UPPER AND LOWER

GIT BLEEDING

DR MOSES KAZEVU

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WARM UP: SINGLE BEST ANSWER

• A 52-year-old man with a history of alcoholism presents
sudden onset bright red hematesis. Upon questioning, the
bleeding is so severe that he is unable to give a detailed
history, though an examination reveals the presence of
spider naevi and ascites. From this information, select the
most likely diagnosis.
A. Hiatus hernia
B. Acute gastritis
C. Mallory-Weiss syndrome
D. Esophageal varices
E. Perforated peptic ulcer

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UPPER GIT BLEEDING

• This is bleeding from the upper gastrointestinal tract
proximal to the ligament of Treitz which anatomically
separates the duodenum from the jejunum.
• Mortality is 10% and usually results from complications of
underlying disease rather than from exsanguination.
• The risk of re-bleeding is low if bleeding occurred more
than 48 hours before presentation.

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ETIOLOGY
• Peptic ulcer disease (50%) (H. pylori and NSAIDs)-ulcer
erosion into blood vessel. Commonly posterior duodenal
ulcer.
• Gastroesophageal varices (15%) (either due to cirrhosis or
schistosomiasis)
• Mallory-Weiss tear (5%) following severe vomiting
• Gastroesophageal reflux disease
• Drugs: Aspirin and NSAIDs
• Inflammation:
➢ Esophagitis (25%)
➢ Gastritis (25%)
➢ Erosive gastritis (in HIV patients consider CMV, HSV,
candida)
➢ Duodenitis (15%)
• Gastric cancer (5%)
• Gastric vascular ectasia
• Cameron’s ulcer
• Dieulafoy’s lesion (submucosal artery)
• Aortoenteric fistula
• Hemobilia (mixture of blood and bile due to surgical and
non-surgical trauma)

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HISTORY
• Nausea
• Retching prior to hematesis (Mallory-Weiss tear)
• Hematemesis (bright red blood or “coffee ground” emesis due to stasis of blood in the stomach)
• Dyspepsia
• Abdominal pain
• Melena: dark tar like stool (as little as 50ml of blood in the GIT can cause melena)
• Hematochezia (from rapid upper GI bleeding or massive bleeding with shock)
• Orthostasis (orthostatic hypotension)
• Chronic slow upper GI bleeding can present with occult blood positive brown stool and chronic
iron deficiency anemia.
• General features: nausea, epigastric pain, syncope, lightheadedness, dizziness, fatigue
• History of alcohol use are usually found among those with variceal hemorrhage, esophagitis, and
Mallory-Weiss tear
• History of NSAID use (peptic ulcer)
• History of prior abdominal aortic graft (aortoenteric fistula)
• History of chronic GERD (esophagitis)
• History of weight loss/iron deficiency (malignancy)

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PHYSICAL EXAMINATION
• Melena or hematochezia
• Pallor
• Hypotension and orthostatic hypotension (>10-point rise in pulse
when the patient goes from the supine to the standing or sitting
position or >20-point drop in systolic blood pressure on change in
position)- there should be at least a minute in between the position
change and the measurement of pulse and blood pressure to allow
time for the normal autonomic discharge to accommodate to the
position change. Orthostasis indicates a 15 to 20% blood loss.
• Tachycardia
• Stigmata of chronic liver disease (spider angioma, ascites, jaundice)
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INVESTIGATIONS
• First determine if the bleed is acute or chronic.
➢ Ask about the number of bleeding episodes, most recent episode, abdominal pain, weight loss, use of ASA, NSAIDs,
alcohol, cirrhosis, risk factors of schistosomiasis.
➢ If the bleed is acute, first evaluate hemodynamic stability. Check blood pressure and heart rate. Ask about lightheadedness,
syncope, dizziness. Check for orthostatic vital signs, they will be positive in patients with significant blood loss.
➢ Do a rectal exam to look for bright red blood or melena.
• Investigations:
➢ Full blood count: chronic or subacute bleeding leads to anemia but hemoglobin concentration may be normal after sudden,
major bleeding until hemodilution occurs. Thrombocytopenia may be a clue to the presence of Hypersplenism in chronic
liver.
➢ Stool for occult blood
➢ Urea, electrolytes and creatinine: this may show evidence of renal failure. The blood urea rises as the absorbed products of
luminal blood are metabolized by the liver, an elevated blood urea with normal creatinine concentration implies severe
bleeding.
➢ Liver enzymes: for chronic liver disease
➢ PT/PTT/INR for coagulopathy
➢ Cross-matching- at least 2 units of blood should be cross-matched.
➢ NG tube lavage: useful if positive (red blood, coffee grounds), if negative (clear or bilious), does not exclude upper GIT
bleeding. 10% of Upper GIT bleeding cases have a negative lavage.
o If you pull out fresh blood (acute and active upper GI bleed)
o If you pull out coffee ground like material (recent upper GI bleed)
o If you pull out non-blood bilious material (this does not exclude an upper GI bleed, the bleed may be lower)
➢ H. pylori testing: perform on all patients with ulcers. (Stool for H. Pylori)
➢ Endoscopy: perform after stabilization and resuscitation, often done <12 hours from admission. Diagnostic, prognostic and
therapeutic.

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MANAGEMENT
• Stabilization:
➢ Oxygen given by facemask
➢ Nil per oral, consider an NG tube and place two large-bore IVs.
➢ If the patient is in shock, treat with aggressive IV fluids (normal saline or Ringer’s
lactate) and cross-matched blood with a hematocrit goal of 25-30% or above in older
patients and in those who may have coronary artery disease. (if you suspect
esophageal variceal bleed, start normal saline cautiously)
➢ Cross match blood and administer packed red blood cells if needed.
➢ In the presence of active bleeding and platelets <50 000/mL or if there is known
impaired function (uremia, aspirin), transfuse platelets or desmopressin. With active
bleeding, increased PT time, and INR> 1.5 transfuse fresh frozen plasma (FFP).
➢ Place a Foley catheter to closely monitor urine output, decreased urine output is a
sign of hypoperfusion and bleeding.
➢ Hourly measurement of pulse, blood pressure and urine output.

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MEDICAL THERAPY
• Give high dose oral proton pump inhibitors twice daily upon presentation. (Omeprazole
40mg BD)
• Initiate an IV proton pump inhibitor drip (8mg/h for 72 hours) if
esophagogastroduodenoscopy (EGD) suggests a high risk of re-bleeding (i.e. active
bleeding, visible vessel, adherent clot). This reduces the relative risk of bleeding by 50%.
• IV octreotide for suspected variceal hemorrhage continue for 3 days if verified by EGD.
This is meant to decrease portal hypertension.
• Correct any coagulopathies, consider giving vitamin K if signs of liver disease. For severe
bleeding give vitamin K 5mg IV stat.
• Propranolol is a non-selective beta blocker that used in the long-term management of
portal hypertension to decrease the frequency of bleeding. Everyone with varices from
portal hypertension and cirrhosis should be on a beta-blocker.
• Broad-spectrum antibiotics in patients with suspected liver disease.

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MANAGEMENT
• Endoscopy: should be carried out after adequate resuscitation, ideally within 24 hours and will yield a diagnosis
in 80% of cases.
➢ Patients can be effectively treated with banding (band ligation for varices), thermal coagulation (heater
probe) sclerosant, epinephrine and/or electrocautery. Predictors of re-bleeding include significant
comorbidities, size of lesion and high risk stigmata (visible vessel, adherent clot).
• Refractory or recurrent upper GIT bleeding:
➢ Esophageal balloon tamponade (Minnesota or Sengstaken-Blakemore tubes) for varices as a bridge to TIPS
(transjugular intrahepatic portosystemic shunting)- a catheter is placed into the jugular vein and guided
radiographically through the liver to form a shunt between the systemic circulation in the hepatic vein and
the portal circulation through the portal vein. TIPS has largely replaced the need to surgically place the
shunt. The most common, long-term complication of TIPS is worsening of hepatic encephalopathy.
➢ Angiogram with intra-arterial embolization or surgery for refractory non-variceal bleeding
• H. pylori eradication: for all peptic ulcer causing upper GIT bleeding with (H. pylori testing).
• Surgery is indicated when endoscopic hemostasis fails to stop active bleeding and if re-bleeding occurs on one
occasion in an elderly or frail patient or twice in a younger fitter patient. If available, angiographic embolization
is an effective alternative to surgery in frail patients. The choice of operation depends on the site and diagnosis
of the bleeding lesion.
• Discharge: The patient’s age, diagnosis on endoscopy, co-morbidity and the presence or absence of shock and
the availability of support in the community should be taken into consideration. In general, all patients who are
hemodynamically stable and have no stigmata of recent hemorrhage on endoscopy can be discharged from
hospital within 24 hours. All shocked patients and patients with co-morbidity need longer inpatient observation.

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LOWER GASTROINTESTINAL TRACT

BLEEDING
• This is bleeding from a source distal to the ligament of
Treitz.
• More 95% of cases are from a colonic source and more
than 85% are self-limited.
• It may be due to hemorrhage from the colon, anal canal or
small bowel.
• It useful to distinguish those patients who present with
profuse, acute bleeding from those who present with
chronic or subacute bleeding of less severity.

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ETIOLOGY
• Diverticulosis (40%)
➢ Diverticular disease
➢ Meckel’s disease
• Angiodysplasia
• Vascular ectasia
• Neoplasm (carcinoma)
• Fissure
• Inflammatory bowel disease
• Ischemic colitis
• Hemorrhoids
• Infectious e.g. hookworms
• Postpolypectomy
• NSAID ulcers
• Radiation colitis
• Rectal varices
• Solitary rectal ulcer syndrome

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CLINICAL FEATURES
• Symptoms:
➢ Usually asymptomatic but may present with abdominal cramps
and to a less extent pain.
➢ Orthostasis is seen in severe cases.
• Signs:
➢ Hematochezia (bright red blood, maroon stool)
➢ Melena
➢ Pallor, chronic bleeding tends to present with anemia (iron
deficiency)
➢ Abdominal distension with mild tenderness
➢ Hypotension and Tachycardia
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DEMOGRAPHICS AND HISTORY

• Age group: distinguish elderly, asymptomatic
patients (diverticular/vascular ectasias) from
young patients who present with pain (infectious,
inflammatory).
• Description of first blood seen by patient: bright
red indicates a distal or rapid proximal source,
black or marron blood points to a more proximal
source.
• Rectal examination

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INVESTIGATIONS
• Full blood count: chronic or subacute bleeding leads to anemia but hemoglobin concentration may be normal after sudden,
major bleeding until hemodiluation occurs. Thrombocytopenia may be a clue to the presence of hypersplenism in chronic liver.
• Stool for occult blood
• Stool microscopy, cultures and sensitivity if infection is suspected.
• Urea, electrolytes and creatinine: this may show evidence of renal failure. The blood urea rises as the absorbed products of
luminal blood are metabolized by the liver, an elevated blood urea with normal creatinine concentration implies severe
bleeding.
• Liver enzymes: for chronic liver disease
• PT/PTT/INR for coagulopathy
• Cross-matching- at least 2 units of blood should be cross-matched.
• Anoscopy to exclude an anal source
• Mild to moderate bleeding: consider nasogastric lavage. Urgent colonic purge (over 4-6 hours then colonoscopy)
• Massive bleeding
• Endoscopy to rule out upper GI bleeding.
• Technetium-labelled RBC scan and/or mesenteric angiography: if >6 units of blood are transfused, consider surgical
intervention.
• Minimum bleeding rates: tagged RBC scan, 0.1-0.5ml/min, mesenteric angiogram, 1.0 ml/min
• Diagnostic colonoscopy: typically performed 12-48 hours after presentation and stabilization.
• Proctoscopy for anorectal disease particularly hemorrhoids
• Flexible sigmoidoscopy or colonoscopy for IBD, cancer, ischemic colitis, diverticular disease, angiodysplasia
• Angiography- vascular abnormality (angiodysplasia): the yield of angiography is low so it is a test of last resort
• If gastroscopy, colonoscopy and duodenal biopsy have not revealed the cause, investigation of the small bowel is necessary.
Capsule endoscopy is the diagnostic investigation of choice but currently has no therapeutic ability. (A capsule with a camera
is swallowed and it takes pictures along the GIT)

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MANAGEMENT
• Stabilization:
➢ Oxygen given by facemask
➢ Nil per oral, consider an NG tube and place two large-bore IVs.
➢ If the patient is in shock, treat with aggressive IV fluids (normal saline or Ringer’s
lactate) and cross-matched blood with a hematocrit goal of 25-30% or above in older
patients and in those who may have coronary artery disease. (if you suspect
esophageal variceal bleed, start normal saline cautiously)
➢ Cross match blood and administer packed red blood cells if needed.
➢ In the presence of active bleeding and platelets <50 000/mL or if there is known
impaired function (uremia, aspirin), transfuse platelets or desmopressin. With active
bleeding, increased PT time, and INR> 1.5 transfuse fresh frozen plasma (FFP).
➢ Place a Foley catheter to closely monitor urine output, decreased urine output is a
sign of hypoperfusion and bleeding.
➢ Hourly measurement of pulse, blood pressure and urine output.

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• Medical therapy: H2 receptor antagonists and PPIs have no role in the treatment
of lower GI bleeding. Discontinue ASA and NSAIDs. Oral iron is given to treat
anemia.
• Urgent therapeutic colonoscopy:
➢ Large volume purge >6L, cautery or injection of epinephrine or clipping.
➢ Colonoscopy is technically challenging with brisk Lower GI bleeding (urgent
colonic purge requires sedation; visualization is often poor)
• Mesenteric angiography/embolization: the intervention of choice for brisk lower
GI bleeding. Associated with 80-90% cessation rates for those with diverticular or
vascular ectasia etiology though 50% experience re-bleeding.
• Surgery: indicated with active lower GI bleeding involve >4-6 units of blood in 24
hours or >10 units in total. If the site is well localized, consider hemicolectomy,
otherwise perform total abdominal colectomy.

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WARM UP: SINGLE BEST ANSWER

• A 52-year-old man with a history of alcoholism presents
sudden onset bright red hematesis. Upon questioning, the
bleeding is so severe that he is unable to give a detailed
history, though an examination reveals the presence of
spider naevi and ascites. From this information, select the
most likely diagnosis.
A. Hiatus hernia
B. Acute gastritis
C. Mallory-Weiss syndrome
D. Esophageal varices
E. Perforated peptic ulcer

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