Stomach Diseases

8/8/2019 Stomach Diseases

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ANATOMY OF THE STOMACH

The stomach lies between the oesophagus and the duodenum(the first part of thesmall intestine). It

is on the left upper part of theabdominal cavity. The top of the stomach lies against the diaphragm.

Lying behind the stomach is thepancreas. The greater omentumhangs down from thegreater

curvature.

Two sphincters, keep the contents of the stomach contained. They are the oesophageal

sphincter(found in the cardiac region, not an anatomical sphincter) dividing the tract above, and

thePyloric sphincterdividing the stomach from the small intestine.

The stomach is surrounded by parasympathetic (stimulant) and orthosympathetic(inhibitor)plexuses (networks of blood vessels and nerves in

theanteriorgastric,posterior,superiorand inferior, celiac and myenteric), which regulate both the

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

In humans, the stomach has a relaxed, near empty volume of about 45 ml. It is a distensible organ.

It normally expands to hold about 1 litre of food, but will hold as much as 2-3 litres (whereas a

newborn baby will only be able to retain 30ml).
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Sections

The stomach is divided into 4 sections, each of which has different cells and functions. The sections

are:

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

Fundus Formed by the upper curvature of the organ.

Body orCorpus

The main, central region.

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

intestine.

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

gastric artery superiorly, which also supplies the cardiac region. The greater curvature is supplied by

theright gastroepiploic artery inferiorly and the left gastroepiploic arterysuperiorly. The fundus of

the stomach, and also the upper portion of the greater curvature, are supplied by the short gastric

artery.

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

from inside to outside:

mucosa

The first main layer. This consists of an epithelium, the lamina propria composed of

loose connective tissue and which has gastric glands in it underneath, and a thin layer

ofsmooth muscle called the muscularis mucosae.

submucosaThis layer lies over the mucosa and consists offibrous connective tissue, separating

the mucosa from the next layer. TheMeissner's plexus is in this layer.

muscularis

externa

Over the submucosa, the muscularis externa in the stomach differs from that of other

GI organs in that it has three layers ofsmooth muscle instead of two.

inner oblique layer: This layer is responsible for creating the motion thatchurns and physically breaks down the food. It is the only layer of the three

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

thicker skin cells in its walls and performs more forceful contractions than the

fundus.

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

circular muscular wall which is normally tonically constricted forming a

functional (if not anatomically discrete) pyloricsphincter, which controls the

movement ofchyme into theduodenum. This layer is concentric to the

longitudinal axis of the stomach.

outer longitudinal layer:Auerbach's plexusis found between this layer and

the middle circular layer.

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

continuous with theperitoneum.
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HISTOLGY

Theepithelium of the stomach forms deep pits. The glands at these locations are named for the

corresponding part of the stomach:

Cardiac glands(at cardia)

Pyloric glands(atpylorus)

Fundic glands(atfundus)

Different types of cells are found at the different layers of these glands:

Layer of

stomachName Secretion

Region of

stomachStaining

Isthmus of

glandMucous neck cells mucus gel layer

Fundic,

cardiac,

pyloric

Clear

Body of

gland

parietal (oxyntic)

cellsgastric acid andintrinsic factor

Fundic,

cardiac,

pyloric

Acidophilic

Base of

gland

chief (zymogenic)

cellspepsinogen Fundic only Basophilic

Base of

gland

enteroendocrine

(APUD) cells

hormones gastrin, histamine,

endorphins, serotonin,cholecystokinin and somatostatin

Fundic,

cardiac,pyloric

-
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Microscopic cross section of the pyloric part of the stomach wall.

Control of secretion and motility

The movement and the flow of chemicals into the stomach are controlled by both theautonomic

nervous system and by the various digestive system hormones:

Gastrin

The hormonegastrin causes an increase in the secretion of HCl from the parietal

cells, and pepsinogen from chief cells in the stomach. It also causes increased

motility in the stomach. Gastrin is released byG-cells in the stomach in response

to distenstion of the antrum, and digestive products(especially large quantities of

incompletely digested proteins). It is inhibited by apH normally less than 4

(high acid), as well as the hormone somatostatin.

Cholecystokinin

Cholecystokinin (CCK) has most effect on the gall bladder, causing gall bladder

contractions, but it also decreases gastric emptying and increases release of

pancreatic juice which is alkaline and neutralizes the chyme.

Secretin In a different and rare manner,secretin, produced in the small intestine, has mosteffects on the pancreas, but will also diminish acid secretion in the stomach.

Gastric inhibitory

peptideGastric inhibitory peptide (GIP) decreases both gastric acid release and motility.

Enteroglucagon enteroglucagon decreases both gastric acid and motility.

Other than gastrin, these hormones all act to turn off the stomach action. This is in response to food

products in the liver and gall bladder, which have not yet been absorbed. The stomach needs only to

push food into the small intestine when the intestine is not busy. While the intestine is full and still

digesting food, the stomach acts as storage for food.

PEPTIC ULCER DISEAESE

Classification

By Region/Location

Stomach (called gastric ulcer)

Duodenum (called duodenal ulcer)

Esophagus (called Esophageal ulcer)

Meckel's Diverticulum (called Meckel's Diverticulum ulcer)Modified Johnson Classification of peptic ulcers:
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Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura

angularis along the locus minoris resistentiae.

Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid

oversecretion.

Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion.

Type IV: Proximal gastroesophageal ulcer

Type V: Can occur throughout the stomach. Associated with chronic NSAID and ASA use.

Pathogenesis.

H. pylori and NSAIDs disrupt normal mucosal defense and repair, making the mucosa more

susceptible to acid.H. pylori infection is present in 50 to 70% of patients with duodenal

ulcers and 30 to 50% of patients with gastric ulcers. IfH. pylori is eradicated, only 10% of

patients have recurrence of peptic ulcer disease, compared with 70% recurrence in patients

treated with acid suppression alone.

NSAIDs now account for > 50% of peptic ulcers. Cigarette smoking is a risk factor for the development of ulcers and their complications.

Also, smoking impairs ulcer healing and increases the incidence of recurrence. Risk

correlates with the number of cigarettes smoked per day.

Although alcohol is a strong promoter of acid secretion, no definitive data link moderate

amounts of alcohol to the development or delayed healing of ulcers. Very few patients have

hypersecretion of gastrin (Zollinger-Ellison syndrome

Signs and symptomsSymptoms of a peptic ulcer can be

abdominal pain, classically epigastric with severity relating to mealtimes, after around 3

hours of taking a meal (duodenal ulcers are classically relieved by food, while gastric ulcers

are exacerbated by it);

bloating and abdominal fullness;

waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus);

nausea, and copious vomiting;

loss of appetite and weight loss;

hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric

ulcer, or from damage to the esophagus from severe/continuing vomiting.

melena (tarry, foul-smelling feces due tooxidized iron fromhemoglobin);

rarely, an ulcer can lead to a gastric or duodenalperforation, which leads toacute peritonitis.

This is extremely painful and requires immediate surgery.

Complications

Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be

life-threatening. It occurs when the ulcer erodes one of the blood vessels.

Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of thegastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the

abdominal cavity. Perforation at the anterior surface of the stomach leads to acuteperitonitis,
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initially chemical and later bacterial peritonitis. The first sign is often sudden intense

abdominal pain. Posterior wall perforation leads topancreatitis; pain in this situation often

radiates to the back.

Penetration is when the ulcer continues into adjacent organs such as the liver andpancreas.

Scarring and swelling due to ulcers causes narrowing in the duodenum andgastric outlet

obstruction. Patient often presents with severe vomiting.

Cancer is included in the differential diagnosis (elucidated bybiopsy),Helicobacterpylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer

from the ulcer.

Diagnosis.

Anesophagogastroduodenoscopy(EGD), a form ofendoscopy, also known as

a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual

identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is

present, EGD can often provide an alternative diagnosis.

The diagnosis ofHelicobacter pylori can be made by:

Urea breath test (noninvasive and does not require EGD);

Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive.

Most labs are not set up to performH. pylori cultures;

Direct detection ofurease activity in a biopsy specimen byrapid urease test;

Measurement ofantibody levels inblood (does not require EGD). It is still somewhat

controversial whether a positive antibody without EGD is enough to warrant eradication

therapy;

Stoolantigen test; Histological examination and staining of an EGD biopsy.

Differential diagnosis of epigastric pain

Peptic ulcer

Gastritis

Stomach cancer

Gastroesophageal reflux disease

Pancreatitis

Hepaticcongestion

Cholecystitis

Biliary colic

Inferior myocardial infarction
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Referred pain (pleurisy,pericarditis)

Superior mesenteric artery syndrome

Treatment

OnceH. pylori is detected in patients with apeptic ulcer, the normal procedure is to eradicate it and

allow the ulcer to heal. The standardfirst-line therapy is a one week "triple therapy" consisting

ofproton pump inhibitors such asomeprazole,lansoprazole and the

antibiotics clarithromycin and amoxicillin.Variations of the triple therapy have been developed over

the years, such as using a different proton pump inhibitor, as withpantoprazole orrabeprazole, or

replacing amoxicillin withmetronidazole for people who are allergic topenicillin.Such a therapy

has revolutionized the treatment of peptic ulcers, and has made a cure to the disease possible;

previously, the only option was symptom control usingantacids, H2-antagonistsor proton pump

inhibitors alone.

An increasing number of infected individuals are found to harbourantibiotic-resistant bacteria. This

results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative

strategies, such as a quadruple therapy, which adds abismuthcolloid, such asbismuthsubsalicylate.For the treatment ofclarithromycin-resistant strains ofH. pylori, the use

oflevofloxacin as part of the therapy has been suggested.

H. pylori colonizes the stomach and induces chronic gastritis, a long-lasting inflammation of the

stomach. The bacterium persists in the stomach for decades in most people. Most individuals

infected byH. pylori will never experience clinical symptoms despite having chronic gastritis.

Approximately 10-20% of those colonized byH. pylori will ultimately develop gastric and

duodenal ulcers.H. pylori infection is also associated with a 1-2% lifetime risk ofstomachcancerand a less than 1% risk of gastric MALT lymphoma.

It is widely believed that in the absence of treatment, H. pylori infectiononce established in its

gastric nichepersists for life. In the elderly, however, it is likely infection can disappear as the

stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. The proportion

of acute infections that persist is not known, but several studies that followed the natural history in

populations have reported apparent spontaneous elimination.

The incidence ofacid reflux disease, Barrett's esophagus, and esophageal cancerhave been rising

dramatically.
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Primary gastric lymphoma

Clinical presentation

Most of the people primary gastric lymphoma affects are over 60 years old. Symptoms

include epigastric pain, early satiety, fatigue and weight loss.

Diagnosis

These lymphomas are difficult to differentiate fromgastric adenocarcinoma. The lesions are usually

ulcers with a ragged, thickened mucosalpattern oncontrast radiographs.

The diagnosis is typically made bybiopsy at the time ofendoscopy. Several endoscopic findings

have been reported, including solitary ulcers, thickened gastric folds, mass lesions and nodules. As

there may be infiltration of the submucosa, largerbiopsyforceps, endoscopic ultrasound guided

biopsy, endoscopic submucosal resection, orlaparotomy may be required to obtain tissue.

Imaging investigations including CT scans orendoscopic ultrasound are useful to stage disease.

Hematological parameters are usually checked to assist with staging and to exclude

concomitant leukemia. An elevated LDH level may be suggestive of lymphom

Histopathology

The majority of gastric lymphomas are non-Hodgkin's lymphoma ofB-cell origin. These tumors

may range from well-differentiated, superficial involvements (MALT) to high-grade, large-cell

lymphomas. Sometimes, it's hard to differentiate poorly differentiated high grade B-cell gastriclymphoma from gastric adenocarcinoma clinically or radiologically, yet histopathology

withimmunohistochemistry is recommended to stain specific markers on the malignant cell that

favor the diagnosis of lymphoma. Immunohistochemistry stains specific clusters of differentiation

that are present on B-cells like CD20.Cytokeratinis also a surface marker that is presented on

epithelial cells, is stained histochemically and favors the diagnosis of epithelial tumors like

adenocarcinoma.

Differentiating poor gastric lymphoma from adenocarcinoma is a must because the prognosis and

modalities of treatment differ significantly.

Other lymphomas involving the stomach include mantle cell lymphomaand T-cell

lymphomas which may be associated with enteropathy; the latter usually occur in the small

bowel but have been reported in the stomach.
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Risk factors

Risk factors for gastric lymphoma include the following:

Helicobacter pylori

Long-term immunosuppressant drug therapy

HIV infection

Treatment

Diffuse large B-cell lymphomas of the stomach are primarily treated

with chemotherapy withCHOP with or withoutrituximab being a usual first choice.

Antibiotic treatment to eradicate H. pylori is indicated as first line therapy forMALT lymphomas.

About 60% of MALT lymphomas completely regress with eradication therapy . Second line therapy

for MALT lymphomas is usually chemotherapy with a single agent, and complete response rates of

greater than 70% have gain been reported

Subtotal gastrectomy, with post-operativechemotherapyis undertaken in refractory cases, or in the

setting of complications, includinggastric outlet obstruction.

STOMACH POLYPS

Stomach polyps are masses of cells that form on the inside lining of your stomach. Stomach polyps,

also called gastric polyps, are rare.

Stomach polyps usually don't cause symptoms. However, as a stomach polyp enlarges, ulcers may

develop on its surface, or rarely, the polyp may block the opening between your stomach and your

small intestine.

If you have stomach polyps, you may experience:

Abdominal pain or tenderness when you press your abdomen

Bleeding

Nausea and vomiting

Classification ; Types of stomach polyps

The most common types of stomach polyps are:
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Hyperplastic polyps. Hyperplastic polyps form as a reaction to chronic inflammation in the cells

that line the inside of the stomach. Hyperplastic polyps are most common in people with stomach

inflammation (gastritis), which has many causes. Most hyperplastic polyps are unlikely to become

stomach cancer. But larger hyperplastic polyps, such as those larger than about 3/4 inch (2

centimeters) in diameter, have a greater risk of becoming cancerous.

Fundic gland polyps. Fundic gland polyps form from the glandular cells that are found on the insidelining of the stomach. Fundic gland polyps occur in people with an inherited colon cancer syndrome

called familial adenomatous polyposis (FAP), but they can also occur in people who don't have this

inherited syndrome. Most fundic gland polyps are unlikely to become stomach cancer, except for

those that occur in people with FAP.

Adenomas. Adenomas form from the glandular cells found on the inside lining of the stomach. But

when adenomas form, their cells develop errors in their DNA. These changes make the cells

vulnerable to becoming cancerous. Though adenomas are the least common type of stomach polyp,

they are the most likely type to become stomach cancer. Adenomas are associated with stomach

inflammation and FAP.

Risk factors

Increasing age. The risk of stomach polyps increases with age. Stomach polyps are more common

among people in their 50s or older.

Bacterial stomach infection. Helicobacter pylori (H. pylori) bacteria are a common cause of the

gastritis that contributes to hyperplastic polyps and adenomas. Experts aren't sure how people

become infected with these bacteria, but H. pylori may be carried in food and water.

An inherited colon cancer syndrome. Familial adenomatous polyposis is an inherited syndrome that

increases the risk of colon cancer and other conditions, such as stomach polyps.

Certain medications. Long-term use of proton pump inhibitors (PPIs), which are medications used

to treat gastroesophageal reflux disease (GERD), has been linked to fundic gland polyps. PPIs

include esomeprazole (Nexium), lansoprazole (Prevacid), omeprazole (Prilosec Rx), pantoprazole

(Protonix) and rabeprazole (Aciphex).

Tests and procedures used to diagnose stomach polyps include:

Using a scope to see inside your stomach. During an upper endoscopy procedure, your doctor

inserts a flexible, lighted tube into your mouth and down your throat. The device has a camera at thetip that allows your doctor to see inside your stomach.

Removing a sample of tissue for testing (biopsy). During the endoscopy procedure, your doctor may

feed special tools through the tube. The tools allow your doctor to remove a small piece of

suspicious tissue for testing in a laboratory. These tests may help your doctor determine what type

of stomach polyps you have


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Treatment may not be necessary

Small polyps that aren't adenomas may not require treatment. These polyps typically don't cause

signs and symptoms and only rarely become cancerous. Instead, your doctor may recommend

periodic monitoring of your stomach polyps. You may undergo endoscopy to see whether your

stomach polyps have grown. Polyps that grow or that cause signs and symptoms can be removed.

Removing adenomas and large stomach polypsTreatment to remove stomach polyps may be recommended if your polyps are adenomas or if they

are larger than 2/5 inch (1 cm) in diameter. Most polyps can be removed during an endoscopy

exam.

Stopping H. pylori infection to treat and prevent polyps

If you have gastritis caused by H. pylori bacteria in your stomach, your doctor will likely

recommend killing the bacteria with antibiotics. Stopping an H. pylori infection may make

hyperplastic polyps disappear. It may also stop polyps from returning in the future. Tests can help

your doctor determine whether you have H. pylori infection. Then, your doctor may prescribe

antibiotics for you to take for several weeks to kill the H. pylori bacteria.

DIEULAFOY'S LESSION

Dieulafoy's Lesions are characterized by a single large tortuousarteriole in thesubmucosa which

does not undergo normal branching or a branch with caliber of 15 mm (more than 10 times the

normal diameter of mucosal capillaries). The lesion bleeds into the gastrointestinal tract through a

minute defect in the mucosa which is not a primary ulcer of the mucosa but an erosion likely caused

in the submucosal surface by protrusion of the pulsatile arteriole.

Approximately 75% of Dieulafoy's lesions occur in the upper part of the stomach within 6 cm of

thegastroesophageal junction, most commonly in the lesser curvature. Extragastric lesions have

historically been thought to be uncommon but have been identified more frequently in recent years,

likely due to increased awareness of the condition. The duodenum is the most common location

(14%) followed by the colon (5%), surgicalanastamoses (5%), thejejunum (1%) and

theesophagus (1%).[4] The pathology in these extragastric locations is essentially the same as that

of the more common gastric lesion.

Interestingly and in contrast to peptic ulcer disease, a history ofalcohol abuse orNSAIDuse is

usually absent in DL.

Dieulafoy's lesions occur twice as often in men as women and patients typically have multiplecomorbidities, including hypertension, cardiovascular disease, chronic kidney disease, and diabetes.
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Symptoms

The symptoms due to bleeding are hematemesisand/ormelena, possibly with shock.

Presenting Symptoms

Recurrent hematemesis with melena 51% of cases

Hematemesis without melena 28% of cases

Melena with no hematemesis 18% of cases

A Dieulafoy's lesion is difficult to diagnose, because of the intermittent pattern of bleeding.

Endoscopically it is not easy to recognize and therefore sometimes multiple views have to be

performed over a longer period. Today angiographyis a good additional diagnostic, but then it can

only be seen during a bleeding at that exact time.

Endoscopic appearance ofnonbleeding Dieulafoys lesion

Therapeutic endoscopy has been used successfully, and is now the modality of choice for the initial

treatment of Dieulafoy lesions.

Endoscopic modalities used include bipolar electrocoagulation, monopolar

electrocoagulation, injection sclerotherapy, heater probe, laser photocoagulation,

epinephrine injection, haemoclipping and banding.

The injection of epinephrine has been used in combination with other modalities, as a means

to slow or stop bleeding and allow better visualisation of the lesion and successful treat-ment.

The specific therapeutic modality used seems to depend on the availability and personal

experience with a particular technique. Endoscopic therapy is said to be successful in

achieving permanent haemostasis in 85% of cases. Of the remaining 15% in whom re-

bleeding occurs, 10% can successfully be treated by repeat endoscopic therapy and 5% may

ultimately require surgical intervention

MALLORY WEISS TEAR
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Mallory-Weiss tear. Retroflexed view of the cardia showing the

typical location of the tear with a clean base.

Mallory-Weiss tear with a pigmented protuberance and active oozing.

Causes

Many underlying disorders that cause vomiting and retching result in a Mallory-Weiss tear.

GI disease

Infectious gastroenteritis

Gastric outlet obstruction

Ulcers

Hiatal hernias

Malrotation

Volvulus

Inflammatory conditions of the stomach and intestine

Pregnancy: Some women develop hyperemesis gravidarum, a syndrome characterized by

persistent severe vomiting and retching, in the first trimester of pregnancy. Gastric

dysrhythmias and prolonged small-bowel motility cause the development of hyperemesis

gravidarum. Some women lose as much as 10% of their body weight during this period.

Hepatitis: Acute inflammation of the liver causes vomiting in 10-20% of patients.

Cirrhosis

Biliary tract disease: Although rare in children, these conditions can cause vomiting

typically associated with meals.

Gallstones

Cholecystitis Biliary cirrhosis
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Renal disease: Vomiting is often associated with diseases affecting the kidneys, including the

following:

Urinary tract infections

Kidney stones

Uteropelvic junction (UPJ) obstruction

Renal failure

Increased intracranial pressure: Intracranial lesions that cause hydrocephalus or increased

intracranial pressure may lead to vomiting in children. Most common causes of

hydrocephalus include tumors, cysts, and congenital abnormalities. Other causes of

increased intracranial pressure consist of trauma, infections (eg, meningitis), medications,

and pseudotumor cerebri.

Iatrogenic causes: Complications of endoscopy may cause esophageal tears (


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In cases of severe bleeding with hemodynamic instability, the patient should be

stabilized prior to performing endoscopy.

Mallory-Weiss tears can heal quickly after the cessation of vomiting and retching and

may not be diagnosed if performance of the upper endoscopy is delayed.

Staging

Predictive factors for recurrent bleeding include the following:

Initial presentation of shock

Liver cirrhosis

Decreased hemoglobin and platelet count

Need for blood transfusion

Intensive care management

Active bleeding noted at the time of endoscopy

Medical Care

Initial medical management is always supportive. Patients in whom conservative medical therapy is

ineffective should have a consultation with a gastroenterologist for possible endoscopy.

Monitor vital signs closely, obtain a CBC count, and place a large-bore intravenous tube for

fluid resuscitation.

Less than 5% of children require a blood transfusion.

Begin workup to determine the underlying cause of the retching and vomiting.

In most cases, Mallory-Weiss tears spontaneously resolve; however, considerpharmaceutical therapy in cases of persistent bleeding or complications

Esophageal balloon tamponade, although useful for patients with esophageal varices, should

be considered only in extreme cases because the use of an esophageal balloon increases the

risk of extending the esophageal tear.

Esophageal clips applied at the site of active bleeding.

Endoscopic band ligation has been used and was shown to be an effective and safe

procedure for patients with severe bleeding.

Angiographic embolization of the vessels supplying blood flow to the esophageal tear has

been reported in the adult literature but should be considered in children only under dire

circumstances.Surgical Care

Only in extraordinary cases should surgical intervention be required. A consultation with a

surgeon should be considered only in patients with persistent bleeding requiring transfusions

and in whom the bleeding cannot be controlled by medication or by therapeutic upper

endoscopy

Consultations

An upper endoscopy (performed by a trained pediatric gastroenterologist) should be

considered for all patients with persistent bleeding for whom medical therapy is

unsuccessful.


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Diet

During the acute problem, keep patients on nothing by mouth (NPO).

Once resolved, provide the patient clear liquids and advance the diet as tolerated.

After complete resolution, no special diet is required. However, foods or liquids that may

have been identified as contributing to the cause of the underlying problem (eg, excessive

alcohol intake, food allergies) should be avoided.

Two types of endoscopic therapy can be used to control severe bleeding in patients who are

hemodynamically unstable because of bleeding from a Mallory-Weiss tear.

Injection therapy is favored as the first-line therapy by most endoscopists for control

of bleeding esophageal lesions because of its ease of use, safety, and cost. Typically,

the injections are made 3-5 mm apart circumferentially around the site of bleeding in

4 areas. The chemical agents used for injection therapy include dilute epinephrine,

sodium morrhuate, ethyl alcohol, or sodium tetradecyl sulfate.

Heater probe or bipolar coagulation therapies use electrical current supplied bycatheters that can be inserted into an endoscope to control bleeding. Approximately

20 joules (10-15 Watts) of current are used per individual pulse, and treatment is

complete when the bleeding has ceased. The current is usually delivered in repeated

time-limited pulses.

Evaluate the underlying cause of vomiting.

Further Outpatient Care

Mallory-Weiss tears almost never rebleed; thus, follow-up is not usually indicated.

Transfer

Transfer children with severe uncontrolled bleeding to a tertiary care hospital with an in-

house pediatric gastroenterologist.

Deterrence/Prevention

Avoid and treat causes of underlying vomiting and retching.

Complications

Anemia

Dehydration

Prognosis

Prognosis is extremely good in children, with a less than 0.01% mortality rate. These tears

almost always respond to conservative therapy and supportive care.

Documents

Stomach Diseases