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Upper Gastrointestinal BleedingAcute gastrointestinal (GI) bleeding is a potentially life-threatening

abdominal emergency that remains a common cause of hospitalization. Theincidence of upper gastrointestinal bleeding (UGIB) is approximately 100 casesper 100,000 population per year (Fallah, 2000). Bleeding from the upper GI tract is

approximately 4 times as common as bleeding from the lower GI tract and is amajor cause of morbidity and mortality. Mortality rates from UGIB are 6-10%overall (Fallah, 2000).

An aging patient population with an increasing prevalence of associatedmedical comorbidities has kept the mortality figures largely unchanged for the past30 years, despite technologic advances in endoscopy and other minimallyinvasive procedures (Peter, 1999). The use of various endoscopic techniques,medical therapies, and visceral angiography has progressively diminished the roleof surgery in the emergent management of UGIB. Nevertheless, operative

intervention still represents the most definitive intervention and remains the finaltherapeutic option for many bleeding lesions of the upper GI tract. Of patients whodevelop UGIB, 3-15% require a surgical procedure (Peter, 1999). With theevolution of laparoscopy, surgeons may have a new dimension to themanagement of GI tract bleeding by developing new techniques performedthrough smaller incisions.

Clinical: The history and physical examination provide crucial informationfor the initial evaluation of a patient presenting with a GI tract hemorrhage. Thehistory findings can be extremely helpful in determining the location of the GIhemorrhage. Alcohol abuse or a history of cirrhosis should elicit consideration ofportal gastropathy or esophageal varices as sources for the bleeding. A history ofrecent nonsteroidal anti-inflammatory drug (NSAID) abuse should elicit concernabout bleeding from a gastric ulcer (Stabile, 2000).

Differential diagnoses for UGIBo Gastric ulcero Duodenal ulcero Esophageal variceso Gastric variceso Mallory-Weiss tearo Esophagitiso Neoplasmo Hemorrhagic gastritiso Dieulafoy lesiono Angiodysplasiao Hemobiliao Pancreatic pseudocysto Pancreatic pseudoaneurysmo Aortoenteric fistula

UGIB is defined as bleeding derived from a source proximal to the ligamentof Treitz. Hematemesis and melena are the most common presentations of acuteUGIB, and patients may present with both symptoms. Occasionally, a brisk UGIB

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manifests as hematochezia. A recent meta-analysis documented theincidence of presenting symptoms in patients with UGIB as follows (Peter, 1999):

History and physical examination findings in acute UGIB at presentationo Hematemesis - 40-50%o Melena - 70-80%o Hematochezia - 15-20%o Either hematochezia or melena - 90-98%o Syncope - 14.4%o Presyncope - 43.2%o Symptoms 30 days prior to admission - No percentage availableo Dyspepsia - 18%o Epigastric pain - 41%o Heartburn - 21%o Diffuse abdominal pain - 10%o Dysphagia - 5%o Weight loss - 12%o Jaundice - 5.2%

As indicated, hematemesis is observed in 40-55% of patients, includingpatients with coffee-ground emesis. Melena is documented in approximately 70-80% of patients, and hematochezia is documented in approximately 15-20%.These clinical signs may also be indicators of the potential source of the GIbleeding, as noted in the following table (Peter, 1999).

Table 1. Probable Source of GI Bleeding Within the Gut

ClinicalIndicator

Probability ofUpper GISource

Probability ofLower GISource

Hematemesis Almost certain Rare

Melena Probable Possible

Hematochezia Possible Probable

Blood-streakedstool Rare Almost certain

Occult blood instool

Possible Possible

Some prognostic indicators that can be detected from the history andphysical examination findings are helpful for developing a scoring system toassess the risk of poor outcome with UGIB. These factors include age, heart rate,systolic blood pressure (SBP) upon admission, orthostatic changes in blood

pressure or pulse rate, and the use of any anticoagulants. Assessing the patientfor hemodynamic instability and clinical signs of poor perfusion is important earlyin the initial evaluation to properly triage patients with massive hemorrhage tointensive care unit (ICU) settings. Worrisome clinical signs and symptoms ofhemodynamic compromise include tachycardia of more than 100 beats per minute

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(bpm), systolic blood pressure of less than 90 mm Hg, cool extremities,syncope, and other obvious signs of shock such as ongoing brisk hematemesis ormaroon or bright-red stools, which requires rapid blood transfusion.

Age older than 60 years is an independent marker for a poor outcome(Peter, 1999). The mortality rate increases to 12-25% in those older than 60 yearscompared to a mortality rate of less than 10% for patients younger than 60 years(Peter, 1999). The American Society for Gastrointestinal Endoscopy (ASGE)grouped patients with UGIB according to age and correlated age category to riskof mortality. The ASGE found a mortality rate of 3.3% for patients aged 21-31years, a rate of 10.1% for those aged 41-50 years, and a rate of 14.4% for thoseaged 71-80 years (Peter, 1999).

Patients who present in hemorrhagic shock have an increased mortality rateof up to 30%. Hemorrhage may be classified based on the amount of blood loss,as noted in the following table (American College of Surgeons Committee onTrauma, 1997).

Table 2. Estimated Fluid and Blood Losses in Shock

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 >120 >140

BloodPressure

Normal Normal Decreased Decreased

RespiratoryRate

Normal orIncreased

Decreased Decreased Decreased

Urine Output,

mL/h 14-20 20-30 30-40 >35

CNS/MentalStatus

Slightlyanxious

Mildlyanxious

Anxious,confused

Confused,lethargic

FluidReplacement,3-for-1 rule

Crystalloid CrystalloidCrystalloidand blood

Crystalloid

and blood

This classification scheme aids in understanding the clinical manifestations

of hemorrhagic shock. In early class 1 shock, the patient may have normal vitalsigns, even with a 15% loss of total blood volume. As the percentage of bloodvolume loss increases, pertinent clinical signs, symptoms, and findings becomemore apparent.

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Although early cardiovascular changes occur as blood loss continues,urine output, as a sign of end organ renal perfusion, is only mildly affected untilclass 3 hemorrhage has occurred. Bornman et al correlated the presence of shock(defined as pulse rate >100 bpm or SBP


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A fibrinogen level of less than 100 mg/dL also indicatesadvanced liver disease with extremely poor synthetic function.

o Liver function tests: Liver function tests are also needed to calculatethe Child-Pugh score. Elevated aminotransferase levels are a result ofhepatocellular injury. Increased levels of alkaline phosphatase andgamma-glutamyltranspeptidase are indicative of cholestatic liverdisease.

o Plasma fibrinogen levelo Serum electrolyte values

Patients generally require blood transfusions because of hypoperfusion andhypovolemia. Patients with significant comorbid conditions (eg, advancedcardiovascular disease) should receive blood transfusions to maintainmyocardial oxygen delivery to avoid myocardial ischemia. One of the criteriaused to determine the need for surgical intervention is the number of units oftransfused blood required to resuscitate the patient. The more units

required, the higher the mortality rate (Larson, 1986). Operative interventionis indicated once the blood transfusion number reaches more than 5 units,as noted in the following table (Larson, 1986).Table 3. Effect of Number of Packed Erythrocyte Transfusions on Need for

Surgery and Mortality from UGIB

Number of UnitsTransfused

Need for Surgery, %

MortalityRate, %

0 4 4

1-3 6 14

4-5 17 28

>5 57 43

Medical therapy:Initial management

Resuscitation of a hemodynamically unstable patient begins with assessingand addressing the ABCs (ie, airway, breathing, circulation) of initial management.Patients presenting with severe blood loss and hemorrhagic shock present withmental status changes and confusion. In such circumstances, patients cannotprotect their airway, especially when hematemesis is present. In these cases,patients are at increased risk for aspiration, which is a potentially avoidablecomplication that can significantly affect morbidity and mortality. This situationmust be recognized early, and patients must be electively, not emergently,intubated in a controlled setting using cricoid pressure.

Once the airway is secured, the next step in evaluation is assessing thepatient's circulation. Intravenous access must be obtained. Bilateral 16-gauge(minimum) upper extremity peripheral intravenous lines are adequate for volumeresuscitative efforts. Poiseuille law states that the rate of flow through a tube isproportional to the fourth power of the radius of the cannula and is inversely

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related to its length (Corson, 2001). Thus, short, large-bore peripheralintravenous lines are adequate for rapid fluid infusion. A rough guideline for thetotal 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. Thisrestores the lost plasma volume. Patients with severe coexisting medicalillnesses, such as cardiovascular and pulmonary diseases, may requirepulmonary artery catheter insertion to closely monitor hemodynamic cardiacperformance profiles during the early resuscitative phase.

Once the ABCs have been addressed, assess the patient's response toresuscitation based on evidence of end organ perfusion and oxygen delivery. Aninteresting study published by Kaplan et al evaluated whether the physicalexamination findings alone or in combination with biochemical markers (arteriallactate levels) can help accurately diagnose hypoperfusion. Their study revealedthat skin temperature upon physical examination in combination with serumbicarbonate levels correlated well with the level of systemic perfusion. The

patients identified as being hypoperfused based on clinical parameters wereconfirmed by following the serum lactate or mixed venous oxygen saturation(SvO2) and cardiac index. Pulmonary artery catheters may be helpful to guidetherapy. Foley catheter placement is mandatory to allow a continuous evaluationof the urinary output as a guide to renal perfusion. This labor-intensivemanagement should be performed only in an ICU setting.

Once the maneuvers to resuscitate are underway, insert a nasogastric tube(NGT) and perform an aspirate and lavage procedure. This should be the firstprocedure 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 ofbleeding may still be possible. In a retrospective review of 1190 patients, Luk et alfound that positive NGT aspirate findings were 93% predictive of an upper GIsource of bleeding.

The ASGE performed a study comparing NGT aspirate findings to theendoscopic findings of the bleeding source (Silverstein, 1981). This studyrevealed that 15.9% of patients with a clear NGT aspirate, 29.9% of patients withcoffee-ground aspirate, and 48.2% of patients with red blood aspirate were

documented as having an active upper GI source of bleeding at the time ofendoscopy. Based on data collected by the ASGE, realize that an NGT aspiratefinding can be negative even in the setting of a large duodenal bleeding ulcer. Arecent study correlated mortality with the color of the fluid from the NGT aspirateand the color of the stool (Kupfer, 2000). As shown in the following table, the colorof the NGT aspirate can be a prognostic indicator.

Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool onUGIB Mortality Rate

Nasogastric

Aspirate Color

Stool

Color

Mortality

Rate, %

ClearBrown orred

6

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Coffee-groundBrown orblack

8.2

Red 19.1

Red blood Black 12.3

Brown 19.4

Red 28.7

Surgical therapy:EndoscopyThe development of endoscopy has provided clinicians with the ability for

both diagnostic and therapeutic approaches to bleeding from the GI tract.Endoscopic examination of the upper GI tract provides useful informationregarding the source and site of bleeding (Silverstein, 1981).

Endoscopic findings and the incidence rate in patients with UGIBo Duodenal ulcer - 24.3%o Gastric erosion - 23.4%o Gastric ulcer - 21.3%o Esophageal varices - 10.3%o Mallory-Weiss tear - 7.2%o Esophagitis - 6.3%o Duodenitis - 5.8%o Neoplasm - 2.9%o Stomal (marginal) ulcer - 1.8%o Esophageal ulcer - 1.7%o Other/miscellaneous - 6.8%

Endoscopy should be performed immediately after endotracheal intubation(if indicated), hemodynamic stabilization, and adequate monitoring in an ICUsetting have been achieved. Studies performed in the 1970s and early 1980squestioned the role for emergent endoscopy because no significant improvementin patient outcomes was noted (Peter, 1999). These studies were performed

during an era before the more advanced therapeutic maneuvers of endoscopywere developed.

Since the late 1980s, endoscopic techniques to achieve hemostasis forbleeding ulcers and varices have continued to evolve. Endoscopy is now themethod of choice for controlling active ulcer hemorrhage. Over the last 10 years,several randomized clinical trials and meta-analyses have demonstrated andsupported that early endoscopic hemostatic therapy significantly reduces rates ofrecurrent bleeding, need for emergent surgery, and mortality in patients with acutenonvariceal UGIB.

Cooper et al studied the effectiveness of performing an early endoscopywithin the first 24 hours of an acute UGIB episode (Cooper, 1999). Earlyendoscopy was associated with reductions in the length of hospital stay, rate ofrecurrent bleeding, and need for emergent surgical intervention. In a retrospectivereview involving more than 30,000 cases, Yavorski et al showed that the mortality

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rates were more than twice as high for those who did not undergo an earlyendoscopic procedure than those who did undergo an early endoscopic procedure(11.1% vs 5.2%). From 1981-1991, the rate of performing endoscopic proceduresin the acute management of UGIB increased from 66.7% to 94%.

The endoscopic techniques used to achieve hemostasis have continued toevolve over the last 15 years as newer, more effective therapies have beendeveloped.

Various techniques currently available for achieving hemostasis (Stabile,2000)

o Injection of vasoactive agentso Injection of sclerosing agentso Bipolar electrocoagulationo Band ligationo Thermal probe coagulationo Constant probe pressure tamponadeo Argon plasma coagulatoro Laser photocoagulationo Rubber band ligationo Application of hemostatic materials, including biologic glue

The 3 most popular methods of hemostasis are injection therapy, coaptivecoagulation, and laser phototherapy.

Injection therapy involves the use of several different solutions injected intoand around the bleeding lesion. The different solutions available for injection areepinephrine, sclerosants, and clot-producing materials such as fibrin glue. The

epinephrine used for injection is diluted (1:10,000) and injected as 0.5- to 1-mLaliquots. Epinephrine is a vasoactive agent that works by inducingvasoconstriction and decreasing blood flow to the area. This allows for increasedplatelet function and clot formation to attain hemostasis. Debate continues overwhether the hemostatic effect of epinephrine is due to the induced vesselvasoconstriction and subsequent platelet aggregation or to the tamponade effectproduced by injecting the volume of drug into the tissue surrounding the bleedinglesion.

Injecting a volume of sterile isotonic sodium chloride solution and providing a

tamponade effect also leads to hemostasis, although not as effectively asepinephrine (Fallah, 2000). Although the injected epinephrine is absorbed into thesystemic circulation, this does not appear to have any adverse effects onhemodynamic status. The sclerosant solutions used today include ethanol,polidocanol, and sodium tetradecyl sulfate.

The sclerosants create hemostasis by inducing thrombosis, tissue necrosis,and inflammation at the site of injection. When large volumes are injected, thearea of tissue necrosis can produce an increased risk of local complications suchas perforation. Combining the various agents into a single injection has not been

shown to be more beneficial than single-agent therapy alone (Fallah, 2000).Combining epinephrine injections with human thrombin (600-1000 IU) reduces therisk of bleeding (Fallah, 2000). The use of fibrin glue has been shown to besuccessful, with results similar to that of epinephrine injections (Vargas, 1999).

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Coaptive coagulation uses direct pressure and thermal therapy toachieve hemostasis. Thermal therapy includes monopolar and bipolarelectrocoagulation and heater-probe application. The bleeding vessel is isolated,compressed, and tamponaded prior to coagulation therapy. By using bothmaneuvers, the depth of tissue injury is minimized. Coaptive coagulation is aseffective as injection therapy in achieving hemostasis (Fallah, 2000).

Laser phototherapy uses an Nd:YAG laser to create hemostasis bygenerating heat and direct vessel coagulation. This is a noncontact thermalmethod. It is not as effective as coaptive coagulation because it lacks the use ofcompression to create a tamponade effect (Fallah, 2000). An additional deterrentto its use is expense.

Although injection therapy and thermal therapy are highly successfulmethods to control a bleeding vessel, rebleeding still occurs in 15-20% of cases.Combining injection therapy with heater-probe coagulation can be used in anattempt to reduce the rebleeding rate in high-risk patients who have spurting

arterial bleeding observed during endoscopy. The epinephrine injection stops thebleeding by vasoconstricting the vessel, which then provides a clearer view for theendoscopist to see the lesion, to apply the heater probe to the appropriate area,and to permanently seal the vessel. Chung et al compared single-agent therapy tocombined epinephrine injection with heater-probe application. The study revealeda reduction in the incidence of rebleeding and the need for emergent surgicalintervention when using combined therapy.

The endoscopic appearance of the bleeding lesion has been used to identifypatients at high risk for recurrent bleeding (Chung, 1994). The indication for

endoscopic therapy is based on the size, site, and stigmata of recent bleeding. Anactively bleeding vessel is treated because it is a high-risk lesion with a 55% riskfor recurrent bleeding. A nonbleeding visible vessel is also a high-risk lesion thatis treated because of its 43% risk for rebleeding. Recurrent bleeding occurs mostcommonly within the first 72 hours.

Treatment of clots adherent to a lesion is based on the patient's risk factorsto withstand and survive another bleeding episode. The risk for rebleeding variesfrom 14-36%. Low-risk lesions are those that appear as flat, pigmented spots andthose that involve a clean ulcer base with no visible vessel. The risk for rebleeding

in these lesions is 10% and 5%, respectively. Endoscopic treatment of these low-risk lesions is not usually performed (Chung, 1994).

Peptic ulcer diseasePeptic ulcer disease (PUD) remains the most common cause of UGIB. In a

literature review involving more than 10,000 patients with UGIB, PUD wasresponsible for 27-40% of all bleeding episodes (Stabile, 2000). High-risk patientpopulations at risk for PUD include those with a history of alcohol abuse, chronicrenal failure, and/or NSAID use.

Duodenal ulcers are more common than gastric ulcers, but the incidence of

bleeding is identical for both. In most cases, the bleeding is caused by the erosionof an artery in the base of the ulcer. Bleeding vessels larger than 1.5 mm indiameter are associated with an increased mortality rate. Initial endoscopicattempts to maintain hemostasis have a high failure rate. In approximately 80% ofpatients, bleeding from a peptic ulcer stops spontaneously (Stabile, 2000). A

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minority of patients experience recurrent bleeding, and these cases areusually associated with risk factors for rebleeding. These factors include age olderthan 60 years, the presence of shock upon admission, coagulopathy, activepulsatile bleeding, and the presence of cardiovascular disease. Thesecircumstances are associated with a poorer prognosis and a higher mortality rate.The appearance of the ulcer at the time of endoscopy provides importantinformation regarding the risk of rebleeding.

Forrest et al were the first to classify the stigmata of hemorrhage from pepticulcers. Based on these classifications, the risk of recurrent bleeding can bepredicted. The ulcers at highest risk for rebleeding are those that involve activearterial bleeding or those with a visible, protuberant, nonbleeding vessel in thebase of the ulcer. The study not only correlated the incidence of rebleeding withthe stigmata of recent bleeding and the endoscopic appearance of an ulcer, butalso determined prognostic information regarding the need for surgery. Mortalitywas also correlated (Corson, 2001).

Table 5. Ulcer Characteristics and Correlations

UlcerCharacteristics

PrevalenceRate, %

RebleedingRate, %

SurgeryRate, %

MortalityRate, %

Clean base 42 5 0.5 2

Flat spot 20 10 6 3

Adherent clot 17 22 10 7

Visible vessel 17 43 34 11

Active bleeding 18 55 35 11

Upper GI endoscopy is the most effective diagnostic tool for PUD and hasbecome the method of choice for controlling active ulcer hemorrhage. Failure ofendoscopy to maintain hemostasis is one of the indications to initiate surgicalintervention, especially in high-risk patients. A recent randomized prospective trialinvolved 92 patients with recurrent ulcer bleeding after initial endoscopic therapy

for hemostasis who were randomized to surgery versus endoscopic re-treatment(Lau, 1999). The group randomized to another endoscopic attempt to controlbleeding was found to have decreased transfusion requirements, 30-day mortalityrates, and duration of ICU stay when compared to the surgical group.

With the exception of a patient in shock who has a life-threatening recurrenthemorrhage, this study supports attempting another trial of endoscopy to control ableeding ulcer. Regardless of the endoscopic therapy, 10-12% of patients withacute ulcerous hemorrhage require an operation as the definitive procedure tocontrol the bleeding ulcer. In most circumstances, the operation is performed

emergently, and the associated mortality rate is as high as 15-25%. Medicaltherapy used in conjunction with endoscopy involves proton pump inhibitoradministration. Proton pump inhibitors decrease rebleeding rates in patients withbleeding ulcers associated with an overlying clot or visible nonbleeding vessel inthe base of the ulcer. Consider transcatheter angiographic embolization in

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patients who are poor surgical candidates. Because of the extensivecollateral circulation of the upper GI tract, ischemic complications are rare.

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 withbleeding 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 historicallyinclude vagotomy, gastric resection, and drainage procedures. Each specific

operative option is associated with its own incidence of ulcer recurrence,postgastrectomy syndrome, and mortality. When making an intraoperative

judgment on how to best manage the bleeding ulcer, it is extremely important forthe surgeon to be aware of these differences (Corson, 2001).

Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operationsfor Duodenal Ulcer

Original OperationRecurrenceRate, %

PostgastrectomySyndrome Rate,

%

MortalityRate, %

Proximal gastric vagotomy 10 5 0.1

Truncal vagotomy and drainage 7 20-30


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Table 7. Effects of Operations for PUD on Gastric Emptying andMotility

OperationAntralInnervation

LiquidEmptying

SolidEmptying

Proximal gastricvagotomy

Preserved Fast Normal

Truncal vagotomy Divided Fast Slow

Truncal vagotomyand drainage

Divided Fast Fast

Truncal vagotomyand antrectomy

Divided Fast Fast

Proximal vagotomy abolishes gastric receptive relaxation and impairsstorage in the proximal stomach. As a result, a more rapid gastric emptying ofliquids occurs. A drainage procedure is not required because the innervation ofthe antrum and pylorus is still intact. Because of this, the gastric emptying of solidfood is not altered. The antropyloric mechanism still functions normally andcontinues to prevent duodenogastric reflux. In addition to having the same effectsas a highly selective vagotomy in the proximal stomach, a truncal vagotomy alsohas marked effects on distal gastric motor function. It weakens distal gastricperistalsis, 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 UGIB in elderly patients with life-threatening hemorrhageand shock. The procedure can be performed rapidly, minimizing the time spent inthe operating room under general anesthesia. The principles of suture ligation of aduodenal bleeding ulcer that involves the gastroduodenal artery require use of the3-point ligation technique.

The gastroduodenal artery is ligated both proximally and distally to thearterial 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 requiresanother emergent laparotomy of the abdomen. Vagotomy with antrectomy isreserved for patients whose conditions have failed to respond to moreconservative attempts at surgical intervention and for those with aggressive andrecurrent duodenal ulcer diathesis such as gastric outlet obstruction.

When performing a highly selective vagotomy, the duodenostomy or thepyloroduodenostomy is closed anatomically, preserving the normal pyloricsphincter muscle. Most commonly, this operation is reserved for young, stable,

low-risk patients. Although long-term follow-up care is still necessary, therecurrent ulcer rate is less than 10% at a mean follow-up of 3.5 years (Stabile,2000).

Much of what is now known about the operations performed for bleedingduodenal ulcers came from the era before the etiologic role for Helicobacter pylori

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and NSAIDs in the development of peptic ulcers was understood.Reducing gastric acidity has been proven to be beneficial, with lower rebleedingrates when using high-dose omeprazole (Fallah, 2000). Although proton pumpinhibitors seem to have an advantage, they have no affect on mortality.

The diagnosis of H pylori infection is important in the management ofpatients with a complicated bleeding peptic ulcer. If a patient with a bleeding ulcerrequires surgery, then knowledge of the patient's H pylori status becomespertinent because it may help guide the decision to choose a particular surgicalprocedure, eg, simply oversewing the ulcer as opposed to performing an antiulceroperation. Many studies support the decision to manage the bleeding ulcer inconjunction with eradication ofH pylori.

In patients with H pyloriinfection, the rate of recurrent bleeding is extremelylow. This is why documenting the presence ofH pyloriand aggressively treatingthe infection are important. Patients who are not infected with H pylorimay requirea subsequent acid-lowering surgical procedure or long-term medical therapy for

recurrent ulcer disease and bleeding. Rates of H pylori infection are reportedlylower in patients with complicated ulcer disease compared to patients withuncomplicated ulcers. Hosking et al reported a 71% incidence ofH pyloriinfectionin patients with bleeding duodenal ulcers; patients with nonbleeding ulcers had anincidence of 93%.

NSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase,which causes decreased mucosal prostaglandin synthesis and results in impairedmucosal defenses. Daily NSAID use causes an estimated 40-fold increase ingastric ulcer creation and an 8-fold increase in duodenal ulcer creation (Corson,

2001). Long-term NSAID use is associated with a 20% incidence in thedevelopment of mucosal ulceration (Corson, 2001). Medical therapy includesavoiding the ulcerogenic drug and beginning a histamine-2 (H2)receptorantagonist or a proton pump inhibitor that provides mucosal protection.

H pyloriis a gram-negative flagellated rod that plays a major etiologic role inthe development of PUD. H pylorican be found in the antrum of the stomach in95% of patients with a duodenal ulcer and in most patients with a gastric ulcer notassociated with NSAID use.

Eradication of H pylori can reduce the risk of rebleeding. Current antiH

pyloriregimens include a variety of drug combinations. Typically, an antimicrobialagent is combined with an H2-receptor antagonist or a proton pump inhibitor. Thetreatment regimens approved by the US Food and Drug Administration (FDA)have eradication rates forH pyloriof 70-90% (Corson, 2001).

Treatment regimens forH pyloriinfection (Corson, 2001)o Omeprazole: Administer 40 mg/d plus clarithromycin at 500 mg q8h for

2 weeks. Then administer omeprazole at 20 mg/d for 2 weeks.o Ranitidine bismuth citrate: Administer 400 mg q12h plus clarithromycin

at 500 mg q8h for 2 weeks. Then administer ranitidine bismuth citrate

at 400 mg q12h for 2 weeks.o Bismuth subsalicylate: Administer 525 mg q6h plus metronidazole at

250 mg q6h plus tetracycline at 500 mg q6h for 2 weeks plus an H2-receptor antagonist for 4 weeks.

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o Lansoprazole: Administer 30 mg plus amoxicillin at 1 g plusclarithromycin at 500 mg q12h for 2 weeks.

Poor compliance with the drug treatment can create antibiotic resistance andcan fail to eradicate H pylori organisms. Diagnostic tests for H pylori can bedivided into 2 groups, ie, (1) tests for patients who will undergo endoscopy andsubsequently have a biopsy of the gastric mucosa performed and (2) tests forthose who do not require endoscopy.

The endoscopic tests include culture, histology, and a rapid urease test(RUT). RUTs are based on the urease-producing activity ofH pylori. If urease ispresent, then urea is hydrolyzed, thus releasing ammonia that raises the pH. TheCLO test and the HP test are 2 of the tests now commercially available. Availablenonendoscopic tests are the urea breath test and serologic testing. The ureabreath test and the endoscopic biopsy results rely on the bacterial load to detectH pylori; therefore, the use of proton pump inhibitors and H2-receptor antagonistsshould be stopped 2-4 weeks before performing these studies. The RUT has an

excellent specificity, approaching 100%, although it has a false-negative rate ofapproximately 10% (Laine, 1999). Therefore, performing a biopsy is important todocument the presence of H pylori or inflammation with a cellular infiltrate(neutrophils).

Bleeding gastric ulcer

The surgical management of bleeding gastric ulcers is slightly different fromthat of duodenal ulcers, but the concepts are identical. The 3 most commoncomplications of a gastric ulcer that mandate emergent surgical intervention arehemorrhage, perforation, and obstruction. The goals of surgery are to correct the

underlying emergent problem, prevent recurrent bleeding or ulceration, andexclude malignancy. A bleeding gastric ulcer is most commonly managed by adistal gastrectomy that includes the ulcer with a gastroduodenostomy or agastrojejunostomy reconstruction. The common operations for the management ofa bleeding gastric ulcer include (1) truncal vagotomy and pyloroplasty with awedge resection of the ulcer, (2) antrectomy with wedge excision of the proximalulcer, (3) distal gastrectomy to include the ulcer with or without truncal vagotomy,and (4) wedge resection of the ulcer only.

The choice of operation depends on the location of the ulcer and the

hemodynamic stability of the patient to withstand an operation. Five types ofgastric ulcers occur, based on their location and acid-secretory status.

Type 1 gastric ulcers are located on the lesser curvature of the stomach ator near the incisura angularis. These ulcers are not associated with ahypersecretory acid state.

Type 2 ulcers represent a combination of 2 ulcers that are associated with ahypersecretory acid state. The ulcer locations occur in the body of thestomach in the region of the incisura. The second ulcer occurs in theduodenum.

Type 3 ulcers are prepyloric ulcers. They are associated with high acidoutput 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.

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Type 5 ulcers are related to the ingestion of NSAIDs or aspirin.These ulcers can occur anywhere in the stomach.A vagotomy is added to manage type 2 or type 3 gastric ulcers. These

ulcers arise in the pyloric channel or the prepyloric area and are associated withacid hypersecretion physiology. Patients who are hemodynamically stable withintermittent bleeding requiring blood transfusions should undergo a truncalvagotomy and distal gastric resection to include the ulcer for type 1, 2, and 3ulcers.

In patients who present with life-threatening hemorrhage and a type 1, 2, or3 ulcer, biopsy and oversew or excision of the ulcer in combination with a truncalvagotomy and a drainage procedure should be considered. Patients with type 4ulcers usually present with hemorrhage. The left gastric artery should be ligated,and a biopsy should be performed on the ulcer. Then, the ulcer should beoversewn through a high gastrotomy.

Rebleeding rates for the procedures that keep the ulcer in situ range from

20-40% (Corson, 2001). Gastric bleeding in the immediate postoperative periodfrom recurrent PUD is initially best managed by endoscopic or angiographicmeans. If reoperation is required, gastric resection is usually indicated because arepeat vagotomy is not reliable. A more definitive solution is warranted.

Stress gastritis

Acute stress gastritis is a disease process characterized by diffusesuperficial mucosal erosions that appear as discrete areas of erythema (Corson,2001). The bleeding is usually mild and self-limiting and rarely progresses to life-threatening hemorrhage. In ICU patients, the incidence of clinically significant GI

bleeding (eg, hypotension, transfusion) from this process was 1.5% (Stollman,2004). Stress gastritis and mucosal ulceration are historically associated with (1)head injuries with associated elevations in intracranial pressure and (2) burninjuries. These stress ulcers are called Cushing ulcer and Curling ulcer,respectively.

Predisposing clinical conditions have the potential to alter local mucosalprotective barriers such as mucus, bicarbonate, blood flow, and prostaglandinsynthesis. Any disease process that disrupts the balance of these factors resultsin diffuse gastric mucosal erosions. This is most commonly observed in patients

who have undergone episodes of shock, multiple trauma, acute respiratorydistress syndrome, systemic respiratory distress syndrome, acute renal failure,and sepsis. The principal mechanisms involved are decreased splanchnicmucosal blood flow and altered gastric luminal acidity.

Knowledge of the predisposing conditions for stress ulceration allows theclinician to identify patients at risk for developing gastritis and GI bleeding.Treatment in this group of high-risk patients should focus on prevention. This isbest accomplished by treating the underlying causes of ulceration. Aggressivesupport of hemodynamic parameters ensures adequate mucosal blood flow. In

addition, several strategies have evolved to treat gastric luminal acidity. Histaminereceptor antagonists (HRAs) have proven to be the most effective at controllingstomach pH. Proton pump inhibitors (PPIs) are superior to the HRAs atsuppressing acid; however, their role in stress ulceration prophylaxis is still beingstudied (Stollman, 2004).

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Stress-related bleeding usually occurs 7-10 days after the initialinsult but may manifest sooner. Initially, endoscopy is the most importantdiagnostic tool. The acute superficial erosions are multiple, begin in the fundus,and progress toward the antrum. Ninety percent of patients stop bleeding withconservative medical therapy that includes NGT lavage and gastric acidcontrolling medications to maintain the gastric luminal pH above 5.0 (Cameron,1995).

Endoscopic hemostasis is attempted using electrocoagulation, laser, orinjection therapy. Selective angiographic catheterization of the left gastric arterymay be attempted with selective infusion of vasopressin (48-72 h) or embolizationusing Gelfoam, coils, or autologous clot to embolize the left gastric artery.Regardless of the angiographic technique used, it is often unsuccessful becauseof the rich and extensive submucosal plexus and collateral circulation within thestomach.

Surgical intervention becomes necessary if nonoperative therapy fails and

blood loss continues. The goals of operative treatment are to control bleeding andto reduce recurrent bleeding and mortality. These patients are at extremely highrisk, and the most expeditious procedure is the best option.

Simply oversewing an actively bleeding erosion is sometimes effectiveenough to control the bleeding. In the setting of life-threatening hemorrhage notamenable to endoscopic control, gastric resection with or without vagotomy withreconstruction 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 30-100%(Cameron, 1995). The choice of the initial operation must be made with anunderstanding of the patient's condition, the amount and location of gastricdisease, and an accurate assessment of one's technical ability to rapidly andsafely perform a gastric resection. Managing the underlying insult causing thegastric stress ulcerations is also important. This involves supportive measures tomaintain acceptable hemodynamic parameters, to provide adequate nutritionalsupport in the critically ill patient, and to treat sepsis if present.

Portal hypertensionrelated bleeding

Variceal bleeding is one of the most alarming life-threatening complicationsof cirrhosis. Sixty percent of patients with cirrhosis develop esophageal varices.Thirty percent of these patients bleed from their varices within 2 years of theirdiagnosis, and 50% bleed at some point during their lifetime. The mortality rate forvariceal bleeding is 30-50%, which is much higher than any other cause of UGIB(Corson, 2001). Patients with portal hypertension but normal liver function (eg,portal vein thrombosis, idiopathic portal hypertension, schistosomiasis) havebetter outcome and survival rates compared to those with liver dysfunction andother organ failure.

The presence of portal vein pressure greater than 10 mm Hg defines portalhypertension. Normal portal venous pressure ranges from 5-10 mm Hg, whichprovides a portal blood flow rate of approximately 1 L/min through the hepaticsinusoids. Portal hypertension can be classified according to the anatomiclocation within the portal system that is the site for increased resistance to portal

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flow. The 3 classifications are presinusoidal, sinusoidal, andpostsinusoidal. This organized classification is clinically useful to differentiatepatients with hepatocellular dysfunction from those with normal liver function, asnoted in the following table (Corson, 2001).

Table 8. Causes and Sites of Block for Portal Hypertension

Presinusoidal Sinusoidal Postsinusoidal

Extrahepatic Cirrhosis Hepatic veins

Congenital Budd-Chiari syndrome

Umbilical sepsis Venoocclusive disease

Trauma

Hypercoagulation state

Malignant occlusion

Intrahepatic

Schistosomiasis

Congenital hepatic

Fibrosis

Primary biliary

Cirrhosis

Patients with presinusoidal portal hypertension have normal liver function;patients with sinusoidal causes for portal hypertension have cirrhosis anddestroyed sinusoidal anatomy. Regardless of the cause of the increased portalpressure, the resistance to portal blood flow leads to the development of 4 well-

recognized collateral vascular systems, ie, (1) the esophageal submucosalvenous plexus, (2) the cardiac vein of the stomach, (3) the retroperitoneal-umbilical system, and (4) the hemorrhoidal system.

The bleeding risk for esophageal varices becomes significant once theintravariceal pressure reaches a threshold level. The increased tension (T) withinthe varices is directly related to its intravascular pressure (P) and radius (R) and isinversely related to its wall thickness (W), ie, T = P X R / W. The life-threateningbleeding that occurs is the result of the high intravascular tension. Of the patientsnewly diagnosed with cirrhosis each year, 30% have compensated disease;however, it is the 60% with uncompensated disease who have varices (Corson,2001). Estimates from prospective studies indicate that the overall incidence ofesophageal varices in patients with cirrhosis is 8% each year (Vargas, 1999). Theclinical implication of this is extremely important because all patients newlydiagnosed with cirrhosis should undergo a screening endoscopy.

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Because the mortality rate associated with an acute variceal bleed isextremely high, varices at high risk for bleeding must be recognized. An Italianprospective study analyzed the endoscopic and clinical features of cirrhosis andpredicted the likelihood of variceal bleeding based on these parameters (NorthItalian Endoscopic Club for the Study and Treatment of Esophageal Varices,1998). The study revealed that the risk of the first variceal bleed may be predictedbased on variceal size, the presence of red wales, and a Child-Pugh score greaterthan or equal to 8 points (Corson, 2001).

Table 9. Child-Pugh Classification

Parameter 1 Point 2 Points 3 Points

Bilirubin 3

Albumin >3.5 2.8-3.5 6

Ascites None Slight Moderate

Encephalopathy None 1-2 3-4

In addition to the Child-Pugh classification system, the model for end-stageliver disease (MELD) score has been used to predict outcomes in this patientpopulation. The MELD score uses 3 objective measurements: creatinine, bilirubin,and INR to quantify the degree of hepatic dysfunction. It is currently used for

allocating patients to liver transplant waiting lists (Amitrano, 2005). In regard topatients with active variceal bleeding, the MELD score can be used to identifyshort-term mortality risk (Amitrano, 2005). This information can then be used todirect a more intense surveillance and therapeutic strategy in these high-riskpatients.

The MELD score calculation is as follows (Kamath, 2001):(0.957 x log(e) (creatinine mg/dl)+0.378 x log(e) (bilirubin mg/dl) +1.120 x

log(e) (INR) +0.643)x10Other studies have studied the correlation between the portal-hepatic vein

gradient (PHVG) and the risk for bleeding. The pressures are measured in thehepatic vein when the vein is both occluded and in the free position. This isperformed using the same principles as those for measuring pulmonary arterypressures and pulmonary artery occlusion pressures. The occluded hepatic veinpressure is an indirect measurement of the hepatic sinusoidal pressure. Thedifference between the occluded and free hepatic vein pressure is called thePHVG. Garcia-Tsao et al observed that all the patients in their study bled whenthe PHVG was greater than 12 mm Hg. Once an initial acute bleed occurs, earlyrebleeding ensues in 20-50% of patients within the first 7-10 days. Within

approximately the first 6 weeks after the initial bleed, the risk for rebleeding dropsto what it was before the initial bleed. The risk for rebleeding within the first year is30%.

The initial management of a patient with an acute variceal bleed involvesaggressive efforts at resuscitation as previously outlined. Admit the patient to an

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ICU setting in which a multidisciplinary team approach can be used totreat the patient. Follow the ABCs, but avoid overhydrating the patient becausevolume overload can increase portal hypertension and provoke more bleeding.Since Gilbert and Vailaret coined the term portal hypertension in 1906, manytherapeutic modalities have been developed to manage acute varicealhemorrhage and subsequent elective treatments for prevention of recurrentbleeding. These treatment strategies can be classified into (1) pharmacologictherapy, (2) endoscopic therapy, (3) tamponade, (4) decompressive therapy(radiologic and surgical), and (5) liver transplantation.

Pharmacologic therapyThe patient with acute variceal bleeding may initially be treated with

intravenous vasopressin and nitroglycerine, somatostatin, or one of its analogs(eg, octreotide). Vasopressin is a potent splanchnic and systemic vasoconstrictor,including coronary vasoconstriction. Nitroglycerin should be concomitantlyadministered to titrate and maintain the SBP in the range of 90-100 mm Hg.

Nitroglycerin should be initiated at 40 mcg/min to protect the coronary arteriesfrom the profound adverse cardiovascular effects of the vasopressin. Theintravenous infusion of vasopressin is started at 0.2-0.4 U/min. A meta-analysisfrom 1995 reviewed vasopressin versus untreated controls and revealed thatvasopressin was clearly superior in arresting hemorrhage but showed no survivalbenefit (D'Amico, 1995).

In Europe, a newly developed prodrug called terlipressin has been used thathas advantages over vasopressin (Vargas, 1999). Terlipressin has a longer half-life with a biphasic vasoconstriction profile. The drug first has systemic vascular

effects that are then steadily converted into a more effective vasoconstriction ofthe splanchnic bed. Randomized control trials comparing terlipressin with placebohave shown clear benefit in terms of bleeding control and survival (Patch, 1997).This drug is not yet available in the United States.

Recombinant coagulation factor VII is a synthetic coagulation factor that iscurrently used to treat acute bleeding episodes in patients with hemophilia. It hasrecently been trialed in randomized studies as an adjunct to standard methods ofcontrolling variceal hemorrhage. Patients in end-stage liver disease lose thesynthetic capacity to produce these coagulation factors, most notably factor VII

(Bosch, 2005). As a result, it has been postulated that replacing factor VII incirrhotics may aid in controlling acute variceal hemorrhage. A recent double-blindtrial has shown increased success at controlling bleeding endpoints in moresevere cirrhotics (classes B and C) treated with factor VII compared to placebo(Bosch, 2005). Although results are promising, cost-effective dosing and timing oftherapy are yet to be determined (Jimenez-Saenz, 2005).

Endoscopy in variceal bleedingSince rigid endoscopy was first introduced in 1939 for the treatment of

variceal bleeding, its evolution into flexible endoscopy has enabled it to become

the cornerstone of current management for acute variceal hemorrhage. The 2main endoscopic techniques available to control variceal bleeding are endoscopicsclerotherapy and endoscopic variceal band ligation. Endoscopic sclerotherapyinvolves injecting a sclerosing agent, such as ethanolamine or polidocanol, intothe varix lumen (intravariceal) or immediately adjacent to the vessel (paravariceal)

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to create fibrosis in the mucosa overlying the varix, which leads tohemostasis. Endoscopic variceal banding ligation consists of the placement of arubber band around the varix. This technique is performed by first sucking thevarix into a sheath attached to the distal end of the endoscope. Once the varix issuctioned into the sheath, a trigger device allows the deployment of a rubber bandaround the varix, a procedure that strangulates the varix.

Each varix is usually ligated as many times as necessary to make it nolonger visible. The rubber bands slough off in the following 24-72 hours, leaving ashallow ulcer behind. Ulceration is less severe than with sclerotherapy.

A recent meta-analysis of all the randomized controlled trials comparingsclerotherapy with variceal banding found significantly lower mortality rates,variceal rebleeding, esophageal perforation, and stricture formation with varicealbanding therapy (Laine, 1995). In addition, evidence accumulating in the literaturedocuments the safety of endoscopic banding in prophylactic therapy for patients athigh risk for esophageal variceal hemorrhage (Lay, 1997). This benefit has not

been established with endoscopic sclerotherapy.The single potential downside to endoscopic variceal banding is poor

visualization of the varices when massive bleeding is present. This is due to the30% reduction in the field of vision through the endoscope caused by the plasticsheath used to deploy the rubber band (Vargas, 1999). The drawback tosclerotherapy is its potential for life-threatening complications such as perforation,ulceration, and stricture of the esophagus.

The initial success in arresting hemorrhage comparing the 2 techniques iscomparableas high as 95% in some studies (Vargas, 1999). Variceal rebleeding

rates are lower with band ligation compared to sclerotherapy, which hasrebleeding rates as high as 50% (D'Amico, 1995).

In summary, endoscopic variceal banding is a more effective techniqueresulting in faster variceal eradication and fewer complications than endoscopicsclerotherapy. Endoscopic surveillance at 3-month intervals during the first year isimportant to detect recurrent and new varices when they are small and have a lowrisk of bleeding (Corson, 2001).

The other available endoscopic option is the use of tissue adhesives, whichare useful for both esophageal and gastric varices. Native cyanoacrylate is a liquid

tissue adhesive used frequently in Europe. It has a consistency similar to water,which makes it easy to manipulate down the endoscope. After injecting thesubstance into the varix, the blood mixes with the adhesive agent and rapidlypolymerizes into a hard glue. The cyanoacrylate then plugs the lumen of the varixand creates hemostasis. Several weeks (ie, 2 wk to 3 mo) after the initial injection,the overlying mucosa sloughs off and the adhesive cast is passed through the GItract.

Cyanoacrylate is 90% successful in achieving hemostasis in patients withacute bleeding from either gastric or esophageal varices (D'Imperio, 1996). The

early rebleeding rate is 0-28%. The risks of using these adhesive agents are thepotential systemic effects and permanent damage to the endoscope fromexposure to the adhesives at the lens of the scope (Sarin, 2001).

The potential systemic effects are related to the risk of thromboticcomplications. Cerebral stroke from anomalous right-to-left shunts, fatal

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pulmonary embolization, portal vein embolization, splenic infarction, andretrogastric abscess have all been reported in the literature (Sarin, 2001).

Oho et al performed a prospective randomized trial involving 53 patients thatcompared cyanoacrylate glue to sclerotherapy in patients with acute gastricvariceal bleeding. Cyanoacrylate was more effective in achieving hemostasis(93% vs 67%). The need for emergent surgical intervention was also reduced inpatients initially injected with the glue tissue adhesive. Other agents used includebovine fibrin or fibrin glue. Polidocanol, a 2-component fibrin glue, has shownpromise as an effective agent with a decreased incidence in mucosal damage orposttherapy ulceration that is characteristic of sclerosants and tissue adhesives(Zimmer, 1998). Bovine thrombin used as an injectable hemostatic agent is notyet approved by the FDA for use in the United States.

Balloon tamponadeSince the 1990s, the use of balloon tamponade for the emergent control of

esophageal variceal bleeding has steadily decreased and is now usually indicated

for only the 10% of patients whose acute bleeding episode is not controlledendoscopically (Corson, 2001). The use of these tubes can be a life-savingmaneuver when medical and endoscopic efforts fail to control the bleeding.Although temporary control of the bleeding is effective in 85% of cases, recurrentbleeding with release of the tamponade occurs in most patients (Kupfer, 2000).

In addition to their limited effectiveness, the tubes are associated with a 20%complication rate that includes airway obstruction, aspiration, and esophagealnecrosis with rupture (Kupfer, 2000). Because of the severe life-threateningcomplications and limited use, the tubes are used only as a temporary measure

while the patient is resuscitated. The tubes act as a bridge to help stabilize thepatient until a time when the patient is prepared for either a repeat endoscopyprocedure or a portal pressure decompression through a radiological or surgicalmethod.

The 2 most commonly used tubes are the Sengstaken-Blakemore tube andthe Minnesota tube. These tubes have an esophageal balloon and a gastricballoon that are inflated to produce a tamponade effect after confirmingappropriate anatomical placement. When deciding to employ this line of therapy,seriously consider endotracheal intubation to secure and protect the patient's

airway. Although balloon tamponade effectively controls acute varicealhemorrhage, a meta-analysis of studies comparing balloon tamponade to drugtherapy and endoscopic sclerotherapy revealed no survival advantage in theballoon group.

The physician must be familiar with the steps involved in placement of thetubes to avoid the unnecessary complications (Kupfer, 2000). Complicationsassociated with balloon tamponade are as follows:

Major complicationso Esophageal ruptureo

Tracheal ruptureo Duodenal ruptureo Respiratory tract obstructiono Aspirationo Hemoptysis

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o Tracheoesophageal fistulao Jejunal ruptureo Thoracic lymph duct obstructiono Esophageal necrosiso Esophageal ulcer

Minor complicationso Nasopharyngeal bleedingo Chest paino Balloon impaction and/or migration (nausea and vomiting)o Alar necrosis

The tube is first introduced into the stomach, and a small amount of air isinjected into the gastric balloon. A radiograph is then obtained to confirmplacement in the stomach. Once proper placement is confirmed, the gastricballoon is inflated with 300-350 mL of air and is pulled up into the gastric fundus,compressing the gastroesophageal junction. The tube is secured to the facemask

of a football helmet placed on the patient's head. The esophageal balloon is theninflated to a pressure of 40 mm Hg. Another radiograph is obtained to confirmproper placement of both tubes. Deflate the esophageal balloon every 4 hours for15 minutes to avoid esophageal pressure necrosis. Do not leave the entire tube inplace for more than 24-48 hours.

Transjugular intrahepatic portosystemic shuntTransjugular intrahepatic portosystemic shunt (TIPS) decompression of the

portal system can be achieved through either radiologic or surgical methods. Thegoal is to reduce intravariceal pressure to less than 12 mm Hg. The TIPS

procedure has become the most frequently employed method; because of itseffectiveness, it is considered the standard of therapy for bleedingesophagogastric varices that are unresponsive to endoscopic and pharmacologicfirst-line treatment. The placement of a TIPS reduces the outflow hepaticresistance, lowers portal pressure, and diverts portal blood flow fromgastroesophageal collaterals through the stent. The procedure takesapproximately 1-2 hours to perform.

The right internal jugular vein is cannulated, and a coaxial catheter system isused to maintain access to either the middle or right hepatic vein. A catheter is

passed over a wire and advanced through the hepatic parenchyma to obtainaccess to the portal system. This track created between the systemic venoussystem and the portal system is balloon-dilated so that a self-expanding metalstent can be inserted and deployed in the track. The wall stent is dilated toapproximately 10-12 mm in diameter. Once the stent is in proper position,pressures are measured in the portal vein, the stent, and the right atrium. Thegoal of the procedure is to reduce the portal-to-atrial pressure gradient to lessthan 12 mm Hg. Another measurement used is the PHVG. Measurement of thefree hepatic and wedged hepatic pressures before and after the procedure should

document a decrease of the PHVG to less than 12 mm Hg.The TIPS procedure controls variceal bleeding in more than 90% of patients(Sarin, 2001). The rebleeding rate is 16-30% at 1-year follow-up, and this is mostcommonly related to stenosis of the intrahepatic shunt or obstruction of the stent

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(Sarin, 2001). Shunt dysfunction occurs in approximately 50-60% ofpatients at 6 months (Sarin, 2001).

Close observation and repeat interventions are required to maintain shuntpatency. Careful monitoring with Doppler ultrasound imaging at regular monthlyintervals has led to better control of bleeding. Redilation of the stent is performedwhen the flow pattern through the shunt changes. This has increased the 1-yearpatency rate to 83-85% (Corson, 2001). The risk of inducing hepaticencephalopathy is 25-35%, but this can usually be managed with proteinrestriction and lactulose (Sanyal, 1994). The 30-day mortality rate is 14-16%, withmost deaths occurring in patients with Child class C cirrhosis as a result ofmultisystem organ failure.

The TIPS procedure is usually considered in patients who have notresponded to first-line treatment using pharmacologic and endoscopic therapy. Itmay also be necessary in patients who required balloon tamponade and haverecurrent bleeding refractory to repeat endoscopic attempts at hemostasis.

The severity of rebleeding and the rate of progression of the underlying liverdisease are major factors that should be considered when determining theappropriate timing for portal decompression and the method to accomplish thetask. For patients who do not respond early and who have recurrent bleeding afteresophageal variceal banding, rapid decompression is indicated. In patients whohave minor rebleeding after variceal obliteration by endoscopic techniques,especially those who have not bled until 1-2 years later, a repeat endoscopicbanding procedure is a more reasonable approach.

The need for liver transplantation should also be considered during the initial

evaluation of patients with UGIB and portal hypertension. For patients with Childclass A or B cirrhosis with preserved liver function, portal decompression ispreferable to transplantation. For patients with Child class C cirrhosis, the TIPSprocedure can be used as a temporizing measure to provide a bridge untiltransplantation can be arranged.

Surgical shuntsSurgery for bleeding esophagogastric varices is the most reliable method to

control acute hemorrhage and is associated with recurrent bleeding rates of lessthan 10% (Corson, 2001). The goal of a surgical shunt is to effectively decrease

the portal venous hypertension and its adverse effects without compromising liverfunction.

Because of the effectiveness and popularity of the available endoscopictherapies and the emergence of the TIPS procedure in the 1990s, the role ofsurgical decompression of the portal system is reserved for patients in whominitial nonsurgical management has failed and who still have preserved liverfunction.

The widespread use of endoscopic techniques and the introduction of theTIPS procedure have made surgery a less attractive choice for acute and chronic

variceal bleeding. The operative approaches for bleeding esophagogastric varicesconsist of 2 general concepts: (1) decompression of the high-pressure portalvenous system into a low-pressure systemic venous system and (2)devascularization of the distal esophagus and proximal stomach (Stabile, 2000).The following options are currently available to the surgeon:

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Portacaval shunt (end-to-side) Portocaval shunt (side-to-side) Small-diameter interposition graft Mesocaval shunt Large-diameter interposition graft Small-diameter interposition graft Distal splenorenal (ie, Warren) shunt Esophagogastric devascularization, esophageal transaction, and

reanastomosis Orthotopic liver transplantation Splenectomy (for splenic vein thrombosis)

Practitioners may well ask whether one shunt is superior to the others andwhether one shunt controls bleeding better than the others. Each type of shunthas a bleeding control rate greater than 90% (Corson, 2001). The differencebetween shunts is the incidence of encephalopathy and the risk of worsening

ascites.Depending on whether the shunt completely decompresses the portal

venous system, portosystemic shunts can be classified as nonselective, selective,or partial. The goal of selective or partial shunts, in addition to decreasing portalvenous hypertension, is to preserve portal blood flow to the liver in order to avoidcompromising liver perfusion and function. Data from many randomized controltrials that have compared the various types of shunts indicate that encephalopathyoccurs in 10-15% of patients after a selective shunt (distal splenorenal), in 10-20%after a partial shunt, and in 30-40% after a total shunt (Corson, 2001). The

differences in survival between all the different shunts are not significantlydifferent, with mortality rates of approximately 5% (Corson, 2001).

Table 10. Surgical Shunts for Treatment of Variceal Hemorrhage

Procedure Advantage Disadvantage

Nonselective shunts

End-to-end portocavalshunt

Low bleeding rate Encephalopathy

Side-to-side portocavalshunt

Low bleeding rateLiverhypoperfusion

Selective shunts

Distal splenorenal shuntFew developencephalopathy

Technically moredifficult

Partial shunts

Polytetrafluoroethyleneinterposition graftportocaval/mesocaval

Maintain liverperfusion; lowerencephalopathy

Graft stenosis or

thrombosis

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shuntrate; low bleedingrate

Nonselective shunts completely divert portal blood flow from the liver.Because the patent shunt has lower resistance to blood flow than the cirrhoticliver, the portal blood flow through the hepatic vein is reversed. None of thenonselective shunts maintains hepatic portal perfusion unless they becomestenotic. Although these shunts are the most effective at alleviating ascites, theirincidence of encephalopathy is 25-50% because of the complete diversion ofportal blood flow from the liver (Corson, 2001).

The current indications for nonselective shunting are (1) in the emergencysetting to control bleeding; (2) as a long-term bridge to liver transplantation inpatients in whom endoscopic, pharmacologic, and TIPS therapies have failed; and(3) in patients who are bleeding from colonic and stomal varices. For patients inwhom liver transplantation is anticipated, avoid dissection in the porta hepatis

when creating a shunt. In this situation, an interposition mesocaval shunt is abetter choice for a nonselective shunt.

Selective shunting decompresses the varices while maintaining hepatopetalblood flow in the remainder of the portal system. The distal splenorenal (Warren)shunt (DSRS) is the most commonly used selective shunt. DSRS placement isperformed by anastomosing the distal end of the splenic vein to the side of the leftrenal vein. The portal venous system is thereby divided into a decompressedgastrosplenic venous circulation and a high-pressure superior mesenteric venouscirculation that maintains hepatopetal blood flow to the liver. The liver maintains

portal perfusion, and the incidence of encephalopathy is lower (10-15%) (Corson,2001).

Worsening of ascites can occur because of the dissecting and dividing oflymphatics near and around the left renal vein. Avoid this shunt in patients withmedically intractable ascites. The splenic vein should be 6-7 mm in diameter toavoid a high risk of shunt thrombosis. Selective shunts are best performed inpatients with nonalcoholic portal hypertension. This is because patients withalcoholic cirrhosis tend to develop collaterals around the shunt, resulting in lessportal flow in 50% of patients at 1-year follow-up (Corson, 2001).

The objective of using partial shunts is the same as that of selective shunts,ie, to decompress varices while maintaining hepatic portal perfusion. This type ofshunt has been popularized by Sarfeh and colleagues over the last 10 years.Sarfeh et al described using a small-diameter, polytetrafluoroethylene,interposition graft portocaval shunt combined with ligation of the coronary vein(Sarfeh, 1983). When the graft diameter is less than or equal to 10 mm, portalperfusion is maintained. Sarfeh et al have shown maintenance of portal perfusionin more than 80% of patients with 8-mm grafts. Shunt stenosis occurs in 15-20%of patients, and thrombosed grafts can be opened and dilated by interventional

radiographic techniques. The incidence of encephalopathy is approximately 15%.One of the major controversies in the surgical management of bleedingvarices has been the role of devascularization procedures. In 1973, Sugiura andFutagawa introduced their experience with a surgical technique that theydeveloped involving gastroesophageal devascularization. The principle of the

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Sugiura procedure is to divide the esophageal and gastric venous plexusfrom the portal system, while intentionally preserving the extra esophagealsystemic venous collaterals to the azygous system. The left gastric vein must bepreserved during the gastric devascularization to allow drainage of the systemicvenous system into the azygous vein. Initially, this was a 2-stage procedure thatfirst involved devascularizing the upper stomach and esophagus up to the leftpulmonary vein through a thoracotomy, followed by a laparotomy a few weekslater. The initial Japanese series reported a low mortality rate (4-12%), witheffectiveness in the prevention of recurrent bleeding (1.5-16%) (Futagawa, 1979).

This procedure has not been as successful in the Western Hemisphere. TheWestern world has not been able to reproduce Sugiura's exceptional results. Oneof the largest series published in the literature was by Orozco et al from MexicoCity, which involved 100 patients. In this series, the overall mortality rate was 22%but reached as high as 80% in the subgroup of patients with Child class Ccirrhosis. In the subgroup of patients with Child class A and B cirrhosis, the

postoperative mortality rate was 12% and 31%, respectively. The rebleeding ratewas 10%, and the incidence of postoperative encephalopathy was 3%. In patientsundergoing the procedure electively versus emergently, the mortality rates weremore than 11% versus 41%.

Several possible explanations may account for the differences between theJapanese results and those observed in the Western Hemisphere (Selzner, 2001).For example, Sugiura had a low percentage of Child class C patients; additionally,alcoholism is a rare cause of portal hypertension in Japan compared to Westernexperiences.

Patients with alcohol abuse and alcoholic cirrhosis are at higher riskbecause of concomitant comorbid illnesses and malnutrition. Lastly, Sugiuraperformed the procedure in an elective setting. The procedure was primarilyperformed for prophylaxis of variceal bleeding.

In 2001, an article by Selzner described the technique of the modifiedSugiura procedure, which involves a 1-stage transabdominal approach. Asplenectomy is first performed. Next, the stomach is devascularized to include theupper two thirds of the lesser and greater curvatures. The devascularization of theesophagus is carried up 6-7 cm through the diaphragmatic hiatus. The left gastric

vein is preserved during this maneuver. Next, a circular stapler is introduced 4-6cm into the esophagus through an anterior gastrotomy. The circular stapler isfired, allowing concomitant transection and reanastomosis of the esophagus. Apyloroplasty is then performed after reinforcing the esophageal anastomosis.Preservation of the anterior and posterior vagus and Nissen fundoplication havebeen described by other authors as part of the procedure.

In this study, the modified Sugiura procedure was offered only to patientswho had Child class A or B cirrhosis with well-preserved synthetic liver functionand contraindications to DSRS, TIPS, and liver transplantation. Patients with Child

class C cirrhosis and those with Child class B cirrhosis with ascites were excludedfrom the procedure. Through appropriate patient selection, the mortality rate inthis study was 9% and the rebleeding rate was 7%. These are satisfactorynumbers considering the high-risk patient population and the dismal outcomesafter exhausting other therapeutic alternatives. Patient selection is extremely

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important when considering surgical intervention. Preserved liver functionand an elective setting are key factors in predicting morbidity and mortality.

An algorithm has been developed for patients with recurrent esophagealvariceal bleeding in whom endoscopic therapy has failed (Selzner, 2001). Patientswith marginal liver function (ie, Child class B or C cirrhosis) should receive TIPSas a bridge to liver transplantation. Patients with preserved liver function (ie, Childclass A or B cirrhosis without ascites) should first be considered for a DSRS. If thepatient is not a candidate for a surgical (ie, DSRS) shunt because of a previoussplenectomy, small splenic vein, or splenic vein thrombosis, then the modifiedSugiura procedure should be considered (Selzner, 2001). The Sugiura procedureis indicated when other therapeutic modalities are not possible or have failed.

Mallory-Weiss syndromeMallory-Weiss tears account for 15% of acute upper GI hemorrhage (Stabile,

2000). Kenneth Mallory and Soma Weiss first described the syndrome in 1929(Cameron, 1995). 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 thegradient between intragastric and intrathoracic pressures, leading to a gastricmucosal tear from the forceful distention of the gastroesophageal junction(Cameron, 1995). In 80-90% of cases, this is a single 1.75- to 2.5-cm mucosaltear along the lesser curve of the stomach just distal to the gastroesophageal

junction (Cameron, 1995).The initial step in management is to first make the correct diagnosis.

Distinguishing Mallory-Weiss syndrome from Boerhaave syndrome is critical.

Although both entities share a common pathogenesis, their management iscompletely different. Boerhaave syndrome represents a full-thickness transmurallaceration with perforation of the esophagus. A Gastrografin swallow helps confirmthe presence of the perforation in most cases, and prompt surgical intervention isnecessary to prevent mediastinitis and sepsis. On the other hand, surgicalintervention in Mallory-Weiss syndrome is required to achieve hemostasis in only10% of cases (Cameron, 1995). The bleeding from a Mallory-Weiss tearspontaneously ceases in 50-80% of patients by the time endoscopy is performed(Cameron, 1995).

For other patients in whom bleeding is visualized at endoscopy, theendoscopic treatment options are electrocoagulation, heater-probe application, orsclerotherapy. In a recent series published by Bataller et al, hemostasis wasachieved in 100% of patients with Mallory-Weiss tears by using endoscopicsclerotherapy with epinephrine (1:10,000) and 1% polidocanol. Othernonoperative therapies are reserved for when the endoscopic attempts at creatinghemostasis have failed. Other available options are angiographic intra-arterialinfusion of vasopressin or transcatheter embolization of branches of the leftgastric artery using Gelfoam. Avoid the balloon tamponade technique using the

Sengstaken-Blakemore tube in this particular circumstance because thisapparatus may extend the mucosal laceration into a transmural laceration withperforation (Cameron, 1995).

Surgical intervention is indicated in patients with continued bleeding afterfailed attempts at nonoperative therapies. Bleeding from the gastroesophageal

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junction is visualized through an anterior gastrotomy. Once the tear islocalized, the bleeding is controlled by oversewing the lesion. The overall mortalityrates of patients who require emergent surgery is 15-25%, in contrast to amortality rate of 3% or less for patients whose bleeding stops by the time of theinitial endoscopy (Cameron, 1995).

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

proximal stomach, usually within 6 cm of the gastroesophageal junction along thelesser curvature of the stomach. However, it can occur anywhere along the GItract. This lesion accounts for 2-5% of acute UGIB episodes (Larson, 1986).Endoscopically, the lesion appears as a large submucosal vessel that hasbecome ulcerated. Because of the large size of the vessel, bleeding can bemassive and brisk. The pathogenesis of the vessel rupture is usually in the settingof chronic gastritis, which may induce necrosis of the vessel wall. Alcoholconsumption 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 theirthird to tenth decade (Reilly, 1991).

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. Contactthermal ablation with a heater probe is the most effective technique, with orwithout the combined use of epinephrine to slow or stop the bleeding prior toapplying the heater probe. No studies have been performed that compare surgicaland endoscopic therapy for Dieulafoy lesions.

Although surgical intervention may be required after failed endoscopictherapy, endoscopy is still an important adjunct for management because anonbleeding Dieulafoy lesion may be undetectable through a gastrotomy.Because of this potential problem, a combined endoscopic and surgical approachhas been adopted. The vascular malformation can be marked with India inkthrough the endoscope. Rebleeding after endoscopic therapy occurs in 11-15% ofcases, with most cases of rebleeding controlled at repeat endoscopy (Reilly,1991). The 30-day mortality rate from the study by Norton et al was 42%, which isa reflection of the severe comorbid conditions associated with patients who have

bleeding from a Dieulafoy lesion.Angiodysplasia

Angiodysplasia of the upper GI tract accounts for 2-4% of bleeding lesions(Stabile, 2000). The condition is also a cause of lower GI bleeding in 6% of cases(Corson, 2000). The lesion is a vascular malformation that represents anabnormal dilation of mucosal and submucosal vessels.

Histologically, angiodysplasias are dilated, thin-walled vascular channelsthat appear macroscopically as a cluster of cherry spots. When located in theupper GI tract, they most commonly involve the stomach and duodenum. Thelesions can be acquired or congenital, as in hereditary hemorrhagic telangiectasiaand Rendu-Osler-Weber syndrome. The acquired lesions are commonly found inpatients with chronic renal failure requiring hemodialysis and with aortic valvulardisease (especially aortic stenosis). Other diseases, such as cirrhosis and vonWillebrand disease, are associated with a higher frequency of angiodysplasia.

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Most lesions are smaller than 1 cm in diameter and can be multiple in66% of patients (Stabile, 2000).

Bleeding from these lesions can range from occult blood loss to life-threatening hemorrhage. Because the lesions are small and superficial,endoscopic therapy is highly successful. Endoscopic methods and devices usedfor hemostasis include lasers, contact heat probes, electrocoagulation, andinjection therapy.

The contact probe coagulators have been the most common form ofendoscopic treatment because of their proven success and ability to target ableeding lesion tangentially. Recurrent bleeding can occur from the mucosal injurycaused by the coagulation. To overcome the possibility of a delayed hemorrhage,endoscopic band ligation has been applied for hemostasis in nonvariceal GIbleeding, including angiodysplasias (Jo, 1999). A recent prospective studycomparing endoscopic band ligation to electrocoagulation for nonvariceal UGIBrevealed that endoscopic band ligation is safer and faster and provides better

results in achieving hemostasis (Matsui, 2002).When endoscopic techniques fail, surgical resection becomes necessary.

When pangastric involvement is the source of bleeding, a total gastrectomy maybe required. Available nonsurgical options include angiography with catheter-directed vasopressin. Combined hormonal therapy with estrogen andprogesterone is reportedly beneficial for patients in whom the diagnosis isunknown and vascular lesions are suggested.

Aortoenteric fistula

An aortoenteric fistula results from the erosion of the aortic graft into the

bowel lumen, usually the third or fourth portion of the duodenum. The result is adirect communication between the aortic graft lumen and the bowel lumen. Mostaortoenteric fistulas involve the proximal aortic anastomotic suture line. Initially,patients most often present with a self-limiting sentinel hemorrhage that is thenfollowed by an exsanguinating massive GI bleed. For the warning lesser sentinelbleed in a patient with a history of an abdominal aortic aneurysm repair or aknown aortic aneurysm, the diagnosis of a graft-enteric fistula should beconsidered. An upper endoscopy is the procedure of choice to help diagnose thefistula. It should be performed to the ligament of Treitz. Upper endoscopy findings

also help exclude other sources of UGIB. CT scanning is useful because imagesmay reveal thickened bowel, perigraft fluid collection, extraluminal gas, orinflammatory changes in the area of the duodenum and aortic graft.

Angiography requires active bleeding (1 mL/min) to be diagnostic. Once thediagnosis is confirmed or seriously considered, emergency surgical intervention isrequired. In most instances, the aortic graft is removed after debridement andclosure of the duodenum, followed by an extra-anatomic vascular bypass tobypass the ligated aorta and revascularize the lower extremities.

The perioperative mortality rate is 25-90%, and major complications are

common. Published opinions state that graft excision is not necessary as long asno gross contamination and purulence are present at the time of laparotomy(Young, 1999). Under these circumstances, antibiotics are administered long-term. Another option emerging in the surgical literature is the use of endovascularstents to repair the fistula (Deshpande, 1999). Endovascular stent management is

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technically feasible and may be used as a bridge to more definitivetreatment after hemodynamic stabilization in high-risk surgical patients.

Stent grafting immediately controls hemorrhage; however, the device isplaced in an infected field. As a result, adjunctive measures, such as long-termantibiotics, percutaneous drainage, and bowel diversion, may be required (Burks,2001). Although endovascular stents have been shown as effective therapy forAEF, case reports are now emerging describing AEFs in AAA patients treatedinitially with stent grafts as well (Abou-Zamzam, 2003).

ConclusionHistorically, UGIB has been a surgical problem. Today, patients are initially

and nonoperatively treated with endoscopic and angiographic methods to helpdiagnose and control the bleeding source. Because of these advances, surgicalintervention is now more targeted to the specific diagnosis and can bepreoperatively planned. Although these technological advances have decreasedthe need for surgical intervention, a need for the traditional operative procedures

will always exist, especially in life-threatening instances.

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