Acute Gastrointestinal Hemorrhage
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Introduction
o Medical emergency
o Common complication of critical illness
o Bleeding from upper or lower GI tract
o Ligament of Treitz: (suspends the intestines and is attached to the diaphragm)
 Bleeding proximal to ligament: Upper GI
 Esophagus, Stomach, and Duodenum
 PUD, SRES, Varices, Mallory Weiss Tears
 Bleeding distal to ligament: Lower GI
 Jejunum, Ileum, Colon, and Rectum
 Diverticula, Cancer, Inflammatory disease
o Gastric Parietal and Mucous Cells
 Parietal cells make hydrochloric acid
 Mucus creates the barrier that protects our stomachs
Functions of Gastric Parietal Cells
o Parietal Cells– forms HCl Acid
 Breaks down food and protein bonds
o pH in the stomach is low (acidic), about 1.5 to 2 from the hydrochloric acid. Need proton pump to push new
hydrochloric acid into the already acidic environment of the stomach. An H2 inhibitor slows production of
hydrochloric acid, PPI prevents transport into the stomach
Functions of Gastric Mucous Cells
o Glycoprotein mucus - forms gel
 Maintains mucosal-luminal pH gradient
o Epithelial mucous cells - secretes bicarbonate
 Augments action of glycoprotein mucus
o Epithelial cell structure
 Protects against damage of gastric secretions
Etiology of Upper GI Bleed
o Peptic Ulcer Disease (PUD)
 Patho
 Breakdown of gastro-duodenal mucosa  gastric secretions auto-digest layers of stomach 
damages blood vessels  hemorrhage
 Primary Causes
 NSAIDS
 Helicobacter pylori
o Bacteria from food, contaminated
o Likes to get into the stomach and lives in the mucousal lining, acts as an agent that
penetrates the epithelial layer, lets the acid come in and deteriorate the lining
o Stress-Related Erosive Syndrome (SRES)
 Patho
 Stress ulcer
 Develop rapidly within hours
 Limited to the stomach
 Primary Causes:
 Increased acid production
 Decreased mucosal blood flow
 High Risk Patients:
 Post-op, Trauma, Shock, Burns (very susceptible), Acute Neurological Disease
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Esophageal Varices
 Portal hypertension
 Vessels become engorged and dilated (varices)  vulnerable to damage from gastric secretions
 rupture and hemorrhage
Etiology of Lower GI Bleed
o Diverticula
 Patho
 Sac-like herniation of the lining of the small intestine or colon - Sigmoid Colon most common
 High fat-Low fiber diet lead to weakening of lining
 Leads to inflammation, bleeding, perforation
 Caused by high fat / low fiber diet
 Complication of this is the diverticula perforating
Assessment
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To Take away from this slide:
  HR.  RR.  urine output. Hypotensive. Confused. Lethargic. Skin: Cool & pale
Assess Type of Bleeding
 Upper GI Bleed S/S
 Hematemesis (two kinds)
o Bright red: Profuse bleeding ( acid contact)
 Varicies
 Coffee-ground: Slow bleed ( acid contact)
o Gastric acid converts bright red hemoglobin to
brown hematin
 PUD
 Melena
o Digestion of blood from an upper GI bleed
 May take several days to clear after the bleeding has stopped
 Looks like tar
 Lower GI Bleed S/S
 Hematochezia
o Massive lower GI hemorrhage
 Blood in GI tract increases peristalsis and diarrhea
 Red colored
 Blood streaked stool
o Hemorrhoids – aka “Piles”
Assess Lab Studies
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If the guaiac strip turns blue, it means it’s positive for blood.
Give calcium gluconate for low Ca levels after the 3rd
transfusion
Hyperkalemia: low or high pulse rate, tall t waves, the pt be
restless and weak
Initially: Normal
Hemoglobin
Hematocrit
Later: Decreased
WBC
Mild elevation
Stool
 Guaiac for Occult blood
Liver Enzymes
Elevated in liver disease
Electrolytes
Watch Ca++ and K+ levels with
blood replacement
BUN
Increased
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Diagnostic Procedures (don’t focus on these, just be aware)
o Endoscopy
 Patient must be hemodynamically stable
 Area to be visualized should be cleared of blood
o Tagged RBC or angiogram
 Done if endoscopy fails to identify source of bleeding
o Wireless Capsule Endoscopy
 Can evaluate the areas of the small intestine
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Management
o Control/Stop Bleeding
 Procedures for bleeding in PUD
 Endoscopic thermal therapy
 Endoscopic injection therapy
o Injecting NS theory behind it is that it puts so much pressure on the vessels it occludes it
and it stops bleeding
 Vagotomy and pyloroplasty
o Vagotomy means they cut the vagas nerve, to stop the production of acetylcholine
 Procedures for bleeding in SRES
 Intraarterial injection
 Total gastrectomy
 Oversew ulcers
 Medications for bleeding in Varices
 Somatostatin (GHI) / Octreotide (Sandostatin): Used in combination to reduce portal HTN
 Vasopressin (Pitressin): Constricts splanchnic arterial bed reducing portal HTN
 Beta blockers: Reduce portal HTN - Prophylactic treatment of varices;
*Not for Acute Bleeding
 Balloon Tamponade
 High risk of airway compromise Occlusion/Aspiration
Gastric Perforation
o Medical Emergency
o Sudden, severe, generalized abdominal pain, rebound tenderness
and rigidity
 Remember abd rigidity
o Fever, leukocytosis, persistent tachycardia
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Stabilization
o IV fluids: Crystalloids, Blood, Blood products
 Hb: 7 gm/dL & Hct: 21%
 How many units of PRBC would be needed to raise the client’s Hb to 9 gm/dL & Hct to 27%?
 2 units of PRBC :  Hb 9 gm/dL &  Hct: 27%.
o Central line
o Supplemental oxygen
o Intubation: Decrease risk for aspiration
o Large-bore NG tube: Gastric lavage
o Urinary catheter: Monitor urine output
o Notes from bottom of slide
 Give IV fluids first! The bleeding is the problem, not the lack of O2. You’ll eventually give them O2, but
they must be fluid resuscitated first
 If a person has esophageal varices, you don’t necessarily want to put an NG tube in, but you have to
because you have to get the blood out of their gut.
 Gastric lavage: the dr will tell you to lavage til clear with room temp water. They used to use ice water to
do this because of the vasoconstriction properties of the cold. But that does something about making
them alkalotic (shift to the left, which is bad). All the vessels constrict, but the constricted cells don’t use
oxygen as easily.
Prophylactic and Treatment
o Antacids - (1-3 hrs after meals and bedtime)
 Work on pH
o Helicobacter pylori - (PUD, SRES)
 Antibiotics - Amoxicillin, Flagyl, Tetracycline
 Work on bacteria causing the problem
o H2 Receptor Antagonists
 Tagamet, Pepcid, Zantac
 Work on reducing production of acid
o Proton Pump Inhibitors - (Parietal Cells)
 Protonix, Nexium, Prilosec
 Slow the transport of HCl down
o Prostaglandin E - (Mucous Cells)
 Cytotec (Increases HCO3, mucous)
 Carafate (Gastric acid Barrier)
 Work on mucous cells, increasing bicarb
Nursing Management
o Assess Gastric Fluid:
 pH monitoring: keep pH > 4
 Litmus paper or direct NG tube probes
o Monitor:
 Presence of bright-red or coffee-ground emesis. Bloody NG aspirate. Bright-red, black, or dark-red stools
o Gastric Lavage:
 Large-bore NG tube. Irrigate (“Clear” return solution)
 Water vs. Normal saline
 Room temperature solutions vs. ice cold solutions
 Document amount instilled and aspirated