Upper gastrointestinal bleeding (UGIB) refers to any bleeding from the GI tract above the ligament of Treitz, presenting in various forms such as hematemesis, melena, and hematochezia. Initial assessment focuses on patient stabilization, rapid treatment, and surgical evaluation when necessary, with endoscopy being the preferred diagnostic and therapeutic approach. Key causes of UGIB include peptic ulcers, gastritis, and neoplasms, with management tailored based on endoscopic findings and clinical features of bleeding severity.

1. Upper gastrointestinal bleed
1. 1. UPPER GASTROINTESTINAL BLEED (HEMATEMESIS)
Anil Haripriya
2. 2. DEFINITION : Any bleed, occurring into the G.I. tract from a source above the ligament of
Treitz is described as ‘upper gastrointestinal bleed’. Blood loss of G.I. tract can manifest in five
ways. § Hematemesis – is bloody vomitus, either fresh and bright red or older and “coffee-
ground” in character. § Malena – is black, tarry, and foul smelling stools. It results from
degradation of blood, minimum of 60 ml of blood which stays in G.I. tract for > 14 hrs cause
malena. § Hematochezia – is passage of bright red or maroon blood from rectum. This is usually
caused by lower G.I. sources but massive upper G.I. bleed (>1000 ml) may also lead to
hematochezia. § Occult blood loss – detected by stool examination. § Symptom of blood
depletion without G.I. symptoms. INITIAL ASSESSMENT OF THE PATIENT Rapid assessment
is carried out to gauge the urgency of the situation. § Whether the bleed is acute or chronic? § Is
the patient haemodynamically stable or unstable? It is helpful to confirm the presence of
bleeding by inspecting the vomit or the nasogastric aspirate or stool. But first goal is always
stabilization of the patient. Blood is sent for CBC, biochemistry, clotting studies typing and
3. 3. cross matching is done. If blood loss is chronic, then depletion of bone marrow iron stores
causes microcytic hypochromic anemia with low MCV. In acute blood loss hematocrit is a poor
indicator of magnitude of loss in the initial hours, because with hemorrhage there is proportional
loss of plasma and RBC (i.e. people bleed whole blood). Hence during this time the MCV will be
normal. It takes 24-72 hours for the extra-vascular fluid to enter the vascular compartment and
subsequently replace the plasma volume causing decrease in hematocrit. This sequence is
modified by preexisting abnormalities in vascular volume or by the administration of exogenous
fluids and blood. RESUSCITATION Resuscitation of an unstable patient is the first goal of
therapy. 1. Two large bone canula are inserted, saline or ringer lactate solution should be in
inferred as a rapidly as the patients cardiopulmonary system will allows. 2. Measurement of
C.V.P. helps prevent fluid overload. 3. O2 inhalation by nasal canula / facemask may be of
benefit in selected patients with inadequate oxygenation. 4. Vital signs and urine output should
be charted frequently. Transfusion is usually indicated in : - 1. Patients who continue to bleed
despite therapy. 2. Who are in shock. 3. Who have very low hematocrit (<20-25%).
4. 4. 4. Who have symptoms related to poor tissue oxygenation (e.g. angina). Hematocrit may be
performed 15 min after the completion of a transfusion to determine the response. Fresh frozen
plasma or platelets should be given to patients who require 10 or more units of blood, who have
demonstrable deficiency of clotting factors, or who have severe thrombocytopenia or platelet
dysfunction. DIAGNOSTIC EVALUATION HISTORY § Any prior h/o bleed? § Illness such as
ulcers, necrosis, cancer, bleeding disorder. § Prior surgery for ulcer disease. § Use of alcohol /
NSAIDS / Anti-coagulants. EXAMINATION § Skin – cutaneous stigmata of cirrhosis. § Evidence
of underlying cancer (acathosis nigricans, Kaposi sarcoma) § Pigmented lip lesion (Peutz-
Jeghars Syn.) § Tumor (blue rubber bleb nevus, neurofibromatosis, Henoch schonlein purpura ).
§ Vascular abnormalities. § Lymphadenopathy (malignancy). § Abdominal masses (malignancy).
5. 5. § Abdominal tenderness (pancreatitis, ulcer). § Splenomegaly (cirrhosis, splenic vein
thrombosis) ENDOSCOPY AND BARIUM RADIOGRAPHY In patients with upper G.I. bleeding
of sufficient magnitude to affect vital signs or necessitate transfusion, urgent endoscopy is the
procedure of choice. Endoscopy is more accurate than barium radiographs1 , and endoscopic
findings, not visible on radiographic studies such as appearance of ulcer base, help determine
subsequent management strategy. Endoscopy should be performed when the haemodynamic
status improves (unless the patient is bleeding massively and not responding to resuscitative
measures) and adequate support personnel are present. The role of gastric lavage in the
management of patient with upper G.I. bleeds is controversial. Although there is no evidence
that lavage help stop bleeding, it may be helpful in cleaning stomach before urgent endoscopy.
Hemostasis is not improved with the use of iced saline solution. 2 Almost all patients with upper

2. G.I. bleeding should undergo endoscopy for several reasons: 1. Endoscopy is more sensitive
than UGI barium radiograph and permits mucosal biopsy as well as hemostatic therapy. 2. It
visualizes the bleeding site or stigmata of recent hemorrhage, thus
6. 6. providing important prognostic information. 3. Barium studies interfere with subsequent
diagnostic tests as endoscopy or angiography. ANGIOGRAPHY The need for angiography as a
diagnostic tool in acute upper G.I. bleed is rare, because endoscopy provides direct mucosal
inspection. On occasion when bleeding is so massive that endoscopy cannot be performed
safely or satisfactorily and surgery is contra-indicated, selective mesenteric angiography
localizes the site of bleeding is above 75% of such patients, after angiographically delivered
therapy may be applied. Blood loss must be about 5 ml/min for extravagation of contrast to be
seen on radiography3 . Radionucleotide imaging is rarely used in Upper G.I. bleed. If bleeding
has cured, radionucleotide study is not helpful, if bleeding is copious, endoscopy or angiography
is a better test. Furthermore, uptake in liver and spleen may obscure bleeding sites in upper G.I.
tract. SPECIFIC BLEEDING LESIONS AND THEIR TREATMENT. PEPTIC ULCERS Peptic
ulcer is the most common cause of hematemesis accounting for about 50% of all cases. Patient
more commonly bleed from duodenal ulcer than from gastric ulcers. Rates of mortality from
bleeding ulcer has remained at about 6% to 12% over last 3 decades5 . The three primary
pathogenic mechanisms for ulcers are acid, H. pylori and NSAIDS. Of these factors only
NSAIDS appear to be an
7. 7. important risk factor for the development of bleeding ulcers. Prognostic factors and Initial
Management Most ulcers cease bleeding spontaneously and patient have an uneventful
recovery; no specific intervention is required. A minority of patients have poorer prognosis.
Various clinical and endoscopic characteristics can be used to help determine which patients are
at highest risk. Clinical features denoting poor prognosis6 : § hemodynamic instability § number
of unit of blood transfused § presence of red blood in the vomitus and stool Characteristics of the
ulcer at endoscopy probably provides the best prognostic information. § Increasing ulcer size (>
1 cm) with endoscopic hemostasis less successful in ulcer > 2 cm7 § Appearance of ulcer base
§ Clean base § Stigmata of recent bleed. § Active bleeding Patients with clean base ulcers may
be discharged within first 24 hrs of endoscopy after stabilization and institution of medical
therapy.
8. 8. Patients with flat spots and adherent clots have higher incidence of re- bleed and they have to
be observed for longer period. Patients with a non-bleeding visible vessel or active bleeding are
at a much higher risk for further bleeding (43% and 55%). Approximately one third require urgent
surgery for re-bleeding if treated conservatively. These patients clearly benefit from endoscopic
hemostatic therapy. Patients without clean-based ulcers should remain in the hospital for a
minimum of 3 days, because most episodes of recurrent bleeding occur within 3 days.
Pharmacological Therapy Endoscopic finding. Prevalence Re-bleed Surgery Mortality Clean
base 42% 5% 0.5% 2% Flat spot 20% 10% 6% 3% Clot 17% 22% 10% 70% Non bleeding
visible vessel 17% 43% 34% 11% Active bleeding 18% 53% 35% 11%
9. 9. Many agents including vasopressors, secretin, H2 receptor antagonist, proton pump inhibitors,
antifibrinolytics, prostaglandins, natural somatostatin and somatostatin analogs have been used
to stop active ulcer bleeding. Although a few studies have suggested a benefit, most have found
no benefit in stopping active ulcer bleeding or preventing early re-bleeding, and at present no
medical therapy can be recommended for acute treatment of bleeding from ulcers. It is
reasonable at present, however to initiate anti-secretory therapy to promote healing, once a
diagnosis of ulcer has been made. Endoscopic hemostatic therapy Endoscopic hemostatic
therapy should be used in patients with high risk for persistent or recurrent bleeding and death
i.e. those who have clinical or endoscopic features suggestive of high risk. Thermal Methods
Lasers Clinical trials of Argon and Nd:YAG laser have yielded variable
10. 10. results but a meta-analysis of prospective controlled trials reveals significantly less need for
urgent surgery and lower mortality with laser therapy than with no endoscopic therapy. 8
Monopolar Electrocoagulation Although these trials have shown benefit in patients with non
bleeding visible vessels or active bleeding, monopolar electrocoagulation is not recommended

3. because of the risk of significant tissue injury. Bipolar or Multipolar Electrocoagulation The
decreased distance between electrodes with bipolar electrocoagulation causes less tissue injury
without decreasing hemostatic efficiency. Prospective randomized trials have shown that BPEC
decreases further re-bleeding, Shorter hospital stay, decreases the number of blood transfusion
and number of patients requiring emergency surgery. 9, 10 Heater Probe The heater probe has
similar theoretical advantages as those for BPEC. The heater probe produces thermal energy
directly for application to bleeding lesions. Several investigations have reported significant
benefit with the heater probe in prospective controlled trials for patients with active bleeding and
non-bleeding invisible vessels. Injection Therapy
11. 11. Injection of epinephrine (1:10000), absolute ethanol, other sclerosing agents (e.g.
polidocanol, sodium tetradecyl sulfate, 50% dextrose), saline solution and water into the base of
a bleeding ulcer, all have been reported to decrease further bleeding. Studies’ reporting that
injection with saline or water provides effective hemostasis suggests that tamponade may be the
most important single factor in the control of bleeding, 11 whether the additional effect of
epinephrine, such as vasoconstriction, also play a role is uncertain. Results of multiple
randomized controlled trials indicate that injection therapy provides significant benefit but it is
unclear whether any agent or combination of agents is best for injection therapy. Other
endoscopic hemostatic Therapies § Microwave coagulation was as effective as bipolar
electrocoagulation and heater probe; and superior to injection therapy in animal models. § Fibrin
glue has been reported to be effective in the treatment of bleeding ulcers in controlled trials. §
Results of uncontrolled studies suggest that endoscopic application of a metallic chip
(Hemochip) may be used successfully to treat patients with bleeding ulcers. Studies comparing
the various endoscopic modalities of hemostasis, viz. bipolar electrocoagulation, heater probe,
laser and injection therapy have demonstrated no significant differences among the four
treatment modalities. 12 RECURRENT BLEEDING AFTER HEMOSTATIC THERAPY
12. 12. Approximately 20% patients with active bleeding or non-bleeding visible vessels, re-bleed
after treatment with bipolar electrocoagulation, heater probe, or injection. 13 Repeat endoscopic
therapy for re-bleeding should achieve permanent hemostasis in 50% of the patients with re-
bleed, but the other half, just over 10% of all patients originally treated with endoscopic therapy,
still require surgery for treatment of bleeding. 13 On balance, offering a second endoscopic
treatment is justified. If it is unsuccessful, patient should be sent for surgical (or angiographic)
therapy. Avoiding surgery, if possible, is desirable today, in view of the importance of H. pylori.
Tiding a patient over without surgery gives the opportunity for eradication of the organism cure of
the ulcer disease, and prevention of recurrent bleeding. ANGIOGRAPHIC THERAPY
Angiographic therapy is seldom used in the treatment of bleeding ulcers and should be reserved
for patients with severe persistent bleeding in whom endoscopic hemostatic therapy is
unsuccessful or unavailable and for whom surgery poses a very high risk. Intra-arterial infusion
of vasopressin may stop ulcer bleeding in upto 50% of cases. Results of uncontrolled studies
suggest that occlusion the bleeding artery with embolic agents such as absorbable gelatin
sponge (Gelfoam), tissue adhesives, autologous clot, or detachable mechanical occlusion
devices may control bleeding identified angiographically in approximately 75% to 80% of cases,
although over half may re-bleed. 14
13. 13. SURGICAL THERAPY Patients with severe ongoing ulcer bleeding in whom endoscopic
therapy has failed or is unavailable should undergo urgent surgery, although controlled trials
have not documented the utility of this approach. A prospective comparison of immediate
operation, selective surgery (based on age and response to transfusion) and no surgery for
patients with massive upper GI bleeding between 1953 and 1963 showed no difference in
mortality rates among the patients with confirmed ulcer disease; immediate surgery, 13/99
(13%); selective surgery 10/86 (12%); and no surgery, 7/51 (14%).15 A more recent randomized
trial revealed no significant difference in mortality rates between early surgery applied for
minimal criteria (e.g. the presence of stigmata of recent episode of re-bleeding) and a policy of
delay that required clinical evidence of severe, persistent bleeding before operating16 . Three
(4%) of 71 patients in the early surgery group died, in comparison with 7(10%) of the 71 patients

4. in the delayed surgery group. All deaths were in patients over 60 years of age, and subgroup
analysis indicated significant benefit of early surgery for patients with gastric ulcers.
HEMORRHAGIC AND EROSIVE GASTROPATHY (“GASTRITIS”) Hemorrhagic and erosive
gastritis refer to endoscopically visualized lesions (subepithelial hemorrhages and erosions) that
may cause bleeding. Because no definite association between these gross abnormalities and
histologic gastritis exists, they should not be labeled
14. 14. gastritis but described more accurately as subepithelial hemorrhages and erosions. Gastritis
frequently has been diagnosed as a cause of upper GI hemorrhage. Gastritis is a relatively
unusual cause of serious upper GI hemorrhage. A prospective endoscopic evaluation of 445
patients at Los Angles Country – USC Medical center revealed that hemorrhagic or erosive
gastritis was diagnosed as the cause of major upper GI hemorrhage in only 3% of cases and
bleeding never was life threatening or necessitated large transfusions. Antacids, H2 receptor
antagonists, and sucralfate appear to decrease bleeding from stress related gastric lesions, as
manifested by occult or overt blood in the nasogastric aspirate. A meta analysis of prophylaxis
for stress induced ulcers indicated that H2 receptor antagonists, antacids, or sucralfate led to a
significant reduction in clinically significant bleeding (defined as hemodynamic changes or a drop
in hemoglobin) plus transfusion. However, no evidence indicates that prophylactic therapy
decreases mortality rates. Endoscopic therapy is unlikely to be helpful or needed in cases of
bleeding subepithelial hemorrhages or erosions because of their diffuse, superficial nature,
although such therapy can be attempted if a small number of isolated erosions appear to be the
sites of bleeding. Selective intra-arterial infusion of vasopressin has been reported to halt
bleeding in 75% to 80% of patients with bleeding from gastritis, whereas trans-catheter
embolization usually is less successful. Surgical therapy seldom is used
15. 15. now for gastritis bleeding. PROLAPSE GASTROPATHY Prolapse gastropathy is a cause of
mild upper GI hemorrhage often seen in alcoholic patients that may be confused with
hemorrhagic gastritis. This syndrome is characterized endoscopically by a focal, well-
demarcated area of subepithelial hemorrhage, sometimes with central erosions, just distal to the
gastroesophageal junction and develops when the gastric mucosa forcefully prolapses into the
distal esophagus. Patients typically have a history of retching preceding hematemesis. In a
prospective evaluation of alcoholic patients undergoing endoscopy for upper GIhemorrhage 5%
had prolapse gastropathy. NEOPLASM Neoplasms of the GI tract often produce chronic occult
bleeding but are unusual causes of profuse acute GI bleeding. Treatment of bleeding neoplasms
usually is aimed at treatment of the neoplasm itself but palliative therapy to stop bleeding may
also be necessary. Surgical resection is generally the first choice if such a procedure is feasible
and the patient is a candidate for surgery. If not, endoscopic therapy (injection) angiographic
therapy or radiation therapy may be tried. HEMOBILIA, HEMOSUCCUS PANCREATICUS
Causes of communication between the vascular and biliary system includes trauma,, liver
biopsy, gallstones, hepatic artery or portal vein aneurysms, ascariasis, hepatic abscess and
neoplasms. Patients classically present with upper GI bleeding accompanied by biliary colic and
16. 16. jaundice. The diagnosis is made endoscopically from the appearance of blood coming from
the ampulla of Vater and/or by angiography. Arterial embolization is the treatment of choice;
hepatic artery irrigation is employed for patients in whom angiographic therapy fails. AORTO-
ENTERIC FISTULAS GI hemorrhage can result from fistulas between any major vascular
structure and the GI tract, but most involve the aorta. Thoracic aortic ancurysms esophageal
foreign bodies, or neoplasms cause aortoesophageal fistulas. Aortoenteric fistulas may involve
any part of the GI tract but about 75% communicate with the duodenum, usually the third portion.
A primary aortoenteric fistula is a rare cause of bleeding that originates from an abdominal aortic
aneurysm, whereas secondary aortoenteric fistulas are more common, developing an average of
3 to 5 years after abdominal aortic re-constructive surgery in 0.4 to 2.4% of patients. Surgery is
mandatory in patients with suspected or confirmed aortoenteric fistulas; the diagnosis may be
established preoperatively in as few as one third of patients. ESOPHAGITIS AND HIATAL
HERNIAS Major hemorrhage from esophagitis is rare, accounting for 2% of patients who
presented with clinically significant upper GI bleeding in one study. Other series have reported

5. esophagitis as a cause of upper GI hemorrhage in 0% to 8% of cases and hiatal hernia in 0% to
12%.
17. 17. MALLORY-WEISS TEARS Mallory-Weiss tears are lacerations in the region of the
gastroesophageal junction that account for about 5% to 15% of cases of upper GI hemorrhage.
The classic history is one of vomiting, retching, or coughing preceding hematemesis in alcoholic
patients. Most Mallory-Weiss tears are located on the gastric side of the gastroesophageal
junction, although 10% to 20% may involve the esophagus. In 10% to 20% of patients two or
more tears are identified. Bleeding from Mallory-Weiss tears stops spontaneously without
specific therapy in 80% to 90% of patients and re- bleeding in this group is uncommon, occurring
in 0% to 5%.17 Thus most patients require only supportive care. Patients without active bleeding
at endoscopy who have been adequately resuscitated and have no other medical problems
necessitating hospitalization may be discharged within 24 hr of admission. Endoscopic therapy
with bipolar electrocoagulation was effective in stopping the active bleeding of Mallory-Weiss
tears in a prospective controlled trial18 . In rare instances, operative therapy with oversewing of
the tear may be required. BLEEDING AS A CONSEQUENCE OF PORTAL HYPERTENSION
VARICEAL § Esophageal varices § Gastric varices § Duodenal varices
18. 18. NON-VARICEAL § Post sclerotherapy ulcers § Portal hypertensive gastropathy Portal
hypertension is responsible for several sources of GI bleeding, including esophageal varices,
gastric varices, ectopic varices in the small and large intestines, and portal hypertensive
gastropathy and enterocolopathy. Portal hypertensive gastropathy rarely causes severe acute
bleeding but is reported to be responsible for 10 to 20% of all bleeding episodes in patients with
portal hypertension. I. Esophageal varices All patients presenting with upper GI bleeding with a
history, physical examination, or laboratory findings that suggest the possibility of liver disease
should undergo early upper endoscopy to determine whether varices are present. Clinical,
biochemical and endoscopic parameters are used to estimate the risk of rebleeding and
expected survival. The risk of variceal bleed is maximum immediately following an acute bleed
and diminishes with time. Clinical risk factors for late rebleeding include overt signs of hepatic
decompensation, hepatocellular carcinoma, and continued use of alcohol. Endoscopic stigmata
of hemorrhage are important signs to assess recent variceal bleeding and to estimate the risk of
rebleeding.19 These endoscopic signs include variceal size and shape (large, nodular), red wale
marks, hematocystic spots, veins on
19. 19. veins, a white nipple, and variceal color tone and red color sign on video endoscopic image
processing. The short-term risk of rebleeding remains high until esophageal varices are
obliterated. The risk of rebleeding can be substantially reduced by follow-up endoscopic
sclerotherapy sessions to obliterate residual varices. 20 II. Gastric and duodenal varices Gastric
varices develop late in the course of cirrhosis. Primary gastric varies develop de novo from
systemic portal hypertension and are usually found in conjunction with esophageal varices
(gastroesophageal varices). Secondary gastric varices may develop after endoscopic obliteration
of esophageal varices. Isolated gastric varices (found in the absence of esophageal varices) can
also develop in the absence of cirrhosis as the result of segmental portal hypertension, owing to
splenic vein thrombosis caused by pancreatic carcinoma, pancreatitis, or hypercoagulable state.
Splenectomy is a curative procedure for isolated gastric varices caused by splenic vein
thrombosis unrelated to malignancy. Duodenal varices are a rare but important cause of massive
UGI bleeding in the cirrhotic patient. Duodenal varices usually develop as a late, secondary
complication following endoscopic obliteration of esophageal varices or underlying hepatocellular
carcinoma. Bleeding from duodenal varices is associated with high mortality rates.
ENDOSCOPIC INJECTION SCLERO-THERAPY TECHNIQUE
20. 20. The authors endoscopic hemostasis technique for esophageal variceal bleeding is to perform
intravariceal injections using the free hand method using ethanol as a sclerosant. Efficacy for
control of acute bleeding is 100% and the stricture rate is only 7% with emergency sclerotherapy.
In a CURE experiment, three session of sclerotherapy were required to obliterate esophageal
varices. In the case of active bleeding from either esophageal or gastric varices, the authors
perform initial injections distal, proximal, and adjacent to the bleeding site. Once active bleeding

6. is controlled, all other non-bleeding distal esophageal varices are injected starting at the GE
junction, then 2.5 and 5.0 cm above the GE junction. Diagnosis and treatment of bleeding fundic
varices must be performed in the retroflexed position. This can be difficult with a stiff therapeutic
endoscope in an actively bleeding patient. The current CURE endoscopic injection sclerotherapy
protocol for gastric variceal bleeding includes (1) combined sclerosing agents with different
mechanism of action, (2) epinephrine solution to minimize back bleeding from injection sites and
to facilitate hemostasis, and (3) aggressive acid suppression with high dose omeprazole to
accelerate ulcer healing. 21 RESULTS OF INJECTION SCLEROTHERAPY Numerous studies
have confirmed the long-term efficacy and safety of endoscopic injection sclerotherapy for acute
hemostasis of bleeding esophageal varices and for prevention of rebuilding. The benefits of
endoscopic injection sclerotherapy of varices include wide availability, low
21. 21. cost, ease and rapidity of use, and outpatient therapy for elective (obliteration) treatment. 21
The authors believe that the advantages of endoscopic injection sclerotherapy over other
modalities for treatment of esophago-gastric varices far outweigh the disadvantages. Emergency
sclerotherapy has been shown to improve short-term survival compare to conventional medical
therapy. The few drawbacks of endoscopic injection sclerotherapy relate to potential
complications of treatment. These complications include local effects (ulceration, bleeding,
stricture, and perforation) as well as systemic effects (bacteremia, sepsis, and pleural effusion).
Emergency Sclerotherapy Endoscopic sclerotherapy has also been shown to be equal or
superior to other non-endoscopic modalities for controlling active bleeding and preventing
variceal rebleeding, including intravenous vasopressin with or without nitroglycerin, somatostatin,
beta– blockers, balloon tamponade, portosystemic shunting, devascular- ization and non
decompressive shunting, and esophageal transection. Elective Sclerotherapy Following acute
hemostasis, elective or serial sclerotherapy is performed at 1- to 3-week intervals to obliterate
remaining varices to prevent bleeding. The risk of rebleeding from esophageal varices varies
from 50% to 80% within 6 to 12 months of the initial bleed if
22. 22. no intervention is undertaken. 22 Prophylactic Sclerotherapy Prophylactic sclerotherapy is
undertaken before any bleeding episodes to prevent initial variceal bleeding. The majority of
randomized, controlled trials comparing prophylactic sclerotherapy to medical therapy have not
demonstrated benefit in terms of preventing first bleeding episode.23,24 Therefore, prophylactic
sclerotherapy should not be performed outside of a study protocol. VARICEAL LIGATION:
Variceal band ligation was developed in the mid-1980s by Stiegmann to treat esophageal
varices endoscopically. The technique is similar in principle to hemorrhoid banding whereby the
varix is drawn into the banding device, and a rubber band is placed around the varix base. The
advantage of band ligation over injection sclerotherapy include fewer local and systemic side
effects, lower rebleeding rates, and fewer endoscopic treatment sessions to obliterate varices.
25 In a meta analysis of seven randomized trials comparing endoscopic ligation with
sclerotherapy for the treatment of patients with bleeding esophageal varices, ligation was
superior to injection sclerotherapy because of lower rates of rebleeding, mortality, and
complications. 26 CYNOACRYLATE Cynoacrylate has been used successfully for treating
actively bleeding
23. 23. esophageal, gastric, and duodenal varices.27 Cynoacrylate is a unique hydrophilic tissue
adhesive that spontaneously polymerizes immediately on contact with water. Therefore, a lipid
based contrast agent (Lipiodol) is used to suspend and chase the cynoacrylate to minimize
polymerization within the injection syringe and endoscope. A single intravariceal injection of
cynoacrylate can achieve immediate variceal hemostasis by mechanical plugging of the bleeding
site with tissue adhesive. It has also been used to obliterate gastric varices. 28 NON-
ENDOSCOPIC THERAPY OF VARICEAL BLEEDING: Mechanical tamponade Esophageal or
gastric balloon tamponade tubes have been used effectively for controlling active esophageal
and gastric variceal bleeding. In a series, initial hemostasis within the first 4 hours was 60%, and
bleeding was controlled over a 24-hour period in 60% patients, these values were not
significantly different to somatostatin infusion. 29 Pharmacological Therapy Pharmacological
agents such as vasopressin, somatostatin, octreotide, and terlipressin decrease portal pressure

7. via constriction of the splanchanic vasculature. These agents are used as a temporary measure
in patients with continued variceal bleeding despite endoscopic therapy. 30 Selective
splanchanic vasoconstrictors such as somatostatin or octreotide, glypressin, and
24. 24. terlipressin are at-least as effective as vasopressin for controlling variceal bleeding and have
fewer side effects. In a randomized trial of 80 consecutive patients, continuos somatostatin
infusion was shown to be as effective as injection sclerotherapy for control of active bleeding.
There was no significant difference between the two treatments in initial or long-term control of
bleeding. Mortality was not significantly different between the two groups, and complications
were minor and less frequent in the somatostatin group. 31 Octreotide is a synthetic
somatostatin analog that has a longer plasma half-life than somatostatin and thus may be
administered subcutaneously as well as by continuos intravenous infusion. In one study,
bleeding was controlled in 88% and 54% of the patients treated with octreotide and vasopressin.
Complete control of bleeding after 24 hours of drug infusion was achieved in 63% patients
receiving octreotide and in 46% patients receiving vasopressin. 32 SURGERY Surgical therapies
for bleeding varices include portosystemic shunts/ esophageal transection and
devascularisation, and liver transplantation. These techniques are associated with high morbidity
and mortality and should be performed only by highly experienced surgeons. Portosystemic
shunting may decrease the risk of rebleeding; however, encephalopathy may worsen Major
causes of upper G.I Bleed
25. 25. Duodenal ulcer 24.3 % Erosive duodenitis 5.8 % Gastric erosions 23.4 % Neoplasm 2.9 %
Gastric ulcers 21.3 % Stomal ulcer 1.8 % Varices 10.3 % Esophageal ulcer 1.7 % Mallory weiss
tear 7.2% Osler-Rendu-Weber telengiactasia 0.5 % Esophagitis 6.3% Others 6.3 %