

Joint Pain

Skin Lesions

Eye Inflammation

Higher Risk of Stones/Malabsorption