gastrointestinal bleeding nursing care planAcute gastrointestinal bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization. The incidence of upper GI bleeding (UGIB) is approximately 100 cases per 100,000 population per year.

Bleeding from the upper GI tract is about 4 times more common than the lower GI tract and is a significant cause of morbidity and mortality. UGIB is twice as common in men as in women and increases in prevalence with age (>60 years). Lower GI bleeding (LGIB) accounts for approximately 20%-33% of episodes of GI hemorrhage, with an annual incidence of about 20-27 cases per 100,000 population in Western countries.

Upper GI bleeding is defined as bleeding derived from a source proximal to the ligament of Treitz. Acute LGIB has been defined as bleeding that is of a recent duration, originates beyond the ligament of Treitz, results in instability of vital signs, and is associated with signs of anemia with or without the need for blood transfusion. The definition of LGIB from the American College of Gastroenterology clinical guideline is “the onset of hematochezia originating from either the colon or the rectum”.

The etiology of GI bleeding is divided into upper GI and lower GI bleeding.

Upper GI bleeding

  • Ulcer-related UGIB. Bleeding peptic ulcers account for the majority of clients presenting with acute upper GI bleeding. Peptic ulcer disease is strongly associated with H. pylori. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on the gastric and duodenal mucosa. As the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm.
  • Vomiting-related UGIB. During vomiting, the lower esophagus and upper stomach are forcibly inverted. Vomiting attributable to any cause can lead to a mucosal tear of the lower esophagus or upper stomach.
  • Mallory-Weiss tears. Mallory-Weiss tears account for 8-15% of acute GI hemorrhages. The occasionally massive UGIB results from a tear in the mucosa of the gastric cardia. The linear mucosal laceration is the result of forceful vomiting, retching, coughing, or straining.
  • Acute stress-related mucosal disease. Acute stress-related mucosal disease or stress ulcer results from predisposing clinical conditions that have the potential to alter the local mucosal protective barriers, such as mucus, bicarbonate, blood flow, and prostaglandin synthesis.
  • Dieulafoy lesions. The Dieulafoy lesion is a vascular formation of the proximal stomach, usually within 6 cm of the gastroesophageal junction along the lesser curvature of the stomach. The lesions appear as a large submucosal vessel that has become ulcerated. Alcohol consumption is reportedly associated with the Dieulafoy lesion.
  • NSAIDs. NSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase, which causes decreased mucosal prostaglandin synthesis and results in impaired mucosal defenses. Daily NSAID use causes an estimated 40-fold increase in gastric ulcer creation and an 8-fold increase in duodenal ulcer creation.

Lower GI bleeding

  • Diverticulosis. Diverticulosis is the dominant etiology of LGIB, reported as the most common reason for massive LGIB in most single-institution publications. Risk factors for diverticular bleeding include lack of dietary fiber, constipation, advanced age, and the use of NSAIDs and aspirin.
  • Angiodysplasia. Angiodysplasia is by far the most common vascular anomaly found in the GI tract. Although the lesions can occur anywhere in the GI tract, they occur most often in the proximal colon. Risk factors for bleeding due to angiodysplasia include earlier bleeding with a high bleeding rate, over anticoagulation, and multiple angiodysplastic lesions.
  • Ischemic and radiation-induced colitis and other vascular diseases. Tissue injury in ischemic colitis is typically caused by hypotension and vasoconstriction, which leads to mucosal friability and endoscopic findings often resembling the changes in IBD. Radiation therapy can cause inflammatory changes in the bowel resulting in mucosal telangiectasias that bleed. Other vascular entities, such as polyarteritis nodosa and Wegener granulomatosis, can also cause LGIB because of the underlying necrotic processes that cause the sloughing of the mucosa.
  • Infectious colitis. The most common causes of colitis worldwide are Salmonella, Shigella, Campylobacter jejuni, E. coli, and Entamoeba histolytica. Such microbial agents cause inflammatory diarrhea characterized by fever, bloody diarrhea, lower quadrant cramps, and tenesmus.
  • Noninfectious colitis. Although IBD due to Crohn disease or ulcerative colitis causes LGIB, it is rarely a massive hemorrhage. Ulcerative colitis can cause mild to moderate bloody diarrhea; in Crohn disease, massive bleeding is less common, occurring in about 2% of clients with Crohn colitis.
  • Neoplasm. Neoplastic bleeding can be from a polyp or carcinoma. Colon cancer is the predominant cause of neoplastic bleeding and is responsible for around 10% of rectal bleeding in clients older than 50 years. The bleeding is usually low-grade and recurrent, occurring as a result of mucosal ulceration or erosion.
  • Anorectal disease. Anorectal diseases, such as hemorrhoids, fistulas, and fissures, typically cause intermittent rectal bleeding.
  • Other causes. Infection with HIV can bleed from hemorrhoids and anal fissures. Most of the LGIB in such cases is caused by HIV-related opportunistic infections and associated etiologies, including cytomegalovirus colitis, idiopathic colon ulcers, Kaposi sarcoma, and lymphoma. Drug-induced bleeding is caused mainly by NSAID and aspirin use. Other uncommon causes of LGIB include stercoral ulcers.

Acute Gastrointestinal Hemorrhage and GI Bleed

The anatomic landmark that separates upper and lower bleeds is the ligament of Treitz, also known as the suspensory ligament of the duodenum. This peritoneal structure suspends the duodenojejunal flexure from the retroperitoneum. Bleeding that originates above the ligament of Treitz usually presents either as hematemesis or melena whereas bleeding that originates below most commonly presents as hematochezia.

Signs and symptoms of GI bleeding include:

  • Resting tachycardia
  • Orthostatic hypotension
  • Supine hypotension
  • Abdominal pain
  • Hematemesis
  • Melena
  • Maroon stools
  • Bright red blood

Acute management of GI bleeding typically involves an assessment of the appropriate setting for treatment followed by resuscitation and supportive therapy while investigating the underlying cause and attempting to correct it. The following are nursing diagnoses associated with a pressure injury.

  • Risk for Bleeding
  • Risk for Shock
  • Acute Pain

Acute Gastrointestinal Hemorrhage and GI Bleed Nursing Care Plan 

Below are sample nursing care plans for the problems identified above.

Risk for Bleeding

Forrest et al was the first to classify the stigmata of hemorrhage from peptic ulcers. Based on these classifications, the risk of recurrent bleeding can be predicted. The ulcers at the highest risk for rebleeding are those that involve active arterial bleeding or those with a visible, protuberant, nonbleeding vessel at the base of the ulcer. In clients with H. pylori infection, the rate of recurrent bleeding is increased.

Nursing Diagnosis

  • Risk for Bleeding

Risk Factors

  • Active fluid loss or hemorrhage
  • Mucosal tears
  • Infectious organisms in the stomach lining

Possibly Evidenced by

  • Not applicable; the presence of signs and symptoms establishes an actual diagnosis

Desired Outcomes

After the implementation of nursing interventions, the client is expected to:

  • Be free of signs of bleeding in GI aspirate or stools.
  • Present stabilization of hemoglobin and hematocrit levels.
  • Demonstrate improved fluid balance.

Nursing Interventions

Assessment Rationale
Assess the color and characteristics of vomitus and stools. The first step in managing bleeding is to determine its location. The bright red blood that does not clear signals recent or acute arterial bleeding, perhaps caused by gastric ulceration; dark red blood may be old blood that has been retained in the intestines or venous bleeding from varices. Coffee-ground appearance is suggestive of partially digested blood from a slowly oozing area. Undigested food indicates obstruction or gastric tumor. In a rapid upper GI bleed, stool color may be red or maroon because of rapid transit time through the GI tract.
Monitor vital signs and compare with normal and previous readings. Pulse and blood pressure should be checked with the client in supine and upright positions to note the effect of blood loss. Significant changes in vital signs with postural changes indicate an acute blood loss of approximately 20% or more of the blood volume.
Monitor intake and output and correlate with weight changes. This provides guidelines for fluid replacement. Because brisk UGIB can present as lower GI bleeding, placement of  a nasogastric tube may be necessary, with the aspirate or lavage examined for the presence of blood and/or bile.
Assess for signs of renewed bleeding after cessation of the initial bleed. Increased abdominal fullness and distention, nausea or renewed vomiting, and bloody diarrhea may indicate a return of the bleeding.
Assess the client’s physiological response to bleeding, such as a change in mentation, weakness, restlessness, anxiety, pallor, diaphoresis, tachypnea, and temperature elevation. Symptomatology is useful in gauging the severity and length of bleeding episodes. Worsening symptoms may reflect continued bleeding, inadequate fluid replacement, and shock.
Maintain bedrest. Schedule the client’s activities and provide uninterrupted periods of rest Activity and vomiting increases intraabdominal pressure and can predispose to further bleeding.
Elevate the head of the bed during gavage. This prevents gastric reflux and aspiration of antacids, which can cause serious pulmonary complications.
Provide clear or bland fluids when intake is resumed. Avoid caffeinated and carbonated beverages. Clear fluids are more easily digested and bland fluids reduce the risk of added irritation to inflamed tissues. Caffeine and carbonated beverages stimulate hydrochloric acid production, possibly potentiating bleeding.
Document and keep accurate records of subtotals of solutions and blood products during replacement therapy. A potential exists for over-transfusion of fluids, especially when volume expanders are given before blood transfusions.
Monitor laboratory studies. A CBC count with platelet count and differential are necessary to assess the level of blood loss in a client with UGIB. Having the client’s previous results as a baseline is useful to gauge this loss. Based on the client’s initial hemoglobin level and clinical assessment of shock, a type, and screen or type and crossmatch should be ordered.
Assist with inserting a nasogastric tube for gastric lavage. Inserting a nasogastric tube should be the first procedure performed to determine whether the GI bleeding is emanating from above or below the ligament of Treitz.
Administer intravenous fluids or volume expanders. Initial resuscitation involves establishing large-bore IV access and administration of normal saline. Clients in shock should receive fluid volume replacement without delay. Colloid or crystalloid solutions may be used to achieve volume restoration before administering blood products.
Administer blood and blood products as appropriate. PRBC transfusions should maintain the hemoglobin level above 7 g/dl, with a threshold of 9 g/dl in those with massive bleeding or significant comorbid conditions. A coagulopathy, such as when an INR is greater than 1.5, may require correction with fresh frozen plasma; thrombocytopenia can be corrected with platelet transfusions.
Administer medications as appropriate. Vasoconstrictive agents reduce the blood flow and facilitate hemostatic plug formation in the bleeding vessel. The relative efficacy of proton-pump inhibitors may be due to their superior ability to maintain a gastric pH at a level above 6.0, thereby protecting an ulcer clot from fibrinolysis. The use of prokinetic agents to empty the stomach of retained blood or clots to improve endoscopic visualization has been extensively studied. H. pylori eradication involves common regimens of “triple therapy” with a PPI, clarithromycin, and amoxicillin, or bismuth “quadruple therapy” consisting of a PPI, bismuth, tetracycline, and nitroimidazole.
Prepare the client for endoscopy. Endoscopy has been the primary method of evaluating and managing UGIB. Urgent endoscopy is indicated when clients present with hematemesis, melena, or postural changes in blood pressure. Early endoscopy is associated with reductions in the length of hospital stay, the rate of recurrent bleeding, and the need for emergent surgical intervention.
Assist with surgery as indicated. Surgery should be considered promptly in clients with massive bleeding or hemodynamic instability who have bleeding that is not amenable to any other treatment. Primary surgical intervention should be considered in clients with a perforated viscus. Endoscopic clipping or sewing techniques can also be used for such clients.
Assist with the insertion of a Blakemore or Minnesota tube. Placement of a Blakemore or Minnesota tube should be considered in clients with hemodynamic instability or massive GI bleeds in the setting of known varices, which should be done only once the airway is secured.

Risk for Shock

Massive LGIB is a life-threatening condition; although this condition manifests as maroon stools or bright red blood from the rectum, clients with massive upper GI bleeding may also present with similar findings. Clients who present with hemorrhagic shock have a mortality rate of up to 30%. Hemorrhage may be classified based on the amount of blood loss. A classification scheme aids in understanding the clinical manifestations of hemorrhagic shock. As the percentage of blood volume loss increases, pertinent clinical signs, symptoms, and findings become more apparent.

Nursing Diagnosis

  • Risk for Shock

Risk Factors

  • Hypovolemia

Possibly Evidenced by

  • Not applicable; the presence of signs and symptoms establishes an actual diagnosis

Desired Outcomes

After the implementation of nursing interventions, the client is expected to:

  • Maintain and improve tissue perfusion.
  • Exhibit normal vital signs and palpable peripheral pulses.
  • Display ABG results and urine output within the normal range.

Nursing Interventions

Assessment Rationale
Assess for any changes in the level of consciousness and reports of dizziness or headache. These changes may reflect inadequate cerebral perfusion as a result of reduced arterial blood pressure.
Assess the client’s vital signs. Assessing the client for hemodynamic instability and clinical signs of poor perfusion is important early in the initial evaluation to properly triage the client with massive hemorrhage to ICU settings. Worrisome clinical signs and symptoms include tachycardia of more than 100 beats/min and systolic blood pressure of less than 90 mm Hg.
Auscultate apical pulse. Monitor cardiac rate and rhythm, if a continuous electrocardiogram is available and indicated. Dysrhythmias and ischemic changes can occur as a result of hypotension, hypoxia, acidosis, electrolyte imbalance, or cooling near the heart if cold saline lavage is used to control bleeding.
Assess the skin for coolness; pallor; diaphoresis; delayed capillary refill; and weak, thready peripheral pulses. Vasoconstriction is a sympathetic response to lowered circulating volume and may occur as a side effect of vasopressin administration.
Note urinary output and specific gravity. Although early cardiovascular changes occur as blood loss continues, urine output, as a sign of end-organ renal perfusion, is only mildly affected until class 3 hemorrhage has occurred.
Observe for reports of abdominal pain, especially sudden, severe pain, or pain radiating to the shoulder. Pain caused by gastric ulcers is often relieved after acute bleeding because of buffering effects of blood. Continued severe or sudden pain may reflect ischemia due to vasoconstrictive therapy, bleeding into the biliary tract, or perforation with the onset of peritonitis.
Investigate reports of chest pain. Note location, quality, duration, and what relieves pain. This may reflect cardiac ischemia related to decreased perfusion. Impaired oxygenation status resulting from blood loss can bring on myocardial infarction in a client diagnosed with cardiac disease.
Change position slowly initially. Vasoconstrictor mechanisms are depressed, and quick movement may lead to orthostatic hypotension, especially in the early periods of shock.
Place the client in a supine position with legs elevated. Current recommendations for shock positioning are having the client supine with the legs passively elevated at 30° to 60° if there is no evidence of trauma or injury.
Insert a Foley catheter, as indicated. Insertion of Foley catheter ensures accurate measurement of the urine. Decreased systemic perfusion may cause kidney ischemia and failure, manifested by decreased urine output.
Monitor ABGs and pulse oximetry. These interventions identify hypoxemia and the effectiveness of and the need for therapy. It may also reveal respiratory alkalosis, compensating for the diminished blood flow through the lungs.
Administer supplemental oxygen, as indicated. Provide supplemental oxygen if the client is hypoxic, typically by nasal cannula, but clients with ongoing hematemesis or altered mental status may require intubation.
Administer IV fluids as indicated. Intravenous access must be obtained. Bilateral, 16-gauge (minimum), upper extremity, peripheral intravenous lines are adequate for volume resuscitative efforts. The 2008 SIGN guideline indicates either colloid or crystalloid solutions may be used to attain volume restoration prior to administering blood products.
Assist with intubation, as indicated. Clients with massive bleeding should be considered for intubation to reduce the increased risk of aspiration. Such clients should be treated in an intensive care setting.

Acute Pain

H. pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt normal mucosal defense and repair, making the mucosa more susceptible to acid. Ulcers may range in size from millimeters to several centimeters. Ulcers are delineated from erosions by the depth of penetration; erosions are more superficial and do not involve the muscularis mucosae (Vakil, 2021). Bleeding peptic ulcers account for the majority of clients presenting with acute UGIB. As the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm. The weakened wall ruptures, producing hemorrhage.

Nursing Diagnosis

  • Acute Pain

Related Factors

  • Chemical burn of gastric mucosa, oral cavity
  • Physical response, such as reflex muscle spasm in the stomach wall

Possibly Evidenced by

  • Communication of pain descriptors
  • Abdominal guarding, rigid body posture, facial grimacing
  • Autonomic responses, such as changes in vital signs in reaction to acute pain

Desired Outcomes

After the implementation of nursing interventions, the client is expected to:

  • Verbalize relief of pain.
  • Demonstrate relaxed body posture and be able to sleep or rest appropriately.
  • Utilize relaxation techniques to reduce discomfort or pain.

Nursing Interventions

Assessment Rationale
Assess the client’s reports of pain, including location, duration, and intensity. Pain is not always present, but if present, should be compared with the client’s previous pain symptoms. This comparison may assist in the diagnosis of the etiology of the bleeding and the development of complications.
Assess for nonverbal pain cues such as restlessness, reluctance to move, abdominal guarding, tachycardia, and diaphoresis. Nonverbal cues may be both physiological and psychological and may be used in conjunction with verbal cues to evaluate the extent of severity of the problem.
Identify factors that aggravate or alleviate pain. This is helpful in establishing diagnosis and treatment needs.
Provide small, frequent meals, as indicated for the individual client. Food has an acid-neutralizing effect and dilutes the gastric contents. Small meals prevent distention and the release of gastrin.
Identify and limit the foods that create discomfort. Specific foods that cause distress vary among individuals. Spicy foods, alcohol, and coffee can precipitate dyspepsia.
Provide frequent oral care and comfort measures including back rubs and position changes. Halitosis from stagnant oral secretions is unappetizing and can aggravate nausea. Gingivitis and dental problems may arise.
Provide and implement prescribed dietary modifications. The client may receive nothing by mouth initially. When oral intake is allowed, food choices depend on the diagnosis and etiology of the bleeding.
Use regular milk rather than skim milk, if milk is allowed. Fat in regular milk may decrease gastric secretions; however, the calcium and protein content especially in skim milk increases secretions.
Administer medications as indicated. Analgesics help relieve acute or severe pain. Morphine also reduces peristaltic activity. Acetaminophen promotes general comfort and rest. Antacids decrease gastric acidity by absorption or by chemical neutralization. Evaluate the choice of antacid in regard to the total health picture, such as sodium restriction.

Acute Gastrointestinal (GI) Hemorrhage Sample Nursing Care Plan

Nursing DiagnosisObjectivesNursing InterventionsRationaleEvaluation
Fluid Volume Deficit (Isotonic)

Possible Etiologies: (Related to)

Active volume loss (hemorrhage)

Defining characteristics: (Evidenced by)

• Pallor
• Cool, clammy skin
• Restlessness/ changes in
• Easy fatigability/ weakness
• Apprehension
• Diaphoresis
• Hypotension, tachycardia,
delayed capillary refill
• Oliguria
• ECG changes
• Syncope
• Hemoconcentration
Short term goal:
Client will be able to participate in
procedures and treatments
necessary for his assumption of
adequate fluid volume.

Long term goal:

Client will be able to maintain
fluid volume at a functional level
as evidenced by client’s adequate
urine output, stable vital signs,
prompt capillary refill, and
laboratory results of hemoglobin
and hematocrit within normal
1. Check for the appearance of vomitus, stool, or drainage.

2. Monitor vital signs and compare with client’s normal and previous data; you may take blood pressure in different positions like when sitting,
lying, and standing positions as much as possible.

3. Assess client’s physiological response to hemorrhage like changes in mentation, weakness,
apprehension, diaphoresis, restlessness, and anxiety.

4. Measure central venous pressure if indicated and available.

5. Strictly monitor fluid intake and output; measure fluid loss through emesis, gastric drainage and stools.

6. Maintain client on bed rest to prevent vomiting and straining when defecation; schedule activities in order to provide adequate rest for the client.

7. Place client in fowler’s position during antacid gavage.

8. Take note for any signs of renewed bleeding after cessation of initial bleeding.

9. Check for signs of secondary bleeding i.e. nose or gums, echymosis.

10. Maintain client on NPO as ordered by the physician.

11. Resume intake with clear/ bland fluids or as indicated by the physician; avoid giving dark colored foods.

12. Administer IV fluids/ volume expanders/ fresh whole blood/platelet/fresh frozen plasma as indicated.

13. Insert NGT as indicated by the physician.
- Perform gastric lavage with cool saline solution until aspirate is pinkish in color or if it is clear.

14. Administer medications like H2 receptors antagonists, antiulcer agents, antacids, Vitamin K,
antiemetic, and anti infective.

15. Monitor laboratory findings like hemoglobin, hematocrit, BUN and creatinine.
1. It helps in differentiating the cause
of gastric distress; bright red blood may be caused by arterial bleeding; dark red blood may be due to esophageal bleeding; coffee ground
may be because of partly digested blood from slowly oozing area.

2. The alterations and fluctuations in blood pressure may be used for rough estimate of blood loss; BP less than 90 mmHg may reflect a
25% volume loss.

3. Worsening in symptomatology may be due to continuous hemorrhage or inadequate fluid

4. It reflects blood volume in the body and cardiac response to bleeding; It may reflect how
effective fluid replacement therapy.

5. It gives the basis for fluid replacement.

6. Vomiting aggravates intra- abdominal pressure and can predispose to further bleeding.

7. It prevents gastric reflux an aspiration of medication.

8. Rebleeding may sometimes occur as evidenced by abdominal fullness, nausea and vomiting.

9. These parameters to know how adequate fluid replacement is; symptoms given may cause DIC.

- That is in order to prevent further gastric distress

10. Foods easily digested reduce the risk for added irritation; to take note for possible rebleeding.

11. Fluid replacement is essential in improving client’s blood volume.

12. It is an avenue for removing gastric secretions, blood, and clots; reduces vomiting and facilitates endoscopy, if applied.

13. It prevents further bleeding by local vasoconstriction.

14. These medications are essential in treating client with acute GI hemorrhage; they have their own specific and actions regarding this

15. It assists in knowing how much blood replacement is needed; BUN greater than 40 with normal creatinine level reflects a major

Client will be able to demonstrate positive and accepting behaviours with regards to treatment interventions like nasogastric tube insertion and blood transfusion and as well participate during necessary procedures like endoscopy, 12 lead ECG, abdominal X - ray and laboratory

Client will demonstrate adequate and improved fluid balance as evidenced by client’s adequate urine output (more than 30 cc which reflects adequate intake) with normal specific gravity, blood pressure ranging from 110/70 mmHg to 120/80mmHg, pulse rate ranging from 72 - 88 beats per minute, capillary refill of less than 2 seconds, and laboratory results showed adequate haemoglobin and hematocrit levels within one week of nursing care.


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  2. DiGregorio, A. M., & Alvey, H. (2022, June 11). Gastrointestinal Bleeding – StatPearls. NCBI. Retrieved August 18, 2022, from
  3. Moorhouse, M. F., Murr, A. C., & Doenges, M. E. (2010). Nursing Care Plans: Guidelines for Individualizing Client Care Across the Life Span. F.A. Davis Company.
  4. Rich, K. (2019, March). Trendelenburg position in hypovolemic shock: A review. Journal of Vascular Nursing, 37(1), 71-73. 10.1016/j.jvn.2019.01.002
  5. Upchurch, B. R. (2021, September 1). Upper Gastrointestinal Bleeding (UGIB): Practice Essentials, Background, Etiology. Medscape Reference. Retrieved August 18, 2022, from
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