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CONTENTS :

1) INTRODUCTION :

2) EPIDIMIOLOGY :

3) ETIOLOGY

4) CLASSIFICATION

5) DIAGOSIS AND DD :

6) TREATMENT :1)init

7) MONITORING

8) PROGNOSIS AND COMPLICATIONS .

1) INTRODUCTION :

Acute gastroduodenal bleeding is a potentially life-threatening abdominal emergency

that remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB)

is defined as bleeding derived from a source proximal to the ligament of Treitz.

The incidence of UGIB is approximately 100 cases per 100,000 population per year.[1] Bleeding from the upper GI tract is approximately 4 times as common as bleeding

from the lower GI tract and is a major cause of morbidity and mortality. Mortality rates

from UGIB are 6-10% overall.[1] (See Epidemiology, below.)

The diagnosis of and therapy for nonvariceal upper gastrointestinal bleeding (UGIB) has

evolved since the late 20th century from passive diagnostic 

In patients with UGIB, comorbid illness, rather than actual bleeding, is the major cause

of death. Comorbid illness has been noted in 50.9% of patients, with similar

occurrences in males (48.7%) and females (55.4%).

One or more comorbid illnesses have been noted in 98.3% of mortalities in UGIB; in

72.3% of patients, comorbid illnesses have been noted as the primary cause of death.[3,

4] (See Epidemiology and Prognosis, below.)

Significant comorbidities have become more prevalent as the patient population with

UGIB has become progressively older. In a retrospective chart review by Yavorski et al,

73.2% of deaths occurred in patients older than 60 years.[4] (See Epidemiology and

Prognosis, below.)

Rebleeding or continued bleeding is associated with increased mortality; therefore,

differentiating the patient with a low probability of rebleeding and little comorbidity from

the patient at high risk for rebleeding with serious comorbidities is imperative. (See

Clinical Presentation and Workup, below.)

Annually, approximately 100,000 patients are admitted to US hospitals for therapy for

UGIB.

UGIB is a common occurrence throughout the world. In France, a report concludes that

the mortality from UGIB has decreased from about 11% to 7%; however, a similar report

from Greece finds no decrease in mortality. In a nationwide study from Spain, UGIB was

6 times more common than lower GI bleeding.[18]

The incidence of UGIB is 2-fold greater in males than in females, in all age groups;

however, the death rate is similar in both sexes.[4]

The population with UGIB has become progressively older, with a concurrent increase

in significant comorbidities that increase mortality. Mortality increases with older age

(>60 y) in males and females

Anatomy of the stomach

The stomach lies between the esophagus and the duodenum (the first part of the small

intestine). It is on the left upper part of the abdominal cavity. The top of the stomach lies

against the diaphragm. Lying behind the stomach is the pancreas. The greater

omentum hangs down from the greater curvature

The stomach is surrounded by parasympathetic (stimulant) and orthosympathetic

(inhibitor) plexuses (networks of blood vessels and nerves in

the anterior gastric, posterior, superior and inferior, celiac and myenteric), which

regulate both the secretions activity and the motor (motion) activity of its muscles.In

adult humans, the stomach has a relaxed, near empty volume of about 45 ml. Because

it is a distensible organ, it normally expands to hold about one litre of food,[4] but can

hold as much as two to three litres. The stomach of a newborn human baby will only be

able to retain about 30 ml.

Sections:The stomach is divided into four sections, each of which has different cells

and functions. The sections are:

Cardia Where the contents of the oesophagus empty into the stomach.

Fundus Formed by the upper curvature of the organ.

Body or

CorpusThe main, central region.

PylorusThe lower section of the organ that facilitates emptying the contents into

the small intestine.

Blood supply

Schematic image of the blood supply to the stomach: left and right gastric

artery, left and right gastro-omental artery and short gastric artery.[5]

Picture 1:

A more realistic image, showing the celiac artery and its branches; the liver has been

raised, and the lesser omentum and anterior layer of the greater omentum removed.

The lesser curvature of the stomach is supplied by the right gastric artery inferiorly, and

the left gastric artery superiorly, which also supplies the cardiac region. The greater

curvature is supplied by the right gastroepiploic artery inferiorly and the left

gastroepiploic artery superiorly. The fundus of the stomach, and also the upper portion

of the greater curvature, is supplied by the short gastric artery which arises from splenic

artery.

Like the other parts of the gastrointestinal tract, the stomach walls are made of the

following layers, from inside to outside:

mucosa

The first main layer. This consists of the epithelium and the lamina

propria (composed of loose connective tissue), with a thin layer ofsmooth

muscle called the muscularis mucosae separating it from the submucosa

beneath.

submucosa

This layer lies over the mucosa and consists of fibrous connective tissue,

separating the mucosa from the next layer. The Meissner's plexus is in

this layer (AKA submucosal plexus).

muscularis

externa

Over the submucosa, the muscularis externa in the stomach differs from

that of other GI organs in that it has three layers of smooth muscle instead

of two.

inner oblique layer: This layer is responsible for creating the motion

that churns and physically breaks down the food. It is the only layer of

the three which is not seen in other parts of the digestive system. The

antrum has thicker skin cells in its walls and performs more forceful

contractions than the fundus.

middle circular layer: At this layer, the pylorus is surrounded by a thick

circular muscular wall which is normally tonically constricted forming a

functional (if not anatomically discrete) pyloric sphincter, which

controls the movement of chyme into the duodenum. This layer is

concentric to the longitudinal axis of the stomach.

Auerbach's plexus  (AKA myenteric plexus) is found between the outer

longitundinal and the middle circular layer and is responsible for the

innervation of both (causing peristalsis and mixing)

outer longitudinal layer

serosaThis layer is over the muscularis externa, consisting of layers of

connective tissue continuous with the peritoneum.

Ref :

* ^ Sherwood, Lauralee (1997). Human physiology: from cells to systems. Belmont,

CA: worth Pub. Co. ISBN 0-314-09245-5. OCLC 35270048.

* ^ Anne M. R. Agur; Moore, Keith L. (2007). Essential Clinical Anatomy (Point

(Lippincott Williams & Wilkins)). Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-

7817-6274-X.OCLC 172964542.; p. 150

Anatomy of duodenum :

The duodenum is the first section of the small intestine. The duodenum precedes the

jejunum and ileum and is the shortest part of the small intestine, where most chemical

digestion takes place. the duodenum is a hollow jointed tube about 10–15 inches (25–

38 centimetres) long connecting the stomach to the jejunum. It begins with the duodenal

bulb and ends at the ligament of Treitz.

Sections

The duodenum is divided into four sections for the purposes of description. The first

three sections curve in a "C"-loop concavity in which the head of the pancreas lies. Only

the first 2 cm of the superior part is mobile (covered by peritoneum) – the distal 3 cm of

the first part along with the rest of the duodenum is retroperitoneal (immobile).

First part

The first (superior) part begins as a continuation of the duodenal end of the pylorus.

From here it passes laterally (right), superiorly and posteriorly, for approximately 5 cm,

before making a sharp curve inferiorly into the superior duodenal flexure (the end of the

superior part). It is the only intraperitoneal portion of the duodenum[8]. Relations:

Anterior

Gallbladder

Quadrate lobe of liver

Posterior

Bile  duct

Gastroduodenal artery

Portal vein

Inferior vena cava

Superior

Neck of gallbladder

Hepatoduodenal ligament (lesser omentum)

Inferior

Neck of pancreas

Greater omentum

Second part

The second (descending) part of the duodenum begins at the superior duodenal flexure.

It passes inferiorly to the lower border of vertebral body L3, before making a sharp turn

medially into the inferior duodenal flexure (the end of the descending part).

The pancreatic duct and common bile duct enter the descending duodenum, commonly

known together as the hepatopancreatic duct (or pancreatic duct in the United States),

through themajor duodenal papilla (known as Ampulla of Vater). This part of the

duodenum also contains the minor duodenal papilla, the entrance for the accessory

pancreatic duct(of Santorini). The junction between the

embryological foregut and midgut lies just below the major duodenal papilla.

Third part

The third (inferior/horizontal) part of the duodenum begins at the inferior duodenal

flexure and passes transversely to the left, crossing the left ureter, left testicular/ovarian

vessels, inferior vena cava, abdominal aorta, superior mesenteric artery and

the vertebral column.

Fourth part

The fourth (ascending) part passes superiorly, either anterior to, or to the left of, the

aorta, until it reaches the inferior border of the body of the pancreas. Then, it curves

anteriorly and terminates at the duodenojejunal flexure where it joins the jejunum. The

duodenojejunal flexure is surrounded by a peritoneal fold containing muscle fibres:

the ligament of Treitz.

Blood supply

The duodenum receives arterial blood from two different sources. The transition

between these sources is important as it demarcates the foregut from the midgut.

Proximal to the 2nd part of the duodenum (approximately at the major duodenal papilla

– where the bile duct enters) the arterial supply is from the gastroduodenal artery and its

branch the superior pancreaticoduodenal artery. Distal to this point (the midgut) the

arterial supply is from the superior mesenteric artery (SMA), and its branch the inferior

pancreaticoduodenal artery supplies the 3rd and 4th sections. The superior and inferior

pancreaticoduodenal arteries (from the gastroduodenal artery and SMA respectively)

form an anastomotic loop between the celiac trunk and the SMA; so there is potential

for collateral circulation here.

The venous drainage of the duodenum follows the arteries. Ultimately these veins drain

into the portal system, either directly or indirectly through the splenic or superior

mesenteric vein.

Ref :

* http://bedahunmuh.wordpress.com/algoritma-bedah/

*van Gijn J, Gijselhart JP (2011). "Treitz and his ligament.". Ned Tijdschr

Geneeskd. 155 (8). PMID 21557825.

* http://books.google.com.pe/books?

id=ZR0RKtr7YBoC&pg=PA187&lpg=PA187&dq=duodenum+retroperitoneal+

portions+anatomy&source=bl&ots=VkFzZ4K6_G&sig=AlvypvJPNyT_DJHi6w

ccaYcro8c&hl=en&sa=X&ei=mWwDUIKKK-

qm6gHWpd3_Bg&ved=0CEsQ6AEwBA#v=onepage&q=duodenum

%20retroperitoneal%20portions%20anatomy&f=false

Etiology of gastroduodenal bleding :

1) Ulcer-related UGIB

Peptic ulcer is the most common cause of acute upper GI bleeding and accounts for

approximately 50% of all upper GI bleeding cases (69).

There are approximately 150,000 hospitalizations per year in the United States for evaluation

and treatment of bleeding ulcers. Although hospitalization and surgery for uncomplicated

ulcers have decreased in the United States and Europe over the past three decades, the

number of hospitalizations for hemorrhage associated with ulcers has remained unchanged

(70). Even though ulcer bleeding stops spontaneously in at least 80% of patients, the overall

mortality is also unchanged over the last 30 years, ranging from 6 to 7% in the United States

(70) and averaging

14% in the United Kingdom (71).

Without specific hemostatic intervention, peptic ulcer bleeding continues or recurs in

approximately

20% of patients (72).

Ulcer bleeding starts when the ulcer base erodes into a blood vessel. Spontaneous hemostasis

occurs when a sentinel clot (what is usually actually referred to as a “visible vessel”) plugs the

“side hole” in the vessel.

The clot may then enlarge, remain attached for some time as it organizes, and eventually slough

off, leaving the underlying vessel covered with a flat pigmented spot that fades to leave a clean

ulcer base (72). This process takes less than 72 hours, and rebleeding occurs if the clot

undergoes lysis or falls off prematurely (72).

The most common cause of peptic ulcer is H. pylori infection. Peptic ulcer can present

silently with complications such as hemorrhage, particularly in patients on NSAIDs. PPIs

are the mainstays of therapy and should be held prior to noninvasive diagnostic tests for

H. pylori. Effective eradication of H. pylori involves regimens utilizing multiple antibiotics.

COX-2 inhibitors have lower incidence of causing peptic ulcers. Upper endoscopy

effectively diagnoses peptic ulcers, reduces rebleeding, and allows for appropriate

triage of patients with upper GI bleeding complications.

2) Tumors :

A ) benign tumors:

Most patients with benign stomach and duodenal tumors remain asymptomatic for

long periods of time. When symptoms are present, these depend on the tumor size,

location and complications arising from the tumor (eg: bleeding and ulceration). The

most common presenting symptoms are bleeding (acute or chronic), abdominal pain

and discomfort, nausea, weight loss, intestinal obstruction and as for periampullary

tumors, such as adenomas in the papilla of Vater, recurrent pancreaticobiliary

complications including jaundice, cholangitis, and pancreatitis may occur. Patients

may be referred by another physician to the out-patient clinics with one of the above

symptoms, or be admitted as an emergency due to massive upper gastrointestinal

bleeding. Rarely, they may also present with intestinal obstruction

Types:

epithelial tumors of the stomach

According to results published by Orlowska in 1995, the potential of these

lesions becoming malignant poses a much more worrying problem than the

clinical symptoms themselves. Orlowska found that 1.3% of Hyperplastic

Polyps (HP) and 10% of Adenomas were malignant. Her results support the

belief that gastric HP, like adenomas, can become malignant, thus she

concluded that it is sensible to differentiate a subgroup of Foveolar

Hyperplasia (FH) from HP, since FH will not become malignant unless their

histology changes to that of HP. The view that FH and HP belong to the same

category accounts mainly for the widespread underestimation of the

malignant potential of HP. While it was believed that polyps that become

malignant exceed 2 cm in diameter, Orlowska found cancer cells in very

small polyps (diameter ≈ 5 mm).

Leiomyoma/Leiomyoblastoma

These tumors constitute 2% of all resected neoplasms of the stomach, and

occur most frequently in males between fifty and seventy years old. 10–20%

of leiomyomas of the small intestine are located in the duodenum. They are

usually asymptomatic, but present with anemia in 50% of cases as a result of

mucosal ulceration. Leiomyomas are usually located in the corpus (40%) or

in the antrum (25%). Even when histopathologic tests are conducted, it is

difficult to distinguish benign lesions from malignant ones, partly because

leiomyomas are not encapsulated. The relationship between Leiomyoma

(LM), Leiomyoblastoma (LMB) and Leiomyosarcoma (LMS) is still unknown.

The “enigma” of LMB is its unusual histology, coupled with a somewhat

unpredictable clinical progression. Important in the assessment of the

malignant potential of LMB is the mitotic count, with counts over 5 for 50

high power fields, implying the possibility of malignancy and subsequent

metastasis. The accepted rate of malignant transformation is around 12%.

Duodenal adenomas in familial adenomatous polyposis (FAP)

This association is being increasingly recognized. Early diagnosis and

longterm surveillance of asymptomatic patients with this disease allows the

opportunity to diagnose and treat duodenal tumors at an early stage,

thereby avoiding the dismal prognosis once invasive cancer has developed in

patients who have survive for a mean period of 13 months.

Duodenal (periampullary) tumors

These tumors are rare. Villous and tubulovillous adenomas remain the most

common of such benign tumors and many have probably undergone

malignant change at the time of diagnosis. The presenting symptoms are

uncharacteristic, and endoscopy and ERCP are the most sensitive tools for

diagnosis. In the post-operative histology of one third of patients with

adenoma, we can observe severe third degree dysplasia (1).

Neurogenic gastric and duodenal tumors

These tumors constitute 4% of all benign neoplasms in stomach and 3% to

6% of all small bowel tumors. The most common tumors are neurilemomas

(schwanomas) and neurofibromas. About 40% of tumors present with

bleeding, and mechanical occlusion is not an unusual manifestation in the

duodenum.

Lipoma

Gastric lipoma is a benign tumor that occurs infrequently (1–3% of all benign

gastric tumors), and it is usually located in the antrum. Most lipomas are

found in the submucosa (95%), and they usually occur singly. The most

common clinical presentation (50– 60%) is gastrointestinal hemorrhage

caused by ulceration of the tumor. Currently, CT scanning is the study of

choice which identifies fatty tissue because of its low attenuation numbers,

but the definitive diagnosis is reached with the excision of the lesion and its

anatomopathologic study. In the duodenum we can observe approximately

35% of small intestine lipomas.

Brunner’s Gland Adenoma

This is the most common hamartoma, often found in the proximal

duodenum. It is believed to indicate hyperplasia of Brunner’s glands, perhaps

in response to excessive gastric acid secretion. Such hyperplasia has not

been associated with malignant degeneration. These tumors are usually

smaller than 1 cm, with multiple and polypoid incidence. As they are

asymptomatic, Brunner’s gland adenomas are often incidental findings

during endoscopy or radiographic examination.

1)Alstrup N, Burcharth F, Hauge C, Horn T. Transduodenal excision of tumors of the

ampulla of Vater. Eur J Surg. (1996);162:961–967. [PubMed]

2)Geis W, Baxt R, Kim H. Benign gastric tumors (Minimally invasive approach). Surg

Endosc. (1996);10:407–410. [PubMed]

b)malignant tumors :

The geographic incidence of gastric cancer has changed dramatically over the last few

decades. Prior to 1950, it was the most common cause of cancer death in men, and the

third leading cause of cancer death in women in the U.S. Mortalityfrom gastric cancer in

the United States has declined, perhaps due to dietary changes. This cancer is twice as

common in men than women, twice as common in blacks than whites, and more

common with advancing age. Gastric cancer is also seen in higher rates in Latin

America, Northern Europe and the Far East. It remains the second leading cause

of cancer death worldwide.

Gastric cancer peaks in the seventh decade of life. Often, a delay in diagnosis may

account for the poor prognosis. Fortunately, dedicated research into

itspathogenesis and identification of new risk factors, treatment, and advanced

endoscopic techniques have led to earlier detection of gastric cancer. Recognition

that Helicobacter pylori infection causes most gastric ulcers has revolutionized the

approach to gastric cancer today. Gastric tumors include adenocarcinoma, non-

Hodgkin’s lymphoma, and carcinoid tumors. 

Adenocarcinoma 

Adenocarcinomas arising from gastric epithelium are the most common malignancies of

the stomach (90% of cases). 

Lymphoma 

Primary gastrointestinal lymphoma may be of B- or T-cell type, with primary Hodgkin’s

disease being extremely uncommon. 

Hemorrhaging occurs in approximately 6%–10% of patients with advanced

cancer [1]. When visible, it can be particularly distressing to patients and

their caregivers [2, 3]. In some patients, it may be the immediate cause of

death. This article focuses on hemorrhaging that is visible, as opposed to

occult bleeding. It reviews treatment options in the context of advanced

cancer

Bleeding may result from local vessel damage and invasion or from systemic

processes such as disseminated intravascular coagulopathy (DIC) or

abnormalities in platelet functioning and number. The underlying causes of

these abnormalities are varied and include liver failure, medications such as

anticoagulants, chemotherapy, radiotherapy, surgery, and the cancer itself

[4]. Occasionally, concurrent diseases, such as idiopathic thrombocytopenia,

may be responsible. Hemorrhaging may manifest in a variety of ways,

including hematemesis, hematochezia, melena, hemoptysis, hematuria,

epistaxis, vaginal bleeding, or ulcerated skin lesions [4]. It may also present

as echymoses, petechiae, or bruising. Hemorrhage may occur as an acute

catastrophic event, episodic major bleeds, or ongoing low-volume oozing.

These characteristics provide clues as to the underlying cause and guide

management.

↵1 Pereira J, Mancini I, Bruera E. The management of bleeding in patients

with advanced cancer. In: Portenoy RK, Bruera E, eds. Topics in Palliative

Care, Volume 4. New York: Oxford University Press, 2000:163–183.

↵ Gagnon B, Mancini I, Pereira J et al. Palliative management of bleeding

events in advanced cancer patients. J Palliat Care 1998;14:50–54.

↵ Hoskin P, Makin W. The role of surgical and radiological intervention in

palliation. In: Oncology for Palliative Medicine. Oxford, UK: Oxford University

Press, 1998:229–234.

3)Acute stress gastritis in UGIB

Acute stress gastritis results from predisposing clinical conditions that have the potential

to alter local mucosal protective barriers, such as mucus, bicarbonate, blood flow, and

prostaglandin synthesis. Any disease process that disrupts the balance of these factors

results in diffuse gastric mucosal erosions.

This is most commonly observed in patients who have undergone episodes of shock,

multiple trauma, acute respiratory distress syndrome, systemic respiratory distress

syndrome, acute renal failure, and sepsis.

The principal mechanisms involved are decreased splanchnic mucosal blood flow and

altered gastric luminal acidity.

4)Mallory-Weiss tears in UGIB

Mallory-Weiss tears account for 15% of acute upper GI hemorrhage.[5] Kenneth Mallory

and Soma Weiss first described the syndrome in 1929.[13] The massive UGIB results

from a tear in the mucosa of the gastric cardia.

This linear mucosal laceration is the result of forceful vomiting, retching, coughing, or

straining. These actions create a rapid increase in the gradient between intragastric and

intrathoracic pressures, leading to a gastric mucosal tear from the forceful distention of

the gastroesophageal junction.[14] In 80-90% of cases, this is a single, 1.75- to 2.5-cm

mucosal tear along the lesser curve of the stomach just distal to the gastroesophageal

junction.[13]

5) Dieulafoy lesions in UGIB

The Dieulafoy lesion, first described in 1896, is a vascular malformation of the proximal

stomach, usually within 6 cm of the gastroesophageal junction along the lesser

curvature of the stomach. However, it can occur anywhere along the GI tract. This

lesion accounts for 2-5% of acute UGIB episodes.[15]

Endoscopically, the lesion appears as a large submucosal vessel that has become

ulcerated. Because of the large size of the vessel, bleeding can be massive and brisk.

The vessel rupture usually occurs in the setting of chronic gastritis, which may induce

necrosis of the vessel wall. Alcohol consumption is reportedly associated with the

Dieulafoy lesion.

In a review of 149 cases, the Dieulafoy lesion mostly occurred in men and mostly in

those in their third to tenth decade.[16]

6) NSAIDs in UGIB

NSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase, which causes

decreased mucosal prostaglandin synthesis and results in impaired mucosal defenses.

Daily NSAID use causes an estimated 40-fold increase in gastric ulcer creation and an

8-fold increase in duodenal ulcer creation.[11]

Long-term NSAID use is associated with a 20% incidence in the development of

mucosal ulceration.[17] Medical therapy includes avoiding the ulcerogenic drug and

beginning a histamine-2 (H2)–receptor antagonist or a proton pump inhibitor that

provides mucosal protection.

7)Vomiting-related UGIB

During vomiting, the lower esophagus and upper stomach are forcibly inverted.

Vomiting attributable to any cause can lead to a mucosal tear of the lower esophagus or

upper stomach. The depth of the tear determines the severity of the bleeding. Rarely,

vomiting can result in esophageal rupture (Boerhaave syndrome), leading to bleeding,

mediastinal air entry, left pleural effusion (salivary amylase can be present) or left

pulmonary infiltrate, and subcutaneous emphysema.

CLASSIFICATION:

The gastrointestinal bleeding can be classified in acute or chronic;

A) ACUTE GI BLEEDING

The cardinal features are haematemesis and melaena. Following a bleed from the upper

GI tract, unaltered blood can appear per rectum, but the bleeding must be massive and

is almost always accompanied by shock.

Peptic ulceration is the commonest cause of serious and life-threatening G.I bleeding.

Drugs.

Aspirin and NSAIDs can produce ulcers and erosions. These agents are also responsible

for GI haemorrhage from both duodenal and gastric ulcers, particularly in the elderly.

Corticosteroids in the usual therapeutic doses probably have no influenceon GI

haemorrhage.

Anticoagulants do not cause acute GI haemorrhage per se but bleeding from any cause

is greater if the patient is anticoagulated.

All cases with a recent (i.e. within 48 hours) significant GI bleed should be seen in

hospital.

B) CHRONIC GI BLEEDING

Usually present with iron-deficiency anaemia (IDA).Chronic blood loss producing IDA in

all men and all women after the menopause is always due to bleeding from the GI tract.

The primary concern is to exclude cancer, articularly of the stomach or right colon,and

coeliac disease. Occult blood tests areunhelpful. Chronic blood loss can occur with any

lesion of the GI tract that produces acute bleeding.

FORMS OF PRESSENTING:1)HEMORAGic SHOKThe goal of the patient's physical examination is to evaluate for shock and blood loss.Assessing the patient for hemodynamic instability and clinical signs of poor perfusion is important early in the initial evaluation to properly triage patients with massive hemorrhage to ICU settings. Worrisome clinical signs and symptoms of hemodynamic compromise include tachycardia of more than 100 beats per minute (bpm),systolic blood pressure of less than 90 mm Hg, cool extremities,syncope, and other obvious signs of shock, such as ongoing brisk hematemesis or the occurrence of maroon or bright-red stools, which requires rapid blood transfusion.[24]Pulse and blood pressure should be checked with the patient in supine and upright positions to note the effect of blood loss. Significant changes in vital signs with postural changes indicate an acute blood loss of approximately 20% or more.Assessment of hemorrhagic shock

As previously mentioned, patients who present in hemorrhagic shock have a mortality rate of

up to 30%. Hemorrhage may be classified based on the amount of blood loss, as noted in the

following table.[25

Table Estimated Fluid and Blood Losses in Shock

This

classification scheme aids in understanding the clinical manifestations of hemorrhagic shock. In

early class 1 shock, the patient may have normal vital signs, even with a 15% loss of total blood

volume. As the percentage of blood volume loss increases, pertinent clinical signs, symptoms,

and findings become more apparent.

Although early cardiovascular changes occur as blood loss continues, urine output, as a sign of

end organ renal perfusion, is only mildly affected until class 3 hemorrhage has occurred.

Bornman et al correlated the presence of shock (defined as a pulse rate >100 bpm or SBP < 100

mm Hg) with the incidence of rebleeding rates after initial nonsurgical intervention.[25] They

found that rebleeding (a marker for increased mortality and need for surgery) occurred in 2% of

patients without shock, in 18% with isolated tachycardia, and in 48% with shock.

Schiller et al determined that SBP is a sensitive clinical marker for helping to predict mortality.

They correlated mortality rates based on the patient's SBP at the time of bleeding and found

mortality rates of 8% for patients with SBP more than 100 mm Hg, rates of 17% for SBP of 80-90

mm Hg, and rates of more than 30% for SBP less than 80 mm Hg.

Unless the patient has evidence of shock, orthostatic testing should be performed to assess and

document a hypovolemic state. A positive tilt test finding is defined as an SBP decrease of 10

mm Hg and a pulse rate increase of 20 bpm with standing compared to the supine position. The

ASGE survey was able to correlate orthostatic changes with the incidence of mortality.[26] The

Class 1 Class 2 Class 3  Class 4

Blood Loss, mL Up to 750 750-1500 1500-2000 >2000

Blood Loss,% blood volume Up to 15% 15-30% 30-40% >40%

Pulse Rate, bpm < 100 >100 >120 >140

Blood Pressure Normal Normal Decreased Decreased

Respiratory Rate Normal or Increased Decreased Decreased Decreased

Urine Output, mL/h >35 30-40 20-30 14-20

CNS/Mental Status Slightly

anxious

Mildly

anxious

Anxious,

confused

Confused,

lethargic

Fluid Replacement, 3-for-1 rule Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood

mortality rate when orthostatic changes are present is 13.6%, compared to 8.7% when they are

absent.

Knopp et al studied the use of the tilt test in phlebotomized healthy volunteers and found that

a positive tilt test result consistently correlated with a blood loss of 1000 mL. This becomes

extremely useful when evaluating patients with class 1 hemorrhagic shock.

2)iron deficiency anemia

Anemia is a condition in which the body does not have enough healthy red blood cells. Iron is

an important building block for red blood cells.

iron deficiency anemia related with chronic gastroduodenal bleeding is appearing when the

body is losing more blood cells and iron than the body can replace.

Most of the time, symptoms are mild at first and develop slowly. Symptoms may include:

Feeling grumpy

Feeling weak or tired more often than usual, or with exercise

Headaches

Problems concentrating or thinking

As the anemia gets worse, symptoms may include:

Blue color to the whites of the eyes

Brittle nails

Light-headedness when you stand up

Pale skin color

Shortness of breath

Sore tongue

Symptoms of the conditions that cause iron deficiency anemia include:

Pain in the upper belly (from ulcers)

Weight loss (in people with cancer)

Dark, tar-colored stools or blood

Ref: Mabry-Hernandez IR. Screening for iron deficiency anemia--including iron supplementation for

children and pregnant women. Am Fam Physician. 2009 May 15;79(10):897-8.

Alleyne M, Horne MK, Miller JL. Individualized treatment for iron-deficiency anemia in adults. Am J Med.

2008;121:943-948..

DIAGNOSIS:

A)CLINICAL DIAGNOSIS:

The history and physical examination of the patient provide crucial information for the

initial evaluation of persons presenting with a GI tract hemorrhage.[5]

History findings include weakness, dizziness, syncope associated with hematemesis

(coffee ground vomitus), and melena (black stools with a rotten odor).

Occasionally, a brisk UGIB manifests as hematochezia (red or maroon stools); the

redder the stool, the more rapid the transit, which suggests a large upper tract

hemorrhage. Laine and Shah found that 15% of patients presenting with hematochezia

had an upper gastrointestinal source of bleeding identified at urgent

esophagogastroduodenoscopy.[21]

Patients may have a history of dyspepsia (especially nocturnal symptoms), ulcer

disease, early satiety, and NSAID or aspirin use. A history of recent aspirin ingestion

suggests that the patient may have NSAID gastropathy with an enhanced bleeding

diathesis from poor platelet adhesiveness.[5]

Many patients with UGIB who are taking NSAIDs present without dyspepsia but with

hematemesis or melena as their first symptom, owing to the analgesic effect of the

NSAID. Low-dose aspirin (81 mg) has been associated with UGIB with or without the

addition of NSAID therapy. Using the lowest effective dose for both short-term and long-

term users is recommended.[22]

Patients with a history of ulcers are at an especially increased risk for UGIB when

placed on aspirin or NSAID therapy and should receive continuous acid suppression

with a proton pump inhibitor (PPI). The patient’s ulcer history is also important because

recurrence of ulcer disease is common, especially if he or she has not been treated

for H pylori gastritis or antibiotic therapy has failed.

Patients may present in a more subacute phase, with a history of dyspepsia and occult

intestinal bleeding manifesting as a positive fecal occult blood test result or as iron

deficiency anemia.

A history of chronic alcohol use of more than 50 g/d or chronic hepatitis (B or C)

increases the risk of variceal hemorrhage, gastric antral vascular ectasia (GAVE), or

portal gastropathy.

The finding of subcutaneous emphysema with a history of vomiting is suggestive of

Boerhaave syndrome (esophageal perforation) and requires prompt consideration of

surgical therapy.

The presence of postural hypotension indicates more rapid and severe blood loss.

A meta-analysis documented the incidence of acute UGIB symptoms as follows (see

also Physical Examination, below)[23] :

Hematemesis - 40-50%

Melena - 70-80%

Hematochezia - 15-20%

Either hematochezia or melena - 90-98%

Syncope - 14.4%

Presyncope - 43.2%

Symptoms 30 days prior to admission - No percentage available

Dyspepsia - 18%

Epigastric pain - 41%

Heartburn - 21%

Diffuse abdominal pain - 10%

Dysphagia - 5%

Weight loss - 12%

Jaundice - 5.2%

b)Lab tests :

CBC With Platelet Count

A complete blood count (CBC) is necessary to assess the level of blood loss in a patient

with upper gastrointestinal bleeding. Where possible, having the patient's previous

results is useful to gauge this loss. CBC should be checked frequently (q4-6h) during

the first day.

Hemoglobin Value and Type and Crossmatch Blood

Based on the patient's initial hemoglobin level and clinical assessment of shock, a type

and screen or type and crossmatch should be ordered. The patient should be

crossmatched for 2-6 units, based on the rate of active bleeding. The hemoglobin level

should be monitored serially in order to follow the trend. An unstable hemoglobin level

may signify ongoing hemorrhage requiring further intervention.

Patients generally require blood transfusions because of hypoperfusion and

hypovolemia. Patients with significant comorbid conditions (eg, advanced

cardiovascular disease) should receive blood transfusions to maintain myocardial

oxygen delivery to avoid myocardial ischemia.

BMP, BUN, and Coagulation

The basic metabolic profile (BMP) is useful in evaluating for renal comorbidity; however,

blood in the upper intestine can elevate the BUN (blood urea nitrogen) level as well.

Measurement of coagulation parameters is necessary to assess for continued bleeding.

Abnormalities should be corrected rapidly.

The BUN-to-creatinine ratio increases with upper gastrointestinal bleeding (UGIB). A

ratio of greater than 36 in a patient without renal insufficiency is suggestive of UGIB.

Coagulation Profile

The patient's prothrombin time (PT), activated partial thromboplastin time, and

International Normalized Ratio (INR) should be checked to document the presence of a

coagulopathy. The coagulopathy may be consumptive and associated with a

thrombocytopenia.

A platelet count of less than 50 with active acute hemorrhage requires a platelet

transfusion and fresh frozen plasma in an attempt to replete lost clotting factors.

The coagulopathy could be a marker for advanced liver disease.

The PT is used in calculating the Child-Pugh score.[11] Elevated aminotransferase levels

are a result of hepatocellular injury. Increased levels of alkaline phosphatase and

gamma–glutamyl transpeptidase are indicative of cholestatic liver disease.

Prolongation of the PT based on an INR of more than 1.5 may indicate moderate liver

impairment.

A fibrinogen level of less than 100 mg/dL also indicates advanced liver disease with

extremely poor synthetic function.

Calcium Level

Assessing patients’ calcium levels is useful in identifying individuals with

hyperparathyroidism as well as in monitoring calcium in patients receiving multiple

transfusions of citrated blood. Hypercalcemia increases acid secretion.

Gastrin level

A gastrin level can identify the rare patient with gastrinoma as the cause of upper

gastrointestinal bleeding and multiple ulcers.

c)imagestic studies :

Radiography

Plain radiographs of the abdomen are not usually helpful in the diagnosis of acute upper

gastrointestinal bleeding (UGIB). The pathophysiology of acute UGIB is often mucosal

erosion with subsequent hemorrhage, which is not detected with plain radiographs.

Occasionally, free air under the diaphragm is seen in cases of perforated viscous, and

this may be accompanied by UGIB. Other etiologies, such as upper GI masses (which

usually result in chronic, not acute, UGIB), aneurysms with calcifications, and ascites

suggestive of portal hypertension, may be seen on radiographs.[12]

The radiographic findings, as outlined above, are usually nonspecific. Calcifications

associated with aneurysms, in the aorta or branch vessels, are reliable but rare findings

regarding a source of upper gastrointestinal bleeding.

Chest radiographs should be ordered to exclude aspiration pneumonia, effusion, and

esophageal perforation.

Barium Contrast Studies

Barium contrast studies are not usually helpful and can make endoscopic procedures

more difficult (ie, white barium obscuring the view) and dangerous (ie, risk of aspiration)

CT Scanning

Computed tomography (CT) scanning and ultrasonography may be indicated for the

evaluation of liver disease with cirrhosis, cholecystitis with hemorrhage, pancreatitis with

pseudocyst and hemorrhage, aortoenteric fistula, and other unusual causes of upper GI

hemorrhage.[29] The 2010 ACR criteria state that CT is particularly useful for localizing

obscure UGIB and for evaluating a patient with UGIB and a history of aortic

reconstruction or pancreaticobiliary procedure.[28]

CT scanning is useful in the diagnosis of aortoenteric fistula because images may

reveal thickened bowel, perigraft fluid collection, extraluminal gas, or inflammatory

changes in the area of the duodenum and aortic graft.

Nuclear Medicine Scanning

Nuclear medicine scans may be useful in determining the area of active hemorrhage.

However, the 2010 ACR criteria state that Tc-99m-labeled erythrocyte scans are of

limited value in diagnosing UGIB, but continue to be useful in certain cases of obscure

UGIB.[28]

D)interventional procedures :

Nasogastric Lavage

This procedure may confirm recent bleeding (coffee ground appearance), possible

active bleeding (red blood in the aspirate that does not clear), or a lack of blood in the

stomach (active bleeding less likely but does not exclude an upper GI lesion).

A nasogastric tube is an important diagnostic tool, and tube placement can reduce the

patient's need to vomit. Placement for diagnostic purposes is not contraindicated in

patients with possible esophageal varices.

The characteristics of the nasogastric lavage fluid (eg, red, coffee grounds, clear) and

the stool (eg, red, black, brown) can indicate the severity of the hemorrhage. Red blood

with red stool is associated with an increased mortality rate from more active bleeding

compared with negative aspirate findings with brown stool.

Endoscopy

The development of endoscopy has provided clinicians with the ability for diagnostic

and therapeutic approaches to bleeding from the GI tract. Endoscopic examination of

the upper GI tract provides useful information regarding the source and site of bleeding.[26]

After a positive NG lavage, and even with a negative one if there is high enough

suspicion, the next step should be performance of an esophagogastroduodenoscopy

(EGD) for localization of the bleeding source. Upper endoscopy is the primary

method of evaluating a patient with UGI bleeding as it has a 90–95% success rate

[72]. There is debate as to the timing of early upper endoscopy [74]. Most agree

that an endoscopy should be performed within 24 hours [73] to evaluate UGIB

but several studies are evaluating whether some patients benefit from even earlier

endoscopy. Clearly, patients who have persistent or severe bleeding should undergo

very early endoscopy to avail themselves of the potential of endoscopic therapy

[74].During the procedure, the endoscopist is looking for any lesion that might have

caused the bleeding and for characteristics that suggest the likelihood of recurrence.

Forrest [16] classified peptic ulcers according to features that were associated with

risk of rebleeding (see Table 1).

Table 1 Forrest classification of peptic ulcers

Type Description

Ia Active spurting bleeding

Ib Active oozing bleeding

IIa Non-bleeding but visible vessel

IIb Non-bleeding with adherent clot

IIc Non-bleeding with pigmented ulcer base

III Clean base, no sign of bleeding

most ulcers

with a clean base, are associated with a 5%risk of rebleed and 2% mortality.

Patients

with ulcers that have a flat, pigmented spot on endoscopy have a 10% risk of

further

bleeding and 3% mortality. The presence of adherent clots on top of an ulcer

is associated with a 22% risk of further bleeding and 7% mortality. A visible,

nonbleeding

vessel is correlated with a 43% risk of rebleed and 11% mortality, while

actively bleeding vessels have the highest risk of recurrence at about 55%

and a

mortality of 11% [1]. Other lesions such as Mallory–Weiss tears are

associated with

a low risk (2%) of further bleeding [75]. These associations suggest that

proper evaluation

via endoscopy is crucial, as endoscopic findings are directly associated with

patients’ prognosis and therefore will aid in decisions concerning therapy.

Endoscopic findings and their incidence rate in patients with UGIB include the following:

Duodenal ulcer - 24.3%

Gastric erosion - 23.4%

Gastric ulcer - 21.3%

Esophageal varices - 10.3%

Mallory-Weiss tear - 7.2%

Esophagitis - 6.3%

Duodenitis - 5.8%

Neoplasm - 2.9%

Stomal (marginal) ulcer - 1.8%

Esophageal ulcer - 1.7%

Other/miscellaneous - 6.8%

Endoscopy should be performed immediately after endotracheal intubation (if indicated),

hemodynamic stabilization, and adequate monitoring in an ICU setting have been

achieved. The 2010 American College of Radiology (ACR) appropriateness criteria for

upper gastrointestinal bleeding recommend upper endoscopy as the initial diagnostic

examination for all patients presumed to have UGIB.[28]

In spite of the excellent results with EGD, the procedure is not without complications.

It can cause gastrointestinal perforations, precipitation of gastrointestinal

bleeding, aspiration pneumonia, respiratory arrest, and cardiovascular complications

[11]. The incidence of complications is low, but it is important to be certain

that in each patient the benefit of the procedure outweighs the risk

Angiography

Angiography may be useful if bleeding persists and endoscopy fails to identify a

bleeding site. According to the 2010 ACR guidelines, angiography along with

transcatheter arterial embolization (TAE) should be considered for all patients with a

known source of arterial UGIB that does not respond to endoscopic management, with

active bleeding and a negative endoscopy.[28]

In cases of aortoenteric fistula, angiography requires active bleeding (1 mL/min) to be

diagnostic.

Differential Diagnoses

Abdominal Aortic Aneurysm Barrett Esophagus and Barrett Ulcer

Esophageal Cancer Esophageal Varices Esophagitis

Pancreatic pseudoaneurysm

Cardiac cirrhosis Celiac sprue Cholecystitis Cirrhosis Disseminated intravascular coagulation Strongyloidiasis Syncope von Willebrand disease Zollinger-Ellison syndrome Dengue fever

Emergency treatment in GD bleeding :

The goal of medical therapy in upper gastrointestinal bleeding (UGIB) is to correct

shock and coagulation abnormalities and to stabilize the patient so that further

evaluation and treatment can proceed

Resuscitation of a hemodynamically unstable patient begins with assessing and

addressing the ABCs (ie, airway, breathing, circulation) of initial management.

(Baradarian et al demonstrated that early, aggressive resuscitation can reduce mortality

in acute UGIB.[30] )

Patients presenting with severe blood loss and hemorrhagic shock present with mental

status changes and confusion. In such circumstances, patients cannot protect their

airway, especially when hematemesis is present. In these cases, patients are at

increased risk for aspiration, which is a potentially avoidable complication that can

significantly affect morbidity and mortality. This situation must be recognized early, and

patients should be electively intubated in a controlled setting.

Intravenous access must be obtained. Bilateral, 16-gauge (minimum), upper extremity,

peripheral intravenous lines are adequate for volume resuscitative efforts. Poiseuille’s

law states that the rate of flow through a tube is proportional to the fourth power of the

radius of the cannula and is inversely related to its length.[17] Thus, short, large-bore,

peripheral intravenous lines are adequate for rapid fluid infusion.

According to the 2008 SIGN guideline, either colloid or crystalloid solutions may be

used to attain volume restoration prior to administering blood products.[27] A rough

guideline for the total amount of crystalloid fluid volume needed to correct the

hypovolemia is the 3-for-1 rule. Replace each milliliter of blood loss with 3 mL of

crystalloid fluid. This restores the lost plasma volume. Patients with severe coexisting

medical illnesses, such as cardiovascular and pulmonary diseases, may require

pulmonary artery catheter insertion to closely monitor hemodynamic cardiac

performance profiles during the early resuscitative phase.

Once the ABCs have been addressed, assess the patient's response to resuscitation,

based on evidence of end organ perfusion and oxygen delivery.

Pulmonary artery catheters may be helpful to guide therapy.

Foley catheter placement is mandatory to allow a continuous evaluation of the urinary

output as a guide to renal perfusion. This labor-intensive management should be

performed only in an ICU setting.

Once the maneuvers to resuscitate are underway, insert a nasogastric tube and perform

an aspirate and lavage procedure. This should be the first procedure performed to

determine whether the GI bleeding is emanating from above or below the ligament of

Treitz. If the stomach contains bile but no blood, UGIB is less likely. If the aspirate

reveals clear gastric fluid, a duodenal site of bleeding may still be possible.

In a retrospective review of 1190 patients, Luk et al found that positive nasogastric-tube

aspirate findings were 93% predictive of an upper GI source of bleeding.[32]

According to a study performed by the ASGE, however, a nasogastric-tube aspirate

finding can be negative even in the setting of a large duodenal bleeding ulcer. The study

compared nasogastric-tube aspirate findings with endoscopic findings of the bleeding

source.[20] The investigation revealed that 15.9% of patients with a clear nasogastric-

tube aspirate, 29.9% of patients with coffee-ground aspirate, and 48.2% of patients with

red blood aspirate had an active upper GI source of bleeding at the time of endoscopy.

A study correlated mortality with the color of the fluid from the nasogastric-tube aspirate

and the color of the stool.[29] As shown in the following table, the color of the nasogastric-

tube aspirate can be a prognostic indicator.

Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIB

Mortality Rate)

Nasogastric Aspirate Color Stool Color Mortality Rate, %

Clear Brown or red 6

Coffee-ground Brown or black 8.2

Red 19.1

Red blood Black 12.3

Brown 19.4

Red 28.7

Surgery

Primary surgical intervention should be considered in patients with a perforated viscus

(eg, from perforated duodenal ulcer, perforated gastric ulcer, or Boerhaave syndrome).

In patients who are poor operative candidates, conservative treatment with nasogastric

suction and broad-spectrum antibiotics can be instituted. Endoscopic clipping or sewing

techniques have also been used in such patients.

Emergency surgery in UBIG typically entails oversewing the bleeding vessel in the

stomach or duodenum (usually preoperatively identified by endoscopy), vagotomy with

pyloroplasty, or partial gastrectomy. Angiographic obliteration of the bleeding vessel is

considered in patients with poor prognoses.

Treatment-related contraindications :

Contraindications to upper endoscopy include an uncooperative or obtunded patient,

severe cardiac decompensation, acute myocardial infarction (unless active, life-

threatening hemorrhage is present), and perforated viscus (eg, esophagus, stomach,

intestine).

Contraindications to emergency surgery include impaired cardiopulmonary status and

bleeding diathesis.

Esophagogastroduodenoscopy may be more difficult or impossible if the patient has

had previous oropharyngeal surgery or radiation therapy to the oropharynx.

The presence of a Zenker diverticulum can make intubation of the esophagus more

difficult.

Patients with Down syndrome are more sensitive to conscious sedation and should

receive much less sedation, or they should be monitored by an anesthesiologist and/or

intubated prophylactically prior to the procedure.

Hypotension may be exacerbated by sedation; therefore, patients who are unstable

should be given less sedation.

Patients with massive bleeding should be considered for intubation to reduce the

increased risk of aspiration. Such patients should be treated in an intensive care setting.

Ideally, the patient should be stabilized prior to endoscopy and abnormalities in

coagulation should be corrected. When this is not possible, the judgment of an

experienced endoscopist is vital.

Endoscopy

Since the late 1980s, endoscopic techniques to achieve hemostasis for bleeding ulcers

and varices have continued to evolve. Endoscopy is now the method of choice for

controlling active ulcer hemorrhage.

Several randomized clinical trials and meta-analyses have demonstrated and supported

the idea that early endoscopic hemostatic therapy significantly reduces rates of

recurrent bleeding, the need for emergent surgery, and mortality in patients with acute

nonvariceal upper gastrointestinal bleeding (UGIB).

In the early history of endoscopy for UGIB, multiple published studies questioned the

cost-effectiveness of endoscopy in this setting, because it was unclear whether the

outcome was changed. In a setting in which 80% of patients respond to conservative

medical management, studies were hampered by type 2 errors because of the large

number of patients needed to demonstrate statistical significance.

In 1989, a National Institutes of Health (NIH) consensus conference on UGIB concluded

that effective therapy was needed in the presence of active bleeding or a visible vessel.

The conference affirmed that the treatment, when performed by an experienced

endoscopist using 1 of 4 techniques (ie, injection of epinephrine or sclerosants, heater-

probe coagulation, bipolar electrode coagulation, laser coagulation), was proven

effective by the published evidence.

Three other techniques have since been developed: (1) endoscopic application of clips,

(2) use of banding devices, and (3) argon plasma coagulation. Aside from ulcer

hemorrhaging, other causes of gastrointestinal bleeding, including mucosal tears in the

esophagus or upper stomach due to vomiting (Mallory-Weiss tears), venous blebs, and

vascular ectasias, can also be treated with endoscopic coagulation.

Patients should be considered for upper endoscopy if blood loss from the upper

gastrointestinal tract is suspected.

The patient should undergo upper endoscopy prior to any operative intervention in order

to diagnose and localize the bleeding site. Most patients (85-90%) respond to

endoscopic therapy.

The bleeding from gastric cancers and ulcers in leiomyomas does not usually respond

to endoscopic therapy; surgical or radiologic intervention is needed.

Much debate has focused on the significance of the nonbleeding visible vessel (ie,

color, size, diagnostic characteristics, risk of rebleeding) in ulcer hemorrhage. These

matters became clarified after the characteristics and significance of the visible vessel in

the ulcer crater were defined and the evidence for endoscopic therapy was established,

demonstrating that patients requiring therapy to control bleeding or rebleeding could be

diagnosed and treated at the time of the upper endoscopy.

During the endoscopy, the patient is monitored according to analgesia and sedation

guidelines formulated by the American Society of Anesthesiology. The characteristics of

the bleeding lesion are noted, and appropriate therapy is applied when necessary for

high-risk lesions or active bleeding.

Urgent endoscopy

Urgent endoscopy is indicated when patients present with hematemesis, melena, or

postural changes in blood pressure. Cooper et al have demonstrated a lower rate of

rebleeding and shorter length of stay when endoscopy is performed within 24 hours of

admission.[39, 32]

Early endoscopy

Cooper et al studied the effectiveness of performing an early endoscopy within the first

24 hours of an acute UGIB episode and found it to be associated with reductions in the

length of hospital stay, rate of recurrent bleeding, and need for emergent surgical

intervention.[39]

According to the 2010 international consensus on nonvariceal upper gastrointestinal

bleeding, early endoscopy (within 24 hours of presentation) is appropriate for most

patients with UGIB.[40] In a retrospective review involving more than 30,000 cases,

Yavorski et al showed that the mortality rates were more than twice as high for patients

who did not undergo an early endoscopic procedure than for those who did undergo the

procedure early on (11.1% vs 5.2%, respectively).

Endoscopic techniques

The following endoscopic techniques have been developed for achieving hemostasis[5] :

Injection of epinephrine or sclerosants

Bipolar electrocoagulation

Band ligation[41]

Heater probe coagulation

Constant probe pressure tamponade

Argon plasma coagulator

Laser photocoagulation

Rubber band ligation

Application of hemostatic materials, including biologic glue

Application of hemoclips or endoclips

Application of nanopowder (experimental)[42]

Treatment using a combination of endoscopic therapies has become more common.

For example, injection therapy can be applied first to better clarify the bleeding site,

especially in the actively bleeding patient, followed by the application of heater probe or

bipolar (gold) probe coagulation. Injection therapy can also be performed prior to

endoscopic placement of hemoclips.

According to the 2008 SIGN guideline, combinations of endoscopy with an injection of

at least 13 mL of 1:10,000 adrenaline, coupled with either a thermal or mechanical

treatment, are more effective than single modalities.[27]

The 2010 international consensus guidelines on UGIB recommend the use of

endoscopic clips or thermal therapy for high-risk lesions.[40] As another example,

injection therapy is useful prior to laser therapy to reduce the heat sink effect of rapidly

flowing blood prior to laser coagulation.

Heater probe coagulation

The heater probe consists of a resistor electrode enveloped by a titanium capsule and

covered by Teflon (to reduce sticking to the mucosa by the probe). The probe

temperature rises to 250°C (482°F).

Bipolar electrocoagulation

The bipolar probe consists of alternating bands of electrodes producing an electrical

field that heats the mucosa and the vessel. The electrodes are coated with gold to

reduce adhesiveness. The probes are stiff in order to allow adequate pressure to the

vessel to appose the walls and thus produce coaptive coagulation when the electrical-

field energy is transmitted. Careful technique is required to heat-seal the perforated

vessel.

Injection therapy

Injection therapy involves the use of several different solutions injected into and around

the bleeding lesion. The different solutions available for injection are epinephrine,

sclerosants, and clot-producing materials, such as fibrin glue.

Laser therapy

Laser phototherapy uses an Nd:YAG laser to create hemostasis by generating heat and

direct vessel coagulation. This is a noncontact thermal method. It is not as effective as

coaptive coagulation, because it lacks the use of compression to create a tamponade

effect.[1] An additional deterrent to its use is expense.

To perform laser coagulation, the area near the vessel is first injected with epinephrine

to reduce blood flow (reducing the heat-sink effect); then, the laser is applied around the

vessel, producing a wall of edema. Caution must be observed to avoid drilling into the

vessel with the laser, causing increased bleeding.

Hemostatic clips and endoclips

Modification of the delivery system has made clip placement much easier than it was in

the original model. With careful placement of the clip, closing the defect in the vessel is

possible. Usually, multiple clips are applied. They vary in the size and the strength of

the clip. Four models of hemoclips are available: QuickClip2, which is rotatable;

Resolution Clip, which can be reopened after closure; TriClip, which has 3 prongs; and

In Scope, which is a multiclip applier with 4 endoclips. The Resolution Clip seems to be

the current clip of choice by experienced endoscopists.

There are some clinical settings in which endoclips may be preferred over other

hemostatic methods. These include the treatment of ulcers in patients who are

coagulopathic or who require ongoing anticoagulation; in such patients,

electrocoagulation will increase the size, depth, and healing time of treated lesions.

Endoclips may also be preferable in the retreatment of lesions that rebleed after initial

thermal hemostasis.

Ulcers on the lesser curvature, the posterior duodenum, or the cardia increase the

difficulty of clip deployment and clip failure rates.

Larger endoclips have advantages over smaller hemoclips for the hemostasis of chronic

ulcers and the closure of larger lesions.

Argon plasma coagulation

Argon plasma coagulation is a technique in which a stream of electrons flows along a

stream of argon gas. The coagulation is similar to monopolar cautery, with the current

flow going from a point of high current density (the point of contact of the gas with the

mucosa) to an area of low current density (the conductive pad on the patient's body).

The current flows through the body in an erratic path to the pad.

Nanopowder

Nanopowder has been found to be effective in a small study using a porcine model of

arterial bleeding.[42] Further trails are awaited.

Endoscopic treatment decisions

The choice of treatment modality is influenced by the size of the vessel. Animal studies

have demonstrated that the heater probe and bipolar probe are effective for vessels as

large as 2 mm in diameter.

Other techniques (eg, clips, band ligation) or a combination of techniques are needed

for larger vessels or vessels that are not approachable by the heater probe or bipolar

probe. (Surgical intervention should be considered when dealing with vessels larger

than 2 mm in diameter, discounting an enlargement due to the development of

pseudoaneurysm.)

Ulcers with an overlying clot

In the patient who has an ulcer with an overlying clot, attempting to remove the clot by

target washing is critical. Endoscopic removal of the clot by washing or cold snare has

been demonstrated to be effective in reducing the recurrence of bleeding.[47] (Cutting

away the adherent clot is somewhat controversial but is recommended based on study

results from experienced centers.)

The findings under the clot (eg, bleeding vessel, visible vessel, flat spot, clean base,

examples of which are seen in the images below) help to determine the therapy needed

and improve efficacy by allowing treatment to be applied directly to the vessel. (See the

table below.)

Ulcer with active bleeding. Ulcer

with a clean base. Diagram of an ulcer with a clean base.

Ulcer with a flat spot. Ulcer with

an overlying clot. Ulcer with a visible vessel.

Diagram of an ulcer with a visible vessel.

Table 5. Ulcer Characteristics and Correlations (Open Table in a new window)

If the clot cannot be removed by washing, then cutting away the clot using a cold snare

can be considered by experienced endoscopists.

Vigorous washing of the clot formed after therapy is useful in determining the adequacy

of coagulation. A combination of injection with heater probe or bipolar coaptive

coagulation is often used and has been shown to be more effective in patients with

active bleeding.

Active bleeding and rebleeding

The endoscopy should not be started unless the endoscopist is equipped for any

potential lesions (eg, ulcer, varix, angioectasia, tear, tumor). The patient should be

monitored for recurrent bleeding and treated a second time if appropriate. A surgical

consultation should be considered for all patients with gastrointestinal hemorrhage.

Rebleeding occurs in 10-30% of endoscopically treated patients. A second attempt at

endoscopic control is warranted. Some authorities have concerns about the perils of a

second esophagogastroduodenoscopy, which may result in delayed surgery,

perforation, and increased morbidity and mortality rates. However, this approach has

been validated in a large, randomized, controlled trial that showed decreased morbidity

and mortality rates.[48]

Specific characteristics at endoscopy can predict rebleeding. Rebleeding occurs in 55%

of patients who have active bleeding (pulsatile, oozing), in 43% who have a nonbleeding

visible vessel, in 22% who have an ulcer with an adherent clot, and in 0-5% who have

an ulcer with a clean base.

At endoscopy, the prevalence rate for a clean base is 42%, for a flat spot is 20%, for an

adherent clot is 17%, for a visible vessel is 17%, and for active bleeding is 18%. (See

the images below.)

Freeman et al have described a pale, visible vessel that appears to have a very high

risk for rebleeding.[49] This must be differentiated from the presence of a clean ulcer

base.

Good visualization is important. The uncleared fundal pool may obscure an ulcer,

mucosal tear, gastric varices, portal gastropathy, or tumor (eg, leiomyoma,

adenocarcinoma, lymphoma). Endoscopic therapy is recommended for ulcers at

increased risk for rebleeding.

According to the 2008 SIGN guidelines, TIPS should be considered to prevent gastric

variceal rebleeding.[27]

Using a combination of techniques is prudent when re-treating the ulcer site because

the first therapy produced necrosis and weakening of the intestinal wall. Ulcers on the

anterior surface of the stomach and duodenum are at increased risk for perforation.

Using injection as the first step increases the thickness of the submucosal layer, thus

providing an extra margin of safety.

Even operative techniques can have a significant rebleeding rate with significant

mortality, as noted in the study of Poxon et al. In this investigation, the rebleeding rate

was 10% (80% mortality for rebleeders) in patients who underwent a conservative

surgical technique in which the ulcer base was undersewn.[50] This more conservative

approach was compared with the standard surgical technique (ie, vagotomy and

pyloroplasty or partial gastrectomy). The comparison of the conservative approach with

a standard gastrectomy resulted in similar mortality rates, ie, 26% versus 19%,

respectively, with no rebleeding after partial gastrectomy.

Postendoscopic monitoring

Postoperatively, the patient is monitored for recovery from conscious sedation after

endoscopy and from general anesthesia after abdominal surgery. Monitor the patient's

mental status, vital signs, chest, cardiac, and abdominal findings to ascertain that the

patient's clinical status has stabilized and that no complications (eg, aspiration,

perforation, recurrent bleeding, myocardial infarction due to hypotension) have

occurred. Monitor the hemoglobin level.

TREATMENT OF MAJOR CAUSES OF GASTRODUODENAL DISEASES :

1)Bleeding Peptic Ulcer Treatment

Upper GI endoscopy is the most effective diagnostic tool for PUD and has become the

method of choice for controlling active ulcer hemorrhage. Failure of endoscopy to

maintain hemostasis is one of the indications to initiate surgical intervention, especially

in high-risk patients.

Regardless of the endoscopic therapy, however, 10-12% of patients with acute ulcerous

hemorrhage require an operation as the definitive procedure to control the bleeding

ulcer. In most circumstances, the operation is performed emergently, and the

associated mortality rate is as high as 15-25%.

Medical therapy used in conjunction with endoscopy involves PPI administration. PPIs

decrease rebleeding rates in patients with bleeding ulcers associated with an overlying

clot or visible, nonbleeding vessel in the base of the ulcer.[52, 53] Consider transcatheter

angiographic embolization in patients who are poor surgical candidates. Because of the

extensive collateral circulation of the upper GI tract, ischemic complications are rare.

Surgical treatment

If 2 attempts at endoscopic control of the bleeding vessel are unsuccessful, avoid

further attempts (ie, because of increased rebleeding and mortality rates) and pursue

surgical intervention. The indications for surgery in patients with bleeding peptic ulcers

are as follows:

Severe, life-threatening hemorrhage not responsive to resuscitative efforts

Failure of medical therapy and endoscopic hemostasis with persistent recurrent

bleeding

A coexisting reason for surgery, such as perforation, obstruction, or malignancy

Prolonged bleeding, with loss of 50% or more of the patient's blood volume

A second hospitalization for peptic ulcer hemorrhage

The operative treatment options for a bleeding duodenal ulcer historically include

vagotomy, gastric resection, and drainage procedures. Each specific operative option is

associated with its own incidence of ulcer recurrence, postgastrectomy syndrome, and

mortality (as seen in the table below). When making an intraoperative judgment on how

to best manage the bleeding ulcer, it is extremely important for the surgeon to be aware

of these differences.[11]

Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations for

Duodenal Ulcer 

Original OperationRecurrence Rate,

%

Postgastrectomy Syndrome

Rate, %

Mortality Rate,

%

Proximal gastric

vagotomy

10 5 0.1

Truncal vagotomy and

drainage

7 20-30 < 1

Truncal vagotomy and

antrectomy

Billroth I or Billroth II

1 30-50 0-5

Truncal vagotomy and

antrectomy

Roux-en-Y

5-10 50-60 0-5

The 3 most common operations performed for a bleeding duodenal ulcer are as

follows[5] :

Truncal vagotomy and pyloroplasty with suture ligation of the bleeding ulcer

Truncal vagotomy and antrectomy with resection or suture ligation of the bleeding

ulcer

Proximal (highly selective) gastric vagotomy with duodenostomy and suture ligation of

the bleeding ulcer

The purpose of the vagotomy is to divide the nerves to the acid-producing body and

fundus of the stomach. This inhibits the acid production that occurs during the cephalic

phase of gastric secretion. Although acid secretion is controlled, gastric motility and

gastric emptying is affected, as indicated in the following table.[11]

Proximal vagotomy abolishes gastric receptive relaxation and impairs storage in the

proximal stomach. As a result, a more rapid gastric emptying of liquids occurs. A

drainage procedure is not required, because the innervation of the antrum and pylorus

is still intact. Because of this, the gastric emptying of solid food is not altered. The

antropyloric mechanism still functions normally and continues to prevent duodenogastric

reflux.

In addition to having the same effects as a highly selective vagotomy in the proximal

stomach, a truncal vagotomy also has marked effects on distal gastric motor function. It

weakens distal gastric peristalsis, thus requiring the creation of a pyloroplasty to

decrease the resistance to outflow from the stomach.

Truncal vagotomy and suture ligation of a bleeding ulcer is a frequently used operation

for treating upper gastrointestinal bleeding (UGIB) in elderly patients with life-

threatening hemorrhage and shock. The procedure can be performed rapidly,

minimizing the time spent in the operating room under general anesthesia.

The principles of suture ligation of a duodenal bleeding ulcer that involves the

gastroduodenal artery require use of the 3-point ligation technique.

The gastroduodenal artery is ligated proximally and distally to the arterial bleeding site.

The third suture is a horizontal mattress placed to control hemorrhage from the

transverse pancreatic branch of the gastroduodenal artery. Failure to place this third

stitch may result in recurrent bleeding that requires another emergent laparotomy of the

abdomen. Vagotomy with antrectomy is reserved for patients whose conditions have

failed to respond to more conservative attempts at surgical intervention and for those

with aggressive and recurrent duodenal ulcer diathesis, such as gastric outlet

obstruction.

When performing a highly selective vagotomy, the duodenostomy or the

pyloroduodenostomy is closed anatomically, preserving the normal pyloric sphincter

muscle. Most commonly, this operation is reserved for young, stable, low-risk patients.

Although long-term follow-up care is still necessary, the recurrent ulcer rate is less than

10% at a mean follow-up of 3.5 years.[5]

Much of what is now known about the operations performed for bleeding duodenal

ulcers came from the era before the etiologic role for H pylori and NSAIDs in the

development of peptic ulcers was understood. Reducing gastric acidity has been proven

to be beneficial, with lower rebleeding rates when using high-dose omeprazole.[1] Although PPIs seem to have an advantage, they have no affect on mortality.

The diagnosis of H pylori infection is important in the management of patients with a

complicated bleeding peptic ulcer. If a patient with a bleeding ulcer requires surgery,

then knowledge of the patient's H pylori status becomes pertinent, because it may help

to guide the decision to choose a particular surgical procedure, eg, simply oversewing

the ulcer as opposed to performing an antiulcer operation. Many studies support the

decision to manage the bleeding ulcer in conjunction with eradication of H pylori.

Bleeding Gastric Ulcer Treatment

The surgical management of bleeding gastric ulcers is slightly different from that of duodenal

ulcers, but the concepts are identical. The 3 most common complications of a gastric ulcer that

mandate emergent surgical intervention are hemorrhage, perforation, and obstruction. The goals

of surgery are to correct the underlying emergent problem, prevent recurrent bleeding or

ulceration, and exclude malignancy.

A bleeding gastric ulcer is most commonly managed by a distal gastrectomy that includes the

ulcer, with a gastroduodenostomy or a gastrojejunostomy reconstruction.

The common operations for the management of a bleeding gastric ulcer include (1) truncal

vagotomy and pyloroplasty with a wedge resection of the ulcer, (2) antrectomy with wedge

excision of the proximal ulcer, (3) distal gastrectomy to include the ulcer, with or without truncal

vagotomy, and (4) wedge resection of the ulcer only.

Types of gastric ulcers

The choice of operation for a bleeding gastric ulcer depends on the location of the ulcer and the

hemodynamic stability of the patient to withstand an operation. Five types of gastric ulcers

occur, based on their location and acid-secretory status.

Type 1 gastric ulcers are located on the lesser curvature of the stomach, at or near the incisura

angularis. These ulcers are not associated with a hypersecretory acid state.

Type 2 ulcers represent a combination of 2 ulcers that are associated with a hypersecretory acid

state. The ulcer locations occur in the body of the stomach in the region of the incisura. The

second ulcer occurs in the duodenum.

Type 3 ulcers are prepyloric ulcers. They are associated with high acid output and are usually

within 3 cm of the pylorus.

Type 4 ulcers are located high on the lesser curvature of the stomach and (as with type 1 ulcers)

are not associated with high acid output.

Type 5 ulcers are related to the ingestion of NSAIDs or aspirin. These ulcers can occur anywhere

in the stomach.

Surgical management according to ulcer type

A vagotomy is added to manage type 2 or type 3 gastric ulcers.

Patients who are hemodynamically stable but have intermittent bleeding requiring blood

transfusions should undergo a truncal vagotomy and distal gastric resection to include the ulcer

for type 1, 2, and 3 ulcers.

In patients who present with life-threatening hemorrhage and a type 1, 2, or 3 ulcer, biopsy and

oversew or excision of the ulcer in combination with a truncal vagotomy and a drainage

procedure should be considered.

Patients with type 4 ulcers usually present with hemorrhage. The left gastric artery should be

ligated, and a biopsy should be performed on the ulcer. Then, the ulcer should be oversewn

through a high gastrotomy.

Rebleeding rates for the procedures that keep the ulcer in situ range from 20-40%.[11]

Gastric bleeding in the immediate postoperative period from recurrent PUD is initially best

managed by endoscopic or angiographic means. If reoperation is required, gastric resection is

usually indicated, because a repeat vagotomy is not reliable. A more definitive solution is

warranted.

According to the 2008 SIGN guidelines, patients with confirmed gastric variceal hemorrhage

require endoscopic therapy, preferably with cyanoacrylate injection.[27]

Stress Gastritis Treatment

Knowledge of the predisposing conditions for stress ulceration allows the clinician to

identify patients at risk for developing gastritis and GI bleeding. Treatment in this group

of high-risk patients should focus on prevention. This is best accomplished by treating

the underlying causes of ulceration.

Aggressive support of hemodynamic parameters ensures adequate mucosal blood flow.

In addition, several strategies have evolved to treat gastric luminal acidity. Histamine

receptor antagonists (HRAs) have proven to be the most effective at controlling

stomach pH. Proton pump inhibitors (PPIs) are superior to the HRAs at suppressing

acid; however, their role in stress ulceration prophylaxis is still being studied.[12]

Stress-related bleeding usually occurs 7-10 days after the initial insult but may manifest

sooner. Initially, endoscopy is the most important diagnostic tool. The acute superficial

erosions are multiple, begin in the fundus, and progress toward the antrum. Ninety

percent of patients stop bleeding with conservative medical therapy that includes NGT

lavage and gastric acid–controlling medications to maintain the gastric luminal pH

above 5.0.[13]

Endoscopic hemostasis is attempted using electrocoagulation, laser, or injection

therapy. Selective angiographic catheterization of the left gastric artery may be

attempted with selective infusion of vasopressin (48-72 h) or embolization using

Gelfoam, coils, or autologous clot to embolize the left gastric artery. Regardless of the

angiographic technique used, it is often unsuccessful because of the rich and extensive

submucosal plexus and collateral circulation within the stomach.

Surgical treatment

Surgical intervention becomes necessary if nonoperative therapy fails and blood loss

continues. The goals of operative treatment are to control bleeding and to reduce

recurrent bleeding and mortality. These patients are at extremely high risk, and the most

expeditious procedure is the best option.

Simply oversewing an actively bleeding erosion is sometimes effective enough to

control the bleeding. In the setting of life-threatening hemorrhage not amenable to

endoscopic control, gastric resection with or without vagotomy with reconstruction may

be necessary.

The type of gastric resection depends on the location of the gastric erosions, ie, whether

they are proximal or distal. The options are antrectomy and subtotal, near total, or total

gastrectomy. Operative mortality rates range from 4-17%.[54] The choice of the initial

operation must be made with an understanding of the patient's condition, the amount

and location of gastric disease, and an accurate assessment of one's technical ability to

rapidly and safely perform a gastric resection. The trend has been to perform less

surgery in general and to minialize the type of surgical procedure performed.[55]

Managing the underlying insult causing the gastric stress ulcerations is also important.

This involves supportive measures to maintain acceptable hemodynamic parameters, to

provide adequate nutritional support in the critically ill patient, and to treat sepsis (if

present).

Mallory-Weiss Syndrome Treatment

Distinguishing Mallory-Weiss syndrome from Boerhaave syndrome is critical. Although

both entities share a common pathogenesis, their management is completely different.

Boerhaave syndrome represents a full-thickness transmural laceration with perforation

of the esophagus. A Gastrografin swallow helps to confirm the presence of the

perforation in most cases, and prompt surgical intervention is necessary to prevent

mediastinitis and sepsis.

On the other hand, surgical intervention in Mallory-Weiss syndrome is required to

achieve hemostasis in only 10% of cases.[13] The bleeding from a Mallory-Weiss tear

spontaneously ceases in 50-80% of patients by the time endoscopy is performed.[13]

For patients in whom bleeding is visualized at endoscopy, the endoscopic treatment

options are electrocoagulation, heater-probe application, hemoclips, epinephrine

injection, or sclerotherapy.

In a series published by Bataller et al, hemostasis was achieved in 100% of patients

with Mallory-Weiss tears by using endoscopic sclerotherapy with epinephrine (1:10,000)

and 1% polidocanol. Other nonoperative therapies are reserved for cases in which

endoscopic attempts at creating hemostasis have failed.

Other available options are angiographic intra-arterial infusion of vasopressin and

transcatheter embolization of branches of the left gastric artery using Gelfoam. Avoid

the balloon tamponade technique using the Sengstaken-Blakemore tube in this

particular circumstance, because this apparatus may extend the mucosal laceration into

a transmural laceration with perforation.[13]

Surgical intervention is indicated in patients with continued bleeding after failed attempts

at nonoperative therapies.

Bleeding from the gastroesophageal junction is visualized through an anterior

gastrotomy. Once the tear is localized, the bleeding is controlled by oversewing the

lesion.

The overall mortality rates for patients who require emergent surgery is 15-25%, in

contrast to a mortality rate of 3% or less for patients whose bleeding stops by the time

of the initial endoscopy.[13]

Dieulafoy Lesion Treatment

The initial endoscopic management of this lesion can be highly successful. In a report

by Norton et al describing their experience with 90 Dieulafoy lesions, endoscopic

management achieved primary hemostasis in 96% of cases.

Contact thermal ablation with a heater probe is the most effective technique, with or

without the combined use of epinephrine to slow or stop the bleeding prior to applying

the heater probe. No studies have been performed that compare surgical and

endoscopic therapy for Dieulafoy lesions.

Although surgical intervention may be required after failed endoscopic therapy,

endoscopy is still an important adjunct for management, because a nonbleeding

Dieulafoy lesion may be undetectable through a gastrotomy.

Because of this potential problem, a combined endoscopic and surgical approach has

been adopted. The vascular malformation can be marked with India ink through the

endoscope.

Rebleeding after endoscopic therapy occurs in 11-15% of cases, with most cases of

rebleeding controlled at repeat endoscopy.[16] (Repeat endoscopy for patients who have

rebleeding has been validated in controlled studies of endoscopy and surgery.)

The 30-day mortality rate from the study by Norton et al was 42%, which is a reflection

of the severe comorbid conditions associated with patients who have bleeding from a

Dieulafoy lesion.

Angiodysplasia Treatment

Bleeding from angiodysplasias can range from occult blood loss to life-threatening

hemorrhage. Because the lesions are small and superficial, endoscopic therapy is

highly successful. Endoscopic treatments and devices used for hemostasis include

lasers, contact heat probes, electrocoagulation, and injection therapy.

The contact probe coagulators have been the most common form of endoscopic

treatment because of their proven success and ability to target a bleeding lesion

tangentially.

Recurrent bleeding can occur from the mucosal injury caused by the coagulation. To

overcome the possibility of a delayed hemorrhage, endoscopic band ligation has been

applied for hemostasis in nonvariceal GI bleeding, including angiodysplasias.[56]

When endoscopic techniques fail, surgical resection becomes necessary. When

pangastric involvement is the source of bleeding, a total gastrectomy may be required;

however, this is extremely rare. Available nonsurgical options include angiography with

catheter-directed vasopressin. Combined hormonal therapy with estrogen and

progesterone for patients in whom the diagnosis is unknown and vascular lesions are

suggested has not been demonstrated to be effective.

Aortoenteric Fistula

Patients with an aortoenteric fistula most often present with a self-limiting sentinel

hemorrhage that is then followed by an exsanguinating, massive GI bleed. For the

warning lesser sentinel bleed in a patient with a history of an abdominal aortic aneurysm

repair or a known aortic aneurysm, the diagnosis of a graft-enteric fistula should be

considered.

An upper endoscopy is the procedure of choice to help diagnose the fistula. It should be

performed to the ligament of Treitz. Upper endoscopy findings also help to exclude

other sources of UGIB.

Once the diagnosis of aortoenteric fistula is confirmed or seriously considered,

emergency surgical intervention is required. In most instances, the aortic graft is

removed after debridement and closure of the duodenum, followed by an extra-

anatomic vascular bypass in order to bypass the ligated aorta and revascularize the

lower extremities.

The perioperative mortality rate is 22-75%,[57] and major complications are common.

Published opinions state that graft excision is not necessary as long as no gross

contamination and purulence are present at the time of laparotomy.[58]Under these

circumstances, antibiotics are administered long-term.

Another option emerging in the surgical literature is the use of endovascular stents to

repair the fistula.[59, 60] Endovascular stent management is technically feasible and may

be used as a bridge to more definitive treatment after hemodynamic stabilization in

high-risk surgical patients.

Stent grafting immediately controls hemorrhage; however, the device is placed in an

infected field. As a result, adjunctive measures, such as long-term antibiotic use,

percutaneous drainage, and bowel diversion, may be required.[61]

According to the 2010 ACR UGIB guidelines, variceal UGIB that does not respond to

endoscopic management should be treated with a transjugular intrahepatic

portosystemic stent shunt (TIPS).[28] The 2008 SIGN guidelines consider TIPS to be the

treatment of choice for uncontrolled variceal bleeding.[27] Primary and secondary TIPS

patency rates have greatly improved with the use of stent grafts in lieu of bare metal

stents. Doppler ultrasonography of the liver is useful for TIPS monitoring, and both

Doppler ultrasonography and CT may be useful for planning TIPS insertion.[28] Although

endovascular stents have been shown to be effective in treating aortoenteric fistulas,

case reports are emerging describing aortoenteric fistulas in patients with abdominal

aortic aneurysm treated initially with stent grafts as well.[62]

Treatment Complications

Complications of endoscopic therapy include aspiration pneumonia and perforation (1%

for the first endoscopic therapy, 3% for the second). Bleeding can be caused by drilling

into the vessel with the laser, by perforating the vessel with an injection, or by removing

the clot with failure to coagulate the vessel.

Tseng et al investigated the cardiovascular effects of emergency endoscopy for UGIB in

patients with stable coronary artery disease (CAD)[63] and found that the patients

commonly experienced, primarily on a subclinical level, ventricular arrhythmias and

myocardial ischemia. The authors' results were as follows:

Incidence of ventricular arrhythmias during endoscopy - 42% (patients with CAD)

versus 16% (controls)

Frequency of ventricular arrhythmias during endoscopy - 1.19 events per minute

(patients with CAD) versus 0.12 events per minute (controls)

Number of patients with ischemic ST changes - 9 patients with CAD versus 1 control

Complications from emergency abdominal surgery include ileus, sepsis, poor wound

healing, and myocardial infarction.

Salvage surgery is associated with a high mortality rate, reflecting the comorbidities of

patients who rebleed or continue to bleed.

Post-treatment Monitoring and Care

The 2010 international consensus guidelines on UGIB state that selected low-risk

patients may be discharged immediately following endoscopy, but high-risk patients

should remain hospitalized for at least 72 hours.[40]

According to the 2008 SIGN guideline, patients with a post-endoscopic Rockall score of

less than 3 have a low risk of rebleeding or death and are candidates for early

discharge and outpatient follow up.[27]

The goal is to maintain the intragastric pH above 6 to maintain the clot. This is most

easily achieved by intravenous proton pump inhibitor (PPI) therapy. After the acute

phase, 72 hours, the coagulated vessel should be stable and the patient can be

switched to oral therapy. If the patient rebleeds or has ongoing bleeding, then repeat of

endoscopic therapy would be considered. If this is not successful, then interventional

radiology is performed to clot the bleeding vessel. If this fails, then surgery would be

considered.

In the subsequent 48-72 hours after endoscopic therapy, the patient should receive

acid-suppressive therapy to maintain a high gastric pH (above 6). A high gastric pH can

be achieved by a continuous infusion of high-dose intravenous PPI therapy.

Patients who do not require endoscopic therapy and do not have other comorbidities

should be considered for discharge.

Patients who did not require endoscopic treatment should receive routine, oral dosing of

a PPI, ie, daily dosing prior to breakfast. Whether high-dose intravenous PPI therapy is

advantageous in this setting remains controversial.

Oral PPI therapy can be achieved with any of the oral PPI preparations.

Patients should be tested for H pylori either by histology of gastric biopsy specimens

taken on initial upper endoscopy or by serologic tests. If positive, H pylori therapy

should be instituted after the patient has been discharged and is in stable condition.

Moreover, H pylori eradication should be confirmed 4-6 weeks later in patients with

UGIB. This can be done by checking the stool for the H pyloriantigen.

Tachyphylaxis may develop within 24 hours if H2-receptor antagonists are

administered.

Data on acid suppression via oral PPI therapy in order to produce a reduction in

rebleeding are limited. High-dose intravenous PPI therapy appears to reduce

rebleeding, but PPIs are not currently approved by the US Food and Drug

Administration (FDA) for such treatment. The patient may be fed after recovery from

local and intravenous anesthesia.

Some patients may require further endoscopic therapy. If repeat endoscopic therapy is

needed, the stomach will empty liquids without residue within 3 hours. The 2008 SIGN

guideline recommends repeat endoscopy and endotherapy within 24 hours when initial

endoscopic treatment is deemed suboptimal or in patients in whom rebleeding will likely

be life threatening.[27]

If the patient remains stable, the patient can then be started on therapy for ulcer

healing.

The patient should continue oral therapy for ulcer disease noted on endoscopy or for

ulcers caused by cautery techniques during endoscopic therapy. The greatest risk for

perforation is usually within the first 48 hours after endoscopic therapy. Long-term acid

suppression therapy should be offered with either full-dose H2-receptor antagonists or

low-dose PPIs to prevent ulcer recurrence or its complications.[64]

Aspirin and NSAID therapies should be avoided in view of their adverse effect on

platelet aggregation and ulcer healing. However, according to the 2010 international

consensus guidelines, resumption of aspirin therapy in patients who require anticlotting

prophylaxis should not be delayed as cardiovascular risks outweigh the risk of

rebleeding.[40]

The 2008 SIGN guidelines state that patients with healed bleeding ulcers who are

negative for H pylori require concomitant PPI therapy at the usual daily dose if NSAIDs,

aspirin, or COX-2 inhibitors are indicated.[27]

If patients must remain on NSAIDs or low-dose aspirin, secondary prophylaxis against

NSAID-induced ulcers should be given. According to the 2010 international consensus

guidelines on UGIB, postdischarge use of aspirin or NSAIDs requires cotherapy with

PPI.[40]

Only lansoprazole (15 mg or 30 mg daily),[65] esomeprazole (20-40 mg daily), and

misoprostol (200 µg 4 times daily)[66] are approved by the FDA for prophylaxis against

NSAID-induced ulcers.

The patient's hemoglobin value should be monitored to assess the efficacy of iron

therapy as an outpatient; further improvement should be noted. Erythropoietin

analogues have been shown to be effective in increasing the rate of hemoglobin

production after ulcer hemorrhage.

Repeat endoscopy should be done in a few weeks in patients with gastric ulcers to

document ulcer healing and to exclude cancer.[67]

Deterrence and Prevention of UGIB

Antibiotic therapy should be given if H pylori is present in the setting of any history of

ulcer disease. Eradication of H pylori has been demonstrated to reduce the risk of

recurrent ulcers and, therefore, recurrent ulcer hemorrhages.

NSAIDs should be avoided. If not possible, they should be used at the lowest dose and

duration.

PPI or misoprostol cotherapy should be used along with NSAIDs.

The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer

hemorrhage, although only when not combined with aspirin therapy. Concerns have

been raised about an increase in myocardial infarction and stroke in patients taking

selective cyclooxygenase-2 inhibitors.

As demonstrated in the study by al-Assi et al, the combination of H pylori infection and

NSAID use may increase the risk of ulcer hemorrhage; however, the treatment of H

pylori in patients who are taking NSAIDs remains controversial.[23]

Medication Summary

Rebleeding is associated with increased morbidity and mortality; therefore, this is the

major goal of therapy.

As advised in the 2008 SIGN guidelines, patients with chronic liver disease who present

with acute UGIB should be started on antibiotic therapy.[27]

The use of H2-receptor antagonists has not been shown to be effective in altering the

course of UGIB. A meta-analysis concluded that there was a possible minor benefit with

intravenous H2 antagonists in bleeding gastric ulcers but no benefit in duodenal ulcers.[68]

The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer

hemorrhage, although only when not combined with aspirin therapy. Concerns have

been raised about an increase in myocardial infarction and stroke in patients taking

selective cyclooxygenase-2 inhibitors.

As demonstrated in the study by al-Assi et al, the combination of H pylori infection and

NSAID use may increase the risk of ulcer hemorrhage; however, the treatment of H

pylori in patients who are taking NSAIDs remains controversial.[23]

The 2008 SIGN guidelines clearly advocate the discontinuation of aspirin and NSAIDs

in patients who present with peptic ulcer bleeding. When ulcer healing and eradication

of H pylori are confirmed, aspirin and NSAIDs should only be resumed if there is a clear

indication for their use.[27]

Eradication of H pylori can reduce the risk of rebleeding. Current anti-H pyloriregimens

include a variety of drug combinations. Typically, an antimicrobial agent is combined

with an H2-receptor antagonist or a PPI.

The treatment regimens approved by FDA have eradication rates for H pylori of 70-

90%.[11]

Drugs used to treat H pylori infection include the following:

Omeprazole

Ranitidine bismuth citrate

Bismuth subsalicylate

Lansoprazole

Consider for admission and early endoscopy (and calculation of full Rockall

score) if:

aged ≥60 years (all patients who are aged >70 years should be admitted); or witnessed haematemesis or haematochezia (suspected continued bleeding); or haemodynamic disturbance (systolic blood pressure <100 mm Hg, pulse ≥100

beats per minute); or liver disease or known varices.

Other significant comorbidity (especially cardiac disease, malignancy) should also lower the

threshold for admission.

RISK ASSESSMENT AND PROGNOSIS IN GASTRODUODENAL BLEEDING:

Recommendations emphasise early risk stratification, using validated prognostic scales, and early

endoscopy (within 24 hours).6 The following formal risk assessment scores are recommended by

the National Institute for Health and Clinical Excellence (NICE) for all patients with acute UGIB:2

the Blatchford score at first assessment, and the full Rockall score after endoscopy.

The Blatchford risk assessment is designed to be used pre-endoscopy. Scores are added using the

level of urea, haemoglobin, systolic blood pressure, pulse rate, presentation with melaena,

presentation with syncope, hepatic disease and cardiac failure. A score of 0 is the cut-off with any

patient scoring >0 being at risk of requiring an intervention.

The Scottish Intercollegiate Guidelines Network (SIGN) guideline on the management of acute upper

and lower gastrointestinal bleeding recommends that an initial (pre-endoscopic) Rockall score be

calculated for all patients presenting with acute UGIB. In patients with an initial Rockall score >0,

endoscopy is recommended for a full assessment of bleeding risk.3

Rockall Numerical Risk Scoring System4

Initial Score Criteria (prior to gastroscopy)

1) Age:AGE <60->O POINT

60-79->1 POINT

>80->2 POINTS

Shock      

Co-morbidity

Additional Criteria for Full Score (after gastroscopy)

"No shock" = (SBP =100 mm Hg, pulse <100/min) - 0 points"Tachycardia" = (SBP =100 mm Hg, pulse =100/min) - 1 point"Hypotension" = (SBP <100 mm Hg) - 2 points

No major comorbidity - 0 pointsCardiac failure, IHD or any major comorbidity - 2 pointsRenal or liver failure, disseminated malignancy - 3 points

Reset

Diagnosis

Major stigmata of recent haemorrhage (SRH)?

PrognosisElderly patients and people with chronic medical conditions withstand acute UGIB less well and have

a higher risk of death.2 Mortality is about 7% in patients admitted with an UGIB. It is as high as 26%

in patients who develop bleeding whilst in hospital having been admitted for another cause.3 A score

of less than 3 using the Rockall system above is associated with an excellent prognosis, whereas a

score of 8 or above is associated with high mortality.4 

Factors which affect the risk of death include:

Age: deaths under age 40 years are rare. 30% of patients over 90 years old with UGIB die as a result of the bleed.

Comorbidity: complications are more likely with comorbid disease. Shock: the presence of signs of shock at presentation confers a worse prognosis. Prognosis is also worse with: liver disease, inpatient, continued bleeding after

presentation, haematemesis, haematochezia and elevated blood urea.3

Endoscopic findings: much work has been done on classifying and identifying endoscopic findings which correlate with high risk - for example:

o Mallory-Weiss tears or clean ulcers have a low risk of re-bleeding and death.o Active bleeding in a shocked patient carries an 80% risk of re-bleeding or death.o Non-bleeding but visible vessel has a 50% risk of re-bleeding.

Mortality is reported to be lower in specialist units, possibly because of adherence to protocols rather

than because of technical advances. The prognosis in liver disease relates significantly to the

severity of the liver disease rather than to the magnitude of the haemorrhage.

REF: Document references

Mallory-Weiss tear, no lesion seen nor SRH - 0 pointsAll other diagnoses - 1 pointMalignancy of upper GI tract - 2 points

None or dark spot only - 0 pointsBlood in the upper GI tract, adherent clot, visible or spurting vessel - 2 points

Reset

1. Holster IL, Kuipers EJ; Management of acute nonvariceal upper gastrointestinal bleeding: current policies World J Gastroenterol. 2012 Mar 21;18(11):1202-7. [abstract]

2. Acute upper GI bleeding, NICE Clinical Guideline (June 2012)3. Management of acute upper and lower gastrointestinal bleeding, Scottish

Intercollegiate Guidelines Network - SIGN (September 2008)4. Rockall TA, Logan RF, Devlin HB, et al; Risk assessment after acute upper

gastrointestinal haemorrhage. Gut. 1996 Mar;38(3):316-21. [abstract]5. Baradarian R, Ramdhaney S, Chapalamadugu R, et al; Early intensive resuscitation

of patients with upper gastrointestinal bleeding decreases mortality. Am J Gastroenterol. 2004 Apr;99(4):619-22. [abstract]

6. Barkun AN, Bardou M, Kuipers EJ, et al; International consensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2010 Jan 19;152(2):101-13. [abstract]

7. Cerulli MA et al, Upper Gastrointestinal Bleeding, Medscape, Nov 20118. Stent insertion for bleeding oesophageal varices, NICE Interventional Procedure

Guideline (April 2011)

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Prakash C,

Edmundowicz S.

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