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222 Part II Abdominal Wall
devices such as metallic clips and band ligation. ermal
coagulation probes include bipolar, monopolar, and heat
probes, with an overall perforation rate of up to 2.5%,
particularly frequent in the thin-walled right hemicolon.
45
Argon plasma coagulation (APC) is a means of noncontact
coagulation with an almost nonexistent risk of perforation
46
in the colon.
Laser-mediated coagulation (such as with the
Nd:YAG laser) uses high-energy laser light to vaporize the
tissue, producing deeper penetration than APC but with a
higher perforation rate.
Injection of a 1:10,000 dilution of epinephrine is an
e ective and inexpensive method of endoscopic treatment,
causing vasoconstriction and physical compression of the vessel. Metallic clips, both in reusable and disposable forms, are
also suitable for arrest of hemorrhage endoscopically. Rubber
band ligation is frequently employed in lower GI bleeding
due to hemorrhoids or rectal varices.
Interventional Angiography
While initial attempts of embolization led to high rates of
bowel infarction due to the use of large-bore catheters for
cannulation, the more recent approach using microcatheters
has circumvented this and produces success rates of 70–90%
without signi cant complications and recurrent hemor-
47
rhage rates of only 15%.
Embolization material includes
microcoils, Gelfoam (gelatin sponge), and polyvinyl alcohol particles. Selective angiographic embolization has been
shown to arrest life-threatening bleeding from gastroduodenal ulcers, with a low rate of early rebleeding and no late
rebleeding, obviating the need for emergency surgery in
48
high- operative-risk patients.
Early bleeding recurrence is associated with coagulation
disorders, longer time to angiography, higher preprocedural
blood transfusion volume, two or more comorbidities, and
49
the use of coils as the only embolic agent.
Embolization has
also been shown to be of value in patients with diverticular
lower GI bleeding, with an 85% success rate, and particularly
successful in the left colon compared to the right colon and
caecum. Less success was noted in nondiverticular lower GI
bleeding, such as from arteriovenous dysplastic lesions, with
50
a greater than 40% rate of rebleeding.
Angiography may also be coupled with selective infusion of
a vasoconstrictor such as vasopressin or the longer-acting analogue terlipressin; however, this is associated with a 50% rate
51
of rebleeding after cessation of the infusion.
e side e ects
of vasopressin and terlipressin, including abdominal pain and
cardiac complications, have meant that this technique is now
only rarely used.
Surgery
Surgery is rarely used as a means of controlling hemorrhage
except when a clear bleeding point has been identi ed, but all
other modalities of hemorrhage control have failed. However,
surgery remains the treatment of choice in patients with
neoplasia and may be used as a last resort in patients with
recurrent bleeding without a de ned bleeding point or in fulminant hemorrhage. Blind segmental colectomy is associated
with unacceptably high rates of rebleeding (up to 75%) and
mortality (up to 50%); hence intraoperative endoscopy should
be used to aid in determination of the source of bleeding,
resulting in a more conservative directed segmental colectomy
52,
(6% rebleeding and 4% mortality).
53
UPPER GI HEMORRHAGE
Causes of Upper GI Hemorrhage
Causes of upper GI hemorrhage can be divided into variceal
and nonvariceal bleeding ( Table 11-2 ), of which the latter is
more common. Nonvariceal bleeding is also more common
than variceal bleeding in patients with portal hypertension;
however, the higher morbidity and mortality of variceal
bleeding means that this should be excluded before bleeding
is attributed to any other source.
NONVARICEAL BLEEDING
Peptic Ulcer Disease and Bleeding. Numerous studies
demonstrated a worldwide reduction in the incidence of peptic
ulcers between 1958 and 1999, attributable to the introduction
of H. pylori eradication therapy and PPIs. A reduction was also
noted in the rate of operation and mortality from peptic ulcer
disease; however, the overall incidence of peptic ulcer bleeding
TABLE 11-2: CAUSES OF UPPER GI
BLEEDING
Causes Frequency (%)
Nonvariceal
upper GI
bleeding (80%)
Portal
hypertensive
upper GI
bleeding (20%)
GAVE, gastric antral vascular ectasia; GI, gastrointestinal.
Peptic ulcer disease
Mallory-Weiss tears
Gastritis/duodenitis
Esophagitis
Dieulafoy’s lesions
GAVE
Malignancy
Others:
Aortoenteric stula
Hemobilia
Hemosuccus pancreaticus
Iatrogenic bleeding
Gastroesophageal varices
Gastric varices
Portal hypertensive
gastropathy
40
15–20
10–15
5–10
1.5
4
2
7.5
>90
Rare
Rare
Chapter 11 Gastrointestinal Bleeding 223
did not show a signi cant decrease over the same period. 12
11,
Peptic ulcer bleeding still carries a mortality rate of 5–10%,
54
and in-hospital care costs more than $2 billion annually in the
55
United States.
Nonvariceal bleeding accounts for 80–90% of acute upper
GI bleeding, the majority of which is due to gastroduodenal
11
peptic ulceration,
upper GI bleeding.
which accounts for 40% of all nonvariceal
24
A large proportion of this is associated
with use of aspirin and NSAIDs, and the majority of cases
occur in the elderly (68% of patients are >60 years of age and
56
27% >80 years of age).
At some point during the course
of the disease, 10–15% of ulcers will bleed. Patients with
bleeding ulcers commonly present with hematemesis and/or
melena, and require early and aggressive uid resuscitation to
replace any existing losses. History, examination, and investigations should proceed as outlined previously ( Fig. 11-2 ).
Both duodenal and gastric ulcers can bleed profusely; however, this predilection is higher in gastric compared to the
more common duodenal ulcers. Bleeding is most signi cant
when involving an artery such as branches of the gastroduodenal or left gastric arteries.
Several risk strati cation scores have been developed to
assist in identi cation of patients who require close monitoring and are at risk of rebleeding. e two most commonly
used tools are the Rockall score and the lesser used Blatchford score ( Table 11-3 ). e Rockall score utilizes clinical as
well as endoscopic ndings to risk-stratify patients. e score
ranges from 0 to 11; a higher score is associated with greater
57
risk of rebleeding or death.
e Blatchford score uses hemoglobin, blood urea nitrogen, systolic blood pressure, pulse,
melena, syncope, hepatic disease, or cardiac failure to produce
a maximum score of 23; again higher scores indicate higher
58
likelihood of rebleeding or death.
Upper gastrointestinal
bleeding
Actively
bleeding
ulcer
Ulcer with adherent
clot or visible
vessel
Ulcer with clean
spot
TABLE 11-3: COMPARISON OF THE
BLATCHFORD AND ROCKALL SCORES
Criteria of the
Blatchford Score
Systolic blood pressure
Blood urea nitrogen
Hemoglobin
Pulse
Melena
Syncope
Hepatic disease
Cardiac failure
Criteria of the Rockall
Score
Age
Shock
Coexisting illness
Endoscopic diagnosis
Endoscopic stigmata of
recent hemorrhage
e endoscopic appearance of a bleeding ulcer alone can
also be used to stratify the risk of rebleeding using the Forrest criteria ( Table 11-4 ).
59
High-grade lesions are those that
are actively spurting or oozing blood, or have a nonbleeding
visible vessel or adherent clot.
Medical Management
STOP ANY CAUSES (EG, DRUGS). All ulcerogenic medication
such as salicylates, NSAIDs, and SSRIs should be stopped
and nonulcerogenic alternatives prescribed. Cyclooxygenase-2 (COX-2) inhibitors, which initially showed promise as
a gastroprotective alternative to NSAIDs have recently been
shown to demonstrate cardiotoxicity without signi cant
bene t on gastric mucosal protection and are therefore infre-
60
quently used.
ERADICATION OF H. PYLORI AND LONG-TERM ACID SUPPRESSION.
e association of bleeding with H. pylori infection is not
as strong as the association reported for perforated ulcers,
with H. pylori infection reported in only 60–70% of bleed-
ing ulcers. However, recent data show that treating patients
positive for H. pylori with eradication therapy reduces the risk
of rebleeding and obviates the need for long-term acid sup-
61
pression
; hence H. pylori eradication is recommended in all
bleeders infected with H. pylori .
Injection/thermal
coagulation + high dose
PPIs and eradication of
H. pylori
Uncontrolled
bleeding
Surgery/repeat
endoscopic therapy
FIGURE 11-2 An algorithm for the management of peptic ulcer
bleeding.
Controlled
bleeding
Conservative
management and
eradication of
H. pylori
Recurrent
bleeding
TABLE 11-4: FORREST CLASSIFICATION
FOR ENDOSCOPIC FINDINGS AND RISK OF
REBLEEDING IN PEPTIC ULCER DISEASE
Classi cation
(Grade)
Ia Active, pulsatile bleeding High
Ib Active, nonpulsatile bleeding High
IIa Nonbleeding visible vessel High
IIb Adherent clot Intermediate
IIc Ulcer with at, pigmented spot Low
III Clean, nonbleeding ulcer bed Low
Endoscopic
Finding
Risk of
Rebleeding
224 Part II Abdominal Wall
Gastric acid has been shown to impair clot formation,
promote platelet disaggregation, and increase brinolysis.
In keeping with this, PPIs have been shown to signi cantly
reduce the risk of ulcer rebleeding, the need for urgent surgery,
and, in patients with high-risk stigmata who have undergone
62,
endoscopic therapy, mortality.
63
Endoscopic Management. Patients with high-risk stigmata
on endoscopy (active bleeding or nonbleeding visible vessel)
require haemostatic intervention, such as injection, and thermal or mechanical therapy such as clips ( Fig. 11-3 ). Addition
of any one of these to adrenaline injection further reduces
64–66
rebleeding rates, the need for surgery, and mortality.
Several factors are predictors of failure of endoscopic
therapy for peptic ulcer bleeding, including previous ulcer
bleeding, shock and presentation, active bleeding during
endoscopy, ulcers greater than 2 cm in diameter, a large
underlying bleeding vessel greater than 2 mm in diameter,
and ulcers on the lesser curve of the stomach or the poste-
67
rior or superior duodenal bulb.
Recent studies suggest that
second-look endoscopy (within 24 hours of the initial endoscopic therapy) provides only a small reduction in the rate of
rebleeding, is not cost-e ective in the presence of acid-sup-
25,
68,
pressing medication, and is overall not recommended.
69
Repeat endoscopy should only be considered in cases of
recurrent hemorrhage or unsuccessful rst treatment.
Surgical Management. Meta-analysis and surgical registry
data show the rate of surgical intervention for bleeding peptic
ulcers has decreased to 6.5–7.5%. An improved understanding of peptic ulcer disease as well as the development of newer
pharmacologic and endoscopic treatments has meant that
surgery is now employed not as rst-line or curative treatment, but instead only when other modalities have failed.
ere are no consensus guidelines on the appropriate
indications for surgery; however in general, persistent blood
TABLE 11-5: POSSIBLE INDICATIONS FOR
SURGICAL INTERVENTION FOR PEPTIC
ULCER BLEEDING
Possible Indications for Surgery in Peptic Ulcer
Bleeding
Absolute indications Persistent blood loss refractory to
endoscopic therapy
Shock with recurrent hemorrhage
Slow blood loss requiring >3 units blood
Relative indications Shock on admission
Transfusion in excess of 6 units
Elderly patient
Severe comorbidity
Rare blood type/refusal of transfusion
Suspicion of malignancy in a gastric ulcer
loss with failure of endoscopic therapy and a blood transfusion requirement in excess of 6 units are often considered an
indication for surgical intervention ( Table 11-5 ). Similarly,
hypovolemic shock associated with recurrent hemorrhage or
a slow continuous blood loss requiring transfusion of more
than 3 units per day is also considered indicative. Shock on
admission, an elderly patient, severe comorbidity, a rare blood
type, refusal of transfusion, and bleeding chronic gastric
ulcer with a suspicion of malignancy are considered relative
indications for surgery.
In stable patients with evidence of rebleeding, a second
attempt at endoscopic hemostasis is often as e ective as surgery
with fewer complications and is the recommended manage-
70
e aim of surgery in both gastric and duodenal
ment.
ulcers is to arrest hemorrhage and perform an acid-reducing
procedure if deemed necessary.
FIGURE 11-3 Metallic clips to arrest bleeding from a duodenal
ulcer.
(Used with permission from Dr Nicola Simmonds, Luton and Dunstable
Hospital, UK.)
OPERATIVE PROCEDURE FOR DUODENAL ULCERS. A longitudi-
nal duodenotomy or duodenopyloromyotomy provides good
exposure of bleeding sites in the duodenal bulb, the most
common site of duodenal ulcers. Direct pressure provides
temporary arrest of the bleeding, and it should be followed by
suture ligation with a nonabsorbable suture such as Prolene.
Four-quadrant suture ligation will achieve hemostasis in
anterior ulcers. Posterior ulcers, particularly if involving the
pancreaticoduodenal or gastroduodenal artery, will require
suture ligation of the artery both proximal and distal to the
ulcer for adequate control of hemorrhage, as well as placement
of a U-stitch underneath the ulcer to control the pancreatic
branches ( Fig. 11-4 ).
e use of an acid-reducing procedure in duodenal ulcers
remains a topic of debate, as theoretically arrest of hemorrhage
and H. pylori eradication is likely to be su cient management.
In the absence of trials and convincing data, however, it is
hard to make any rm recommendations, and the decision
is best left to the surgeon taking into account each patient’s
condition and their experience with such operations. Surgical
Chapter 11 Gastrointestinal Bleeding 225
be an option. Management of bleeding ulcers at the cardioesophageal junction and the proximal stomach is more challenging. While optimal resection would involve a proximal
or near-total gastrectomy, this results in increased morbidity
and mortality in patients acutely bleeding. More conservative
options may suce, such as distal gastrectomy with resection
of a tongue of proximal stomach to ensure excision of the
ulcer, or a wedge resection of the ulcer or simple oversewing
with a vagotomy and pyloroplasty.
Mallory-Weiss Tears. e sensation of nausea is accompanied
by closure of the pylorus, gastric distension, and retrograde
propulsion of gastric contents toward the cardia. When this is
followed by vomiting, the diaphragm moves abruptly upward,
associated with rapid increase in intra-abdominal pressure
that pushes the gastric cardia into the thorax through the
diaphragmatic hiatus. With sucient force, a longitudinal
71
laceration of the esophagus or stomach can result.
Hiatus
hernias coexist in more than 75% of patients with MalloryWeiss tears, and the amount of herniated stomach determines
the point of maximal dilation (law of Laplace) and therefore
72,73
the position of the tear.
Large hiatus hernias are associated
with more distal tears, while in patients with small or absent
hiatus hernias, tears occur at or below the gastroesophageal
junction. e majority of tears are situated within 2 cm of the
gastroesophageal junction on the lesser curvature.
e highest incidence of Mallory-Weiss tears occurs in
patients between 30 and 50 years of age and in men more
than women. Some 40–75% of patients have a history of
FIGURE 11-4 Suture control of bleeding duodenal ulcers. A
longitudinal pyloric incision is made and gure-of-eight sutures are
placed at the cephalad and caudad aspects of the ulcer to occlude the
gastroduodenal artery.
alcohol use
cally present with a history of several episodes of vomiting or
retching followed by hematemesis with fresh red blood. Ten
percent of patients may present with only melena.
74
and 30% a history of aspirin use.75 Patients typi-
EGD usually identies a single tear on the lesser curve
of the cardia, or occasionally on the greater curvature of the
cardia. Retroexion during the endoscopic examination is
options for acid reduction in bleeding duodenal ulcer management include pyloroplasty with truncal vagotomy, parietal cell
vagotomy, or antrectomy with truncal vagotomy. e former
is the most frequently used as it is facilitated by the longitudinal approach to the pylorus for arrest of hemorrhage. Parietal
cell vagotomy is limited by surgeon inexperience. Antrectomy
with truncal vagotomy may be suitable in patients refractory
to conservative surgery but is a complex procedure that is
unsuitable in the shocked patient. Ulcer surgery is covered in
greater detail in Chap. 26.
an important maneuver in these patients to ensure the distal gastroesophageal junction and cardia are visualized. e
majority of lesions heal spontaneously; hence management
is largely supportive, with emphasis on antiemesis and acid
suppression. Patients with persistent bleeding may require
endoscopic injection or thermocoagulation, or angiographic embolization. Surgery may be required should
these options prove unsuccessful, and hemorrhage can be
arrested operatively by a high gastrotomy and suture of the
mucosal laceration.
OPERATIVE PROCEDURE FOR GASTRIC ULCERS. Management of
the bleeding gastric ulcer also prioritizes arrest of the bleeding.
However, because of the risk of rebleeding and the 10% risk
of malignancy in gastric ulcers, gastrotomy and suture ligation
are insucient in these patients. Resection of the ulcer alone
is associated with a 20% rebleeding rate; hence a distal gastrectomy is recommended for ulcers in the antrum and distal
stomach. In patients who may be unt for a distal gastrectomy,
resection of the ulcer itself combined with an acid-reducing
procedure in the form of a vagotomy and pyloroplasty may
Stress-Related Mucosal Bleeding. Critically ill patients
are at risk for the development of diuse mucosal injury of
the stomach, resulting in upper GI bleeding with signicant
morbidity and mortality. is phenomenon, termed “stressrelated mucosal bleeding” or occasionally “stress gastritis,” is
a result of a combination of mucosal ischemia and reperfusion injury and impairment of host cytoprotective defenses,
and ultimately results in a prolonged ICU stay in a vulner-
65
able population of patients.
While this phenomenon was
previously common, the incidence of clinically signicant
226 Part II Abdominal Wall
bleeding in the critically ill population has now decreased to
less than 3.5% with the use of prophylaxis.
76
e most important risk factors for stress-related mucosal
bleeding are prolonged mechanical ventilation (>48 hours)
and coagulopathy. Other factors include shock, severe sepsis, neurologic injury/neurosurgery, greater than 30% burns,
and multiorgan failure. Patients with these risk factors require
prophylaxis with antacids, H
-receptor blockers, PPIs, or
2
Carafate.
Acid suppression is often sucient to control hemorrhage in stress-related mucosal bleeding. For persistent
bleeding, options include selective infusion of octreotide
or vasopressin via the left gastric artery, endoscopic measures, or angiographic embolization. Surgery is now rarely
performed but, if necessary, involves vagotomy and pyloroplasty with oversewing of discrete regions of hemorrhage or
subtotal gastrectomy.
Esophagitis. In rare cases bleeding may originate in the
esophagus and is then often due to esophagitis. Gastroe-
mucosa to irritant acidic gastric content, causing chronic
inammation and blood loss (Fig. 11-5). Occasionally ulceration may follow, presenting as occult bleeding with anemia
or guaiac-positive stool. While GERD is the most common
cause, other causes include Crohn’s disease, certain drugs,
and radiotherapy. Immunocompromised patients may have
esophagitis of an infective etiology; causes most commonly
include herpes simplex, Candida, and cytomegalovirus
(CMV), but esophagitis can occasionally be due to ulceration directly induced by human immunodeciency virus
(HIV) or Epstein-Barr virus, or secondary involvement of
the esophagus in mycobacterial infection of adjacent lymph
77
nodes.
Infective esophagitis is uncommon but may lead to
torrential hemorrhage.
Management, particularly of GERD-induced esophagitis,
hinges on acid-suppressive therapy, occasionally requiring
therapeutic endoscopy to arrest the bleeding. Treatment of
the infective cause is often successful at managing the bleeding in immunocompromised infected patients.
Dieulafoy’s Lesion. Dieulafoy’s lesions are an arterial vascu-
lar anomaly featuring abnormally large (“caliber persistent”)
submucosal end arteries, likely congenital in origin, and with
the potential for massive, potentially life-threatening hemorrhage upon erosion of the overlying gastric mucosa. ese
lesions are most commonly located in the stomach within
5–7 cm of the cardia but may present in small bowel, duodenum, and colon. ese account for 1.5% of upper GI bleeding and are more commonly encountered in men.
78
Dieulafoy’s lesions appear as reddish-brown protrusions
on endoscopy with no ulceration. Endoscopic therapy is
often successful provided good visualization of the lesion is
obtained; mechanical methods such as clipping or banding
have been shown to work better than injections for control of
79,80
hemorrhage.
Angiographic embolization or surgery may
be employed for endoscopic failures. Surgical intervention
may require prior endoscopic tattooing to facilitate identication of the site, followed by wedge resection of the lesion.
78
Gastric Antral Vascular Ectasia (GAVE). GAVE, or
“watermelon stomach,” is so named for the dilated, tortuous
mucosal capillaries and veins present in the antrum, converging onto the pylorus, and resembling the surface of a watermelon (Fig. 11-6). is condition is more common in women
than in men and often presents with occult blood loss and iron
FIGURE 11-5 Gastroesophageal reux disease (GERD) viewed on
endoscopy.
FIGURE 11-6 Gastric antral vascular ectasia (GAVE) can be seen in
the gastric antrum, giving the stomach a watermelon appearance.
with permission from Dr Nicola Simmonds, Luton and Dunstable Hospital,UK.)
(Used
Chapter 11 Gastrointestinal Bleeding 227
FIGURE 11-8 Intraoperative appearance of an aortoenteric stula.
e photograph demonstrates a large hole (black arrow) in the posterior aspect of the third part of the duodenum after it was medialized
FIGURE 11-7 A gastrointestinal stromal tumor (GIST) of the
stomach on endoscopy.
Luton and Dunstable Hospital, UK.)
(Used with permission from Dr Nicola Simmonds,
and peeled o of the graft. e photograph has been taken from left side
of the table with the patient in supine position.
from Neal Barshes, MD, MPH, Brigham and Women’s Hospital, Boston, MA.)
(Used with permission
deciency anemia. APC is the treatment of choice for GAVE;
treatment may need to be repeated for recurrences, and PPI
cover is recommended for 1 month following treatment.
78,81
Patients refractory to APC should be considered for surgical
intervention in the form of an antrectomy.
Malignancy. Malignant upper GI lesions rarely present with
overt signicant hemorrhage and instead are more likely
to present with hemoccult-positive stool or iron deciency
anemia. Endoscopy occasionally reveals a recurrent bleeding
ulcer, a common feature of GI stromal tumors, which characteristically appear as a submucosal tumor with central umbilication and ulceration (discussed further in Chap. 24), and on
occasion leiomyomas and lymphomas (Fig. 11-7). Surgery is
necessary as the rate of rebleeding in these malignant lesions
is high, and may involve full curative resections or in unt
patients, palliative wedge resections for hemorrhage control.
Aortoenteric Fistula. Aortoenteric stula is an impor-
tant clinical condition, often presenting with torrential
GI hemorrhage. Primary stulae are rare; most commonly
stulation occurs following a previous abdominal aortic aneurysm (AAA) repair and is seen in approximately 1% of these
cases. e pathophysiology behind this is likely to be infective
in origin, leading to the development of a pseudoaneurysm
at the proximal suture line, resulting in stulization into the
duodenum (Fig. 11-8).
Early diagnosis of this problem is critical but can be
dicult. A high index of suspicion is required in all patients
presenting with GI hemorrhage with known aortic aneurysms or a history of previous aortic aneurysm repair. Often,
patients present with several smaller, self-limiting episodes of
GI hemorrhage (“sentinel bleeds”). Urgent endoscopy at this
stage is essential to preempt a subsequent torrential, often
fatal bleed, and usually reveals bleeding at the third or fourth
part of the duodenum (Fig. 11-9). CT with IV contrast is
a useful adjunct in these patients, often demonstrating air
within the aortic thrombus or around the graft (particularly
in the context of an infected graft), and rarely a pseudoaneurysm or contrast within the duodenal lumen.
Surgical repair involves extra-anatomic bypass grafting and
aortic ligation for primary aortoenteric stula. For secondary aortoenteric stula, surgery involves excision of the graft
with extra-anatomic bypass or in situ aortic reconstruction. By
necessity these procedures are often performed in critically ill,
FIGURE 11-9 Endoscopic view of the aortoenteric stula on EGD
showing the stulous track (black arrow) into the aneurysmal sac from
the third part of the duodenum.
MD, MPH, Brigham and Women’s Hospital, Boston, MA.)
(Used with permission from Neal Barshes,
228 Part II Abdominal Wall
severely exsanguinated, and septic patients and hence associated with high morbidity and mortality.
With the advent of endovascular stenting for primary AAA
repair, various studies have been performed to determine the
eectiveness of endovascular stenting for aortoenteric stula.
is has been associated with a high incidence of recurrent
bleeding and infection, particularly in the presence of preprocedural infection.
82
Hemobilia. Hemobilia is a rare cause of GI bleeding. Causes
include trauma, hepatic neoplasms, instrumentation of the
biliary tree, percutaneous radiofrequency liver ablation, and
following liver transplant. A high index of suspicion is required
in patients with these risk factors, as the classic presentation of
hemorrhage, right upper quadrant pain, and jaundice is only
seen in a minority of patients. Endoscopy may reveal blood
at the ampulla, but angiography and embolization remain the
diagnostic and therapeutic modality of choice.
Hemosuccus Pancreaticus. Bleeding from the pancre-
atic duct (hemosuccus pancreaticus) is another rare cause of
upper GI bleeding, due to stulation of a pancreatic pseudo-
83
cyst into the splenic or other peripancreatic artery.
A presentation of abdominal pain, hematemesis, and melena in
patients with a previous history of pancreatitis should raise
suspicion of hemosuccus pancreaticus. Angiography is again
both diagnostic and therapeutic, although in some cases distal
pancreatectomy may be employed.
Iatrogenic Bleeding. Upper GI endoscopy or surgery is
another cause of bleeding. Percutaneous gastrostomy is often
necessary as a means of nutritional support in certain conditions but is accompanied by a 3% rate of GI hemorrhage.
Bleeding may have tracked into the stomach from the incision site but may also be from the stomach mucosa; both
causes can be managed endoscopically.
Endoscopic sphincterotomy is increasingly common as a
means of accessing the biliary tree during an endoscopic retrograde cholangiopancreatography and facilitates endoscopic
clearance of the common bile duct, but it is associated with a
2% risk of bleeding. Bleeding may occur after 48 hours but
can often be arrested by local injection of epinephrine, rarely
requiring surgical intervention. Bleeding following upper GI
surgery may occur from suture or staple lines. is can occasionally be treated endoscopically, with minimal insuation
to avoid disruption of the anastomosis.
and is one of the most important complications of hepatic
cirrhosis. Variceal bleeding is associated with increased risk
of rebleeding and transfusion requirement, greater length
of hospital stay, and higher morbidity and mortality compared with nonvariceal bleeding.
17,84
Gastroesophageal varices represent one site of portosystemic anastomosis, which is dilated as the portal circulation
tries to decompress to the systemic circulation. Other sites
of portosystemic collaterals are the stomach, the umbilical region (collateral formation leads to formation of caput
medusae), and the distal rectum.
Factors that determine variceal bleeding include high
variceal wall tension (determined by vessel diameter) and
variceal pressure, in turn related to hepatic venous pressure
gradient (HPVG). Patients with a HPVG of less than 12 mm
Hg are unlikely to develop variceal bleeding.
85
Isolated gastric varices (IGV) can occur in the absence of
esophageal varices and are located along the gastric fundus
84
(IGV1), or along the body, antrum, or pylorus (IGV2).
Risk
factors for gastric variceal bleeding include variceal size and
area or spots on the mucosal surface of a varix).
86
In addition to varices, portal hypertension can also cause
the development of portal hypertensive gastropathy, diuse
dilation of the mucosal, and submucosal venous plexus of
the stomach with overlying gastritis. e stomach develops
a snake-skin appearance with cherry-red spots on endoscopy,
and rarely may be the site of major hemorrhage (Fig. 11-10).
e management of variceal upper GI bleeding follows the
same principles as those of nonvariceal upper GI bleeding, with
VARICEAL BLEEDING AND
PORTAL HYPERTENSION
Portal hypertension is a serious cause of upper GI bleeding, often the result of cirrhosis that is the end stage of
chronic liver disease. e pathophysiology of portal hypertension is discussed further in Chap. 47 and hence is not
covered here. Approximately 50% of patients with cirrhosis
will develop gastroesophageal varices as a result of portal
84
hypertension.
Variceal bleeding occurs in 30% of patients
FIGURE 11-10 Endoscopic view of portal hypertensive gastropathy.
Note the snake-skin appearance of the stomach and the associated
cherry-red spots.
Dunstable Hospital, UK.)
(Used with permission from Dr Nicola Simmonds, Luton and
Chapter 11 Gastrointestinal Bleeding 229
Prophylaxis
Pharmacological management
Acute variceal bleeding
Endoscopic therapy
Evaluation
Good liver function Poor liver function
No
Transplant candidate
Banding + a block
Rebleed
DSRS or TIPS
Progressive liver disease
Transplant candidate
FIGURE 11-11 An algorithm for the management of variceal
bleeding. DSRS, distal splenorenal shunt; TIPS, transjugular intrahepatic portosystemic shunt.
Ye s
Transplant
emphasis on urgent resuscitation and therapeutic endoscopy
because of the higher morbidity and mortality associated with
variceal bleeds (Fig. 11-11).
EGD remains the gold standard for diagnosing variceal
bleeding. e diagnosis of variceal hemorrhage is based
onmeeting one of the following criteria: active bleeding from
a varix, a “white nipple” overlying a varix, clots overlying a
varix, or varices with no other potential source of bleeding.
87
Management. Treatment of variceal bleeding requires a
combination of medical and endoscopic management.
Medical. Somatostatin or its analogues octreotide or terlip-
ressin should be administered as a bolus immediately in cases
where there is a high index of suspicion, and continued for 3–5
84
days after endoscopic conrmation of diagnosis.
Fluids and
blood products should be administered judiciously to maintain
a hemoglobin level of greater than 8 g/dL. Current recommendations are that any patients with cirrhosis and GI bleeding
should be given up to 7 days of antibiotic prophylaxis, specically a uoroquinolone such as noroxacin or ciprooxacin.
Endoscopic. Variceal bleeding should be diagnosed
and treated by EGD, either with variceal ligation or
sclerotherapy.
84
In patients with variceal bleeding, endos-
copy should be performed as soon as possible (within
88,89
12hours of admission).
is is of particular importance
in patients with hemodynamic instability or features of cirrhosis. Early endoscopy also excludes nonvariceal causes of
bleeding, which occur in 15% of patients with varices.
90
Variceal ligation is the endoscopic treatment of choice as it
has been shown to have lower rates of complications compared to sclerotherapy, which can cause perforation, mediastinitis, and stricture formation. Variceal ligation involves
the placement of rubber bands on the varices to completely
interrupt blood ow into the ligated varix and arrest hemorrhage acutely. e mucosa and submucosa develop ischemic
necrosis and granulation and sloughing of the rubber rings,
and necrotic tissue results in replacement of varices by scar
tissue. Sequential treatments may be required, as many as
three treatments over 24hours, but will achieve control of
hemorrhage in up to 90% of patients.
Mechanical tamponade devices may be useful in temporarily controlling bleeding from esophageal varices where
endoscopy and medical management have failed. One example is the Sengstaken-Blakemore tube, which consists of a
gastric tube with gastric and esophageal balloons. Ination
of the gastric and esophageal balloons compresses the esophagogastric venous plexus, arresting bleeding, but at the risk
of ischemic necrosis and perforation. Deation of the tube
can be associated with recurrent bleeding in 50% of patients;
hence this technique is reserved as a temporizing measure in
massive hemorrhage before more denitive intervention is
commenced.
Gastric varices should be managed initially by pharmacotherapy. Endoscopic therapy is not as successful in gastric
varices because of the diuse nature of portal hypertensive gastropathy. Patients with refractory bleeding should be referred
early for decompressive therapy such as TIPS (transjugular
intrahepatic portosystemic shunt) or shunting.
IGVs, without associated portal hypertension, can occur
in the setting of splenic vein thrombosis, often associated
with pancreatitis. Varices occur in the presence of normal central portal pressures due to left-sided hypertension, rerouted
from the spleen to the short gastric vessels. Splenectomy may
relieve the hypertension, but the risk of variceal bleeding in
these patients is low and hence splenectomy should not be
routinely undertaken.
91
PREVENTION OF REBLEEDING. Prevention of rebleeding is of the
utmost importance in this patient population. Rebleeding
may occur in up to 70% of patients within 2 months without
92
further denitive therapy.
e highest risk of rebleeding is in
the rst few days following the initial episode. A combination
of nonselective beta-blockers with isosorbide mononitrate has
been shown to be more eective than beta-blockers alone in
93
preventing rebleeding.
e addition of prophylactic endoscopic band ligation to combination pharmacotherapy did
not reduce the risk of rebleeding but instead was associated
with more adverse events in a recent randomized controlled
94
trial.
230 Part II Abdominal Wall
Radiologic or Surgical Portal Decompression. In
approximately 10% of cases of variceal bleeding, endoscopic
management is unsuccessful, necessitating urgent decompression of the portal system. A TIPS procedure involves the
creation of an articial anastomosis between the hepatic and
portal veins under uoroscopic guidance with the use of a
covered stent, shunting blood away from the hepatic sinu-
95
soids and relieving portal pressure.
TIPS is, however, associated with a 30-day mortality of up to 30% in the emergency
setting, usually a result of hepatic encephalopathy from diver-
96
sion of blood away from the liver parenchyma.
Rebleeding
may occur in 20% of patients and is often due to occlusion
of the anastomosis. Surgery is another therapeutic option for
decompression of the portal system. Surgical shunts, such
as the selective distal splenorenal shunt (DSRS), have lower
rates of rebleeding compared to endoscopic therapy but do
97
not demonstrate any dierence in survival.
DSRS patients
have an in-hospital mortality of approximately 5%, a 5–8%
97
rate of rebleeding, and a 75–80% 3-year survival.
A recent
randomized controlled trial comparing TIPS with DSRS in
patients with failed medical or endoscopic therapy showed
no signicant dierence in the rate of rebleeding, hepatic
encephalopathy, or overall survival, but identied a need
for close follow-up and a greater need for reintervention in
patients subjected to TIPS, suggesting that in patients with
relatively limited access to health care facilities, DSRS may
98
be a more suitable therapeutic option.
Further details on
surgical decompression for portal hypertension are covered
in Chap. 47.
LOWER GI HEMORRHAGE
Lower GI bleeding can occur from any site distal to the
ligament of Treitz, most commonly from the colon.
Occasionally bleeding can also occur from the small bowel.
Diculty in diagnosis of lower GI bleeding stems from the
large surface area of colon and small intestine, intermittent
bleeding, occasional lack of visible mucosal lesions, and difculties in endoscopic visualization as lesions are obscured
by forward movement of blood. e majority of patients
with lower GI bleeding experience self-limiting episodes;
only 10–20% of patients present with massive unremitting lower GI bleeding. Patients with self-limited bleeding
can usually be managed with initial resuscitation, exclusion of an upper GI source, and further investigation using
colonoscopy and, if necessary, angiography or nuclear scintigraphy. Younger patients with suspected hemorrhoidal
bleeding should be followed up and the hemorrhoids
managed appropriately, while older patients should be
investigated for malignancy before bleeding is attributed
to a benign pathology. Bleeding from the anus or rectum
can be identied by digital rectal examination (DRE) and
proctoscopy and may on occasion require sigmoidoscopy.
Upper GI bleeding can be eectively excluded in the presence of a blood-free bilious NG aspirate; however, an EGD
is required for denitive exclusion.
Management of Lower GI Hemorrhage
Lower GI bleeding is often less severe than upper GI bleeding;
however, the same principles for resuscitation should be followed (Fig. 11-12), guided by the hemodynamic stability of
the patient. Accurate identication of the source of bleeding
can be dicult in patients with lower GI bleeding—more than
one source for bleeding is found in 40% of patients and in
up to 25% of patients no source is identied. A management
algorithm is outlined in Fig. 11-13. Patients with hematochezia who are hemodynamically stable should undergo colonoscopy in the rst instance to identify a cause for the bleeding.
If a bleeding site is identied, endoscopic therapy should be
attempted to control the bleeding. If no bleeding site is identied, an EGD should be performed, followed by capsule or
deep enteroscopy if this is unsuccessful. Hemodynamically
unstable patients should undergo EGD in the rst instance as
severe upper GI bleeding may often present as hematochezia.
Patients with bleeding refractory to endoscopic management or those with signicant hemodynamic instability may
require urgent operative intervention. In these patients an
exploratory laparotomy is required, and attempts made to
determine the location of blood within the GI tract. Although
this is relatively nonspecic, it may assist in broadly localizing
the origin of bleeding; for instance if blood is only present
beyond the ileocecal valve, bleeding is likely to be colonic
in origin. e GI tract should be thoroughly examined to
exclude bleeding from small bowel tumors or Meckel’s
diverticulum. A segmental bowel resection is appropriate in
localized bleeding, and in relatively t patients this may be
combined with a primary anastomosis. In unt patients with
preexisting hemodynamic instability or severe malnutrition,
a mucous stula and end stoma is a more appropriate option.
Segmental colectomies should not be performed as “blind”
procedures without localization of the bleeding source, as
these have been associated with unacceptably high mortality
99
rates and rebleeding rates between 20 and 50%.
A better
alternative in patients without localization of the bleeding
source is a “blind” subtotal colectomy, with a primary ileorectal anastomosis, associated with a less than 10% mortality
rate and less than 10% rebleeding rate with the benet of
normal postoperative bowel control. is procedure further
allows irrigation of the rectal segment with repeat proctoscopy to rule out rectal bleeding.
On-table lavage may allow identication of a bleeding
source, facilitating segmental colectomy, but is best attempted
in stable patients who may not retain acceptable bowel function after a total or subtotal colectomy and not advised in the
unstable patient.
Causes of Lower GI Hemorrhage
OVERT LOWER GI BLEEDING
e majority of lower GI bleeding originates from the colon
as a result of common pathologies such as diverticular disease
Chapter 11 Gastrointestinal Bleeding 231
Acute lower gastrointestinal bleeding
Ye s
Begin necessary treatment
Anorectal outlet bleeding confirmed
on DRE and anoscopy
No
Ye s
Persistent bleeding, large amounts
Manage as upper GI bleeding
Hemodynamically unstableHemodynamically stable
Transfer to operating room
Source of
bleeding
undetermined
Localization of
bleeding with
serial damping or
intraoperative
enteroscopy then
resection of
affected segment
Bleeding from
colon/small
bowel
Subtotal
colectomy with
ileorectal
anastomosis or
small bowel
resection
Intermittent bleeding, small amounts
Colonoscopy
Source of bleeding
identified
Begin necessary
treatment
Positive
Negative
Fur ther colonoscopy
Blood in NG aspirate
No
No source of bleeding
seen, persistent bleeding
Small bowel investigations
• Small bowel series
• Enterodysis
• Deep/capsule enteroscopy
Negative
Tagged red cell scan
Positive
Angiography and
embolization +/−
segmental resection
FIGURE 11-12 An algorithm for the management of lower gastrointestinal bleeding. DRE, digital rectal examination; GI, gastrointestinal; NG,
nasogastric. (
Adapted from Fig. 46-12, Sabiston Textbook of Surgery, 18th ed. Townsend, Beauchamp, Evers, and Mattox, Elsevier.)
and neoplasia (Table 11-6). Early identication of the cause
of bleeding is essential to initiate appropriate management, in
particular for cases of malignancy.
Diverticular Disease. Diverticular disease is an extremely
prevalent and often asymptomatic disease of Western countries.
e incidence increases with age; up to 60% of patients older
100
than 80 years have diverticulae.
In Western countries, 95% of
diverticula are in the sigmoid and left colon; however, in Asian
101,102
countries 70% of cases are in the right colon.
Colonic
diverticular are usually pulsion-type pseudodiverticula—
outpouchings of the mucosa and submucosa through the
muscular layer of the bowel at the sites of penetration of the
vasa recta—resulting from high intraluminal pressure and
bowel segmentation. Only 4–17% of patients with diverticu-
103
lar disease develop symptoms of bleeding
; however, the fre-
quency of diverticular disease means that diverticular bleeding
104
accounts for 30–40% of lower GI bleeding.
Eighty percent
of diverticular bleeds stop spontaneously, but a small minority
will require hemostatic intervention. Ten percent of patients
willrebleed within a year and 50% within 10 years.
104
FIGURE 11-13 An inamed diverticulum with associated bleeding
(black arrow) seen on colonoscopy.
Simmonds, Luton and Dunstable Hospital, UK.)
(Used with permission from Dr Nicola