5.2 Core Workflows and Decision Points

Distinguishing Upper from Lower GI Bleeding

Gastrointestinal hemorrhage is the highest-yield workflow in this domain. The first step is to localize the source, because it changes the differential and the disposition.

Melena indicates blood has been in the gut long enough to be digested, so it points upper. Coffee-ground emesis is blood altered by gastric acid. Brisk upper bleeding can also produce hematochezia, so hemodynamic instability with apparent lower bleeding still warrants an upper source workup. Peptic ulcer disease remains the single most common cause of acute upper GI bleeding.

Resuscitation Priorities and Sequence

Manage every significant GI bleed as hemorrhagic shock until proven otherwise. The ordered priorities:

1. Airway — active hematemesis risks aspiration; have suction ready and consider intubation for airway protection before endoscopy in the obtunded patient.
2. Access and fluids — establish two large-bore (16-18 gauge) peripheral IVs; begin isotonic crystalloid while blood is prepared.
3. Blood work — type and crossmatch, CBC, coagulation studies, comprehensive metabolic panel, and lactate. Remember an initial hemoglobin can be normal in acute hemorrhage before hemodilution.
4. Transfusion — use a restrictive threshold of about 7 g/dL for hemodynamically stable patients (higher for active ischemia); for massive hemorrhage activate the massive transfusion protocol with a balanced 1:1:1 ratio of packed red cells, plasma, and platelets.
5. Reverse anticoagulation — hold and reverse warfarin (vitamin K, PCC), direct oral anticoagulants (specific reversal agents), and consider platelets/DDAVP for antiplatelet agents.
6. Pharmacology — start an IV proton pump inhibitor (pantoprazole) for suspected ulcer bleeding; do not delay resuscitation for it.

The Glasgow-Blatchford score (using BUN, hemoglobin, blood pressure, heart rate, melena, syncope, and comorbidities) risk-stratifies who needs urgent intervention.

Variceal Bleeding: The Special Case

Esophageal and gastric varices form when portal hypertension (usually from cirrhosis) forces blood through collateral veins. A variceal bleed is often massive and has in-hospital mortality near 50%, so it gets its own pathway:

• Start a vasoactive agent — octreotide (a somatostatin analog that reduces splanchnic blood flow) — as soon as variceal bleeding is suspected, before endoscopy.
• Give prophylactic antibiotics (e.g., ceftriaxone); bacterial infection is common in cirrhotic GI bleeds and antibiotics reduce mortality.
• Arrange urgent endoscopy; endoscopic band ligation is the definitive therapy of choice for esophageal varices.
• For uncontrolled hemorrhage, balloon tamponade with a Sengstaken-Blakemore tube is a temporizing bridge. It carries serious risks: airway obstruction if the balloon migrates (keep scissors at the bedside to deflate/cut emergently) and esophageal rupture from over-inflation. The airway is typically secured first.
• Definitive salvage includes TIPS (transjugular intrahepatic portosystemic shunt).

Transfuse variceal bleeds cautiously toward the restrictive target; over-transfusion raises portal pressure and worsens rebleeding.

Non-Variceal Sources and Lower GI Bleeding

Outside of varices, peptic ulcer disease is the dominant cause of upper GI hemorrhage, driven by Helicobacter pylori infection and NSAID use. A bleeding ulcer is managed with IV proton pump inhibitors and endoscopic hemostasis (clipping, thermal coagulation, or injection). A Mallory-Weiss tear is a mucosal laceration at the gastroesophageal junction after forceful vomiting; it usually causes self-limited hematemesis but can bleed briskly. Distinguish it from Boerhaave syndrome, which is full-thickness rupture (covered in 5.4) and far more lethal.

Lower GI bleeding arises distal to the ligament of Treitz and most often presents as hematochezia. The leading causes are diverticulosis (typically painless, brisk) and angiodysplasia; others include hemorrhoids, ischemic or infectious colitis, inflammatory bowel disease, and colorectal cancer. Workup may include CT angiography, tagged red-cell scan, or colonoscopy to localize the source. The resuscitation priorities are identical to upper bleeding: airway, large-bore access, crystalloid then blood, and reversal of anticoagulation.

Recognizing Hemorrhagic Shock

Do not wait for hypotension. Class I-II hemorrhagic shock shows tachycardia, anxiety, and a narrowing pulse pressure while the systolic blood pressure is still normal because of compensatory vasoconstriction. Hypotension is a late sign, especially in young patients who compensate well until they crash. Frequent reassessment of heart rate, mental status, skin signs, urine output, and lactate detects ongoing blood loss earlier than a single blood pressure reading. The nurse treats the trend toward shock aggressively rather than waiting for the numbers to confirm it.

Positioning, monitoring, and disposition

While resuscitating, place the actively vomiting patient in a position that protects the airway (upright or lateral with suction at hand), apply continuous cardiac and pulse-oximetry monitoring, and keep the patient warm because hypothermia worsens coagulopathy. Insert a urinary catheter to trend urine output as a marker of end-organ perfusion, target a mean arterial pressure adequate for organ perfusion, and avoid over-resuscitating a variceal patient.

Most significant GI bleeds need GI/endoscopy consultation and admission, frequently to an intensive care setting; the emergency nurse's role is to keep the patient alive and stable until definitive endoscopic or surgical control is achieved, while documenting the volume and character of ongoing losses.