Acute Gastrointestinal Hemorrhage PDF

# Acute Gastrointestinal Hemorrhage Acute Gastrointestinal Hemorrhage is a potentially life-threatening emergency that remains a common complication of critical illness. Cause of death is from exacerbation of the medical illness. May occur from upper or lower gastrointestinal tract. ## Causes of A...

# Acute Gastrointestinal Hemorrhage Acute Gastrointestinal Hemorrhage is a potentially life-threatening emergency that remains a common complication of critical illness. Cause of death is from exacerbation of the medical illness. May occur from upper or lower gastrointestinal tract. ## Causes of Acute Gastrointestinal Hemorrhage ### Upper Gastrointestinal Tract * **Peptic ulcer disease:** Most common or leading cause; Often result from the breakdown of the gastromucosal lining. * Gastric or Duodenal Ulcer * **Possible factor:** * Chronic ingestion of NSAID, aspirin and alcohol which weaken the gastric mucosal barrier against acids and pepsin. * Action of the stomach that would damage the mucosal wall of the duodenal area. * **Proliferation of H.Pylori in the stomach:** PRIMARY FACTOR * H.Pylori would disrupt the mucosa layer, it would release enzymes and toxins wherein the enzymes and toxins adhere to the gastric epithelium causing the damage of the gastric epithelium. * **Absence of H.Pylori infection:** use NSAIDs, aspirin and alcohol to be the second factors that could cause the development of peptic ulcer disease. * **Stress-related erosive syndrome:** * Stress ulcer * Stress Gastritis * **Px with Acute Erosive Gastritis:** Result into the ischemia of the mucosal lining and degeneration of the mucosal lining. * The main cause in the development of the disruption of the gastric mucosal is the increase acid production and decrease mucosal blood flow. * **Possible factor/Cause in the increased production of the hydrochloric acid and possible ischemia:** * **High Physiologic Stress:** Most common factor * Because of the following condition: * Use of mechanical ventilator * Px with severe, massive or extensive burns - would develop *curling's ulcer* because of ischemia and physiologic stress. * With severe trauma * Undergone major surgery * Shock and sepsis * Co-agulopathy * Acute neuro conditions - would develop *Cushing's Ulcer*. ### Lower Gastrointestinal Tract * **Diverticulosis:** Outpouching of the bowel wall, may possibly cause infection because of the entrapment of the small stools refer as fecalith. The outpouching is commonly located in the sigmoid colon because of the increasing pressure. * **Inflammatory bowel disease** * Crohn's * Ulcerative Colitis: cause friability of the bowel wall. * **Hallmark characteristic of ulcerative colitis:** *rectal bleeding* or bloody stool. * **Trauma** * **Neoplasm** * **Infectious colitis** * **Radiation colitis:** Secondary to exposure to radiation. * **Angiodysplasia** * **Ischemia** * **Aortoenteric fistula** * **Hemorrhoids:** Presence of varicosities in the rectal and anal vein ⇒ could lead to possible damage on the wall of the rectum or anus. ## Pathophysiology Gl hemorrhage is a life-threatening disorder that is characterized by acute, massive bleeding. Gl hemorrhage results in hypovolemic shock, initiation of the shock response, and development of multiple organ dysfunction syndrome if left untreated. ## Clinical Classification of Hemorrhage | Class | Blood Loss (%) | Clinical Signs and Symptoms | |---|---|---| | 1 | ≤15 | Pulse rate: normal or <100 beats/min (supine), Capillary refill <3 seconds, Urine output: adequate (30-35 mL/hr), Orthostatic hypotension, Apprehensive | | 2 | 15-30 | Pulse rate: increased (>100 beats/min), Capillary refill: sluggish, Pulse pressure: decreased, Blood pressure: normal (supine), Tachypnea, Urine output: low (25-30 mL/hr) | | 3 | 30-40 | Pulse rate: 120+ beats/min (supine), Hypotension, Skin: cool & pale, Confused, Hyperventilating, Urine output: low (5-15 mL/hr) | | 4 | ≥40 | Profoundly hypotensive, Pulse rate: 140+ beats/min, Confused, lethargic, Urine output minimal | ## Hallmarks of Gastrointestinal Hemorrhage * **Hematemesis:** Bright red or coffee ground or brownish vomit, it would depend on the amount of the gastric contents at the time of the bleeding and the length of time the blood has been exposed to gastric secretion. The gastric acid converts the bright red hemoglobin to brown hematin that would account for the presence of brownish or coffee ground vomitus. * **Hematochezia:** Presence of bright red stool and would occur for massive lower GI hemorrhage and if rapid enough it could be related to upper GI hemorrhage also. * **Melena:** Black tarry or dark red stool. Would occur from digestion of blood from an upper GI hemorrhage and may take several days to clear after the bleeding has stopped. ## Assessment Findings: Acute Gastrointestinal Hemorrhage The initial clinical presentation of the patient with acute GI hemorrhage is signs and symptoms of hypovolemic shock depending on the amount of blood lost ## Laboratory/diagnostic Studies: Acute Gastrointestinal Hemorrhage * **Hemoglobin and Hematocrit:** Baseline * Poor indicators of severity of blood loss if the bleeding is acute - decreased. * It may take 24 to 72 hours for the redistribution of the plasma from the extravascular to intravascular space to occur that can cause patient's level and hematocrit value to decrease. * **Mild leukocytosis:** Elevation of the WBC. * **Endoscopy:** To isolate and treat the source of bleeding. To visualize the GI mucosa. May advise for esophagogastroduodenoscopy (EDG) or colonoscopy or enteroscopy (visualization of the small intestine). * **Other Lab test:** * BUN - increased for 24 hours after GI bleed. * FBS - increased because of physiologic stress. * LFT (liver function test) - impaired depending on the primary condition of the px. * S. Electrolytes- *hypokalemia* * ABG - *hypoxemia* in relation to bleeding and px will be (+) for *metabolic alkalosis* and *metabolic acidosis*. * **Coagulation Studies:** * Patient's with portal hypertension with esophageal viruses that cause the hemorrhage: * Platelet - decreased. * PT- prolonged * PTT- prolonged ## Medical Management: Acute Gastrointestinal Hemorrhage To reduce mortality: Identification of clients at risk and implementations of interventions to reduce gastric acidity and support the gastric mucosal defense mechanisms. Management of the patient at risk for Gl hemorrhage should include prophylactic administration of pharmacologic agents for neutralization of gastric acids. * **Administration of antacids, H2 antagonists and proton pump inhibitor (pantoprazole)** * **Cytoprotective agent:** Sucralfate or isoprene - Would adhere to the ulcer side and would protect from the acids or enzymes and bile salts and it would prevent further damage of the mucosa lining or the ulcer area. It can heal the ulcer but it will not prevent future ulcer from occuring. ## Priorities in the medical management of the patient with Gastrointestinal Hemorrhage * Airway protection * Fluid resuscitation - to achieve hemodynamic stability * Correction of co-morbid conditions (e.g., coagulopathy) * Therapeutic procedures to control or stop bleeding and diagnostic procedures to determine the exact cause of the bleeding. ## Stabilization: Initial Treatment Priority * **Initiate fluid resuscitation by:** * administration of intravenous infusions of crystalloids, blood, and blood products. * **blood loss is >1500mL:** need a blood replacement therapy *(Plain LR and Plain NSS)* - fluid of choice to restore the circulating blood volume and to prevent possible progression to hypovolemic shock. * **gauge 14 and 16:** to facilitate rapid administration of fluid for resuscitation. * **If blood is available:** usual component of blood that is used is the → *Packed RBC*, to reestablish the oxygen carrying capacity of the blood or other blood products as ordered. * **If no available packed RBC:** advise for *fresh whole blood*. * **Administration of Vit. K 10mL IM/IV:** px with coagulopathy, to restore the normal prothrombin time level. * **Vasopressor medications:** dopamine, epinephrine or norepinephrine ← to maintain the BP of the px thereby maintaining the perfusion and the vital signs. * **Supplemental oxygen therapy:** * To increase oxygen delivery and to improve the tissue perfusion thereby preventing multi-organ dysfunction syndrome to occur. * **Monitor the hemodynamic parameters:** to help guide fluid replacement therapy particularly in px at risk of heart failure. * **Insertion of a large nasogastric tube** ← to confirm the diagnosis of active bleeding, to facilitate gastric lavage, decrease the risk for aspiration and to prepare the esophagus, stomach, and proximal duodenum for endoscopic evaluation. * **Controlling the Bleeding** ← Second priority. Dependent on the primary problem that caused the bleeding. * **PUD (Peptic Ulcer Disease)** * **Endoscopic injection therapy in conjunction with thermal or hemostatic clips.** * **Thermal:** *Heat probe/Bipolar coagulation* - to cauterize the bleeding vessel thereby stopping the bleeding. * **Application of hemostatic clips:** - used to ligate the bleeding blood vessels thereby stopping the bleeding. * **Endoscopic thermal therapy** ← uses heat to cauterize the bleeding vessel, and endoscopic injection therapy with variety of agents such as hypertonic saline, epinephrine, ethanol, and sclerosants. * **Intra-arterial infusion of vasopressin into the gastric artery or intra-arterial injection of an embolizing agent (e.g., Gelfoam pledgets, polyvinyl alcohol particles, coils).** * **Intra-arterial infusion of vasopressin:** * **Vasopressin also referred as “Petrosine”** ← initial mode of therapy in urgent situation and produces constriction of the splanchnic arterial bed and would decrease the portal pressure. * It can also reduce the coronary blood flow and decrease the blood pressure and may increase the oxygen demand causing coronary artery constriction that could potentiate the development of cardiac dysrhythmias. Reduce the mesenteric circulation causing bowel ischemia to minimize the side effect and the doctor would advise for the use of IV/sublingual/topical nitroglycerin to prevent these side effects of vasopressin. Intra-arterial injection of an embolizing agent (e.g., Gelfoam pledgets, polyvinyl alcohol particles, coils). Can be performed during arteriography to stop the bleeding. This is an emergent intervention in **high risk patients and patients who are refractory to endoscopic treatment.** **Indications:** * px with muscle bleeding that require blood transfusion of at least 4 units of blood in 24 hours. * px with hemodynamic instability wherein the blood pressure is <100 mmHg systolic and HR of 100bpm. * px with clinical shock. * px who is not responsive to conservative medical treatment including endoscopic treatment. * **STRESS-RELATED MUCOSAL DISEASE** ← intra-arterial infusion of vasopressin and intraarterial embolization. * **ESOPHAGOGASTRIC VARICES** * In acute variceal hemorrhage: control of bleeding may be done initially through the use of pharmacologic agents and endoscopic therapies. * **Intravenous administration of vasopressin, somatostatin, and octreotide** * **Somatostatin** ← lower the portal venous pressure by vasoconstriction or splanchnic circulation. * **Octreotide** ← decrease bleeding of the esophageal varices. * **Endoscopic therapies:** endoscopic injection sclerotherapy (EIS) and endoscopic variceal ligation (EVL). * **EIS - Endoscopic Injection Sclerotheraphy** ← controls bleeding by the injection of a sclerosing agent in or around the varices. This creates an inflammatory reaction that induces vasoconstriction and results in the formation of a venous thrombosis. * **The most commonly used agent is epinephrine** - which results in localized vasoconstriction and enhanced platelet aggregation. * **Sclerosing agents that may also be used:** such as ethanolamine, alcohol, and polidocanol - cause an inflammatory reaction in the vessel - results in thrombosis and eventually produces a fibrous band. * **EVL- Endoscopic Variceal Ligation** ← application of bands or metal clips around the circumference of the bleeding varices - induce venous obstruction and control bleeding. After 1-2 days necrosis and scar formation would occur that would promote the sloughing off of the band and the tissue. * **Treatment of choice in the management of px with esophageal varices If EIS and EVL fails:** *Transjugular Intrahepatic Portosystemic shunting (TIPS)* - a channel between the systemic and portal venous systems is created to redirect portal blood, thereby reducing portal hypertension and decompressing the varices to control bleeding. * **Portal hypertension is confirmed if the pressure is > 10 mmHg.** * **Indicated:** Acute episode of uncontrolled variceal bleeding refractory to pharmacological and endoscopic therapies. * **Postprocedural care includes:** * observation for overt or covert bleeding. * hepatic or portal vein laceration – result in rapid blood loss volume. * inadvertent puncture of surrounding organs. * Observe for other complications include hepatic encephalopathy, liver failure, bacteremia, and stent stenosis. * **SURGICAL INTERVENTION: AGH** - for patient who remains hemodynamically unstable. * **PUD: VAGOTOMY AND PYLOROPLASTY** * **Vagotomy** ← involve the severing of the vagus nerve that would eliminate the autonomic stimulus to the gastric cells and reduce hydrochloric acid production. * **Pyloroplasty** ← provide for gastric emptying. Incision of the pyloric sphincter to widen the pylorus. * **ESOPHAGEAL VARICES:** * **Decompression procedures** ← result to the diversion of the portal blood away from the liver and decompress the portal system; to decrease or reduce the portal pressure. * **Portacaval shunt procedure:** * **End-to-side portacaval shunt procedure** involves the ligation of the hepatic end of the portal vein with subsequent anastomosis to the vena cava. * **Side-to-side portacaval shunt procedure** - the side of the portal vein is anastomosed to the side of the vena cava. * **Mesocaval shunt procedure** ← involves the insertion of a graft between the superior mesenteric artery and the vena cava. ## Nursing Management: Acute Gastrointestinal Hemorrhage ### Nursing Diagnoses * Deficient Fluid Volume, related to absolute loss * Decreased Cardiac Output, related to alterations in preload * Risk for Aspiration * Imbalanced Nutrition: Less Than Body Requirements, related to lack of exogenous nutrients and increased metabolic demand * Risk for Infection ### Nursing Interventions: Acute Gastrointestinal Hemorrhage * **Administering Volume Replacement** * Measures to facilitate volume replacement include obtaining intravenous access and access and administering prescribed fluids and blood products. * Two large-diameter peripheral intravenous catheters should be inserted to facilitate the rapid administration of prescribed fluids. * **Controlling the Bleeding** * Gastric lavage and irrigate with normal saline or water until return flow is clear. It is used to decrease gastric mucosal blood flow and evacuate blood from the stomach. * Keep accurate records of the amount of fluid instilled and aspirated to ascertain the true amount of bleeding. * Iced saline NOT used: low-temperature fluids shift the oxyhemoglobin dissociation curve to the left, decrease oxygen delivery to vital organs, and prolong bleeding time and prothrombin time. Iced saline also may further aggravate bleeding. * **Maintaining Surveillance for Complications** * Continuously observed for signs of gastric perforation. * Signs and symptoms include sudden, severe, generalized abdominal pain with significant rebound tenderness and rigidity. *Perforation* should be suspected when fever, leukocytosis, and tachycardia persist despite adequate volume replacement. * **Educating the Patient and Family** * Teaching should focus on the interventions: * How to reduce further bleeding episodes * Importance of taking medications * Lifestyle changes * Stress management * Diet modifications * Alcohol cessation * Smoking cessation ## Notes from Ma'am * Bicarbonate in a very high concentration - bone demineralization * Diverticulosis - outpouching in the colon * Cancer - you will feel the pain at the end. * If you want to save patient - apply pressure to area and insert a large-bore catheter for IV.