COMPLICATIONS OF GASTRODUODENAL ULCERS

Peptic ulcers are open sores

include :
1. Gastric ulcers
2. Esophageal ulcers
3.Duodenal ulcers

CAUSES
H. pylori infections are now uncommon.
(NSAIDs).
Smoking, alcohol.
Mental stress.
Genetics.
This is because these types of ulcers do not always cause obvious symptoms, so
are left untreated.
Gastric and duodenal ulcers usually cannot be differentiated based on history
alone, although some findings may be suggestive. Epigastric pain is the most
common symptom of both gastric and duodenal ulcers, characterized by a
gnawing or burning sensation and that occurs after meals—classically, shortly
after meals with gastric ulcers and 2-3 hours afterward with duodenal ulcers.
Gastric and duodenal ulcers are two kinds of peptic ulcers. A peptic ulcer is a
sore that’s on the inside of the stomach lining — a gastric ulcer — or the upper
part of the small intestine — a duodenal ulcer.
A person can have one or both types of ulcers at the same time. Having both
types is known as gastroduodenal.
One way of telling if you may have a gastric or duodenal ulcer is to figure out
where and when your symptoms occur. For some, the time between meals
aggravates an ulcer. For others, eating may be a trigger for the pain.The exact
location of the pain doesn’t always match up with the location of the ulcer,
though. Sometimes the pain is referred. This means that a person may have pain
in a location away from the actual ulcer.
H. Pylori is the most common cause of gastric and duodenal ulcers. This
bacterium affects the mucus that protects your stomach and small intestine,
allowing for stomach acid to damage the lining.

H. pylori is the most common cause of gastric and duodenal ulcers. This
bacterium affects the mucus that protects your stomach and small intestine,
allowing for stomach acid to damage the lining.
An untreated gastric or duodenal ulcer can develop into a serious problem,
especially if you have certain existing medical conditions.

It is estimated that around 1 in 50 people with a NSAID-related stomach ulcer

will develop a complication

SYMPTOMS OF COMPLICATED PUD

sudden, sharp pain that doesn’t stop
black or bloody stools
bloody vomitus
vomit that looks like coffee grounds
COMPLICATIONS OF PUD
1. Perforation
2. Bleeding
3. Penetration
4. Malignization
5. Obstruction

The most common complications of ulcers are:

Perforation: Peptic ulcers can eat a hole through (perforate) the wall of your
stomach or small intestine, putting you at risk of serious infection of your
abdominal cavity (peritonitis).

Bleeding Ulcer: Bleeding can occur as slow blood loss that leads to anemia or
as severe blood loss that may require hospitalization or a blood transfusion.
Severe blood loss may cause black or bloody vomit or black or bloody stools.

Pyloroduodenal Stenosis: It occurs as a result of peryulcer infiltrate, scaring

because of healing of the ulcer, hypostasis and spasm.

Penetrated and callous Ulcer: It’s a chronic non-healing ulcer;floor contains non
unhealthy, flabby whitish yellow granulation tissue and a thin scanty serous
discharge or with indurated non tender edge; base is indurated, non tender and
often fixed. Ulcer does not show any tendency to heal. It lasts for many months
to years. Tissue destruction is more with absence of or only minimal
regeneration.

PEPTIC ULCER PERFORATION

It affects around 1 in 350 people with a stomach ulcer.
Annual incidence of ulcer perforation is 4 to 14 cases per 100,000 individuals
Operative treatment
– risk status
– definitive surgery vs. simple closure
– laparoscopy

Nonoperative treatment
• Water soluble contrast study documenting
sealed perforation
• Age<70
• NG tube, antibiotics, acid suppression, IVF
• Improving exam and clinical signs within 12 hours
• 70% success rate in avoiding surgery, 35% longer hospital stay

Operative treatment—risk assessment

• Multiple studies show mortality a function of risk status, independent of
operation performed
– Age>70, perforation>24 hours, SBP<100, poorly controlled comorbid
conditions define high risk patient
Benefits of definitive operation
• High risk of recurrent ulcer disease (48-60%) if simple closure done, though
this can be lowered by long term acid suppression
• PCV lowers above to 3-7%, can be combined with patch closure
• Not advised in setting of shock, significant comorbidity, gross peritonitis

Parietal Cell Vagotomy

What about laparoscopy?
• Small series published detailing feasibility and efficacy of laparoscopic (and
combined endoscopic/laparoscopic) patch procedures in selected patients
• Laparoscopic vagotomies also described and reported in small series (Taylor,
truncal, true PCV)
• Remember for gastric lesions, excision or biopsy as a minimum advised

H. pylori?
• 83 patients with perforated DU
– 47% H. pylori + (similar to non-ulcer controls)
– No differences in age, smoking, EtOH, prior hx DU, and NSAID use
– Concluded that unlike chronic uncomplicated DU, perforation has no
correlation with H. pylori positive status
47 consecutive perforated ulcer patients
– 73% H. pylori +
– 38% closed laparoscopically, all treated with simple closure
• Morbidity and mortality significantly higher in laparoscopic group
– Eradicative rx successful in 96% (triple rx)
– No recurrence or delayed mortality at median of 43.5 month follow up
BLEEDING FROM PEPTIC ULCER
Melena
Tachycardia
Hypotension
Main possible reasons:
Peptic ulcer;
Gastritis;
Portal hypertension
Stops spontaneously in 75%.Reminder will require surgery or die

Peptic ulcer hemorrhage is on the order of 19 to 57 cases per 100,000

individuals
Internal bleeding is the most common complication of stomach ulcers. Internal
bleeding can occur when an ulcer develops at a site of a blood vessel. You
are at an increased risk of bleeding if:
on continued use of non-steroidal anti-inflammatory drugs (NSAIDs)
60 years old or over
Clinical predictors of continued/recurrent bleeding
• Shock (SBP < 100 mmHg)
• Anemia (hemoglobin <7, <10)
• High transfusion requirement (2000 cc/24,5 units total)
• Age > 60 (comorbidities)
• Bleeding rate of > 600cc/hour as measured hematemesis

Forrest Classification of Bleeding Activity (Endoscopy, 1989)

Type of bleeding Forrest Type Description
Active bleeding Ia Spurtingbleed
Ib Oozing bleed
Recent bleeding IIa Nonbleeding
Visible vessel
IIb adherent clot
No bleeding III Clean, no stigmata

Choice of operation—gastric ulcers

• Generally higher rebleeding rate with gastric lesions (30% with
simple oversew),also increased risk of neoplasia (10%)compared to
duodenal
• Location and setting influence choice of operation

Billroth I (gastroduodenostomy)
Billroth II (gastrojejunostomy)

Choice of operation
• Pauchet procedure (distal gastectomy with lesser curve tongue-
extension to incorporate higher ulcer and Billroth I reconstruction)
• Csendes operation (gastrectomy incorporating portion of GE
junction onlesser curve side and esophagogastrojejunostomy
• Kelling-Madlener procedure (antrectomy with oversew/bx of ulcer
left in situ)
Csendes operation
Billroth I most “anatomic”
– No afferent loop or retained antrum issues
• Billroth II if inadequate length, duodenal status marginal
• Roux en Y if reflux a major concern; risk of Roux stasis/emptying
difficulty must be considered--best if very small gastric remnant
Operation for bleeding duodenal ulcer
• Support for PCV with oversewing of ulcer bed in this setting,
particularly in stable,younger, healthier patient population
– Miedema, Jordan (both 1991): one death in 79 patients, 1.3%
rebleeding risk (combined series)
• Caveat that relatively few patients in era of endoscopic hemostasis
come to surgery with above credentials
Truncal vagotomy and pyloroplasty with oversew most attested and
efficient operation in less stable patient
• Antrectomy a useful alternative in stable patient with large ulcers
(>2 cm)
– Increased bleeding and rebleeding with giant ulcers
– Nissen closure technique can be a helpful adjunct with large
posterior ulcers into pancreas or adjacent structure

Gastric outlet obstruction

OBSTRUCTION BY PEPTIC ULCER
Symptoms:
• Vomiting – Usually right after eating yellow or green.
contains foods eaten more than 12 hours earlier.
• Epigastric pain
• Constipation
• Loss of weight
• Hypokalemia and metabolic acidosis –Due to vomiting.
• Hypertrophy of stomach muscles
• Acute vs. chronic, natural history
• Nonsurgical options
• Surgical options
• 68% of acute obstructions and 98% chronic obstructions ultimately
require surgery Balloon dilation
22 consecutive patients with benign peptic stenosis (16 duodenal, 6
pyloric)
• Eradicative triple therapy followed by 8 weeks PPI
• 20/22 fully resolved clinically and endoscopically within 2 months
• No recurrence at mean follow up of 12 months

type of drainage procedure

• Duodenal status limits procedures which directly approach site of
obstruction
• Extended pyloroplasties make reoperation more challenging, if
required
• Antrectomy irreversible, contributes to higher incidence
postgastrectomy sequelae
• Overall, gastrojejunostomy appears to be best choice for GOO due
to duodenal ulcer

Gastrojejunostomy
• Near greater curve, retrocolic, with distal aspect approximately 3
cm proximal to pylorus
– Posterior and near antroduodenal pump for emptying, short and
undistorted afferent limb

Gastrointestinal bleeding

Gastrointestinal bleeding describe every form of haemorrhage in the

GIT,from the pharynx to the rectum.
Can be divided into 2
clinical syndromes:-
- upper GI bleed(pharynx to ligament of Treitz)
- lower GI bleed(ligament of Treitz to rectum)

Pathogenesis
The celiac axis and the superior mesenteric artery (SMA) are the first
two branches of the abdominal aorta and provide a rich and well-
collateralized network of branch vessels that supply blood to the
upper gastrointestinal tract.
Extensive collateralization between the celiac artery and the SMA
protects the upper gastrointestinal tract from ischemic insult and
permits surgical and embolization procedures to be carried out with
a relatively low risk of ischemic injury.
Similarly, branch vessels of both the SMA and the inferior mesenteric
artery (IMA) form a series of interconnected arcades that provide a
means of collateral flow throughout the lower gastrointestinal tract.

Gastrointestinal bleeding can also have venous sources. Venous

bleeding within the upper gastrointestinal tract is typically due to
gastric or esophageal varices arising from the coronary vein
or the short gastric veins in the setting of portal hypertension.
However, approximately 30% of patients with portal hypertension
and coexistent varices who present with upper gastrointestinal
bleeding will have an arterial source of bleeding . Venous
bleeding within the lower gastrointestinal tract is commonly due to
hemorrhoids involving either the internal or external rectal venous
plexus

CLINICAL FEATURES
Haematemesis : Vomiting of blood whether fresh and red or digested
and black.
Melaena : Passage of loose, black tarry stools with a characteristic
foul smell.
Coffee ground vomiting : Blood clot in the vomitus.
Hematochezia : Passage of bright red blood per rectum (if the
haemorrhage is severe)
Haematemesis without malaena is generally due to lesions proximal
to the ligament of Treitz, since blood entering the GIT below the
duodenum rarely enters the stomach.
Malaena without haematemesis is usually due to lesions distal to
the pylorus
Approximately 60mL of blood is required to produced a single black
stool.

BLEEDING IN DIFFERENT LOCATIONS Oesophagus

LOCAL
Oesophageal varices
Oesophageal CA
Reflux oesophagitis
Mallory-Weiss syndrome stomach
Gastric ulcer
Erosive gastritis
Gastric CA
gastric lymphoma
gastric leiomyoma
Dielafoy’s syndrome
Duodenum
Duodenal ulcer
Duodenitis
Periampullary tumour
Aorto-duodenal fistula
Gastrointestinal bleeding is typically categorized
as either upper or lower gastrointestinal bleeding
depending on the anatomic location of the
bleeding site.
Upper gastrointestinal bleeding occurs proximal
to the ligament of Treitz and may involve the
esophagus, stomach, and duodenum.
Lower gastrointestinal bleeding occurs distal to
the ligament of Treitz and may involve the small
bowel, colon, and rectum.
Lower gastrointestinal bleeding is less common
than upper gastrointestinal bleeding and accounts
for approximately 30% of all gastrointestinal
bleeding.
Lower gastrointestinal bleeding tends to affect
elderly patients and is 200 times more likely to
occur in an 80-year-old than in a 20-year-old

Common causes of upper GI bleeding

Erosion or ulcer 55–74
Variceal bleeding 5–14
Mallory-Weiss tear 2–7
Vascular lesions 2–3
Neoplasms 2–5
Common causes of lower GI bleeding
Diverticular disease 20–55
Angiodysplasia 3–40
Neoplasms 8–26
Colitis 6–22
Benign anorectal lesions 9–10

MANAGEMENT OF GI BLEEDING
Endoscopic hemostasis is an established technique as a first choice
for treating GI bleeding. Lower GI bleeding can be observed
conservatively, assuming the amount of bleeding is slight and the
circulatory condition is stable; the majority of lower GI bleeding
stops spontaneously. In contrast, upper GI bleeding should be
addressed because continuous bleeding may be likely to cause
hemorrhagic shock. The success rate of hemostasis under endoscopy
is reported to be 90% . Approximately half of acute GI bleeding is
caused by gastric and duodenal ulcers . Currently, the first option for
treating GI bleeding is endoscopic hemostasis, including endoscopic
clipping, injection of epinephrine or hypertonic saline-epinephrine
(HSE), and argon plasma coagulation. Endoscopic treatment with GI
bleeding from peptic ulcers by epinephrine injection reportedly
yields high rates of successful hemostasis ranging from 97.4% to
100% . Clearly, endoscopic hemostasis is effective and feasible if
circulatory conditions are stable and visual fields are secured.
However, there are several cases where endoscopic hemostasis may
fail in unfavorable conditions, including unstable hemodynamic
status, respiratory failure, and poor visual fields. GI bleeding that is
difficult to hemostasis under endoscopy or re-bleed may necessitate
IVR or surgical intervention. It is reported that 10-30% of GI bleeding
that is staunched by endoscopy may re-bleed . Patients with massive
GI bleeding may be at risk for deterioration of their general condition
due to several postoperative complications; therefore, IVR is the
optimal secondary option for treating GI bleeding.

Candidates for IVR include the following: 1) acute GI bleeding that is

refractory to endoscopic management, 2) massive bleeding that
requires transfusion of more than 4 units of blood over 24 h, or
unstable hemodynamic status or hemorrhagic shock in which systolic
blood pressure is < 100 mm Hg and heart rate is > 100 bpm, and 3)
recurrent bleeding.
In case , empirical embolization was adopted due to lack of
angiographic evidence of bleeding. Because of the intermittent
nature of GI bleeding, the detection of culprit vessels is sometimes
challenging in angiographic examinations. The literature concerning
patients with acute upper and lower GI bleeding reports that 52% of
angiography reveals normal or negative results [6]. Frequency of
angiographic negative results is significantly higher in patients with
lower GI bleeding and stable hemodynamic conditions. In such cases,
provocative angiographic investigations or empirical embolization
are attempted. Provocative angiographic examination is a method to
localize bleeding arteries with the use of intra-arterial tissue
plasminogen activator, heparin, or trazoline
While empirical embolization is a method taken as a preventative
measure for re-bleeding . With the superselective catheterization of
patients with GI bleeding, the percentage of positive angiography
may increases to 93.4%. However, it is noted that empirical
embolization is controversial because of the increased possibility of
re-bleeding and ischemia .
Transarterial embolization (TAE) in the upper GI tract above the Treiz
ligament is unlikely to cause intestinal infarction because of the rich
collateral arteries to the stomach and duodenum. However, with the
wide range
Surgically:
Severe gastrointestinal bleeding has historically been a clinical
problem primarily under the purview of the general surgeon.
Diagnostic advances made as the result of newer technologies, such
as fiberoptic and video endoscopy, selective visceral arteriography,
and nuclear scintigraphy, have permitted more accurate and
targeted operations. More importantly, they have led to safe,
effective nonoperative therapeutic interventions that have obviated
the need for surgery in many patients. Today, most gastrointestinal
bleeding episodes are initially managed by endoscopic or
angiographic control measures. Such interventions are often
definitive in obtaining hemostasis. Even temporary cessation or
attenuation of massive bleeding in an unstable patient permits a
safer, more controlled operative procedure by allowing an adequate
period of preoperative resuscitation. Despite the less frequent need
for surgical intervention, traditional operative approaches, such as
suture ligation, lesion or organ excision, vagotomy, port systemic
anastomosis, and devascularization procedures, continue to be life-
saving in many instances. The proliferation of laparoscopic surgery
has fostered the application of minimally invasive techniques to
highly selected patients with gastrointestinal bleeding.
Intraoperative endoscopy has greatly facilitated the accuracy of
laparoscopic surgery by endoscopic localization of bleeding lesions
requiring excision. It is anticipated that the evolving technologies
pertinent to the diagnosis and management of gastrointestinal
bleeding will continue to promote collaboration and cooperation
between gastroenterologists, radiologists, and surgeons.

You may reduce your risk of peptic ulcer if you follow

the same strategies recommended as home remedies to treat ulcers. It
also may be helpful to:
 Protect yourself from infections. It's not clear just how H. pylori
spreads, but there's some evidence that it could be transmitted from
person to person or through food and water.
You can take steps to protect yourself from infections, such as H.
pylori, by frequently washing your hands with soap and water and by
eating foods that have been cooked completely.
 Use caution with pain relievers. If you regularly use pain relievers
that increase your risk of peptic ulcer, take steps to reduce your risk
of stomach problems. For instance, take your medication with meals.
Work with your doctor to find the lowest dose possible that still
gives you pain relief. Avoid drinking alcohol when taking your
medication, since the two can combine to increase your risk of
stomach upset.
If you need an NSAID, you may need to also take additional
medications such as an antacid, a proton pump inhibitor, an acid
blocker or cytoprotective agent. A class of NSAIDs called COX-2
inhibitors may be less likely to cause peptic ulcers, but may increase
the risk of heart attack.

Usually treatment will involve killing the H. pylori bacterium if present,

eliminating or reducing use of NSAIDs if possible, and helping your ulcer to
heal with medication.
Medications can include:
 Antibiotic medications to kill H. pylori. If H. pylori is found in
your digestive tract, your doctor may recommend a combination of
antibiotics to kill the bacterium. These may include amoxicillin
(Amoxil), clarithromycin (Biaxin), metronidazole (Flagyl),
tinidazole (Tindamax), tetracycline and levofloxacin.
 The antibiotics used will be determined by where you live and
current antibiotic resistance rates. You'll likely need to take
antibiotics for two weeks, as well as additional medications to
reduce stomach acid, including a proton pump inhibitor and possibly
bismuth subsalicylate (Pepto-Bismol).
 Medications that block acid production and promote
healing. Proton pump inhibitors — also called PPIs — reduce
stomach acid by blocking the action of the parts of cells that produce
acid. These drugs include the prescription and over-the-counter
medications omeprazole (Prilosec), lansoprazole (Prevacid),
rabeprazole (Aciphex), esomeprazole (Nexium) and pantoprazole
(Protonix).
Long-term use of proton pump inhibitors, particularly at high doses,
may increase your risk of hip, wrist and spine fracture. Ask your
doctor whether a calcium supplement may reduce this risk.
 Medications to reduce acid production. Acid blockers — also
called histamine (H-2) blockers — reduce the amount of stomach
acid released into your digestive tract, which relieves ulcer pain and
encourages healing.
Available by prescription or over the counter, acid blockers include
the medications famotidine (Pepcid AC), cimetidine (Tagamet HB)
and nizatidine (Axid AR).
 Antacids that neutralize stomach acid. Your doctor may include
an antacid in your drug regimen. Antacids neutralize existing
stomach acid and can provide rapid pain relief. Side effects can
include constipation or diarrhea, depending on the main ingredients.
Antacids can provide symptom relief but generally aren't used to
heal your ulcer.
 Medications that protect the lining of your stomach and small
intestine. In some cases, your doctor may prescribe medications
called cytoprotective agents that help protect the tissues that line
your stomach and small intestine.
Options include the prescription medications sucralfate (Carafate)
and misoprostol (Cytotec).