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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.