Sandbox:Aditya

Definitions

• Haematemesis: vomiting fresh red blood.
• Coffee ground emesis: vomiting of altered black blood.
• Melaena: passage of black tarry stools.
• Haemochezia: Passage of red blood per rectum (usually due to bleeding from the lower gastrointestinal tract but occasionally can be due to massive upper gastrointestinal bleeding).
• Rebleeding: Defined as fresh haematemesis and/or melaena associated with the development of shock (pulse greater than 100 beats/min, systolic pressure less than 100 mm Hg), a fall in CVP greater than 5 mm Hg, or a reduction in haemoglobin concentration greater than 20 g/l over 24 hours. Rebleeding should always be confirmed by endoscopy

HAS-BLED score

Components	Points
Hypertension	1
Abnormal renal/liver functions Dialysis, Kidney transplantation, Creatinine >2.6 mg/dl Cirrhosis, total bilirubanc>2X, AST/ALT >3e	1
Stroke	1
Bleeding history	1
Liable INR	1
Elderly( >65 years)	1
Drugs	1
INTERPRETATION OF HAS-BLED score
1	3%
2	4%
3	5%
4	8%
5	9%

Causes

Common causes

• Peptic ulcer disease
  • Responsible for around 33%-50% of upper GI bleeding
  • Peptic ulcer disease is most commonly due to H.pylori or nonsteroidal anti-inflammatory drugs (NSAIDs).
  • Upper GI bleeding is the most common complication of peptic ulcer disease and may be the initial presentation.
• Esophageal varices
  • Responsible for around 14% of upper GI bleeding
  • These dilated veins within the esophagus are usually secondary to portal hypertension from cirrhosis.
  • Massive variceal hemorrhage is responsible for acute life-threatening upper GI bleeding which is an medical emergency .
• Mallory-Weiss syndrome :
  • Responsible for around 5% of upper GI bleeding
  • A longitudinal mucosal laceration in the distal esophagus and/or proximal stomach that usually results from forceful retching

Less common causes

• Neoplasms
  • gastric cancer
  • esophageal tumors
• Esophagitis (complications due to erosive or necrotizing infectious esophagitis )
• Gastric erosions/gastropathy
  • Acute erosive gastritis caused by drugs, radiation, infection, or direct trauma.
  • Reactive gastropathy may be due to bile reflux, particularly after partial gastrectomy.
  • Portal hypertensive gastropathy, which results in increased friability of gastric mucosa in patients with cirrhosis.
• Dieulafoy lesions
  • Dilated aberrant submucosal vessels that erode the overlying epithelium in the absence of an ulcer
• Gastric varices
• Gastric antral vascular ectasia
  • Dilated gastric vessels of unknown etiology that cause chronic UGIB and iron-deficiency anemia

Rare causes

• Bleeding from the hepatobiliary tract
  • Most commonly secondary to a liver or biliary tract injury, from trauma or following procedures or surgery.
  • Diagnosed by endoscopic retrograde cholangiopancreatography (ERCP) and treated with arteriography
• Aortoenteric fistulas,
  • Most commonly involves the lower duodenum.
  • Common causes include aortic aneurysms or prosthetic vascular grafts, syphilis and tuberculosis
  • Presents with frank UGIB along with a pulsatile mass and abdominal pain radiating to the back.
  • Diagnosed by endoscopy.
• Crohn disease involving the upper gastrointestinal tract
• Metastatic malignancy involving the upper gastrointestinal tract, such as melanoma or renal cell carcinoma
• Hemosuccus pancreaticus
  • Pancreatic inflammation or cancer may result in bleeding into the pancreatic duct, which connects to the duodenum

Risk factors

• Advancing age
• Previous history of gastrointestinal bleed
• Chronic kidney disease
• Underlying cardiovascular disease
• Cirrhosis and portal hypertension
• Presence of H.pylori
• NSAID or aspirin use in patients with a history of ulcer disease
  • Those on dual antiplatelet therapy; those on anticoagulant therapy; or those with two or more of the following risk factors
    • Age 60 years or older
    • Glucocorticoid use
    • Dyspepsia
    • Gastroesophageal reflux disease
• Critical illness
  • Nosocomial stress ulcers due the to the use of mechanical ventilation for more than 48 hours, and coagulopathy
  • Other risk factors for nosocomial stress ulcerations in critically ill patients include a history of gastrointestinal ulceration or bleeding within the past year; or two or more of the following risk factors: presence of sepsis, ICU admission lasting longer than 1 week, occult gastrointestinal bleeding lasting 6 days or longer, and administration of more than 250 mg of hydrocortisone or equivalent glucocorticoid therapy
• Rare conditions associated with gastric acid hypersecretion, such as Zollinger-Ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy.

Causes of Acute Upper GI bleeding
Esophagus	Esophagitis Mallory–Weiss tear Esophageal varices Esophageal ulcers Esophageal cancer
Gastric	Gastric ulcer Gastric cancer Gastritis Gastric varices Portal hypertensive gastropathy Gastric antral vascular ectasia Dielafuoy lesions
Duodenal	Duodenal ulcer Vascular malformations, including aorto-enteric Fistulae Bleeding from the bile duct due to Liver biopsy Trauma Arteriovenous malformations Liver tumors

Associated Conditions

• Heyde syndrome, aortic valve stenosis with associated gastrointestinal bleeding thought to be due to acquired reduction of von Willebrand factor.

History

Obtaining the history is the most important aspect of making a diagnosis of upper GI bleed. It provides insight into the cause, precipitating factors and associated comorbid conditions and also helps in determining the severity of the bleed as well as in identifying the potential source of bleed:

• A history of epigastric pain, dyspepsia, or prior peptic ulcer may suggest the diagnosis of peptic ulcer disease.
• A history of documented prior upper GI bleeding is important because approximately 60% of upper GI bleeders are rebleeding from the same site.
• Prior use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is important because these patients have an increased risk of gastric ulcer and a fourfold risk of significant GI bleeding compared with other patients.
• A history of alcoholism increases the likelihood of cirrhosis and consequently of bleeding from esophageal varices or congestive gastropathy but alcoholics also frequently have peptic ulcers or gastritis.
• Cigarette smokers have a significantly higher rate of the recurrent duodenal ulcer as compared with nonsmokers and a history of cigarette smoking should be elicited.
• Vomiting, coughing, or retching before bleeding is suggestive of a Mallory-Weiss tear.

A directed history may also alert to consider unusual causes.

• A history of pancreatitis suggests possible hemorrhage from a pancreatic pseudocyst. Erosion of a pancreatic pseudocyst into the duodenum or stomach may cause massive hematemesis, and the patient may present in shock.
• Patients with prior abdominal aortic aneurysm repair may present with severe GI hemorrhage from an aortoenteric. This fistula often presents with a herald bleed followed within 4 to 96 hours by massive bleeding.
• A personal or family history of recurrent epistaxis may suggest the diagnosis of Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia), and a careful examination for skin telangiectasias should be performed.
• Patients with renal failure frequently have GI bleeding. This bleeding is often due to peptic ulcer disease or angiodysplasia. This bleeding may be severe because of clotting dysfunction associated with renal disease.

Symptoms

• Hematemesis
• Melena
• Hematochezia
• Syncope
• Presyncope
• Dyspepsia
• Epigastric pain
• Heartburn
• Diffuse abdominal pain
• Dysphagia
• Weight loss
• Jaundice

Primary Prevention

Effective measures for the primary prevention of upper GI bleeding include administration of PPI in patients with an increased risk due to critical illness or use of NSAIDs or aspirin. In patients with cirrhosis and suspected portal hypertension, who found to have esophageal varices patients are given prophylactic treatment with a nonselective β-blocker or undergo endoscopic variceal ligation (EVL) with surveillance endoscopy.

Patients with stress ulcers

• The American Society of Health-System Pharmacists developed clinical practice guidelines that recommend prophylaxis with a PPI or with a histamine-2 receptor antagonist (H2RA) for ICU patients at high risk for UGIB.

Patients on NSAID, aspirin, or antiplatelet therapy

• Joint gastroenterology and cardiology society practice guidelines recommend gastroprotective therapy with a PPI for patients considered to be at increased risk of bleeding from chronic NSAID and aspirin therapy.

Patients with cirrhosis and varices

• EGD is used to screen for the presence of varices in patients with cirrhosis complicated by portal hypertension.
• In patients with cirrhosis who do not have varices, no prophylaxis is indicated.
• In patients with cirrhosis and varices that have not bled, prophylactic treatment with nonselective β-blockers, such as nadolol or propranolol, may decrease portal blood flow and thus decrease the risk of variceal bleed.
• In patients with cirrhosis who have medium or large varices that have not bled, EVL is an alternative prophylactic treatment.
• EVL is repeated every several weeks until obliteration of varices is seen.
• Surveillance EGD should then be performed 1 to 3 months after obliteration and then every 6 to 12 months to check for variceal recurrence.

Secondary Prevention

Effective measures for the secondary prevention of UGIB include discouraging the use of NSAIDS in all patients with a history of UGIB.

Seondary Prevention

• NSAID use in all patients with a history of UGIB should be discouraged.

UGIB from peptic ulcer disease

• Avoid NSAIDs.
• For patients who are at high risk for rebleeding (elderly patients; those taking anticoagulant and antiplatelet medications), indefinite use of a PPI may be recommended.
• H pylori status should be determined, and patients should be treated if positive.
• Eradication is confirmed with stool sample or repeat endoscopy with biopsy.

UGIB from varices

• A combination of nonselective β-blockers plus EVL is the best option for secondary prophylaxis of UGIB from varices.
• The nonselective β-blocker should be titrated up as tolerated.
• Variceal banding should be repeated every 2 to 3 weeks until the varices are obliterated.
  • EGD must be performed 1 to 3 months after initial obliteration then every 6 to 12 months to check for variceal recurrence.

Prognosis

• Prognosis is generally good with appropriate treatment, and the 1-year mortality rate of patients with nonvariceal UGIB is approximately 10%.
• In UGIB, the prognosis doesn't depend on the severity of bleeding but depends upon patients age and comorbid conditions.
• The majority of patients with UGIB will stop bleeding spontaneously.
• A clean ulcer base has less than a 3% chance of rebleeding; therefore, these lesions are not usually treated or scoped again.
• In otherwise stable patients, patients with a clean ulcer base has less than a 3% chance of rebleeding and are good candidates for early discharge.
• Treatment includes management of underlying liver disease and prevention of complications of cirrhosis.
• Despite advances in gastric acid suppression as well as improved endoscopic diagnostic and therapeutic techniques, the mortality rate from UGIB has remained stable.

Scoring systems

Two scoring systems identify those at risk for adverse outcomes from UGIB:

• The Glasgow Blatchford Score (GBS)
• The Rockall score

The Glasgow Blatchford Score (GBS)

• The Glasgow Blatchford Score (GBS) helps in identifying low-risk patients with UGIB who can be managed safely as outpatients without an urgent endoscopy.
• GBS parameters include
  • Blood urea nitrogen level
  • Hematocrit level
  • Heart rate
  • Systolic blood pressure
  • Presence of syncope or melena, as well as presence of comorbid heart and liver disease.
• GBS is the more effective system for predicting the need for transfusion in patients with UGIB.

The Glasgow Blatchford Score (GBS)
Admission risk markers			Score
Blood urea nitrogen level (mg/dl)		≥ 18.2 to < 22.4	2
		≥ 22.4 to < 28	3
		≥ 28 to < 70	4
		≥ 70	6
Hemoglobin level (g/dl)	Men	≥ 12 to < 13	1
		≥ 10 to < 12	3
		< 10	6
	Women	≥ 10 to < 12	1
		< 10	6
Systolic blood pressure (mmHg)		≥ 100 to < 109	1
		≥ 90 to < 99	2
		< 90	3
Other markers		Pulse rate ≥ 100 beats/min	1
		Presentation with melena	1
		Presentation with syncope	2
		Hepatic disease	2
		Heart failure	2
Scores of 0-2 -Low-risk group Score of >6- High risk group

The Rockall score

• The complete Rockall score identifies those patients with evidence of acute UGIB on endoscopy who are at low risk for further bleeding or death.
• The score is based upon
  • Age
  • Presence of shock
  • Comorbidity diagnosis
  • Endoscopic ulcer characteristics
  • Stigmata of recent hemorrhage.

The Rockall score
Markers			Score
Age		<60	0
		60 - 79	1
		≥ 80	2
Shock stage	Blood pressure	>120	0
		100-119	1
		<100	2
	Heart rate	>100	0
		<100	1
Comorbidity		No major comorbidity	0
		Cardiac failure Ischemic heart disease Any major comorbidity	2
		Renal failure Liver failure Disseminated malignancy	3
Diagnosis		Mallory-Weiss tear, no lesion identified and no SRH	0
		All other diagnosis	1
		Malignancy of upper GI tract	2
Major SRH		None or dark spot only	0
		Blood in upper GI tract, adherent clot, visible or spurting vessel	2
GI: Gastrointestinal, SRH: Signs of recent hemorrhage. Range of score is 0-11. Score of ≤ 3 predicts low mortality risk, while ≥ 8 is a predictor of high mortality risk.

Complications

Complications of UGIB include:

• End-organ damage
  • Cardiac ischemia
  • Renal failure
  • Ischemic hepatitis
  • Anoxic brain injury
• Iron-deficiency anemia

Classification

According to The American Gastroenterological Association, upper GI bleeding can be classified based on the rate of blood loss into overt(acute), occult or obscure(chronic) forms.

• Overt GI bleeding:- Overt GI bleeding is defined as acute bleeding which is visible and can present in the form of hematemesis, “coffee-ground” emesis, melena, or hematochezia.
  
• Occult or chronic GI bleeding:- Occult GI bleeding is defined as a microscopic hemorrhage which can present as Hemoccult-positive stools with or without iron deficiency anemia. It is the initial presentation in patients with no evidence of visible blood loos and is positive on fecal occult blood test(FOBT).
• Obscure GI bleeding:- Obscure GI bleeding is defined as recurrent bleeding in which a source is not identified after upper endoscopy and colonoscopy. It can be either overt or occult.

Epidemiology and Demographics

Incidence

The incidence of acute UGIB is approximately 50 to 100 per 100,000 individuals worldwide.

Gender

Males are more commonly affected by UGIB than females. The males to female ratio is approximately 2 to 1.

Pathophysiology

Blood supply of Foregut

The digestive system is supplied by the celiac artery. The celiac artery is the first major branch from the abdominal aorta, and is the only major artery that nourishes the digestive organs.

Foregut		Blood supply
Esophagus	Upper esophageal sphincter Cervical esophagus	Inferior thyroid artery
	Thoracic esophagus	Aortic esophageal arteries or branches of the bronchial arteries
	Distal esophagus Lower esophageal sphincter	Left gastric artery and left phrenic artery
Stomach	Lesser curvature	Right and left gastric arteries
	Greater curvature	Right and left gastroepiploic arteries
	Gastric fundus	Short gastric arteries
Duodenum	First and second parts	Gastroduodenal artery (GDA) and Superior pancreaticoduodenal artery
	Third and fourth parts	Inferior pancreaticoduodenal artery

Blood supply of stomach
Source: By Mikael Häggström.https://commons.wikimedia.org/w/index.php?curid=3416062

Mucosal barrier

• The gastric mucosa is protected from the acidic environment by mucus, bicarbonate, prostaglandins, and blood flow.
• This mucosal barrier consists of three protective components which include:
  • Layer of epithelial cell lining.
  • Layer of mucus, secreted by surface epithelial cells and foveolar cells.
  • Layer of bicarbonate ions, secreted by the surface epithelial cells.

Diagram of alkaline Mucous layer in stomach with mucosal defense mechanisms
Source: By M•Komorniczak (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

The following table demonstrates the defense mechanisms of gastric mucosal barrier

Defense mechanisms of gastric mucosal barrier
Mucus layer	Forms a protective gel-like coating over the entire gastric mucosal surface
Epithelial layer	Epithelial cell layer are bound by tight junctions that repel fluids
Bicarbonate ions	Neutralize acids

Pathogenesis

The main inciting event in the pathogeneis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding.

Etiology	Frequency of occurance
Peptic ulcer disease	50%
Variceal bleeding	20%
Esophagitis, gastritis, and duodenitis	10-15%
Mallory-Weiss tear	15%
Malignancy	3-5%
Arteriovenous malformation	<3%
Gastric antral vascular ectasia	<1%
Dieulafoy lesion	<1%

Pathogenesis

• Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage.
  • Varices are large, tortuous veins and protrude into the lumen, rupturing.
  • Helicobacter pylori disrupts the mucosal barrier and causes inflammation of the mucosa of the stomach and duodenum.
  • As the ulcer progresses beyond the mucosa to the submucosa the inflammation causes weakening and necrosis of arterial walls, leading to pseudoaneurysm formation followed by rupture and hemorrhage.
  • NSAIDs inhibit cyclooxygenase, leading to impaired mucosal defenses by decreasing mucosal prostaglandin synthesis.
  • During stress, there is acid hypersecretion; therefore, the breakdown of mucosal defenses leads to injury of the mucosa and subsequent bleeding.
  • Mucosal defects along with dilated and tortuous vessels in dieulafoy lesion put them at risk for rupture because of necrosis of the arterial wall from exposure to gastric acid.

NSAIDS

Inhibits cycloxygenase pathway

COX-1

COX-2

Reduced mucosal blood flow

Reduced mucosal and bicarbonate secreation

Impaired platelet aggregation

Reduced angiogenesis

Increased leucocyte adherence

Impaired defence Impaired healing

Mucosal Injury

Gross and Microscopic Pathology

		Gross Pathology	Microscopic Pathology
Varices		Large and tortuous veins that protrude into the lumen	Varices may be difficult to demonstrate in surgical specimens
Mallory-Weiss Tear		Isolated or multiple cleft like mucosal defects	Defects in the esophageal squamous mucosa. Cells of acute inflammation. Multiple ruptured blood vessels in the lamina propria or submucosa. Prior lacerations may show various degrees of healing Granulation tissue Fibrosis Epithelial regeneration.
Esophagitis	Herpes esophagitis	Shallow ulcers Sharp and raised edges Normal intervening erythematous mucosa	Ground glass inclusion bodies
	Cytomegalovirus esophagitis	Superficial ulcers Well-circumscribed CMV infects mesenchymal cells in the lamina propria and submucosa	Intranuclear inclusions
	Fungal esophagitis	Erythematous Hyperemic Friable Discrete and raised white plaque	Neutrophils within the squamous epithelium
	Pill esophagitis	Discrete ulcers	Not specific and include Necrosis Prominent eosinophilic infiltrate Spongiosis
	Toxic esophagitis	Mucosal erythema, Edema Hemorrhage Necrosis	Acid injury Coagulative necrosis Eschar Alkaline injury Liquefactive necrosis Acute inflammation Abundant granulation tissue
Gastroesophageal Reflux Disease			Basal cell hyperplasia Elongation of the lamina propria papillae Mixed intraepithelial inflammation Neutrophils, eosinophils, and lymphocytes Squamous cell degeneration.
Barrett Esophagus			Columnar metaplasia Mucinous columnar cells Goblet cells, and enterocyte-like cells, among others. Cells of acute inflammation
Acute Gastritis		Mucosal hyperemia associated with Bleeding Erosions Ulcers	Dilation and congestion of mucosal capillaries, edema, and hemorrhage in the lamina propria. Ischemic-type changes such as Degenerated and necrotic epithelium Fibrinoid necrosis Adherent fibrinopurulent debris
Gastric Ulcers		Solitary, typically less than 2 cm in diameter, and have sharply defined borders. The ulcer edges are usually flat, and the base of the ulcer usually appears smooth. The presence of a radiating pattern of rugal folds is characteristic of peptic ulcers	Fibrinopurulent debris Necrosis Granulation tissue
Portal Hypertensive Gastropathy		Mosaic pattern of congestion Most commonly involves the fundus	Dilation, tortuosity, and thickening of small submucosal arteries and veins. Mucosal capillaries may also show congestion, dilation, and proliferation.
Gastric Antral Vascular Ectasia		Linear pattern of mucosal congestion in the antrum termed “watermelon stomach	Antral biopsies show Congestion Dilated mucosal capillaries Vascular microthrombi The mucosa also shows Foveolar hyperplasia Fibromuscular hyperplasia Edema and regenerative changes
Reactive (Chemical) Gastropathy		Stomach Edema Surface erosions Polypoid changes, and friability	The mucosa shows Congestion Edema Fibromuscular hyperplasia Foveolar hyperplasia
Peptic Disease		Wide range of findings From normal/slightly edematous mucosa to increased friability, erosions, and ulcers	Increased plasma cells Neutrophilic infiltrate Reactive epithelial changes, including villous blunting. The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
Ischemia		Hypoperfused ulcers	Acute ischemia Mucosal edema Congestion Superficial necrosis Coagulative necrosis Chronic ischemia Fibrosis Strictures
Structural Abnormalities of Blood Vessels		Large-caliber artery within the submucosa	Dilated venules and arteriole in direct communication with each other
Inflammatory Bowel Disease			Lymphoplasmacytic infiltrate with numerous neutrophils

Diagnosis

In patients with acute Upper GI bleeding who are unstable rapid assessment and resuscitation should be initiated even before diagnostic evaluation. Once hemodynamic stability is achieved, a proper clinical history, physical examination, and initial laboratory findings are crucial not only in determining the likely sources of bleeding but also in directing the appropriate intervention. The hematocrit level is measured soon after the onset of bleeding, but will not accurately reflect the amount of blood loss. Equilibration between the intravascular and extravascular spaces is not complete until 24 to 72 hours after bleeding has occurred. Low mean corpuscular volume, low iron and ferritin levels, and high transferrin and total iron-binding capacity (TIBC) confirm iron deficiency. Blood urea nitrogen (BUN) level may be elevated out of proportion to any increase in the creatinine level in patients with UGIB, secondary to the breakdown of blood proteins to urea by intestinal bacteria. Platelet count and coagulation studies should be checked, especially in patients with known or suspected coagulopathy. Nasogastric lavage should be performed if the presence or source of bleeding is unknown. Upper gastrointestinal endoscopy is the primary diagnostic tool, performed for both diagnosis and treatment of active bleeding. The American Society of Gastrointestinal Endoscopy guidelines recommend that upper endoscopy be performed within 24 hours of presentation in all patients with UGIB. Angiography and tagged erythrocyte scan are rarely needed, but may be used to diagnose (and embolize) active UGIB, particularly in patients who cannot tolerate EGD. Also, upper gastrointestinal tract radiographic studies using barium are generally not advised, as they may obscure visualization during EGD.

Initial Laboratory Studies

• The hematocrit level is used to identify the degree of blood loss and suggests the acuity or chronicity of blood loss.
• Serial complete blood count (CBC) tests are important for monitoring the presence of ongoing blood loss.
• Initial CBC may not fully reflect the actual degree of acute blood loss.
• Qualitatively, on peripheral blood smear prepared with Wright-Giemsa stain, normal erythrocytes should be smaller than the nucleus of a normal lymphocyte, and the central clear area should not be overly prominent.
• In iron-deficiency anemia associated with chronic blood loss, erythrocytes are smaller (microcytic) and appear lighter (hypochromic) than normal cells.
• Mild to moderate thrombocytopenia (>30 × 103/µL) does not usually result in spontaneous bleeding, although patients with a pre-existing lesion may bleed in the presence of even mild thrombocytopenia.
• Platelet count may rise in response to significant gastrointestinal bleeding and may fall with multiple blood transfusions.
• Low ferritin level is the most specific test for iron-deficiency anemia. This finding together with a low iron and high TIBC levels are helpful in diagnosing iron-deficiency anemia, a common complication of ongoing or significant UGIB.
• BUN level may be elevated out of proportion to any increase in the creatinine level in patients with UGIB, secondary to breakdown of blood proteins to urea by intestinal bacteria.
• In patients with esophageal varices, acquired coagulopathies are common due to cirrhosis.

Naso-Gastric Lavage

• Nasogastric lavage is only indicated when the diagnosis of UGIB doubtful.
• It is rarely used now
• Nasogastric lavage also helps in documenting active or recent UGIB and the need for urgent endoscopy.
• Occasionally used to empty gastric contents in preparation for endoscopy.

Complicatiions

Complications of the procedure include:

• Bleeding from trauma during tube passage in patients with coagulopathy is a possible complication.
• Other rare complications include
  • Pharyngeal and esophageal perforation
  • Cardiac arrest
  • Ethmoid sinus fracture with brain trauma
  • Bronchial intubation.

Interpretation

• Evidence of old (brown colored or 'coffee grounds') or fresh blood documents presence of UGIB.
• Evidence of bilious material rules out bleeding distal to the pylorus.
• Any other appearances of GI contents are non-diagnostic.
• There is no evidence that performing a nasogastric lavage to clear clots or otherwise manage bleeding improves clinical outcome.

Contraindications

• Avoid gastric lavage in patients with suspected perforated abdominal viscus.

Upper GI Endoscopy

• Upper GI Endoscopy is considered investigation of choice for diagnosing and assessing the source of UGIB.
• The American Society of Gastrointestinal Endoscopy guidelines recommend that upper gastrointestinal endoscopy be performed within 24 hours of presentation in all patients with UGIB

Indications

• Active UGIB
• Used for biopsy lesions for tissue diagnosis and to treat currently bleeding lesions.

Complications

Complications include

• Aspiration
• Esophageal perforation
• Cardiopulmonary complications secondary to anesthesia
• Increased bleeding while attempting therapeutic intervention

If upper GI Endoscopy undiagnostic

Patient’s hemodynamic stability

Stable with low volume bleeding

Unstable with large volume bleeding

Repeat endoscopy

Surgery exploration and partial gastrectomy

Other Diagnostic studies

In cases where the source of bleeding is unidentified after upper endoscopy, the utilization of subsequent diagnostic modalities depends upon the hemodynamic stability of the patient. Other diagnostic studies include:

• CT angiography
• Catheter angiography
• Radionuclide imaging

	CT angiography	Catheter angiography	Radionuclide imaging
Bleeding at rates detection	At least 0.5 mL/min	0.5 to 1.5 mL/min	0.1 mL/min
Indications	Hemodynamically stable Endoscopy undiagnostic	Endoscopy not feasible due to severe bleeding with hemodynamic instability Persistent or recurrent GI bleeding Non-diagnostic upper endoscopy
Advantages	Minimally invasive  Demonstrate neoplasms or vascular malformations Can provide evidence of recent bleeding	Diagnostic and therapeutic Allows for infusion of vasoconstrictive drugs and/or embolization. Does not require bowel preparation.	Most sensitive imaging modality for GI bleeding More commonly utilized for investigation of patients with obscure, intermittent bleeding
Disadvantages	Lacks therapeutic capability Risk of contrast induced nephropathy in patients with renal impairment and contrast allergy	Access-site hematoma or pseudoaneurysm Arterial dissection Spasm, bowel ischemia Contrast-induced nephropathy or allergic reaction	Poor anatomic localization of the bleeding site Unable to diagnose the pathological cause of GI bleeding

Differentiating UGIB

Blood that originates from the oro-pharynx, if swallowed, can present as melena, leading to a false concern of a gastrointestinal source. Examination of nasal area and mouth will help to identify source of bleeding.

	History	Physical Examination	Laboratory Results
Peptic ulcer disease	Dyspepsia Early satiety NSAID use Previous ulcer disease	Hematemesis Possible hematochezia, melena Hemodynamic instability Tachycardia Hypotension	Decreased hemoglobin Increased BUN/creatinine Increased WBC's Helicobacter pylori positive
Mallory-Weiss tear	Vomiting/retching Weakness Dizziness	Hematemesis Possible hematochezia, melena Hemodynamic instability Tachycardia Hypotension	Decreased hemoglobin Increased creatinine Increased WBCs
Stress gastritis	History of head injury, severe burns, trauma Mechanical intubation Chronic steroid use Coagulopathy	Hematemesis (coffee grounds more common) Melena	Decreased hemoglobin Increased WBCs
Dieulafoy lesion	Dyspepsia Weakness Dizziness, syncope, May have no prior history before bleed.	Hematemesis (bright red) Hematochezia or melena Hemodynamic instability	Decreased hemoglobin Decreased hematocrit Increased WBCs
Gastro-esophageal varices	Alcohol/tobacco use, Weakness, dizziness, syncope	Stigmata of chronic liver disease Hematemesis, hematochezia or melena Hemodynamic instability	Decreased hemoglobin Decreased hematocrit Electrolyte abnormalities Increased bilirubin/liver enzymes
Gastric cancer	Alcohol/tobacco use Often asymptomatic	Hematemesis, Melena, Lymphadenopathy Palpable supraclavicular or anterior axillary lymph node Palpable firm stomach	Decreased hemoglobin Electrolyte abnormalities May have elevated CEA or CA 19-9
Hemobilia	Recent trauma Bliary tree instrumentation Gallstones	RUQ abdominal pain Jaundice Hematemesis, melena	Decreased hemoglobin, Increased bilirubin Increased WBCs
Aortoduodenal fistula	Abdominal pain Back pain History of AAA repair May be asymptomatic	Hematemesis or melena (herald bleed) Pulsatile abdominal mass	Decreased hemoglobin Increased WBCs

Management

The management of GI bleeding includes

• Initial resuscitation and pharmacotherapy
• Risk stratification
• Surgery
  • Pre-endoscopy management
    • Initial management of antithrombotic agents (anticoagulants and antiplatelet agents)
    • Pharmacological therapy
    • Role of gastric lavage and prophylactic endotracheal intubation
    • Timing of endoscopy
  • Endoscopic management
    • Endoscopic diagnosis
    • Endoscopic therapy
• Management following endoscopy/endoscopic hemostasis

Initial resuscitation

• The initial steps in the management of a patient with UGIB is to assess the severity of bleeding, and then institute fluid and blood resuscitation as needed.
• Any patient with hemodynamic instability or who is actively bleeding should be admitted to the ICU for monitoring and resuscitation
• The patient’s hemodynamic status is of great importance in determining the degree of severity and triage status.
• The rate of fluid resuscitation is proportional to the severity of bleeding with the goal of restoring and maintaining the patient’s blood pressure.
• Two large caliber (16-gauge or larger) peripheral catheters or a central venous line should be inserted in patients who are hemodynamically unstable. *Supportive care includes administration of supplemental oxygen and monitoring of urine output.
• Patients with severe bleeding will need to be transfused; the indications for transfusion in patients with less severe bleeding should be based on the patient’s age and presence of comorbid conditions.
• The target hematocrit value varies according to age and clinical conditions.
  • In the elderly patient, the target hematocrit is 30%.
  • In younger, healthy patients, the target hematocrit is 25%.
  • In patients with portal hypertension, the target hematocrit should not be above 27% or 28%, so as not to raise portal venous pressure.
• Fresh frozen plasma, platelets, or both should be given to patients with coagulopathy who are actively bleeding and to those who have received more than 10 units of packed erythrocytes

WORKUP AND INITIAL TREATMENT Initial Resuscitation
Basic ABC Airway Breathing, Circulation
Ensure patent and protected airway Intubate if needed Consider mechanical ventilation 2 large-bore, peripheral intravenous lines Can consider large-bore central venous catheter or intraosseous line if rapid transfuser will be needed Resuscitate with 1:1:1 of packed red blood cells (PRBCs) to fresh frozen plasma (FFP) to platelets. Consider massive transfusion protocol Resuscitate to a target hemoglobin of 7 mg/dL. Consider Sengstaken-Blakemore tube for control of immediately life-threatening upper GI bleeding

Acute GI bleeding

Initial evaluation and resuscitation

Uppe GI endoscopy

Source found

Undiagnostic

Specific Treatment

Unstable

Stable

Urgent CT

Repeat Endoscopy/Angiograpghy

No source identified

Angioembolization

Endoscopic intervention

TIPS

Surgery

Surgery (Laprotomy)

Sclerotherapy

Banding

Injection

Thermocoagulation

Clips

Pharmacotherapy

Correlation between physical signs and the severity of upper gastrointestinal bleeding
Physical signs	Bleeding severity
	Mild	Moderate	Severe
Blood loss	<1L	1-2L	>2L
Systolic blood pressure	<120	100-119	<99
Orthostasis	-	-	+
Tachycardia	<100	101-120	>140
Skin	Warm, well perfused	Diaphoretic	Cool–cold, clammy
Urine output(ml/hour)	>25	10-25	Negligible
Respiratory rate	14-20	20-30	>35
Sensorium	Alert	Anxious	Confused/Drowsy

Physical examination

Common physical exam findings include:

Vitals

• Hypotension
• Tachycardia
• Thready pulse
• Hypoxia

Abdomen

• +Bowel sounds
• Abdominal tenderness
• Hepatomegaly
• Splenomegaly
• Caput medusa
• Spider angiomata

Skin

• Palmar erythema
• Cold clammy extremities

Neurological examination

• Altered sensations
• Poor mentation
• Drowsiness

Rectal examination

• Occult blood
• Gross blood
  • Bright red blood per rectum
  • Melena
  • Burgundy stools
  • Blood coating stools versus within stools
  • Bloody diarrhea

Extremities

• Peripheral edema

Disease/Cause		Bleeding manifestations				Associated signs and symptoms	Risk factors	Endoscopic findings
		Hematemesis	Melena	Hematochezia	Occult blood
Ulcerative/erosisve	Peptic ulcer disease	+	+	+	+	Abdominal pain Pain associated with eating Dyspepsia	NSAIDs Infections: Helicobacter pylori CMV HSV Stress ulcer Excess gastric acid production (ZES) Idiopathic	Ulcer with smooth, regular, rounded edges Ulcer base often filled with exudate Examination of the ulcer may reveal: Active bleeding or oozing Nonbleeding visible vessel Adherent clot Flat pigmented spot Clean ulcer base
	Esophagitis	+	+	-	+	Dysphagia Odynophagia Retrosternal pain	Gastroesophageal reflux disease Medications: Tetracycline Doxycycline Clindamycin Trimethoprim-sulfamethoxazole NSAIDs Oral bisphosphonates Potassium chloride Quinidine Iron supplements  Infections: HSV CMV Candida albicans HIV	Peptic esophagitis The ulcerations are usually irregularly shaped or linear, multiple, and distal; may be accompanied by Barrett's esophagus Pill-induced: Ulcerations are usually singular and deep, occurring at points of stasis (especially near the carina), with sparing of the distal esophagus Infectious esophagitis: HSV – Discrete, superficial ulcers, with well-demarcated borders that tend to involve the upper or mid-esophagus; vesicles may be seen CMV – Ulcers range from small and shallow to large (>1 cm) and deep; most patients have multiple lesions Candida – Diffuse white plaques HIV – Tends to involve the mid to distal esophagus, ulcers may be shallow or deep, and may be large
	Gastritis/gastropathy