GASTRITIS

http://www.webmd.com/digestive-disorders/digestive-diseases-gastritis

Gastritis is an inflammation, irritation, or erosion of the lining of the stomach. It can occur
suddenly (acute) or gradually (chronic).

What Causes Gastritis?

Gastritis can be caused by irritation due to excessive alcohol use, chronic vomiting, stress, or the
use of certain medications such as aspirin or other anti-inflammatory drugs. It may also be
caused by any of the following:

Helicobacter pylori (H. pylori): A bacteria that lives in the mucous lining of the
stomach. Without treatment the infection can lead to ulcers, and in some people, stomach
cancer.
Pernicious anemia: A form of anemia that occurs when the stomach lacks a naturally
occurring substance needed to properly absorb and digest vitamin B12.

Bile reflux: A backflow of bile into the stomach from the bile tract (that connects to the
liver and gallbladder).

Infections caused by bacteria and viruses.

If gastritis is left untreated, it can lead to a severe loss in blood and may increase the risk of
developing stomach cancer.

What Are the Symptoms of Gastritis?

Symptoms of gastritis vary among individuals, and in many people there are no symptoms.
However, the most common symptoms include:

Nausea or recurrent upset stomach

Abdominal bloating

Abdominal pain

Vomiting

Indigestion

Burning or gnawing feeling in the stomach between meals or at night

Hiccups

Loss of appetite

Vomiting blood or coffee ground-like material

Black, tarry stools

How Is Gastritis Diagnosed?

To diagnose gastritis, your doctor will review your personal and family medical history, perform
a thorough physical evaluation, and may recommend any of the following tests.

Upper endoscopy. An endoscope, a thin tube containing a tiny camera, is inserted

through your mouth and down into your stomach to look at the stomach lining. The
doctor will check for inflammation and may perform a biopsy, a procedure in which a
tiny sample of tissue is removed and then sent to a laboratory for analysis.
Blood tests. The doctor may perform various blood tests such as checking your red blood
cell count to determine whether you have anemia, which means that you do not have
enough red blood cells. He or she can also screen for H. pylori infection and pernicious
anemia with blood tests.
Fecal occult blood test (stool test). This test checks for the presence of blood in your
stool, a possible sign of gastritis.

What Is the Treatment for Gastritis?

Treatment for gastritis usually involves:

Taking antacids and other drugs to reduce stomach acid, which causes further irritation to
inflamed areas.
Avoiding hot and spicy foods.

For gastritis caused by H. pylori infection, your doctor will prescribe a regimen of several
antibiotics plus an acid blocking drug (used for heartburn).

If the gastritis is caused by pernicious anemia, B12 vitamin shots will be given.

Eliminating irritating foods from your diet such as lactose from dairy or gluten from
wheat.

Once the underlying problem disappears, the gastritis usually does, too.
You should talk to your doctor before stopping any medicine or starting any gastritis treatment
on your own.

What Is the Prognosis for Gastritis?

Most people with gastritis improve quickly once treatment has begun.

Pediatric Hypertrophic Pyloric Stenosis

Background
Hirschsprung wrote the first complete description of hypertrophic pyloric stenosis (HPS) in
1888. He believed the disease was congenital and represented fetal pyloric development failure.
In 1907, Ramstedt described an operation to alleviate this condition. He suggested splitting the
pyloric muscle and leaving it open to heal secondarily. This procedure has been used to treat
infantile hypertrophic pyloric stenosis (IHPS) since that time. Although this curious disease is
treated easily with surgery, its etiology remains undetermined. Hypertrophic pyloric stenosis is
inherited by a multifactorial threshold model, and the generalized occurrence risk for siblings is
5-9%. Associated congenital anomalies are reported in 6-20% of patients with pyloric stenosis. A
rare association with developmental delay has also been reported.[1]

Pathophysiology
HPS occurs secondary to hypertrophy and hyperplasia of the muscular layers of the pylorus,
which cause a functional gastric outlet obstruction. Diffuse hypertrophy and hyperplasia of the
smooth muscle of the antrum of the stomach and pylorus proper narrow the channel, which then
can become easily obstructed. The antral region is elongated and thickened to as much as twice
its normal size. In response to outflow obstruction and vigorous peristalsis, stomach musculature
becomes uniformly hypertrophied and dilated. Gastritis may occur after prolonged stasis.
Hematemesis is occasionally noted. The patient may become dehydrated as a result of vomiting
and develop marked hypochloremic alkalosis.
Researchers have investigated the cause of this muscle hypertrophy for several decades. Many
believe the problem is induced by the pyloric musculature failing to relax. Results of studies of
pyloric muscle innervation are inconclusive, possibly showing a tendency toward fewer or more
immature ganglion cells in affected individuals. Deregulation of vasoactive intestinal peptide
(VIP) and nitric oxide both have been demonstrated in patients with pyloric stenosis, although
whether these factors are associative or causative is unclear.
No definitive cause for hypertrophic pyloric stenosis has been found. However, various
environmental and hereditary factors have been implicated. Suspected environmental factors
include infantile hypergastrinemia, abnormalities in the myenteric plexus innervation, cow's milk
protein allergy, and exposure to macrolide antibiotics. Hereditary factors may also play a role;
hypertrophic pyloric stenosis occurs in as many as 7% of infants of affected parents. The
etiology is probably multifactorial, with both genetic and environmental factors contributing.
Recognition that hypertrophic pyloric stenosis is an acquired disorder and not a congenital
disorder is increasing. Recently, genetic studies have identified susceptibility loci for infantile
HPS and molecular studies have concluded that smooth muscle cells are not properly innervated
in infantile HPS.[2]

Epidemiology

Frequency
United States

Pyloric stenosis is the most common cause of gastric outlet obstruction in infants. It is also the
most common surgical cause of vomiting in infants. The prevalence of hypertrophic pyloric
stenosis ranges from 1.5-4 cases per 1000 live births among whites, although it is less prevalent
among blacks and Asian Americans.

Mortality/Morbidity
Operative therapy for hypertrophic pyloric stenosis has remained unchanged for nearly 100
years. Outcomes have improved through advances in early diagnosis, preoperative resuscitation,
operative anesthetics, and nutritional management. Mortality may rarely result from late
diagnosis, resulting in dehydration and shock. Mortality is also rare after pyloromyotomy.
Wound infection occurs in fewer than 1% of patients. Perforation of the pyloric mucosa is also
unusual, occurring in fewer than 3% of reported cases. Long-term sequelae from the disease or
treatment are also minimal.

Race
Reported prevalence of hypertrophic pyloric stenosis among whites ranges from 1.5-4 cases
1000 live births; hypertrophic pyloric stenosis is less prevalent among blacks, Asians, and
Hispanics.

Sex
Pyloric stenosis has a well-known predilection for occurring more often in males than in females,
with reported ratios ranging from 2:1 to 5:1. First-born male children are believed to have the
highest risk of developing hypertrophic pyloric stenosis.

Age
Newborns typically develop signs of gastric outlet obstruction at 3-4 weeks. Cases of
hypertrophic pyloric stenosis have been documented from the first week of life to 3 months.
Approximately 95% of infantile hypertrophic pyloric stenosis cases are diagnosed in those aged
3-12 weeks. Premature infants generally develop symptoms later than full-term infants, which
may lead to a delay in diagnosis.

History

Typical presentation of an infant with hypertrophic pyloric stenosis (HPS) is

onset of initially nonbloody, always nonbilious vomiting at 4-8 weeks.
Although vomiting may initially be infrequent, over several days it becomes

more predictable, occurring at nearly every feeding. Vomiting intensity also

increases until pathognomonic projectile vomiting ensues. Slight
hematemesis of either bright red flecks or a coffee-ground appearance is
sometimes observed.
Patients are usually not ill-looking or febrile. The baby in the early stage of
the disease remains hungry and sucks vigorously after episodes of vomiting.

Prolonged delay in diagnosis can lead to dehydration, poor weight gain,

malnutrition, metabolic alterations, and lethargy.

Parents often report trying several different baby formulas because they (or
their physicians) assume vomiting is due to intolerance.

Physical

Careful physical examination provides a definitive diagnosis for most infants

with hypertrophic pyloric stenosis. However, some of the classic signs that
would lead to diagnosis may be absent due, in part, to the early diagnosis of
hypertrophic pyloric stenosis.
An enlarged pylorus, classically described as an "olive," can be palpated in
the right upper quadrant or epigastrium of the abdomen in 60-80% of infants.
[3]
In order to assess the pylorus, the patient must be calm and cooperative. A
pacifier or small amount of dextrose water may help. If the stomach is
distended, aspiration using a nasogastric tube is necessary. With the infant
supine and the examiner on the child's left side, gently palpate the liver edge
near the xiphoid process. Then displace the liver superiorly; downward
palpation should reveal the pyloric olive just on or to the right of the midline.
To be assured of the diagnosis, the physician should be able to roll the
pylorus beneath the examining finger. The tumor (mass) is best felt after
vomiting or during, or at the end of, feeding. The diagnosis is easily made if
the presenting clinical features are typical, with projectile vomiting, visible
peristalsis, and a palpable pyloric tumor.
When diagnosis is delayed, the infant may develop severe constipation
associated with signs of dehydration, malnutrition, lethargy, and shock.

Causes
Despite numerous hypotheses, the exact etiology of HPS is not fully understood. Genetic,
extrinsic and hormonal factors have been implicated. In addition, abnormalities of various
components of the pyloric muscle, such as smooth muscle cells, growth factors, extracellular
matrix elements, nerve and ganglion cells, neurotransmitters, and interstitial cells of Cajal, have
been reported. Recently, genetic studies have identified susceptibility loci and molecular studies
have concluded that smooth muscle cells are not properly innervated in this condition.[4]

Differential Diagnoses

Adrenal Insufficiency
Alkalosis, Metabolic

Bowel Obstruction in the Newborn

Duodenal Atresia

Failure to Thrive

Gastroenteritis

Gastroesophageal Reflux

Intestinal Malrotation

Sandifer Syndrome

Laboratory Studies

Serum electrolytes: Document adequacy of fluid resuscitation and correction

of electrolyte imbalances before surgical repair of hypertrophic pyloric
stenosis (HPS). See Medical Care. Infants with severe vomiting can develop
profound hypochloremia and hypokalemia. The classic biochemical
abnormality in hypertrophic pyloric stenosis is hypochloremic, hypokalemic
metabolic alkalosis.

Imaging Studies

Ultrasonography has become the criterion standard imaging technique for

diagnosing hypertrophic pyloric stenosis. It is reliable, highly sensitive, highly
specific, and easily performed. An experienced ultrasonographer increases
the test's predictive value. Necessary measurements include pyloric muscle
thickness and pyloric channel length. Muscle wall thickness 3 mm or greater
and pyloric channel length 14 mm or greater are considered abnormal in
infants younger than 30 days.
Barium upper GI (UGI) study is an effective means of diagnosing HPS when
ultrasonography is not diagnostic. It should demonstrate an elongated
pylorus with antral indentation from the hypertrophied muscle. The UGI may
demonstrate the "double track" sign when thin tracks of barium are
compressed between thickened pyloric mucosa or the "shoulder" sign when
barium collects in the dilated prepyloric antrum. After UGI barium study,
irrigating and removing any residual barium from the stomach is advisable to
avoid aspiration.
Although UGI endoscopy would demonstrate pyloric obstruction, physicians
would find it difficult to differentiate accurately between hypertrophic pyloric
stenosis and pylorospasm. Endoscopy is reserved for patients with atypical
clinical signs when ultrasonography and UGI studies are nondiagnostic.
Endoscopic dilatation has rarely been used as a method of treatment. This
treatment is not standard for hypertrophic pyloric stenosis; endoscopy should
be used rarely, if ever.

Medical Care

Surgical repair of hypertrophic pyloric stenosis (HPS) is fairly straightforward

and without many complications, yet properly preparing the infant for this
procedure is vitally important. Most infants with hypertrophic pyloric stenosis

do not have complete gastric outlet obstruction and can tolerate their
inherent gastric secretions.
Repeated episodes of vomiting following attempts to feed the infant cause
progressive dehydration and loss of hydrogen chloride from the gastric juices.
Preoperative management is directed at correcting the fluid deficiency and
electrolyte imbalance.
o

Base fluid resuscitation on the infant's degree of dehydration. Most

infants can have their fluid status corrected within 24 hours; however,
severely dehydrated children sometimes require several days for
correction.

If necessary, administer an initial fluid bolus of 10 mL/kg with lactated

Ringer solution or 0.45 isotonic sodium chloride solution. Continue
intravenous (IV) therapy at an initial rate of 1.25-2 times the normal
maintenance rate until adequate fluid status is achieved.

Adequate amounts of both chloride and potassium are necessary to

correct metabolic acidosis. Unless renal insufficiency is a concern,
initially add 2-4 mEq of KCL per 100 mL of IV fluid. Adequate chloride
for resuscitation can usually be provided by 5% dextrose in 0.4%
sodium chloride solution. Avoid adding hypertonic chloride or
ammonium chloride.

Urine output and serial electrolyte determinations are performed

during resuscitation. Correction of serum chloride level to 90 mEq/L or
greater is usually adequate to proceed with surgical intervention.

Before induction of anesthesia, aspirate the infant's stomach with a

large-caliber suction tube to remove any residual gastric fluid or
barium. Saline irrigation is occasionally necessary to remove a large
quantity of barium.

Surgical Care
Pyloromyotomy remains the standard of treatment, and outcome is excellent. [5] The best surgical
outcome and lowest complications are more likely when the surgeon has specialist pediatric
surgical training.

Ramstedt pyloromyotomy remains the standard procedure of choice for

hypertrophic pyloric stenosis because it is easily performed and is associated
with minimal complications. The usual approach is via a right upper quadrant
transverse incision that splits the rectus muscle and fascia.
Some authorities report that laparoscopic pyloromyotomy has a significantly
shorter recovery time compared with open pyloromyotomy but that open
pyloromyotomy has higher efficacy and fewer complications. However, a
small (N=98) 2011 prospective, randomized trial found no difference in
operating time, length of stay, or difference in time to full feeds between
open and laparoscopic pyloromyotomy. While complication rates were similar
between the 2 groups, significantly superior long-term cosmetic results were

noted in the laparoscopic group. [6] A systematic review of 502 patients echoed
these results, finding laparoscopic pyloromyotomy does not lead to significant
postoperative complications compared to open pyloromyotomy. [7]

Endoscopic pyloromyotomy is a simple procedure and can be performed as

an outpatient procedure.

Recently, endoscopic balloon dilatation of hypertrophic pyloric stenosis after

failed pyloromyotomy has been used with greater frequency.

Several other approaches have been described. A supraumbilical curvilinear

approach has gained popularity with good cosmetic results.

Postoperative management
o

Continue IV maintenance fluid until the infant is able to tolerate enteral

feedings. In most instances, feedings can begin within 8 hours
following surgery. Graded feedings can usually be initiated every 3
hours, starting with Pedialyte and progressing to full-strength formula.

Although schedules that advance the volume of feeds more quickly or

those that begin with ad lib feeds are associated with more frequent
episodes of vomiting, they do not increase morbidity and actually may
decrease the time to hospital discharge.

Addition of a histamine 2 (H2) receptor blocker sometimes can be

beneficial.

Treat persistent vomiting expectantly because it usually resolves within

1-2 days.

Avoid the temptation to repeat ultrasonography or UGI barium study;

these invariably demonstrate a deformed pylorus and results are
difficult to interpret.

Consultations
Early consultation with a surgeon familiar with neonatal care is warranted because treatment is
essentially surgical. Early consults facilitate decisions for diagnostic studies, fluid resuscitation,
and scheduling the operative procedure. This is especially important if the child requires transfer
to another facility for surgical care. The American Pediatric Surgical Association offers
guidelines for appropriate consultation and transfer of small infants. Good outcome has been
shown to depend on the quality of preoperative correction of fluid and electrolyte abnormalities,
availability of a pediatric anesthetist, and training level of the surgeon.

Diet
Feedings are usually resumed 6-8 hours after operation.[8] In most instances, gradually increasing
the volume and strength of feedings is recommended (see Surgical Care).

Further Inpatient Care

Feeding can be resumed and advanced over a 24-hour period for most
patients with hypertrophic pyloric stenosis (HPS). Premature infants
sometimes require apnea monitoring if they have a history of apnea spells.
Narcotic pain medications should be avoided in the postoperative period
because opioids may precipitate apnea in the alkalotic newborn.
Infants can be discharged from hospital care once they can remain hydrated
and have adequate enteral intake.

Further Outpatient Care

Infants generally recover rapidly after operative correction of HPS. Advise

parents to increase food volume in the days after discharge. A single
postoperative visit 1-2 weeks after surgery is often all that is necessary to
document weight gain. Long-term sequelae from pyloromyotomy are virtually
unheard of. Studies have documented normal function returns in months to
years after surgery.

Inpatient & Outpatient Medications

Postoperative analgesics are used as with any other surgical patient.

Once oral intake has resumed, acetaminophen usually suffices.

Complications

Undetected mucosal perforation: Perform a diligent search for mucosal

transgressions at the time of operation and examine the infant again before
initiating feedings. In those rare cases where a perforation was not detected,
the infant develops fever, tenderness in the abdomen, and abdominal
distention. Return to the operating room if perforation is suspected.
Bleeding: In most instances, venous oozing from the myotomy site is selflimited and is not a concern in the postoperative period. Reports of continued
bleeding are exceedingly rare but can occur, especially in children with
undetected coagulopathy.
Persistent vomiting: Incomplete pyloromyotomy is rare in the hands of an
experienced pediatric surgeon and usually presents as persistent vomiting
until after the second week postsurgery. This problem is confounded when
repeat studies performed after surgery provide a confusing picture. Patient
observation resolves the problem in most cases.

ESOPHAGEAL ATRESIA

Background
Esophageal atresia refers to a congenitally interrupted esophagus. One or more fistulae may be
present between the malformed esophagus and the trachea.
For patient education resources, see the Esophagus, Stomach, and Intestine Center and
Procedures Center, as well as Choking and Bronchoscopy.

History of the Procedure

The condition was first described anecdotally in the 17th century.[1] In 1670, Durston described
the first case of esophageal atresia in one conjoined twin. In 1696, Gibson provided the first
description of esophageal atresia with a distal tracheoesophageal fistula (TEF). In 1862,
Hirschsprung (a famous pediatrician from Copenhagen) described 14 cases of esophageal atresia.
In 1898, Hoffman attempted primary repair of the defect but was not successful and resorted to
the placement of a gastrostomy.
At the start of the 20th century, surgeons were theorizing about how the lesion could be repaired.
In 1939 and 1940, Ladd of Boston and Lever of Minnesota first achieved surgical success in
stages; success meant that the affected children survived and skin-lined pharyngogastric conduits
were eventually constructed. In 1941, Haight of Michigan successfully repaired esophageal
atresia in a 12-day-old baby using a primary single-stage left-sided extrapleural approach.
Subsequent to that child's survival and with advances in surgical and anesthetic techniques,
esophageal atresia is now regarded as an eminently correctable congenital lesion.

Problem
The lack of esophageal patency prevents swallowing. In addition to preventing normal feeding,
this problem may cause infants to aspirate and literally drown in their own saliva, which quickly
overflows the upper pouch of the obstructed esophagus. If a TEF is present, fluid (either saliva
from above or gastric secretions from below) may flow directly into the tracheobronchial tree.

Epidemiology

Frequency
The incidence of esophageal atresia is 1 case in 3000-4500 births. This frequency may be
decreasing for unknown reasons.[2]
Internationally, the highest incidence of this disorder is in Finland, where it is 1 case in 2500
births.

Etiology
No human teratogens that cause esophageal atresia are known. Esophageal atresia that occurs in
families has been reported. A 2% risk of recurrence is present when a sibling is affected. The
occasional association of esophageal atresia with trisomies 21, 13, and 18 further suggests
genetic causation. Also, twinning occurs about 6 times more frequently in patients with
esophageal atresia than in those without the condition.
Currently, most authorities believe that the development of esophageal atresia has a nongenetic
basis.[3] Debate about the embryopathologic process of this condition continues, and little about it
is known. The old His theory that lateral infoldings divide the foregut into the esophagus and
trachea is attractively simple, but findings from human embryology studies do not support this
theory.
In 1984, O'Rahilly proposed that a fixed cephalad point of tracheoesophageal separation is
present, with the tracheobronchial and esophageal elements elongating in a caudal direction from
this point.[4] This theory does not easily account for esophageal atresia but explains TEF as a
deficiency or breakdown of esophageal mucosa, which occurs as the linear growth of the organ
exceeds the cellular division of the esophageal epithelium.
In a 1987 report, Kluth eschews the concept that tracheoesophageal septation has a key role in
the development of esophageal atresia.[5] Instead, he bases the embryopathologic process on the
faulty development of the early, but already differentiated, trachea and esophagus, in which a
dorsal fold comes to lie too far ventrally; thus, the early tracheoesophagus remains undivided. He
also suggests that esophageal vascular events, ischemic events, or both may be causes in cases of
esophageal atresia without fistula.
In 2003, Spilde et al reported esophageal atresia-TEF formations in the embryos of rat models of
Adriamycin-induced teratogenesis.[6] Specific absences of certain fibroblast growth factor (FGF)
elements have been reported, specifically FGF1 and the IIIb splice variant of the FGF2R
receptor.[7] These specific FGF-signaling absences are postulated to allow the nonbranching
development of the fistulous tract from the foregut, which then establishes continuity with the
developing stomach.
In 2001, Orford et al postulated that the ectopic, ventrally displaced location of the notochord in
an embryo at 21 days' gestation can lead to a disruption of the gene locus, sonic hedgehogsignaled apoptosis in the developing foregut, and variants of esophageal atresia.[8] This situation
may be due to various early gestation teratogenic influences such as twinning, toxin exposure, or
possible abortion. More studies are required.

Pathophysiology
The variants of esophageal atresia have been described using many anatomic classification
systems. To avoid ambiguity, the clinician should use a narrative description. Nevertheless, Gross
of Boston described the classification system that is most often cited (see the image below).[9]

Esophageal atresia classification according to Gross.

According to this system, the types of esophageal atresia and the approximate incidence in all
infants born with esophageal anomalies is as follows:

Type A - Esophageal atresia without fistula or so-called pure esophageal

atresia (10%)
Type B - Esophageal atresia with proximal TEF (< 1%)

Type C - Esophageal atresia with distal TEF (85%)

Type D - Esophageal atresia with proximal and distal TEFs (< 1%)

Type E - TEF without esophageal atresia or so-called H-type fistula (4%)

Type F - Congenital esophageal stenosis (< 1%) (This is not discussed in this
article.)

A fetus with esophageal atresia cannot effectively swallow amniotic fluid, especially when TEF
is absent.[10] In a fetus with esophageal atresia and a distal TEF, some amniotic fluid presumably
flows through the trachea and down the fistula to the gut. Polyhydramnios may be the result of
this change in the recycling of amniotic fluid through the fetus. Polyhydramnios, in turn, may
lead to premature labor. The fetus also appears to derive some nutritional benefit from the
ingestion of amniotic fluid; thus, fetuses with esophageal atresia may be small for their
gestational age.
The neonate with esophageal atresia cannot swallow and drools copious amounts of saliva.
Aspiration of saliva or milk, if the baby is allowed to suckle, can lead to an aspiration
pneumonitis. In a baby with esophageal atresia and a distal TEF, the lungs may be exposed to
gastric secretions. Also, air from the trachea can pass down the distal fistula when the baby cries,
strains, or receives ventilation.[11] This condition can lead to an acute gastric perforation, which is
often lethal. Prerepair esophageal manometric studies have revealed that the distal esophagus in
esophageal atresia is essentially dysmotile, with poor or absent propagating peristaltic waves.
This condition results in variable degrees of dysphagia after the repair and contributes to
gastroesophageal reflux.
The trachea is also affected by the disordered embryogenesis in esophageal atresia. The
membranous part of the trachea, the pars membranacea, is often wide and imparts a crosssectional D shape to the trachea, as opposed to the usual C shape. These changes cause
secondary anteroposterior structural weakening of the trachea, or tracheomalacia. This
weakening can result in a sonorous cough as the intrathoracic trachea resonates and partially

collapses with forceful expiration. Secretions can be difficult to clear and may lead to frequent
pneumonias. Also, the trachea can partially collapse during feeding, after repair, or with episodes
of gastroesophageal reflux; this partial collapse can lead to ineffective respiration; hypoxia; and,
somewhat inexplicably, apnea.

Presentation
A mother who is carrying a fetus with esophageal atresia may have polyhydramnios, which
occurs with approximately 33% of mothers with fetuses with esophageal atresia and distal TEF
and with virtually 100% of mothers with fetuses with esophageal atresia without fistula.
Characteristically, the neonate born with esophageal atresia drools and has substantial mucus,
with excessive oral secretions. If suckling at the breast or bottle is allowed, the baby appears to
choke and may have difficulty maintaining an airway. Significant respiratory distress may result.
In the delivery room, the affected infant may have the sonorous seal-bark cough that indicates
concomitant tracheomalacia. If an oral tube is placed to suction the stomach, as it is in some
delivery rooms, it characteristically becomes blocked 10-11 cm from the lips.
Vertebral defects, anorectal malformations, cardiovascular defects, tracheoesophageal defects,
renal anomalies, and limb deformities (VACTERL) are associated anomalies that should be
readily apparent upon physical examination.[12, 13] If any of these anomalies are present, the
presence of the others must be assessed. The VACTERL syndrome occurs when 3 or more of the
associated anomalies are present. This syndrome occurs in approximately 25% of all patients
with esophageal atresia. Anomalies in this syndrome include the following:

Vertebral defects - Multiple or single hemivertebrae, scoliosis, rib deformities

Anorectal malformations -Imperforate anus of all varieties, cloacal deformities

Cardiovascular defects -Ventricular septal defect (most common), tetralogy of

Fallot, patent ductus arteriosus, atrial septal defects, atrioventricular canal
defects, aortic coarctation, right-sided aortic arch, single umbilical artery

Tracheoesophageal defects - Esophageal atresia

Renal anomalies - Renal agenesis including Potter syndrome, bilateral renal

agenesis or dysplasia, horseshoe kidney, polycystic kidneys, urethral atresia,
ureteral malformations

Limb deformities - Radial dysplasia, absent radius, radial-ray deformities,

syndactyly, polydactyly, lower-limb tibial deformities

Other associated conditions include coloboma, heart defects, atresia choanae, developmental
retardation, genital hypoplasia, and ear deformities (CHARGE).
The following anomalies also occur with increased frequency in esophageal atresia

Neurologic defects -Neural tube defects, hydrocephalus, tethered cord,

holoprosencephaly

GI defects -Duodenal atresia, ileal atresia, hypertrophic pyloric stenosis,

omphalocele, malrotation, Meckel diverticulum

Pulmonary defects - Unilateral pulmonary agenesis, diaphragmatic hernia

Genitalia defects - Undescended testicles, ambiguous genitalia, hypospadias

Also, trisomies 13, 21, or 18 and Fanconi syndrome may be present. The overall incidence of
associated anomalies is approximately 50%. Cardiovascular anomalies occur in 35% of cases,
genitourinary anomalies occur in 20% of cases, and associated gastrointestinal anomalies occur
in approximately 20% of cases. A tethered cord is usually detectable with ultrasonography in the
newborn period or later in life with MRI (or less desirably with CT scanning) if findings are
equivocal.

Indications
The indication and timing of surgical repair may be determined by using the Waterston, Spitz, or
Poenaru prognostic classification system.
In 1962, Waterston developed a prognostic classification system for esophageal atresia that is
still used today.[14] Category A includes patients who weigh more than 5.5 lb (2.5 kg) at birth and
who are otherwise well; category B includes patients who weigh 4-5.5 lb (1.8-2.5 kg) and are
well or who have higher birth weights, moderate pneumonia, and congenital anomalies; and
category C includes patients who weigh less than 4 lb (1.8 kg) or have higher birth weights,
severe pneumonia, and severe congenital anomalies. Management strategies are as follows:

Category A - Immediate primary repair

Category B - Delayed repair

Category C - Staged repair

In 1994, after analyzing findings in 387 patients, Spitz et al recognized that the presence or
absence of cardiac disease is a proven major prognostic factor.[15] Spitz et al suggested the
following groups, which are analogous to those in the Waterston classification system:

Group I - Birth weight more than 1.5 kg and no major cardiac disease
Group II - Birth weight less than 1.5 kg or major cardiac disease

Group III - Birth weight less than 1.5 kg and major cardiac disease

In 1993, Poenaru proposed a simpler, 2-group classification system based on logistic regression
analysis findings in 95 patients.[16] Note that birth weight is not a factor. Class I includes patients
who are low risk and do not meet criteria in class II, and class II includes patients who are high
risk and ventilator-dependent or who have life-threatening anomalies, regardless of pulmonary
status.
In 1989, Randolph et al refined the Waterston classification and reported a clinically helpful
system that used a patient's physiologic status to determine the surgical management (ie,

immediate repair, delayed primary repair, or staged repair).[17] Weight, gestational age, and
pulmonary condition were not considered. If the patient's physiologic parameters were good,
they were managed with immediate repair. Staged repairs were used for infants who were severe
compromised infants, especially those with severe cardiac anomalies. In this group, the survival
rate was 77%, and the overall survival was 90%.
The above prognostic groupings can allow for the stratification of high-risk patients with
esophageal atresia in planning for delayed repair, staged repair, or both; low-risk babies can
usually undergo early (first 24-48 h) primary single-stage repair. For instance, a 2-kg baby with
esophageal atresia and distal tracheoesophageal fistula (TEF) who also has tetralogy of Fallot is
in Waterston category C, Spitz group II, and Poenaru class II; in this patient, delayed or staged
repair may be best.
These classification systems help physicians to compare results in an organized and meaningful
way. When comparing the 3 prognostic classification systems, the Spitz classification appears to
have the most applicability in current practice.[18] Ductal-dependent cardiac lesions still seem to
significantly affect the survival of children born with esophageal atresia.

Relevant Anatomy
The treatment plan for each baby must be individualized. The prognostic classifications can
provide guidance in patients with multiple problems, but decisions in identifying the most lifethreatening anomaly must be made early.
Management plans for a delayed repair of the esophageal atresia may include placing a 10F
Replogle double-lumen tube through the mouth or nose well into the upper pouch to provide
continuous suction of pooled secretions from the proximal portion of the atretic esophagus. The
baby may be positioned in the 45 sitting position. Prophylactic broad-spectrum antibiotics such
as ampicillin and gentamicin may be used. General supportive care and total parenteral nutrition
are needed.
With careful bedside attendance, these measures may permit a delay of days to perhaps weeks.
Some have described cases in which the baby was discharged home with a Replogle tube in situ
while waiting for staged repair of an esophageal atresia. However, deaths have been reported in
infants in whom the tube did not maintain an empty upper pouch. A gastrostomy, distal
tracheoesophageal fistula (TEF) ligation, or cervical esophagostomy may permit longer delays in
the esophageal atresia repair. However, each intrusion carries a price.
A gastrostomy may be created if no distal TEF is present. In such cases, the stomach is small,
and laparotomy is required. In all cases of esophageal atresia in which a gastrostomy is created,
care should be taken to place it near the lesser curve to avoid damaging the greater curve, which
can be used in the formation of an esophageal substitute. When a baby is ventilated with high
pressures, the gastrostomy may offer a route of decreased resistance, causing the ventilation
gases to flow through the distal fistula and out the gastrostomy site. This condition may
complicate the use of ventilation.

In cases such as those above or in cases in which a distal fistula continues to cause lung soiling,
consider distal TEF ligation. This ligation is performed by means of a right-sided thoracotomy,
ideally performed via an extrapleural approach. The fistula may be clipped or simply ligated. If it
is ligated and divided, subsequent staged repair of the esophageal atresia may be difficult
because the distal esophageal segment tends to retract inferiorly to a substantial degree when it is
detached from its tracheal mooring. However, simple fistula ligation may allow subsequent
reopening of the fistula. Division of the fistula and attempts to anchor it at the mid chest with
sutures are usually unsuccessful.
A cervical esophagostomy or spit fistula may be constructed in the right or left side of the neck,
depending on the choice for subsequent esophageal substitution. It allows drainage of the upper
pouch and precludes aspiration from the upper pouch. Sham feeding may be commenced in cases
in which a long delay to repair is anticipated. This feeding may prevent subsequent oral aversion,
which is a real problem in babies who have not been fed by mouth in their early weeks to months
of life. However, cervical esophagostomy usually dooms the child to some form of esophageal
substitution.
Please see Preoperative details for a discussion of aortic arch position and surgery.

Contraindications
Potter syndrome is bilateral renal agenesis and has a 100% mortality rate; therefore, repair of
esophageal atresia is contraindicated.

Laboratory Studies
In babies with esophageal atresia, samples should be obtained to determine baseline values of the
following:

CBC count
Electrolyte levels

Venous gas concentrations

BUN and serum creatinine levels

Blood glucose level

Serum calcium level

ABG concentrations, as necessary

Imaging Studies

Prenatal ultrasonography may reveal the size of the gastric bubble,

polyhydramnios, and VACTERL anomalies, all of which may indicate
esophageal atresia in the fetus.
o The sensitivity of prenatal ultrasonography is approximately 40%.

A prenatal diagnosis of esophageal atresia may be associated with a

worse prognosis.

Chest radiography (see the images below) is mandatory and should be

performed as soon as possible if esophageal atresia is suspected.

This chest radiograph reveals esophageal atresia and

distal tracheoesophageal fistula. Note the Replogle tube in the upper pouch

and the GI air below the diaphragm.

This chest
radiograph reveals esophageal atresia without tracheoesophageal fistula.
Note the absence of gas below the diaphragm.
o

The value of the chest radiography is enhanced if a Replogle tube is in

place and if 5-10 mL of air is injected to distend the upper pouch.

Great caution should be exercised if liquid contrast material is injected

into the proximal pouch. First, only about 1 mL of isotonic water-soluble
contrast should be used to prevent spillage into the airway. A catheter
with an end-hole should be used. Second, if an upper pouch fistula is
present, the contrast material flows directly into the airway. Usually, a
contrast-enhanced study is unnecessary.

The heart shadow and size should be assessed.

Vertebral and rib anomalies should be assessed.

The lung fields should be assessed for possible aspiration pneumonitis

and for the rarely associated diaphragmatic hernia or congenital lung
lesion.

The presence or absence of GI air below the diaphragm is an important

finding. Complete absence of gas in the GI tract denotes the absence
of a distal tracheoesophageal fistula (TEF); however, distal fistulae
simply occluded by mucous plugs have been rarely reported. In cases
of esophageal atresia without fistula, assume that the distance
between the ends of the atretic esophagus is too long for early singlestage primary repair. These infants require a delayed repair (see
discussion about gastrostomy in Relevant Anatomy and about gap-ogram below).

Early renal ultrasonography is mandatory and is used to evaluate associated

kidney anomalies, ureteral anomalies, or both.

Echocardiography is indicated early in the care of infants with esophageal

atresia who have clinical signs of cardiovascular disease. [19] However, a 1-dayold neonate with significant congenital heart disease may have normal
findings upon physical examination. Therefore, some argue that
echocardiography should be performed in all infants with esophageal atresia.
This examination also provides the surgeon with information regarding the
side of the aortic arch. A right-sided aortic arch is not uncommon in cases of
esophageal atresia, and the surgeon should be aware of this finding.

Limb radiography (see the image below) is indicated if the limbs appear
abnormal. The possibility of associated radial-ray deformities should be

investigated.
without a radial ray deformity.

This radiograph reveals a radius

Spinal ultrasonography is a simple test that takes advantage of the neonate's

relatively transparent lumber lamina in the assessment of an associated
tethered cord. This examination may be performed when the baby is younger
than 1 month, although it is not critically important in the early care of the
infant.

In cases in which the distance between the 2 atretic ends of the esophagus is
suspected to be too long for a primary repair, a gap-o-gram (see the image

below) is useful in assessing that distance.

Contrast material
has been administered, and a probe has been placed through the
gastrostomy in this child with pure esophageal atresia. The air-filled upper
pouch can be observed superiorly, with a Replogle tube within it. This gap-ogram reveals a very wide gap (>5 vertebral bodies), which requires
esophageal replacement. This study is a dynamic investigation, one in which
the surgeon and radiologist should be present to view the real-time
fluoroscopic images.
o

A gastrostomy is created, and the upper pouch is intubated with a 10F

Replogle tube with radiopaque markings. A small-diameter Bakes
dilator is introduced into the gastrostomy and directed superiorly under
fluoroscopic guidance into the distal esophageal segment. With gentle
but definite force on both the Bakes dilator and the Replogle tube, the
2 ends are pushed toward each other under fluoroscopic control.

At the point of least separation, an image is obtained, and the distance

between the 2 ends is determined in terms of vertebral bodies, which
provide an inherent reference for measurement.

Generally, a separation distance of 2 (some say 3) vertebral bodies or

fewer is usually small enough for an anastomosis. If greater distances
separate the ends, a delay of weeks to months may be required for the
ends to grow closer together, for reassessment with gap-o-grams
every 4-6 weeks, or for esophageal replacement or lengthening
surgery.

--------------------------------------

VOMITING

Nausea and vomiting facts

Nausea and vomiting are symptoms of a disease or condition. The underlying cause of the
illness causing nausea and vomiting should be identified and treated.
Nausea and vomiting symptom control is important both for comfort's sake and to
prevent dehydration.

Dehydration can worsen nausea and vomiting.

Medication may be available to control symptoms of nausea and vomiting.

Introduction to nausea and vomiting

Nausea and vomiting are symptoms of an underlying illness and not a specific disease. Nausea is
the sensation that the stomach wants to empty itself, while vomiting (emesis) or throwing up, is
the act of forcible emptying of the stomach. The term "dry heaves" refers to an episode of
vomiting where there is no food in the stomach to vomit, and only clear secretions are vomited.
Vomiting is a violent act in which the stomach almost turns itself inside out - forcing itself into
the lower portion of the esophagus (the tube that connects the mouth to the stomach) during a
vomiting episode, expelling food and secretions.

What causes nausea or vomiting?

There are numerous causes of nausea and vomiting. These symptoms may be due to the
following:

Acute gastritis (direct irritation of the stomach lining)

Central causes in which signals from the brain cause nausea and vomiting

Other illnesses not due to stomach problems

Medications and medical treatments

Mechanical obstruction of the bowel

Acute gastritis and nausea and vomiting

Acute gastritis is often caused by an something that irritates the lining of the stomach. Examples
of these circumstances include:

Infections: Infections are often the cause of stomach irritation, whether it is a common
virus or another type of infection. There may be associated crampy upper abdominal pain
that is associated with the nausea and vomiting. Fever ,and chills may be present.

Common viral infections include noroviruses and rotavirus. Infection by bacteria in the
Helicobacter family (such as H. Pylori) can also be the infectious agent.
Stomach flu: Stomach flu (gastroenteritis) is when vomiting and diarrhea occur together
that is associated with a viral infection. It should not be confused with influenza
(symptoms include fever, chills, cough, and muscle pain.

Food poisoning: Food poisoning may cause significant vomiting, and the most common
cause is a toxin released by the bacteria Staphylococcus aureus. Symptoms of food
poisoning begin within a couple hours of eating contaminated or poorly prepared food.
Other bacterial causes of food poisoning include Salmonella, Campylobacter, Shigella,
E. coli, Listeria, or Clostridium botulinum (botulism).

Other stomach irritants: alcohol, smoking, and nonsteroidal anti-inflammatory

medications (NSAIDs) such as aspirin and ibuprofen may irritate the stomach lining and
cause nausea and vomiting.

Peptic ulcer disease: Peptic ulcer disease can range from mild irritation of the stomach
lining to the formation of a defect in the protective lining of the stomach called an ulcer.

Gastroesophageal reflux disease (GERD, reflux esophagitis): Nausea or vomiting is

also associated with GERD (acid from the stomach is refluxed into the esophagus).

Central causes of nausea and vomiting

Headache: especially migraine, is commonly associated with nausea and vomiting.

Inner ear: Motion sickness, labyrinthitis, benign positional vertigo, or Meniere's disease

Increased intracranial pressure: Any illness or injury that increases the pressure within
the skull can cause vomiting.

Brain swelling due to trauma (includes bleeding within the brain)

Infection (meningitis or encephalitis)

Tumors (benign or malignant)

Abnormal electrolyte concentrations in the bloodstream and associated water

imbalance

Concussion, patients with head injuries do not have to have detectable bleeding in
the brain or brain swelling to have symptoms of brain irritation, which can include
headache, nausea, vomiting, changes in vision, confusion, difficulty
concentrating, difficulty sleeping, among other symptoms.

Noxious stimulus: Certain smells or sounds can cause centrally mediated nausea and
vomiting that originates in the brain. Whether it is the pain of a broken bone or the
emotional shock of observing an event, vasovagal events can cause significant symptoms.
In a vasovagal episode, the vagus nerve (one of the nerves that helps control basic body
functions like heart rate, breathing, and blood pressure) is overly stimulated can cause the

heart rate to slow and blood vessels to dilate. This decreases the blood flow to the brain
and can cause fainting, known as a syncopal episode.

Heat related illness: For example heat exhaustion, extreme sunburn, or dehydration

Nausea and vomiting associated with illness

Diabetes: Persons with diabetes may develop nausea because of gastroparesis, a

condition in which the stomach fails to empty properly and is likely due to the
generalized neuropathy (failure of the nerves in the body to send proper signals to and
from the brain) that is a complication of the disease.

People with diabetes can also develop nausea and vomiting should their blood sugars become
abnormally high or low (hyperglycemia or hypoglycemia) because the sugar and insulin balance
is disturbed.

Diseases or illness: Many illnesses associated with the intra-abdominal organs can
produce the symptoms of nausea and vomiting. These include digestive organ
diseasessuch as:
o Hepatitis
o

Gallbladder disease

Pancreatitis

Crohn's disease

Kidney diseases (for example, kidney stones, infection, kidney failure)

Some forms of cancer

Vomiting as an atypical symptom of another disease: Some illnesses will cause nausea
and vomiting, even though there is no direct involvement of the stomach or
gastrointestinal tract.
o

Heart attack victims may experience nausea and vomiting as an atypical symptom
of angina, especially if the heart attack affects the inferior or lower part of the
heart.

Lung infections, for example, pneumonia and bronchitis, may also cause nausea
and vomiting, especially if the area of lung involved is near the diaphragm, the
muscle that separates the chest form the abdomen.

Sepsis: An overwhelming body infection spread through the bloodstream may also be
associated with nausea and vomiting.

Eating disorders: Patients with bulimia will have self-induced vomiting, purging as part
of their psychiatric illness

Nausea and vomiting from medications and medical treatments

Side effects from medications: The side effect of many medications include stomach
irritation and/or nausea and vomiting. Anti-cancer dugs used for chemotherapy
commonly cause nausea and vomiting that is not easily relieved. Narcotic pain
medications, anti-inflammatory medications, steroids, and antibiotics all have nausea and
vomiting listed as common side effects.
Radiation therapy: Nausea and vomiting can be associated with radiation therapy.

Nausea and vomiting and bowel obstruction

Abdominal pain and distention, nausea and vomiting, and inability to pass flatus (gas) or have a
bowel movement are symptoms of bowel obstruction. Due to a variety of potential reasons, the
small intestine becomes blocked and doesn't allow contents to pass through to the colon. This
acts like a dam where food, fluid, and secretions back up, causing the symptoms of an
obstruction. Common causes of bowel obstruction include previous surgery with the formation
of adhesions, hernias, abnormal twisting of the GI tract (volvulus), tumors, and inflammatory
bowel disease (IBD).

Nausea and vomiting in pregnancy (morning sickness)

Vomiting in pregnancy is especially common in the first trimester due to hormone level changes
in the bloodstream.

Vomiting in infants
It may be hard to decide if an infant is vomiting or spitting up. If the episodes occur shortly after
feeding and only a small amount comes up, this may be spitting up.

Forceful vomiting: In the first two or three months, if the vomiting is forceful after
eating (imagine it flying across the room), this may be a sign of pyloric stenosis, or an
abnormal narrowing of the pylorus, the location where the stomach empties into the
duodenum (the first part of the small intestine). The vomiting is impressive and is
described as projectile. The diagnosis is often made by history and physical examination,
confirmed by ultrasound. The treatment is surgery.
Vomiting associated with pain: if the infant cries uncontrollably, and if the stool is
bloody or red, the diagnosis may be an intussusception (the pushing of one segment of
the bowel into an adjacent segment). The stool is classically described as like being
currant jelly, but any blood in the stool is not normal and should always be a cause for
concern. It is reasonable to seek medical care for any inconsolable infant.
Viral infection: If there is vomiting with associated diarrhea that is not bloody, then a
viral infection is a possibility. Alternatively, there may be an issue with intolerance to the
type of baby formula. Infants and children are at greater risk of dehydration if the
vomiting episodes last for more than 24 hours. If dehydration is suspected, seek medical

care. Signs and symptoms of dehydration in an infant include dry mouth, lack of sweat in
the armpits and groin, suken eyes, weakness with a poor cry, and decreased muscle tone.

What are home remedies for nausea or vomiting?

It is important to rest the stomach and yet still avoid dehydration. Clear fluids should be
attempted for the first 24 hours of an illness, and then the diet should be advanced as tolerated.
Clear fluids are easy for the stomach to absorb and include:

Water
Sports drinks

Clear broths

Popsicles

Jello

It is important not to take too much fluid at one time since stretching the stomach may cause the
nausea to worsen. One to two ounces of fluid at a time, taken every 10-15 minutes, may be all
that the stomach will be able to tolerate. In infants and children, the amount may be as little as 5
or 10 cc's or less than a third of an ounce at a time.
Milk products should be avoided for the first 24-48 hours during an episode of nausea and
vomiting. The enzyme that helps digest milk is located in cells lining the stomach. With
vomiting, the body can become relatively lactose intolerant. Abdominal pain, bloating, vomiting,
and diarrhea may occur. As the affected individual begins to feel better, they can begin to
reintroduce foods, but to help the stomach readjust, health care professionals often recommend
limiting the diet to bland foods such as bananas, applesauce, rice, toast (the BRAT diet).

When should I call the doctor regarding nausea and vomiting?

If the symptoms last for more than 24 hours, if the diagnosis is uncertain, if there is concern
about dehydration, or if the patient has underlying medical conditions that make them more
fragile, medical care should be accessed sooner, rather than later.
Infants and children are more susceptible to dehydration and may not have as much reserve as an
adult. If there is concern about dehydration or the inability to tolerate fluids, a health care
professional should be contacted.
If nausea and vomiting are associated with pain, fever, vomiting blood, or having bloody or
black, tarry bowel movements, medical care should be sought immediately.
Vomiting is a symptom of an illness, if the symptom persists for more than 24-48 hours, it may
be wise to contact a health care professional.

How is the source of nausea or vomiting diagnosed?

Diagnosis often can be made when the health care professional takes a careful history and
performs a physical examination. Any tests that need to be ordered will be based on the direction
from the history and physical exam, and sometimes no further testing is required to make the
diagnosis.
Laboratory tests and X-rays may be ordered to assess the stability of the patient and not
necessarily to make the diagnosis. For example, a patient with food poisoning may need blood
tests ordered to measure the electrolytes and other chemicals, since the patient may lose
significant amounts of sodium, potassium, and chloride from the body from persistent vomiting
and diarrhea.
Urinalysis may be helpful in assessing hydration status. Concentrated, dark urine is associated
with dehydration because the kidneys try to preserve as much water as possible in the body.
Ketones in the urine are also a sign of dehydration.

What is the treatment for nausea or vomiting?

Nausea and vomiting can be treated with medication at the same time as the search for the
underlying diagnosis is being carried out. Ideally, these symptoms should resolve when the
underlying illness is treated and controlled.
Nausea and vomiting are often made worse when the patient is dehydrated, resulting in a vicious
cycle. The nausea makes it difficult to drink fluid, making the dehydration worse, which then
increases the nausea. Intravenous fluids may be provided to correct this issue and break the
cycle.
There are a variety of anti-nausea medications (antiemetics) that may be prescribed. They can be
administered in different ways depending upon the patient's ability to take them. Medications are
available by pill, liquid, or tablets that dissolve on or under the tongue, by intravenous or
intramuscular injection, or by rectal suppository.
Common medications used to control nausea and vomiting include:

promethazine (Phenergan),
prochlorperazine (Compazine),

droperidol (Inapsine)

metoclopramide (Reglan), and

ondansetron (Zofran).

The decision as to which medication to use will depend on the patient's condition.

H PYLORI

H. pylori infection
By Mayo Clinic staff

Original Article: http://www.mayoclinic.com/health/h-pylori/DS00958

Definition
H. pylori infection occurs when a type of bacteria called Helicobacter pylori (H. pylori) infects
your stomach, usually during childhood. A common cause of peptic ulcers, H. pylori infection is
present in about half the people in the world.
Most people don't realize they have H. pylori infection, because they never get sick from it. If
you develop signs and symptoms of a peptic ulcer, your doctor will probably test you for H.
pylori infection, because it can be treated with antibiotics.

Symptoms
Most people with H. pylori infection will never have any signs or symptoms. It's not clear why
this is, but scientists believe some people may be born with more resistance to the harmful
effects of H. pylori.
When signs or symptoms do occur with H. pylori infection, they may include:

An ache or burning pain in your abdomen

Nausea

Vomiting

Frequent burping

Bloating

Weight loss

When to see a doctor

Make an appointment with your doctor if you notice any persistent signs and symptoms that
worry you. Seek immediate medical help if you experience:

Severe or persistent abdominal pain

Difficulty swallowing

Bloody or black tarry stools

Bloody or black vomit or vomit that looks like coffee grounds

Causes
H. pylori bacteria can be passed from person to person through direct contact with saliva, vomit
or fecal matter. H. pylori can also be spread through contaminated food or water. The infection is
usually acquired during childhood.

Risk factors
Many people contract H. pylori as children. Contracting H. pylori in adulthood is much less
common. Risk factors for H. pylori infection are related to living conditions in your childhood,
such as:

Living in crowded conditions. You have a greater risk of H. pylori infection

if you live in a home with many other people.
Living without a reliable supply of hot water. Having a reliable hot water
supply can help you keep your living area clean and reduce your risk of H.
pylori.

Living in a developing country. People living in developing countries,

where crowded and unsanitary living conditions may be more common, have
a higher risk of H. pylori infection.

Living with someone who has an H. pylori infection. If someone you

live with has H. pylori, you're more likely to also have H. pylori.

Complications
Ulce
rs

Complications associated with H. pylori infection include:

Ulcers. H. pylori can damage the protective lining of your stomach and small
intestine. This can allow stomach acid to create an open sore (ulcer).
Inflammation of the stomach lining. H. pylori infection can irritate your
stomach, causing inflammation (gastritis).
Stomach cancer. H. pylori infection is a strong risk factor for certain types of
stomach cancer.

Preparing for your appointment

You're likely to first see your family doctor or a general practitioner if you have signs or
symptoms that indicate a complication of H. pylori infection. Your doctor may refer you to a
specialist who treats diseases of the digestive system (gastroenterologist).
Because appointments can be brief, and because there's often a lot of ground to cover, it's a good
idea to be well prepared for your appointment. Here's some information to help you get ready for
your appointment, and what to expect from your doctor.
What you can do
At the time you make the appointment, be sure to ask if there's anything you need to do in
advance, such as restrict your diet. Before your appointment, you might want to write a list that
answers the following questions:

When did your symptoms begin? Does anything make them better or worse?
Have your parents or siblings ever experienced similar problems?

What medications or supplements do you take regularly?

Your time with your doctor is limited, so preparing a list of questions will help you make the
most of your time together. For H. pylori infection, some basic questions to ask your doctor
include:

How did H. pylori infection cause the complications I'm experiencing?

Can H. pylori cause other complications?

What kinds of tests do I need?

Do you have any brochures on this topic?

In addition to the questions that you've prepared to ask your doctor, don't hesitate to ask
questions during your appointment at any time that you don't understand something.
What to expect from your doctor
Your doctor is likely to ask you a number of questions. Being ready to answer them may allow
more time to cover other points you want to address. Your doctor may ask:

Have your symptoms been continuous or occasional?

How severe are your symptoms?

Do you regularly take medications such as aspirin or ibuprofen (Advil, Motrin,

others)?

Tests and diagnosis

Tests and procedures used to determine whether you have an H. pylori infection include:

Blood test. Analysis of a blood sample may reveal evidence of an active or

previous H. pylori infection in your body. A blood sample is usually collected
by pricking your finger.
Breath test. During a breath test, you swallow a pill, liquid or pudding that
contains radioactive carbon molecules. If you have an H. pylori infection, the
radioactive carbon is released when the solution is broken down in your
stomach. Your body absorbs the radioactive carbon and expels it when you
exhale. You exhale into a bag and your doctor uses a special device to detect
the radioactive carbon.

Stool test. A laboratory test called a stool antigen test looks for foreign
proteins (antigens) associated with H. pylori infection in your stool.

Scope test. During an endoscopy exam, your doctor threads a long flexible
tube equipped with a tiny camera (endoscope) down your throat and
esophagus and into your stomach and duodenum. Using this instrument, your
doctor can view any irregularities in your upper digestive tract and remove
tissue samples (biopsy). These samples are analyzed for H. pylori infection.

Treatments and drugs

H. pylori infections are usually treated with two varieties of antibiotics at once, to help prevent
the bacteria from developing a resistance to one particular antibiotic. Your doctor also will
prescribe an acid suppression drug, to help your stomach lining heal.
Your doctor may recommend that you undergo testing for H. pylori several weeks after your
treatment. If the tests show the treatment was unsuccessful, you may undergo another round of
treatment with a different combination of antibiotic medications.

Prevention
In areas of the world where H. pylori infection and its complications are common, doctors
sometimes test healthy people for H. pylori. Whether there is a benefit to treating H. pylori when
you have no signs or symptoms of infection is controversial among doctors. If you're concerned
about H. pylori infection or think you may have a high risk of stomach cancer, talk to your
doctor. Together you can decide whether you may benefit from H. pylori screening.
http://www.mayoclinic.com/print/h-pylori/DS00958/METHOD=print&DSECTION=all
PEPTIC ULCER

Background
Gastric and duodenal ulcers usually cannot be differentiated based on history alone, although
some findings may be suggestive (see Diagnosis). Epigastric pain is the most common symptom
of both gastric and duodenal ulcers. It is characterized by a gnawing or burning sensation and
occurs after mealsclassically, shortly after meals with gastric ulcer and 2-3 hours afterward
with duodenal ulcer.

In uncomplicated peptic ulcer disease (PUD), the clinical findings are few and nonspecific.
Alarm features" that warrant prompt gastroenterology referral[1] include bleeding, anemia, early
satiety, unexplained weight loss, progressive dysphagia or odynophagia, recurrent vomiting, and
family history of GI cancer. Patients with perforated PUD usually present with a sudden onset of
severe, sharp abdominal pain. (See Clinical Presentation.)
In most patients with uncomplicated PUD, routine laboratory tests usually are not helpful;
instead, documentation of PUD depends on radiographic and endoscopic confirmation. Testing
for H pylori infection is essential in all patients with peptic ulcers. Rapid urease tests are
considered the endoscopic diagnostic test of choice. Of noninvasive tests, fecal antigen testing is
more accurate than antibody testing and is less expensive than urea breath tests. A fasting serum
gastrin level should be obtained in certain cases to screen for Zollinger-Ellison syndrome. (See
Workup.)
Upper GI endoscopy is the preferred diagnostic test in the evaluation of patients with suspected
PUD. Endoscopy provides an opportunity to visualize the ulcer, to determine the presence and
degree of active bleeding, and to attempt hemostasis by direct measures, if required. Perform
endoscopy early in patients older than 45-50 years and in patients with associated so-called alarm
features.
Most patients with PUD are treated successfully with cure of H pylori infection and/or avoidance
of nonsteroidal anti-inflammatory drugs (NSAIDs), along with the appropriate use of
antisecretory therapy. In the United States, the recommended primary therapy for H pylori
infection is proton pump inhibitor (PPI)based triple therapy.[1] These regimens result in a cure of
infection and ulcer healing in approximately 85-90% of cases.[2] Ulcers can recur in the absence
of successful H pylori eradication. (See Treatment and Management.)
In patients with NSAID-associated peptic ulcers, discontinuation of NSAIDs is paramount, if it
is clinically feasible. For patients who must continue with their NSAIDs, proton pump inhibitor
(PPI) maintenance is recommended to prevent recurrences even after eradication of H pylori.[3, 4]
Prophylactic regimens that have been shown to dramatically reduce the risk of NSAID-induced
gastric and duodenal ulcers include the use of a prostaglandin analog or a PPI. Maintenance
therapy with antisecretory medications (eg, H2 blockers, PPIs) for 1 year is indicated in high-risk
patients. (See Medication.)
The indications for urgent surgery include failure to achieve hemostasis endoscopically, recurrent
bleeding despite endoscopic attempts at achieving hemostasis (many advocate surgery after 2
failed endoscopic attempts), and perforation.
Patients with gastric ulcers are also at risk of developing gastric malignancy.

Anatomy
Because many surgical procedures for peptic ulcer disease (PUD) entail some type of vagotomy,
a discussion concerning the vagal innervation of the abdominal viscera is appropriate (see image
below). The left (anterior) and the right (posterior) branches of the vagus nerve descend along

either side of the distal esophagus. As they enter the lower thoracic cavity, they can communicate
with each other through several cross-branches that comprise the esophageal plexus. However,
below this plexus, the 2 vagal trunks again become separate and distinct before the anterior trunk
branches to form the hepatic, pyloric, and anterior gastric (also termed the anterior nerve of
Latarjet) branches. The posterior trunk branches to form the posterior gastric branch (also termed
the posterior nerve of Latarjet) and the celiac branch.
The parietal cell mass of the stomach is segmentally innervated by the terminal branches from
each of the anterior and posterior gastric branches. These terminal branches are divided during a
highly selective vagotomy. The gallbladder is innervated from efferent branches of the hepatic
division of the anterior trunk. Consequently, transection of the anterior vagus trunk (performed
during truncal vagotomy) can result in a dilated gallbladder with inhibited contractility and
subsequent cholelithiasis. The celiac branch of the posterior vagus innervates the entire midgut
(with the exception of the gallbladder). Thus, division of the posterior trunk during truncal
vagotomy may contribute to postoperative ileus.

Vagal innervation of stomach.

Pathphysiology
Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis
mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation
of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the
gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and
pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that
lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role,
because PGE increases the production of both bicarbonate and the mucous layer.
In the event of acid and pepsin entering the epithelial cells, additional mechanisms are in place to
reduce injury. Within the epithelial cells, ion pumps in the basolateral cell membrane help to
regulate intracellular pH by removing excess hydrogen ions. Through the process of restitution,
healthy cells migrate to the site of injury. Mucosal blood flow removes acid that diffuses through
the injured mucosa and provides bicarbonate to the surface epithelial cells.
Under normal conditions, a physiologic balance exists between gastric acid secretion and
gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance
between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors,

such as NSAIDs, H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal
defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury. The
defensive mechanisms include tight intercellular junctions, mucus, mucosal blood flow, cellular
restitution, and epithelial renewal.
The gram-negative spirochete H pylori was first linked to gastritis in 1983. Since then, further
study of H pylori has revealed that it is a major part of the triad, which includes acid and pepsin,
that contributes to primary peptic ulcer disease. The unique microbiologic characteristics of this
organism, such as urease production, allows it to alkalinize its microenvironment and survive for
years in the hostile acidic environment of the stomach, where it causes mucosal inflammation
and, in some individuals, worsens the severity of peptic ulcer disease.
When H pylori colonizes the gastric mucosa, inflammation usually results. The causal
association between H pylori gastritis and duodenal ulceration is now well established in the
adult and pediatric literature. In patients infected with H pylori, high levels of gastrin and
pepsinogen and reduced levels of somatostatin have been measured. In infected patients,
exposure of the duodenum to acid is increased. Virulence factors produced by H pylori, including
urease, catalase, vacuolating cytotoxin, and lipopolysaccharide, are well described.
Most patients with duodenal ulcers have impaired duodenal bicarbonate secretion, which has
also proven to be caused by H pylori because its eradication reverses the defect[5] . The
combination of increased gastric acid secretion and reduced duodenal bicarbonate secretion
lowers the pH in the duodenum, which promotes the development of gastric metaplasia (ie, the
presence of gastric epithelium in the first portion of the duodenum). H pylori infection in areas of
gastric metaplasia induces duodenitis and enhances the susceptibility to acid injury, thereby
predisposing to duodenal ulcers. Duodenal colonization by H pylori was found to be a highly
significant predictor of subsequent development of duodenal ulcers in one study that followed
181 patients with endoscopy-negative, nonulcer dyspepsia[6] .

Etiology
Peptic ulcer disease (PUD) may be due to any of the following:

H pylori infection
Drugs

Lifestyle factors

Severe physiologic stress

Hypersecretory states (uncommon)

Genetic factors

H pylori infection

H pylori infection and NSAID use account for most cases of PUD. The rate of H pylori infection
for duodenal ulcers in the United States is less than 75% for patients who do not use NSAIDs.
Excluding patients who used NSAIDs, 61% of duodenal ulcers and 63% of gastric ulcers were
positive for H pylori in one study. These rates were lower in whites than in nonwhites.
Prevalence of H pylori infection in complicated ulcers (ie, bleeding, perforation) is significantly
lower than that found in uncomplicated ulcer disease.

Drugs
NSAID use is a common cause of PUD. These drugs disrupt the mucosal permeability barrier,
rendering the mucosa vulnerable to injury. As many as 30% of adults taking NSAIDs have GI
adverse effects. Factors associated with an increased risk of duodenal ulcers in the setting of
NSAID use include history of previous peptic ulcer disease, advanced age, female sex, high
doses or combinations of NSAIDs, long-term NSAID use, concomitant use of anticoagulants,
and severe comorbid illnesses.
A long-term prospective study found that patients with arthritis who were older than 65 years
who regularly took low-dose aspirin were at an increased risk for dyspepsia severe enough to
necessitate the discontinuation of NSAIDs.[7] This suggests that better management of NSAID
use should be discussed with older patients in order to reduce NSAID-associated upper GI
events.
Although the idea was initially controversial, most evidence now supports the assertion that H
pylori and NSAIDs are synergistic with respect to the development of peptic ulcer disease. A
meta-analysis found that H pylori eradication in NSAID-naive users before the initiation of
NSAIDs was associated with a decrease in peptic ulcers[8] .
Although the prevalence of NSAID gastropathy in children is unknown, it seems to be
increasing, especially in children with chronic arthritis treated with NSAIDs. Case reports have
demonstrated gastric ulceration from low-dose ibuprofen in children, even after just 1 or 2
doses[9] .
Corticosteroids alone do not increase the risk for PUD; however, they can potentiate ulcer risk in
patients who use NSAIDs concurrently.
The risk of upper GI tract bleeding may be increased in users of the diuretic spironolactone[10] or
serotonin reuptake inhibitors with moderate to high affinity for serotonin transporter[11] .

Lifestyle factors
Evidence that tobacco use is a risk factor for duodenal ulcers is not conclusive. Support for a
pathogenic role for smoking comes from the finding that smoking may accelerate gastric
emptying and decrease pancreatic bicarbonate production. However, studies have produced
contradictory findings. In one prospective study of more than 47,000 men with duodenal ulcers,
smoking did not emerge as a risk factor.[12] However, smoking in the setting of H pylori infection

may increase the risk of relapse of PUD.[13] Smoking is harmful to the gastroduodenal mucosa,
and H pylori infiltration is denser in the gastric antrum of smokers.[14]
Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis. Evidence that
consumption of alcohol is a risk factor for duodenal ulcer is inconclusive. A prospective study of
more than 47,000 men with duodenal ulcer did not find an association between alcohol intake
and duodenal ulcer.[12]
Little evidence suggests that caffeine intake is associated with an increased risk of duodenal
ulcers.

Severe physiologic stress

Stressful conditions that may cause PUD include burns, CNS trauma, surgery, and severe
medical illness. Serious systemic illness, sepsis, hypotension, respiratory failure, and multiple
traumatic injuries increase the risk for secondary (stress) ulceration.
Cushing ulcers are associated with a brain tumor or injury and typically are single, deep ulcers
that are prone to perforation. They are associated with high gastric acid output and are located in
the duodenum or stomach. Extensive burns are associated with Curling ulcers.
Stress ulceration and upper-GI hemorrhage are complications that are increasingly encountered
in critically ill children in the intensive care setting. Severe illness and a decreased gastric pH are
related to an increased risk of gastric ulceration and hemorrhage.

Hypersecretory states (uncommon)

The following are among hypersecretory states that may, uncommonly, cause PUD:

Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia type

I (MEN-I)
Antral G cell hyperplasia

Systemic mastocytosis

Basophilic leukemias

Cystic fibrosis

Short bowel syndrome

Hyperparathyroidism

Physiologic factors
In up to one third of patients with duodenal ulcers, basal acid output (BAO) and maximal acid
output (MAO) are increased. In one study, increased BAO was associated with an odds ratio
[OR] of up to 3.5, and increased MAO was associated with an OR of up to 7 for the development

of duodenal ulcers. Individuals at especially high risk are those with a BAO greater than 15
mEq/h. The increased BAO may reflect the fact that in a significant proportion of patients with
duodenal ulcers, the parietal cell mass is increased to nearly twice that of the reference range.[15]
In addition to the increased gastric and duodenal acidity observed in some patients with duodenal
ulcers, accelerated gastric emptying is often present. This acceleration leads to a high acid load
delivered to the first part of the duodenum, where 95% of all duodenal ulcers are located.
Acidification of the duodenum leads to gastric metaplasia, which indicates replacement of
duodenal villous cells with cells that share morphologic and secretory characteristics of gastric
epithelium. Gastric metaplasia may create an environment that is well suited to colonization by
H pylori.

Genetics
More than 20% of patients have a family history of duodenal ulcers, compared with only 5-10%
in the control groups. In addition, weak associations have been observed between duodenal
ulcers and blood type O. Furthermore, patients who do not secrete ABO antigens in their saliva
and gastric juices are known to be at higher risk. The reason for these apparent genetic
associations is unclear.
A rare genetic association exists between familial hyperpepsinogenemia type I (a genetic
phenotype leading to enhanced secretion of pepsin) and duodenal ulcers. However, H pylori can
increase pepsin secretion, and a retrospective analysis of the sera of one family studied before the
discovery of H pylori revealed that their high pepsin levels were more likely related to H pylori
infection.

Additional etiologic factors

Any of the following may be associated with PUD:

Hepatic cirrhosis
Chronic obstructive pulmonary disease

Allergic gastritis and eosinophilic gastritis

Cytomegalovirus infection

Graft versus host disease

Uremic gastropathy

Henoch-Schnlein gastritis

Corrosive gastropathy

Celiac disease

Bile gastropathy

Autoimmune disease

Crohn disease

Other granulomatous gastritides (eg, sarcoidosis, histiocytosis X,

tuberculosis)

Phlegmonous gastritis and emphysematous gastritis

Other infections, including Epstein-Barr virus, HIV, Helicobacter heilmannii,

herpes simplex, influenza, syphilis, Candida albicans,histoplasmosis,
mucormycosis, and anisakiasis

Chemotherapeutic agents, such as 5-fluorouracil (5-FU), methotrexate (MTX),

and cyclophosphamide

Local radiation resulting in mucosal damage, which may lead to the

development of duodenal ulcers

Use of crack cocaine, which causes localized vasoconstriction, resulting in

reduced blood flow and possibly leading to mucosal damage

Epidemiology

United States statistics

In the United States, PUD affects approximately 4.5 million people annually. Approximately
10% of the US population has evidence of a duodenal ulcer at some time. Of those infected with
H pylori, the lifetime prevalence is approximately 20%. Only about 10% of young persons have
H pylori infection; the proportion of people with the infection increases steadily with age.
Overall, the incidence of duodenal ulcers has been decreasing over the past 3-4 decades.
Although the rate of simple gastric ulcer is in decline, the incidence of complicated gastric ulcer
and hospitalization has remained stable, partly due to the concomitant use of aspirin in an aging
population. The hospitalization rate for PUD is approximately 30 patients per 100,000 cases.
The prevalence of PUD has shifted from predominance in males to similar occurrences in males
and females. Lifetime prevalence is approximately 11-14% in men and 8-11% in women. Age
trends for ulcer occurrence reveal declining rates in younger men, particularly for duodenal ulcer,
and increasing rates in older women. Trends reflect complex changes in risk factors for PUD,
including age-cohort phenomena with the prevalence of H pylori infection and the use of
NSAIDs in older populations.

International statistics
The frequency of PUD in other countries is variable and is determined primarily by association
with the major causes of PUD: H pylori and NSAIDs.[16]

Prognosis
When the underlying cause is addressed, the prognosis is excellent. Most patients are treated
successfully with eradication of H pylori infection, avoidance of NSAIDs, and the appropriate
use of antisecretory therapy. Eradication of H pylori infection changes the natural history of the
disease, with a decrease in the ulcer recurrence rate from 60-90% to approximately 10-20%.
However, this is a higher recurrence rate than previously reported, suggesting an increased
number of ulcers not caused by H pylori infection.
With regard to NSAID-related ulcers, the incidence of perforation is approximately 0.3% per
patient year, and the incidence of obstruction is approximately 0.1% per patient year. Combining
both duodenal ulcers and gastric ulcers, the rate of any complication in all age groups combined
is approximately 1-2% per ulcer per year.
The mortality rate for PUD, which has decreased modestly in the last few decades, is
approximately 1 death per 100,000 cases. If one considers all patients with duodenal ulcers, the
mortality rate due to ulcer hemorrhage is approximately 5%. Over the last 20 years, the mortality
rate in the setting of ulcer hemorrhage has not changed appreciably despite the advent of
histamine-2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs). However,
evidence from meta-analyses and other studies has shown a decreased mortality rate from
bleeding peptic ulcers when intravenous PPIs are used after successful endoscopic therapy.[17, 18,
19, 20]

Emergency operations for peptic ulcer perforation carry a mortality risk of 6-30%.[21] Factors
associated with higher mortality in this setting include the following:

Shock at the time of admission

Renal insufficiency

Delaying the initiation of surgery for more than 12 hours after presentation

Concurrent medical illness (eg, cardiovascular disease, diabetes mellitus

Age older than 70 years

Cirrhosis

Immunocompromised state

Location of ulcer (mortality associated with perforated gastric ulcer is twice

that associated with perforated duodenal ulcer.)

Patient Education
Patients should be warned of known or potentially injurious drugs and agents. Some examples
are as follows:

NSAIDs

Aspirin

Alcohol

Tobacco

Caffeine (eg, coffee, tea, colas)

Obesity has been shown to have an association with peptic ulcer disease (PUD), and patients
should be counseled regarding benefits of weight loss. Stress reduction counseling might be
helpful in individual cases but is not needed routinely.
For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine
Center. In addition, see eMedicine's patient education articles Peptic Ulcers, Heartburn, and
Understanding Heartburn/GERD Medications.

History
Obtaining a medical history, especially for peptic ulcer disease, H pylori infection, ingestion of
NSAIDs, or smoking, is essential in making the correct diagnosis. 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. It is
characterized by a gnawing or burning sensation and occurs after mealsclassically, shortly
after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer. Food or antacids
relieve the pain of duodenal ulcers but provide minimal relief of gastric ulcer pain.
Duodenal ulcer pain often awakens the patient at night. About 50-80% of patients with duodenal
ulcers experience nightly pain, as opposed to only 30-40% of patients with gastric ulcers and 2040% of patients with nonulcer dyspepsia (NUD). Pain typically follows a daily pattern specific to
the patient. Pain with radiation to the back is suggestive of a posterior penetrating gastric ulcer
complicated by pancreatitis.
Patients who develop gastric outlet obstruction as a result of a chronic, untreated duodenal ulcer
usually report a history of fullness and bloating associated with nausea and emesis that occurs
several hours after food intake. A common misconception is that adults with gastric outlet
obstruction present with nausea and emesis immediately after a meal.
Other possible manifestations include the following:

Dyspepsia, including belching, bloating, distention, and fatty food intolerance

Heartburn

Chest discomfort

Hematemesis or melena resulting from gastrointestinal bleeding. Melena may

be intermittent over several days or multiple episodes in a single day.

Rarely, a briskly bleeding ulcer can present as hematochezia.

Symptoms consistent with anemia (eg, fatigue, dyspnea) may be present

Sudden onset of symptoms may indicate perforation.

NSAID-induced gastritis or ulcers may be silent, especially in elderly patients.

Only 20-25% of patients with symptoms suggestive of peptic ulceration are

found on investigation to have a peptic ulcer.

Alarm features that warrant prompt gastroenterology referral[1] include the following:

Bleeding or anemia
Early satiety

Unexplained weight loss

Progressive dysphagia or odynophagia

Recurrent vomiting

Family history of GI cancer

Physical Examination
In uncomplicated PUD, the clinical findings are few and nonspecific and include the following:

Epigastric tenderness (usually mild)

Right upper quadrant tenderness may suggest a biliary etiology or, less
frequently, PUD.

Guaiac-positive stool resulting from occult blood loss

Melena resulting from acute or subacute gastrointestinal bleeding

Succussion splash resulting from partial or complete gastric outlet obstruction

Patients with perforated PUD usually present with a sudden onset of severe, sharp abdominal
pain. Most patients describe generalized pain; a few present with severe epigastric pain. As even
slight movement can tremendously worsen their pain, these patients assume a fetal position.
Abdominal examination usually discloses generalized tenderness, rebound tenderness, guarding,
and rigidity. However, the degree of peritoneal findings is strongly influenced by a number of
factors, including the size of perforation, amount of bacterial and gastric contents contaminating
the abdominal cavity, time between perforation and presentation, and spontaneous sealing of
perforation.

These patients may also demonstrate signs and symptoms of septic shock, such as tachycardia,
hypotension, and anuria. Not surprisingly, these indicators of shock may be absent in elderly or
immunocompromised patients or in those with diabetes. Patients should be asked if retching and
vomiting occurred before the onset of pain.

Diagnostic Considerations
Nonulcer dyspepsia (NUD) or functional dyspepsia
Functional dyspepsia is a diagnosis of exclusion made in patients with chronic persistent
epigastric pain in whom a thorough evaluation shows no organic disease. Patients may primarily
have epigastric pain, which is referred to as ulcerlike dyspepsia, or they may have symptoms of
postprandial bloating, which is referred to as motility-like dyspepsia.
Crohn disease
Crohn ulceration can involve any part of the GI tract from the buccal mucosa to the rectum.
Isolated Crohn ulceration of the stomach is rare, although it may cause duodenal or ileal
ulcerations.
Zollinger-Ellison syndrome
Zollinger-Ellison syndrome (ZES) is a rare disorder that can cause gastric or duodenal ulcers
(usually multiple) from excessive acid secretion. Consider ZES if a patient has severe peptic
ulceration, kidney stones, watery diarrhea, or malabsorption. ZES can also be associated with
multiple endocrine neoplasia type I, which occurs earlier than isolated ZES. Patients with ZES
usually have fasting serum gastrin levels of more than 200 pg/mL and basal gastric acid
hypersecretion of more than 15 mEq/h. Proton pump inhibitor (PPI) therapy should be
discontinued at least 2 weeks before the gastrin level is measured.

Differential Diagnoses

Acute Coronary Syndrome

Aneurysm, Abdominal

Cholangitis

Cholecystitis

Cholecystitis and Biliary Colic in Emergency Medicine

Cholelithiasis

Diverticular Disease

Esophageal Perforation, Rupture and Tears

Esophagitis

Gastritis, Acute

Gastritis, Chronic

Gastroenteritis

Gastroesophageal Reflux Disease

Inflammatory Bowel Disease

Viral Hepatitis

H pylori Infection
In the United States, the recommended primary therapy for H pylori infection is proton pump
inhibitor (PPI)based triple therapy.[1] These regimens result in a cure of infection and ulcer
healing in approximately 85-90% of cases.[2] Ulcers can recur in the absence of successful H
pylori eradication.
Dual therapies, which are alternative regimens for treating H pylori infection, are usually not
recommended as first-line therapy, because of a variable cure rate that is significantly less than
the cure rate achieved with triple therapy.
Spouses and H pylori positive family members of H pylori positive persons should be
considered for testing and treatment of H pylori infection,[39] since mother-to-child transmission
may be a major route of H pylori infection.[40]

Triple-therapy regimens
PPI-based triple therapy regimens for H pylori consist of a PPI, amoxicillin, and clarithromycin
for 7-14 days. A longer duration of treatment (14 d vs 7 d) appears to be more effective and is
currently the recommended treatment. Amoxicillin should be replaced with metronidazole in
penicillin-allergic patients only, because of the high rate of metronidazole resistance.[41] In
patients with complicated ulcers caused by H pylori, treatment with a PPI beyond the 14-day
course of antibiotics and until the confirmation of the eradication of H pylori is recommended.
PPI-based triple therapies are a 14-day regimen as shown below:
Omeprazole (Prilosec): 20 mg PO bid
or
Lansoprazole (Prevacid): 30 mg PO bid
or
Rabeprazole (Aciphex): 20 mg PO bid

or
Esomeprazole (Nexium): 40 mg PO qd
Plus
Clarithromycin (Biaxin): 500 mg PO bid
and
Amoxicillin (Amoxil): 1 g PO bid

Alternative triple-therapy regimens

The alternative triple therapies, also administered for 14 days, are as follows:
Omeprazole (Prilosec): 20 mg PO bid
or
Lansoprazole (Prevacid): 30 mg PO bid
or
Rabeprazole (Aciphex): 20 mg PO bid
or
Esomeprazole (Nexium): 40 mg PO qd
Plus
Clarithromycin (Biaxin): 500 mg PO bid
and
Metronidazole (Flagyl): 500 mg PO bid

Quadruple therapy
Quadruple therapies for H pylori infection are generally reserved for patients in whom the
standard course of treatment has failed.
Quadruple treatment includes the following drugs, administered for 14 days:

PPI, standard dose, or ranitidine 150 mg, PO bid

Bismuth 525 mg PO qid

Metronidazole 500 mg PO qid

Tetracycline 500 mg PO qid

Consider maintenance therapy with half of the standard doses of H2-receptor antagonists at
bedtime in patients with recurrent, refractory, or complicated ulcers, particularly if cure of H
pylori has not been documented or if an H pylori negative ulcer is present.

Complications of Peptic Ulcer Disease

Refractory, symptomatic peptic ulcers, though rare after eradication of H pylori infection and the
appropriate use of antisecretory therapy, are a potential complication of PUD. Obstruction is
particularly likely to complicate PUD in cases refractory to aggressive antisecretory therapy, H
pylori eradication, or avoidance of NSAIDs. Obstruction may persist or recur despite endoscopic
balloon dilation. Perforation is also a possibility. Penetration, particularly if not walled off or if a
gastrocolic fistula develops, is a potential complication. In addition, ulcer bleeding, particularly
in patients with a history of massive hemorrhage and hemodynamic instability, recurrent
bleeding on medical therapy, and failure of therapeutic endoscopy to control bleeding is a serious
complication.
Patients with gastric ulcers are also at risk of developing gastric malignancy. The risk is
approximately 2% in the initial 3 years. One of the important risk factors is related to H pylori
infection. H pylori is associated with atrophic gastritis, which, in turn, predisposes to gastric
cancer. H pylori infection is associated with gastric lymphoma or mucosa-associated lymphoid
tissue (MALT) lymphoma. Normal gastric mucosa is devoid of organized lymphoid tissue. H
pylori infection promotes acquisition of lymphocytic infiltration and often the formation of
lymphocytic aggregates and follicles from which MALT lymphoma develops. Eradication of H
pylori is very important in this group of patients because eradication of H pylori has been shown
to cause a remission of MALT lymphoma.
Malignancy should be strongly considered in the case of a persistent nonhealing gastric ulcer.
Endoscopic ultrasound examination may be helpful for assessing mucosal invasion or detecting
associated adenopathy in such patients. Surgical resection should be considered if evidence of
cancerous transformation is present.

Emergency Department Care

Presentations of peptic ulcer disease and gastritis usually are indistinguishable in the ED, and
thus, the management is generally the same. Treatment goals in the acute setting are the relief of
discomfort and protection of the gastric mucosal barrier to promote healing. Administer
supportive therapy as needed. Most patients with gastritis or peptic ulcer disease do not require
acute interventions.
High-risk patients include those with the following characteristics:

Bleeding with hemodynamic instability

Repeated hematemesis or any hematochezia

Failure to clear with gastric lavage

Coagulopathy

Comorbid disease (especially cardiac, pulmonary, or renal)

Advanced age

Drug treatments
Antacids or a GI cocktail (typically an antacid with an anesthetic such as viscous lidocaine
and/or an antispasmodic) may be used as symptomatic therapy; however, relief of symptoms
with a GI cocktail is not a diagnostic indicator.
Empiric treatment of H pylori is not recommended. Therapy is indicated only after confirmation
of infection. These tests are not performed in the ED. Empiric trial of acid suppression in patients
younger than 55 years without alarm features may be initiated with PPI for 4-8 weeks.
Appropriate follow-up is required to assess response in 2-4 weeks.[47]
Anticholinergic agents are contraindicated.

Bleeding
Massive gastric bleeds are the most difficult complication to treat. Mainstays of resuscitation
include the following:

Establishment of adequate IV access and volume replacement, initially with

crystalloid; in the face of continued hypotension after 2 L, consider blood
transfusion.
A central venous catheter to monitor such resuscitation may be considered.

Airway protection with intubation should be considered in the case of massive

bleeding.

NG suction helps to keep the stomach empty and contracted.

IV PPI has been shown to reduce mortality in upper GI bleeds and reduces the
incidence of rebleeding and the need for surgical intervention [48] ; emergent
surgical or endoscopic intervention may be required

Patients with significant or potentially significant hemorrhage require admission, usually to the
intensive care unit.

Surgical Care for Perforated Peptic Ulcer

With the success of medical therapy, surgery has a very limited role in the management of PUD.
Elective peptic ulcer surgery has been virtually abandoned. In the 1980s, the number of elective
operations for peptic ulcer disease dropped more than 70%, and emergent operations accounted
for more than 80%.[49] In general, 5% of bleeding ulcers eventually require operative
management. The indications for urgent surgery include the following:

Failure to achieve hemostasis endoscopically

Recurrent bleeding despite endoscopic attempts at achieving hemostasis
(many advocate surgery after 2 failed endoscopic attempts)

Perforation

The appropriate surgical procedure depends on the location and nature of the ulcer. Many
authorities recommend simple oversewing of the ulcer with treatment of the underlying H pylori
infection or cessation of NSAIDs for bleeding PUD. Additional surgical options for refractory or
complicated PUD include vagotomy and pyloroplasty, vagotomy and antrectomy with
gastroduodenal reconstruction (Billroth I) or gastrojejunal reconstruction (Billroth II), or a highly
selective vagotomy.
Only one prospective randomized trial has compared laparoscopic surgery with open surgery for
perforated ulcer. The study found that the only difference between the 2 groups was reduced
need for analgesia and an increased operative time in the laparoscopic group. Contraindications
for laparoscopic repair for perforated peptic ulcer include large perforations, a posterior location
of the perforation, and a poor general state of health.[34]
Surgical complications include pneumonia (30%), wound infection, abdominal abscess (15%),
cardiac problems (especially in those >70 y), diarrhea (30% after vagotomy), and dumping
syndromes (10% after vagotomy and drainage procedures).
To see complete information on Surgical Treatment of Perforated Peptic Ulcer, please go to the
main article by clicking here.

Medication Summary
The goals of pharmacotherapy are to eradicate H pylori infection, to reduce morbidity, and to
prevent complications in patients with peptic ulcers. Acid suppression is the general
pharmacologic principle of medical management of acute bleeding from a peptic ulcer, using
histamine-2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs).[33] Both classes are
available in intravenous or oral preparations. Discontinuation of NSAIDs is paramount, if it is
clinically feasible. For patients who must continue with their NSAIDs, PPI maintenance is
recommended to prevent recurrences even after eradication of H pylori.
The recommended primary therapy for H pylori infection is proton pump inhibitor (PPI)based
triple therapy. Antacids or a GI cocktail (typically an antacid with an anesthetic such as viscous
lidocaine and/or an antispasmodic) may be used as symptomatic therapy in the ED. Maintenance
treatment with antisecretory medications (eg, H2 blockers, PPIs) for 1 year is indicated in highrisk patients. High-risk patients include those with recurrent ulcers and those with complicated or

giant ulcers. If H pylori eradication is not achieved despite repeat treatment, maintenance
antisecretory therapy should be recommended. Patients with refractory ulcers may continue
receiving once-daily PPI therapy indefinitely. In this setting, if H pylori is absent, consider a
secondary cause of duodenal ulcer, such as Zollinger-Ellison syndrome.
Primary prevention of NSAID-induced ulcers includes avoiding unnecessary use of NSAIDs,
using acetaminophen or nonacetylated salicylates when possible, and using the lowest effective
dose of an NSAID and switching to less toxic NSAIDs.

What is a peptic ulcer?

H. pylori bacteria can cause peptic ulcerssores on the

lining of the stomach or duodenum.
A peptic ulcer is a sore on the lining of the stomach or duodenum, the beginning of the small
intestine. Less commonly, a peptic ulcer may develop just above the stomach in the esophagus,
the tube that connects the mouth to the stomach.
A peptic ulcer in the stomach is called a gastric ulcer. One that occurs in the duodenum is called
a duodenal ulcer. People can have both gastric and duodenal ulcers at the same time. They also
can develop peptic ulcers more than once in their lifetime.
Peptic ulcers are common. Each year in the United States, about half a million people develop a
peptic ulcer.1

Ramakrishnan K, Salinas RC. Peptic ulcer disease. American Family Physician.

2007;76(7):10051012.
[Top]

What causes peptic ulcers?

A bacterium called Helicobacter pylori (H. pylori) is a major cause of peptic ulcers. Nonsteroidal
anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, are another common cause.
Rarely, cancerous or noncancerous tumors in the stomach, duodenum, or pancreas cause ulcers.
Peptic ulcers are not caused by stress or eating spicy food, but both can make ulcer symptoms
worse. Smoking and drinking alcohol also can worsen ulcers and prevent healing.
[Top]

What is H. pylori?
H. pylori is a type of bacteriaa germ that may cause infection. H. pylori infection is common,
particularly in developing countries, and often begins in childhood. Symptoms usually don't
occur until adulthood, although most people never have any symptoms.
H. pylori causes more than half of peptic ulcers worldwide.2 The bacterium causes peptic ulcers
by damaging the mucous coating that protects the stomach and duodenum. Damage to the
mucous coating allows powerful stomach acid to get through to the sensitive lining beneath.
Together, the stomach acid and H. pylori irritate the lining of the stomach or duodenum and
cause an ulcer.
Yet, most people infected with H. pylori never develop ulcers. Why the bacterium causes ulcers
in some people and not in others is not known. Most likely, development of ulcers depends on
characteristics of the infected person; the type, or strain, of H. pylori present; and factors
researchers have yet to discover.
2

Helicobacter pylori and peptic ulcer disease; economics of peptic ulcer disease and H. pylori
infection. Centers for Disease Control and Prevention website.
www.cdc.gov/ulcer/economic.htm. Accessed February 23, 2009.
[Top]

How is H. pylori spread?

Researchers are not certain how H. pylori is transmitted, although they think it may be spread
through contaminated food or water. People may pick up the bacterium from food that has not
been washed well or cooked properly or from drinking water that has come from an unclean
source.

Other research is exploring how infection spreads from an infected person to an uninfected
person. Studies suggest that having contact with the stool or vomit of an infected person can
spread H. pylori infection. And H. pylori has been found in the saliva of some infected people,
which means infection could be spread through direct contact with saliva.
[Top]

What are the symptoms of a peptic ulcer?

Abdominal discomfort is the most common symptom of both duodenal and gastric ulcers. Felt
anywhere between the navel and the breastbone, this discomfort usually

is a dull or burning pain

occurs when the stomach is emptybetween meals or during the night

may be briefly relieved by eating food, in the case of duodenal ulcers, or by

taking antacids, in both types of peptic ulcers

lasts for minutes to hours

comes and goes for several days or weeks

Other symptoms include

weight loss
poor appetite

bloating

burping

nausea

vomiting

Some people experience only mild symptoms or none at all.

Emergency Symptoms

A person who has any of the following symptoms should call a doctor right away:

sharp, sudden, persistent, and severe stomach pain

bloody or black stools

bloody vomit or vomit that looks like coffee grounds

These alarm symptoms could be signs of a serious problem, such as

bleedingwhen acid or the peptic ulcer breaks a blood vessel

perforationwhen the peptic ulcer burrows completely through the stomach

or duodenal wall

obstructionwhen the peptic ulcer blocks the path of food trying to leave the
stomach

[Top]

How is an H. pylori-induced ulcer diagnosed?

Noninvasive Techniques

If a patient has peptic ulcer symptoms, the doctor first asks about use of over-the-counter and
prescription NSAIDs. Patients who are taking an NSAID are asked to stop, reduce the dose, or
switch to another medication.
Then the doctor tests to see if H. pylori is present. Testing is important because H. pylori-induced
ulcers are treated differently than ulcers caused by NSAIDs.
Doctors use one of three simple, noninvasive tests to detect H. pylori in a patient's blood, breath,
or stool. Because the breath test and stool test more accurately detect H. pylori than the blood
test, some doctors prefer to use one of these two tests. Each test described below is easily
performed, often in an outpatient setting such as a doctor's office or lab.
Blood test. A blood sample is taken from the patient's vein and tested for H. pylori antibodies.
Antibodies are substances the body produces to fight invading harmful substancescalled
antigenssuch as the H. pylori bacterium.
Urea breath test. The patient swallows a capsule, liquid, or pudding that contains urea labeled
with a special carbon atom. After a few minutes, the patient breathes into a container, exhaling
carbon dioxide. If the carbon atom is found in the exhaled breath, H. pylori is present, as this
bacterium contains large amounts of urease, a chemical that breaks urea down into carbon
dioxide and ammonia.
Stool antigen test. The patient provides a stool sample, which is tested for H. pylori antigens.
Invasive Techniques

If a patient has any alarm symptoms, the doctor orders an endoscopy or upper gastrointestinal
(GI) series. Many doctors also recommend these tests for patients who first experience peptic
ulcer symptoms around age 50. Often performed as outpatient procedures in a hospital, both
procedures are painless and allow the doctor to look inside the patient's stomach and duodenum.
For an endoscopy, the patient is lightly sedated. The doctor passes an endoscopea thin, lighted
tube with a tiny camera on the endinto the patient's mouth and down the throat to the stomach
and duodenum. With this tool, the doctor can closely examine the lining of the esophagus,
stomach, and duodenum.

The doctor can use the endoscope to take photos of ulcers or remove a tiny piece of tissueno
bigger than a match headto view with a microscope. This procedure is called a biopsy. The
biopsied tissue is examined to see if H. pylori is present.
If an ulcer is bleeding, the doctor can use the endoscope to inject medicines that help the blood
clot or to guide a heat probe that burns tissue to stop bleedinga process called cauterization.
For an upper GI series, the patient drinks a white, chalky liquid called barium. The barium makes
the esophagus, stomach, and duodenum and any ulcers show up on an x ray. Sedation is not
necessary for this procedure.
[Top]

How is an H. pylori-induced ulcer treated?

Peptic ulcers caused by H. pylori are treated with drugs that kill the bacteria, reduce stomach
acid, and protect the stomach and duodenal lining.
Antibiotics are used to kill H. pylori. Antibiotic regimens may differ throughout the world
because some strains of H. pylori have become resistant to certain antibioticsmeaning that an
antibiotic that once destroyed the bacterium is no longer effective. Doctors closely follow
research on antibiotic treatments for H. pylori infection to know which treatment strategy will
destroy which strain.
Medicines that reduce stomach acid include proton pump inhibitors (PPIs) and histamine
receptor blockers (H2 blockers). Both acid-reducing medicines help relieve peptic ulcer pain
after a few weeks and promote ulcer healing. PPIs and H2 blockers work in different ways:

PPIs suppress acid production by halting the mechanism that pumps acid into
the stomach.
H2 blockers work by blocking histamine, which stimulates acid secretion.

While PPIs cannot kill H. pylori, research shows they do help fight the H. pylori infection.
Research also shows that after 4 weeks of treatment, patients taking PPIs had earlier pain relief
and better healing rates than those taking H2 blockers.
Bismuth subsalicylate (Pepto-Bismol) coats ulcers, protecting them from stomach acid. Although
bismuth subsalicylate may kill H. pylori, it is used withnot in place ofantibiotics in some
treatment regimens.
In the United States, clarithromycin-based triple therapytriple therapy, for shortis the
standard treatment for an ulcer caused by H. pylori. The doctor prescribes the antibiotic
clarithromycin, a PPI, and the antibiotics amoxicillin or metronidazole for 10 to 14 days.
Because research shows higher cure rates with 14 days of treatment, some doctors now prescribe
triple therapy for this longer period.

Bismuth quadruple therapy is another treatment strategy used in the United States. The patient
takes a PPI, bismuth subsalicylate, and the antibiotics tetracycline and metronidazole for 10 to 14
days. Bismuth quadruple therapy is used to treat patients in one of several situations, including if
the patient

cannot take amoxicillina penicillin-like antibioticbecause of a penicillin

allergy
has been treated before with a macrolide antibiotic, such as clarithromycin

is still infected with H. pylori because triple therapy failed to kill the bacteria

Triple therapy and bismuth quadruple therapy may cause nausea and other side effects, including

stomach upset
diarrhea

headache

a metallic taste

a darkened tongue or stools

flushing when drinking alcohol

sensitivity to the sun

Patients should discuss any bothersome side effects with their doctor, who may prescribe other
medicines to kill the bacteria and cure the ulcer.
Although antibiotics can cure 80 to 90 percent of ulcers caused by H. pylori, eliminating the
bacteria can be difficult. Patients must take all medicines exactly as prescribed, even when the
peptic ulcer pain is gone.
At least 4 weeks after treatment, doctors test patients using a breath or stool test to be sure the H.
pylori infection has been cured. Blood tests are not useful after treatment because a patient's
blood can test positive for H. pylori even after the bacteria have been eliminated.
If infection is still present, ulcers could recur or, less commonly, stomach cancer could develop.
Thus, some patients need to take more than one round of medicines to kill the H. pylori bacteria.
Bismuth quadruple therapy is one of several treatments used after initial treatment has faileda
strategy called rescue or salvage therapy. In the second round of treatment, the doctor
prescribes different antibiotics than those used in the first round. Amoxicillin, however, can be
used again to treat H. pylori infection because H. pylori resistance to this antibiotic is rare.
[Top]

Can antacids or milk help a peptic ulcer heal?

An antacid may make the ulcer pain go away temporarily, but it will not kill H. pylori. People
being treated for an H. pylori ulcer should check with their doctor before taking antacids. Some
of the antibiotics used to kill H. pylori may not work as well if combined with an antacid.
People used to believe drinking milk helped peptic ulcers heal. But doctors know now that while
milk may make an ulcer feel better briefly, it also increases stomach acid, which can make ulcers
worse. Patients should talk with their doctor about drinking milk while an ulcer is healing.
[Top]

Can H. pylori infection be prevented?

No one knows for sure how H. pylori spreads, so prevention is difficult. Researchers are trying to
develop a vaccine to preventand even cureH. pylori infection. To help prevent infection,
doctors advise people to

wash their hands with soap and water after using the bathroom and before
eating
eat food that has been washed well and cooked properly

drink water from a clean, safe source

[Top]

Points to Remember

A peptic ulcer is a sore in the lining of the stomach or duodenum.

Most peptic ulcers are caused by H. pylori. Use of NSAIDssuch as aspirin and
ibuprofenis another common cause.

Neither stress nor spicy food causes ulcers. Smoking or drinking alcohol, however, each
can worsen ulcers and prevent their healing.

The abdominal discomfort of peptic ulcers

feels like a dull or burning pain
occurs when the stomach is emptybetween meals or during the night
may be briefly relieved by eating food, in the case of duodenal ulcers, or by taking
antacids, in both types of peptic ulcers
lasts for minutes to hours
comes and goes for several days or weeks

A combination of antibiotics and acid-reducing medicines is the most effective treatment

for H. pylori-induced peptic ulcers.

Testing after treatment is needed to be sure the H. pylori infection is gone.

To help prevent an H. pylori infection, people should

wash their hands after using the bathroom and before eating
eat properly prepared food
drink water from a clean, safe source

[Top]

Hope through Research

While H. pylori infection is becoming less common in developed countries, some strains of the
bacteria have become resistant to antibiotics that are used to destroy it. Researchers have
identified and continue to study new antibiotic combinations that can kill these types of H.
pylori.
Other promising research may help identify treatments that

kill the H. pylori bacteria with fewer medicines in less time

use different antibiotic combinations in back-to-back treatment

better protect the stomach lining when eliminating H. pylori

Researchers also are studying

characteristics of H. pylori bacteria

traits of people who develop H. pylori ulcers

transmission of H. pylori infection

vaccines to prevent and cure H. pylori infection

Participants in clinical trials can play a more active role in their own health care, gain access to
new research treatments before they are widely available, and help others by contributing to
medical research. For information about current studies, visit www.ClinicalTrials.gov.

GERD PEDS

Background
Gastroesophageal reflux represents the most common gastroenterologic disorder that leads to
referral to a pediatric gastroenterologist during infancy. In pediatric gastroesophageal reflux,
immaturity of lower esophageal sphincter (LES) function is manifested by frequent transient
lower esophageal relaxations (tLESRs), which result in retrograde flow of gastric contents into
the esophagus. (See Etiology and Pathophysiology.)
Although minor degrees of gastroesophageal reflux are noted in children and adults, the degree
and severity of reflux episodes are increased during infancy. Thus, gastroesophageal reflux
represents a common physiologic phenomenon in the first year of life. As many as 60-70% of
infants experience emesis during at least 1 feeding per 24-hour period by age 3-4 months. (See
Epidemiology and Prognosis.)
The distinction between this "physiologic" gastroesophageal reflux and "pathologic"
gastroesophageal reflux in infancy and childhood is determined not merely by the number and
severity of reflux episodes (when assessed by intraesophageal pH monitoring), but also, and
most importantly, by the presence of reflux-related complications, including failure to thrive,
erosive esophagitis, esophageal stricture formation, and chronic respiratory disease. (See
Prognosis, Presentation, and Workup.)
Other complications noted in adults with gastroesophageal reflux, including Barrett esophagus
and esophageal mucosal dysplasia, are uncommon in childhood.
Gastroesophageal reflux is classified as follows (see Presentation, Workup, Treatment, and
Medication):

Physiologic (or functional) gastroesophageal reflux - These patients have no

underlying predisposing factors or conditions; growth and development are
normal, and pharmacologic treatment is typically not necessary
Pathologic gastroesophageal reflux or gastroesophageal reflux disease
(GERD) - Patients frequently experience the complications noted above,
requiring careful evaluation and treatment [1]
Secondary gastroesophageal reflux - This refers to a case in which an
underlying condition may predispose to gastroesophageal reflux; examples
include asthma (a condition which may also be, in part, caused by or
exacerbated by reflux) and gastric outlet obstruction

Patient education

For patient education information, see the Heartburn and GERD Center and the Children's
Health Center, as well as Spitting Up in Infants, Gastroesophageal Reflux Disease (GERD)
FAQs, Acid Reflux (GERD), Heartburn and GERD Medications, and Sudden Infant Death
Syndrome (SIDS).
In addition, extremely useful patient information and provider-focused information can be
accessed by visiting the North American Society for Pediatric Gastroenterology, Hepatology, and
Nutrition (NASPGHAN) Web site.

Etiology and Pathophysiology

Risk factors
Reflux after meals occurs in healthy persons; however, these episodes are generally transient and
are accompanied by rapid esophageal clearance of refluxed acid. Some consider the small
reservoir capacity of the infant's esophagus to be a predisposing factor to vomiting. The causes
and risk factors for gastroesophageal reflux in children are frequently multifactorial.
Anatomic factors that predispose to gastroesophageal reflux include the following:

The angle of His (made by the esophagus and the axis of the stomach) is
obtuse in newborns but decreases as infants develop; this ensures a more
effective barrier against gastroesophageal reflux
The presence of a hiatal hernia may displace the lower esophageal sphincter
(LES) into the thoracic cavity, where the lower intrathoracic pressure may
facilitate gastroesophageal reflux; however, the presence of a hiatal hernia
by itself does not predict gastroesophageal reflux, which means that many
patients who have a hiatal hernia do not have gastroesophageal reflux
Resistance to gastric outflow raises intragastric pressure and leads to reflux
and vomiting; examples include gastroparesis, gastric outlet obstruction, and
pyloric stenosis

Other factors that predispose individuals to gastroesophageal reflux include the following:

Medications - Eg, diazepam, theophylline; methylxanthines exacerbate reflux

secondary to decreased sphincter tone.
Smoking

Alcohol

Poor dietary habits - Eg, overeating, eating late at night, assuming a supine
position shortly after eating

Food allergies

Certain foods - Eg, greasy, highly acidic

Motility disorders (postulated to potentially cause reflux) - These include

antral dysmotility and delayed gastric emptying; such disorders are
considered functional problems and frequently do not have an identifiable
anatomic or organic cause

Transient lower esophageal sphincter relaxation (tLESR) - This is currently

believed to be the main mechanism of gastroesophageal reflux, accounting
for 94% of reflux episodes in children and adults; poor basal LES tone was
previously thought to be a cause

Obesity -Obesity has been cited as a major risk factor for gastroesophageal
reflux; in studies conducted with adult patients, weight loss has been
demonstrated to be one of the lifestyle modifications that can decrease the
severity and frequency of reflux

Supine position

Decreased gastric emptying and reduced acid clearance from the esophagus
- These can cause abnormal reflux

Neurodevelopmental disabilities - Children with neurodevelopmental

disabilities, including cerebral palsy, Down syndrome, and other heritable
syndromes associated with developmental delay, have an increased
prevalence of gastroesophageal reflux

Chronic LES laxity

Reflux is facilitated when an increase in intraabdominal pressure occurs. In some cases, and
particularly in children with neurodevelopmental disabilities, the presence of a chronically lax
LES associated with decreased or even absent sphincter tone results in severe gastroesophageal
reflux.
Transient lower esophageal relaxations
For many years, gastroesophageal reflux during infancy and childhood was thought to be a
consequence of absent or diminished LES tone. However, studies have shown that baseline LES
pressures are normal in pediatric patients, even in preterm infants.
The major mechanism in infants and children has now been demonstrated to involve increases in
tLESRs. Factors that may promote gastroesophageal reflux during tLESRs include increased
intragastric liquid volume and supine and "slumped" seated positioning.
Fluid diet
Likely because of reduced viscosity and increased gastric volumes, the fluid diet of the infant
facilitates the process of regurgitation compared with solid meals ingested by older children and
adults.
Esophageal clearance

Esophageal clearance is similar in infants and adults, although evidence of reduced peristaltic
activity in preterm infants has been reported.

Differences between adults and infants

The volume ratio of meal-stomach-esophagus differs between adults and infants. Necessary
amounts of infant caloric requirements easily overwhelm gastric capacity. Reflux occurs when
esophageal capacity is exceeded by refluxate.
Decreased gastric compliance is believed to lead to LES relaxation at lower intragastric volumes
in infants. This aspect, in conjunction with abdominal wall muscle contraction (if it occurs
during periods of LES relaxation) propels refluxate into the esophagus, with subsequent
regurgitation.
An association between gastroesophageal reflux and delayed gastric emptying is recognized.
This is more common in premature infants.

Respiratory symptoms
Gastroesophageal reflux has been associated with significant respiratory symptoms in infants and
children. The infant's proximal airway and esophagus are lined with receptors that are activated
by water, acid, or distention. Activation of these receptors can increase airway resistance, leading
to the development of reactive airway disease.[2]
In 1892, Osler first postulated a relationship between asthma and gastroesophageal reflux,
manifested by a bidirectional cause-and-effect presentation. Accordingly, although
gastroesophageal reflux may be involved in the etiology and progression of reactive airway
disease, the asthmatic condition (in addition to antiasthmatic medications) may play a role in
exacerbation of gastroesophageal reflux.
One postulated mechanism for gastroesophageal refluxmediated airway disease involves
microaspiration of gastric contents that leads to inflammation and bronchospasm. However,
experimental evidence also supports the involvement of esophageal acidinduced reflex
bronchospasm, in the absence of frank aspiration. In such cases, gastroesophageal reflux therapy
using either histamine 2 (H2) blockers or proton pump inhibitors has been shown to benefit
patients with steroid-dependent asthma, nocturnal cough, and reflux symptoms.

Other associated conditions

Two major areas of controversy surround the relationship between gastroesophageal reflux and
both apnea and otolaryngologic disease. Early studies appeared to demonstrate a link between
gastroesophageal reflux and obstructive apnea (including an association with apparent lifethreatening events [ALTEs]); however, recent investigations now suggest only a weak
relationship between these disorders.[3] Although the relationship between gastroesophageal
reflux and ALTEs is controversial, where an association with apnea has been found, it is as likely
to occur with nonacid as with acid reflux. Accordingly, a comprehensive evaluation of this

phenomonenon will likely require a bioelectrical impedance study (to identify nonacid reflux;
see below) in conjunction with respiratory monitoring.
Laryngeal tissues are exquisitely sensitive to the noxious effect of acid, and studies support a
significant relationship between laryngeal inflammatory disease (manifested by hoarseness,
stridor, or both) and gastroesophageal reflux.
Conversely, no conclusive clinical evidence supports a link between gastroesophageal reflux and
other supraesophageal problems, including otalgia, recurrent otitis media, and chronic sinusitis.

Epidemiology
Gastroesophageal reflux is most commonly seen in infancy, with a peak at age 1-4 months.
However, it can be seen in children of all ages, even healthy teenagers.

Occurrence in the United States

Approximately 85% of infants vomit during the first week of life, and 60-70% manifest clinical
gastroesophageal reflux at age 3-4 months.
Symptoms abate without treatment in 60% of infants by age 6 months, when these infants begin
to assume an upright position and eat solid foods. Resolution of symptoms occurs in
approximately 90% of infants by age 8-10 months.

Prognosis
During infancy, the prognosis for gastroesophageal reflux resolution is excellent (although
developmental disabilities represent an important diagnostic exception); most patients respond to
conservative, nonpharmacologic treatment.
Indeed, most cases of gastroesophageal reflux in infants and very young children are benign, and
80% resolve by age 18 months (55% resolve by age 10 mo), although some patients require a
step-up to acid-reducing medications. Symptoms that persist after age 18 months suggest a
higher likelihood of chronic gastroesophageal reflux; in such cases, the long-term risks of the
condition are increased.[4]
In refractory cases of gastroesophageal reflux or when complications related to reflux disease are
identified (eg, stricture, aspiration, airway disease, Barrett esophagus), surgical treatment
(fundoplication) is typically necessary. The prognosis with surgery is considered excellent. The
surgical morbidity and mortality is higher in patients who have complex medical problems in
addition to gastroesophageal reflux.
As previously mentioned, children with neurodevelopmental disabilities, including cerebral
palsy, Down syndrome, and other heritable syndromes associated with developmental delay,
have an increased prevalence of gastroesophageal reflux. When these disorders are associated
with motor abnormalities (particularly spastic quadriplegia), medical gastroesophageal reflux

management is often particularly difficult, and suck and/or swallow dysfunction is often present.
Infants with neurologic dysfunction who manifest swallowing problems at age 4-6 months may
have a very high likelihood of developing a long-term feeding disorder.

Strictures
Gastroesophageal reflux strictures typically occur in the mid-esophagus to distal esophagus.
Patients present with dysphagia to solid meals and vomiting of nondigested foods. As a rule, the
presence of any esophageal stricture is an indication that the patient needs surgical consultation
and treatment (usually surgical fundoplication). When patients present with dysphagia, barium
esophagraphy is indicated to evaluate for possible stricture formation. In these cases, especially
when associated with food impaction, eosinophilic esophagitis must be ruled out prior to
attempting any mechanical dilatation of the narrowed esophageal region.

Barrett esophagus
Barrett esophagus, a complication of GERD, greatly increases the patients risk of
adenocarcinoma. As with esophageal stricture, the presence of Barrett esophagus indicates the
need for surgical consultation and treatment (usually surgical fundoplication).

Physical Examination
No classic physical signs of gastroesophageal reflux are recognized in the pediatric population
(although an infant or toddler arriving in the office wearing a bib is often a sure tip off). One
exception would be the relatively uncommon Sandifer syndrome, which is often misdiagnosed as
spastic torticollis.
In toddlers and older children, excessive regurgitation may lead to significant dental problems
caused by acid effects on tooth enamel. In the vast majority of cases, a diagnosis of
gastroesophageal reflux is typically made once the primary care provider has obtained a clinical
history that suggests this disorder.
Esophagitis may manifest as crying and irritability in the nonverbal infant. Failure to thrive can
result from insufficient caloric intake secondary to repeated vomiting and nutrient losses from
emesis. Hiccups, sleep disturbances, and Sandifer syndrome (arching) have also been shown to
be associated with gastroesophageal reflux and esophagitis.

Diagnostic Considerations
Vomiting is a symptom associated with many disorders. Accordingly, gastroesophageal reflux
cannot be assumed to be the primary problem in infants and children who present with a history
of emesis. Warning signals that herald the requirement for additional evaluation include the
following:

Bilious or forceful vomiting

Hematemesis or hematochezia

Vomiting with diarrhea

Abdominal tenderness or distention

Onset of vomiting after 6 months of life

Fever, lethargy, hepatosplenomegaly

Macrocephaly, microcephaly, seizures

The occurrence of any of these signs and symptoms indicates the need to consider a
comprehensive metabolic, neurologic, and/or surgical evaluation, in addition to a
gastroenterologic workup.
Conditions to consider in the differential diagnosis of gastroesophageal reflux include the
following:

Antral web
Intestinal motility disorders

Irritable bowel syndrome

Peptic ulcer disease

Sudden infant death syndrome

Tracheoesophageal fistula

Differential Diagnoses

Duodenal Atresia and Stenosis: Surgical Perspective

Eosinophilic Esophagitis

Esophageal Motility Disorders

Food Allergies

Gastric Ulcers

Gastritis, Acute

Gastritis, Chronic

Helicobacter Pylori Infection

Hiatal Hernia

Intestinal Malrotation

Medication Summary
A therapeutic response to treatment for gastroesophageal reflux may take up to 2 weeks. If
treatment is successful, weight increases and vomiting episodes decrease. Recurrent aspiration
pneumonia or apnea is cause for decreased length of medical therapy. Note that the so-called
prokinetic agents have been omitted from the following drug list. No currently available
prokinetic drug (eg, metoclopramide) has been demonstrated to exert a significant influence on
the number or frequency of reflux episodes.

DYSPEPSIA

What is dyspepsia (indigestion)?

Dyspepsia is one of the most common ailments of the bowel (intestines), affecting an estimated
20% of persons in the United States. Perhaps only 10% of those affected actually seek medical
attention for their dyspepsia. Dyspepsia is not a particularly good term for the ailment since it
implies that there is "dyspepsia" or abnormal digestion of food, and this most probably is not the
case. In fact, another common name for dyspepsia is indigestion, which, for the same reason, is
no better than the term dyspepsia! Doctors frequently refer to the condition as non-ulcer
dyspepsia.
Dyspepsia (indigestion) is best described as a functional disease. (Sometimes, it is called
functional dyspepsia.) The concept of functional disease is particularly useful when discussing
diseases of the gastrointestinal tract. The concept applies to the muscular organs of the
gastrointestinal tract-esophagus, stomach, small intestine, gallbladder, and colon. What is meant
by the term, functional, is that either the muscles of the organs or the nerves that control the
organs are not working normally, and, as a result, the organs do not function normally, and the
dysfunction causes the symptoms. The nerves that control the organs include not only the nerves
that lie within the muscles of the organs but also the nerves of the spinal cord and brain.
Some gastrointestinal diseases can be seen and diagnosed with the naked eye, such as ulcers of
the stomach. Thus, ulcers can be seen at surgery, on X-rays, and by endoscopy. Other diseases
cannot be seen with the naked eye but can be seen and diagnosed under the microscope. For
example, gastritis (inflammation of the stomach) can be diagnosed by microscopic examination
of biopsies of the stomach. In contrast, gastrointestinal functional diseases cannot be seen with
the naked eye or with the microscope. In some instances, the abnormal function can be
demonstrated by tests (for example, gastric emptying studies or antro-duodenal motility studies).
However, the tests often are complex, are not widely available, and do not reliably detect the
functional abnormalities. Accordingly, and by default, functional gastrointestinal diseases are
those that involve abnormal function of gastrointestinal organs in which the abnormalities cannot
be seen in the organs with either the naked eye or the microscope.
Occasionally, diseases that are thought to be functional are ultimately found to be associated with
abnormalities that can be seen. Then, the disease moves out of the functional category. An
example of this would be Helicobacter pylori (H. pylori) infection of the stomach. Some patients
with mild upper gastrointestinal symptoms who were thought to have abnormal function of the
stomach or intestines have been found to have stomachs infected with H. pylori. This infection
can be diagnosed under the microscope by identifying the bacterium. When patients are treated
with antibiotics, the H. pylori and symptoms disappear. Thus, recognition of infections with
Helicobacter pylori has removed some patients' systems from the functional disease category.
The distinction between functional disease and non-functional disease may, in fact, be blurry.
Thus, even functional diseases probably have associated biochemical or molecular abnormalities

that ultimately will be able to be measured. For example, functional diseases of the stomach and
intestines may be shown ultimately to be associated with reduced or increased levels of normal
chemicals within the gastrointestinal organs, the spinal cord, or the brain. Should a disease that is
demonstrated to be due to a reduced or increased chemical still be considered a functional
disease? In this theoretical situation, we can't see the abnormality with the naked eye or the
microscope, but we can measure it. If we can measure an associated or causative abnormality,
should the disease no longer be considered functional, even though the disease (symptoms) are
being caused by abnormal function? The answer is unclear.
Despite the shortcomings of the term, functional, the concept of a functional abnormality is
useful for approaching many of the symptoms originating from the muscular organs of the
gastrointestinal tract. To repeat, this concept applies to those symptoms for which there are no
associated abnormalities that can be seen with the naked eye or the microscope.
While dyspepsia is a major functional disease(s), it is important to mention several other
functional diseases. A second major functional disease is the irritable bowel syndrome, or IBS.
The symptoms of IBS are thought to originate primarily from the small intestine and/or colon.
The symptoms of IBS include abdominal pain that is accompanied by alterations in bowel
movements (defecation), primarily constipation or diarrhea. In fact, dyspepsia and IBS may be
overlapping diseases since up to half of patients with IBS also have symptoms of dyspepsia. A
third distinct functional disorder is non-cardiac chest pain. This pain may mimic heart pain
(angina), but it is unassociated with heart disease. In fact, non-cardiac chest pain is thought to
result from a functional abnormality of the esophagus.
Functional disorders of the gastrointestinal tract often are categorized by the organ of
involvement. Thus, there are functional disorders of the esophagus, stomach, small intestine,
colon, and gallbladder. The amount of research that has been done with functional disorders is
greatest in the esophagus and stomach (for example, non-cardiac chest pain, dyspepsia), perhaps
because these organs are easiest to reach and study. Research into functional disorders affecting
the small intestine and colon (IBS) is more difficult to conduct and there is less agreement
among the research studies. This probably is a reflection of the complexity of the activities of the
small intestine and colon and the difficulty in studying these activities. Functional diseases of the
gallbladder (referred to as biliary dyskinesia), like those of the small intestine and colon, also are
more difficult to study, and at present they are less well-defined. Each of the functional diseases
is associated with its own set of characteristic symptoms.

What are the symptoms of dyspepsia (indigestion)?

We usually think of symptoms of dyspepsia as originating from the upper gastrointestinal tract,
primarily the stomach and first part of the small intestine. These symptoms include:

upper abdominal pain (above the navel),

belching,

nausea (with or without vomiting),

abdominal bloating (the sensation of abdominal fullness without objective distention),

early satiety (the sensation of fullness after a very small amount of food), and,

abdominal distention (swelling as opposed to bloating).

The symptoms most often are provoked by eating, which is a time when many different
gastrointestinal functions are called upon to work in concert. This tendency to occur after meals
is what gave rise to the notion that dyspepsia might be caused by an abnormality in the digestion
of food.
It is appropriate to discuss belching in detail since it is a commonly misunderstood symptom
associated with dyspepsia. The ability to belch is almost universal. Belching, also known as
burping or eructating, is the act of expelling gas from the stomach out through the mouth. The
usual cause of belching is a distended (inflated) stomach that is caused by swallowed air or gas.
The distention of the stomach causes abdominal discomfort, and the belching expels the air and
relieves the discomfort. The common reasons for swallowing large amounts of air (aerophagia)
or gas are gulping food or drink too rapidly, anxiety, and carbonated beverages. People often are
unaware that they are swallowing air. Moreover, if there is not excess air in the stomach, the act
of belching actually may cause more air to be swallowed. "Burping" infants during bottle or
breastfeeding is important in order to expel air in the stomach that has been swallowed with the
formula or milk.
Excessive air in the stomach is not the only cause of belching. For some people, belching
becomes a habit and does not reflect the amount of air in their stomachs. For others, belching is a
response to any type of abdominal discomfort and not just to discomfort due to increased gas.
Everyone knows that when they have mild abdominal discomfort, belching often relieves the
problem. This is because excessive air in the stomach often is the cause of mild abdominal
discomfort; as a result, people belch whenever mild abdominal discomfort is felt-whatever the
cause.
If the problem causing the discomfort is not excessive air in the stomach, then belching does not
provide relief. As mentioned previously, it even may make the situation worse by increasing air
in the stomach. When belching does not ease the discomfort, the belching should be taken as a
sign that something may be wrong within the abdomen and that the cause of the discomfort
should be sought. Belching by itself, however, does not help the physician determine what may
be wrong because belching can occur in virtually any abdominal disease or condition that causes
discomfort.

What causes dyspepsia (indigestion)?

It's not surprising that many gastrointestinal diseases have been associated with dyspepsia.
However, many non-gastrointestinal diseases also have been associated with dyspepsia.
Examples of the latter include diabetes, thyroid disease, hyperparathyroidism (overactive
parathyroid glands), and severe kidney disease. It is not clear, however, how these nongastrointestinal diseases might cause dyspepsia. A second important cause of dyspepsia is drugs.
It turns out that many drugs are frequently associated with dyspepsia, for example, nonsteroidal
anti-inflammatory drugs (NSAIDs such as ibuprofen), antibiotics, and estrogens). In fact, most
drugs are reported to cause dyspepsia in at least some patients.
As discussed previously, most dyspepsia (not due to non-gastrointestinal diseases or drugs) is
believed to be due to abnormal function of the muscles of the organs of the gastrointestinal tract

or the nerves controlling the organs. The nervous control of the gastrointestinal tract, however, is
complex. A system of nerves runs the entire length of the gastrointestinal tract from the
esophagus to the anus in the muscular walls of the organs. These nerves communicate with other
nerves that travel to and from the spinal cord. Nerves within the spinal cord, in turn, travel to and
from the brain. (The gastrointestinal tract is exceeded in the numbers of nerves it contains only
by the spinal cord and brain.) Thus, abnormal function of the nervous system in dyspepsia might
occur in a gastrointestinal muscular organ, the spinal cord, or the brain.
The nervous system controlling the gastrointestinal organs, as with most other organs, contains
both sensory and motor nerves. The sensory nerves continuously sense what is happening
(activity) within the organ and relay this information to nerves in the organ's wall. From there,
information can be relayed to the spinal cord and brain. The information is received and
processed in the organ's wall, the spinal cord, or the brain. Then, based on this sensory input and
the way the input is processed, commands (responses) are sent to the organ over the motor
nerves. Two of the most common motor responses in the intestine are contraction or relaxation of
the muscle of the organ and secretion of fluid and/or mucus into the organ.
As already mentioned, abnormal function of the nerves of the gastrointestinal organs, at least
theoretically, might occur in the organ, spinal cord, or brain. Moreover, the abnormalities might
occur in the sensory nerves, the motor nerves, or at processing centers in the intestine, spinal
cord, or brain.
Some researchers argue that the cause of functional diseases is abnormalities in the function of
sensory nerves. For example, normal activities, such as stretching of the small intestine by food,
may give rise to sensory signals that are sent to the spinal cord and brain, where they are
perceived as painful. Other researchers argue that the cause of functional diseases is
abnormalities in the function of motor nerves. For example, abnormal commands through the
motor nerves might produce painful spasm (contraction) of the muscles. Still others argue that
abnormally functioning processing centers are responsible for functional diseases because they
misinterpret normal sensations or send abnormal commands to the organ. In fact, some
functional diseases may be due to sensory dysfunction, motor dysfunction, or both sensory and
motor dysfunction. Others may be due to abnormalities within the processing centers.
An important concept that is relevant to these several potential mechanisms (causes) of
functional diseases is the concept of "visceral hypersensitivity". This concept states that diseases
affecting the gastrointestinal organs (viscera) "sensitize" (alter the responsiveness of) the sensory
nerves or the processing centers to sensations coming from the organ. According to this theory, a
disease such as colitis (inflammation of the colon) can cause permanent changes in the sensitivity
of the nerves or processing centers of the colon. As a result of this prior inflammation, normal
stimuli are perceived (felt) as abnormal (for example, as being painful). Thus, a normal colonic
contraction may be painful. It is not clear what prior diseases might lead to hypersensitivity in
people, although infectious diseases (bacterial or viral) of the gastrointestinal tract are mentioned
most often. Visceral hypersensitivity has been demonstrated clearly in animals and people. Its
role in the common functional diseases, however, is unclear.

Another potential cause of dyspepsia is bacterial overgrowth of the small intestine (small
intestinal bacterial overgrowth or SIBO), although the frequency with which this condition
causes dyspepsia has not been determined, and there is little research in the area. The relationship
between overgrowth and dyspepsia needs to be pursued, however, since many of the symptoms
of dyspepsia are also symptoms of bacterial overgrowth. Overgrowth can be diagnosed by
hydrogen breath testing and is treated primarily with antibiotics.
Other diseases and conditions can aggravate functional diseases, including dyspepsia. Anxiety
and/or depression are probably the most commonly-recognized exacerbating factors for patients
with functional diseases. Another aggravating factor is the menstrual cycle. During their periods,
women often note that their functional symptoms are worse. This corresponds to the time during
which the female hormones, estrogen and progesterone, are at their highest levels. Furthermore,
it has been observed that treating women who have dyspepsia with leuprolide (Lupron), an
injectable drug that shuts off the body's production of estrogen and progesterone, is effective at
reducing symptoms of dyspepsia in premenopausal women. These observations support a role for
hormones in the intensification of functional symptoms.

What is the course of dyspepsia (indigestion)?

Dyspepsia is a chronic disease that usually lasts years, if not a lifetime. It does, however, display
periodicity, which means that the symptoms may be more frequent or severe for days, weeks, or
months and then less frequent or severe for days, weeks, or months. The reasons for these
fluctuations are unknown. Because of the fluctuations, it is important to judge the effects of
treatment over many weeks or months to be certain that any improvement is due to treatment and
not simply to a natural fluctuation in the frequency or severity of the disease.

What are the complications of dyspepsia (indigestion)?

The complications of functional diseases of the gastrointestinal tract are relatively limited. Since
symptoms are most often provoked by eating, patients who alter their diets and reduce their
intake of calories may lose weight. However, loss of weight is unusual in functional diseases. In
fact, loss of weight should suggest the presence of non-functional diseases. Symptoms that
awaken patients from sleep also are more likely to be due to non-functional than functional
disease.
Most commonly, functional diseases interfere with patients' comfort and daily activities.
Individuals who develop nausea or pain after eating may skip breakfast or lunch because of the
symptoms they experienc. Patients also commonly associate symptoms with specific foods (for
example, milk, fat, vegetables). Whether or not the associations are real, these patients will
restrict their diets accordingly. Milk is the most common food that is eliminated, often
unnecessarily, and this can lead to inadequate intake of calcium and osteoporosis. The
interference with daily activities also can lead to problems with interpersonal relationships,
especially with spouses. Most patients with functional disease live with their symptoms and
infrequently visit physicians for diagnosis and treatment.

How is dyspepsia diagnosed (indigestion)?

Dyspepsia is diagnosed primarily on the basis of typical symptoms and the exclusion of nonfunctional gastrointestinal diseases (including acid-related diseases), non-gastrointestinal
diseases, and psychiatric illness. There are tests for identifying abnormal gastrointestinal function
directly, but they are limited in their ability to do so.

Exclusion of other diseases

Exclusion of non-functional gastrointestinal disease
As always, a detailed history from the patient and a physical examination frequently will suggest
the cause of dyspepsia. Routine screening blood tests often are performed looking for clues to
unsuspected diseases. Examinations of stool also are a part of the evaluation since they may
reveal infection, signs of inflammation, or blood and direct further diagnostic testing. Sensitive
stool testing (antigen/antibody) for Giardia lamblia would be reasonable because this parasitic
infection is common and can be acute or chronic. Some physicians do blood testing for celiac
disease (sprue), but the value of doing this is unclear. (Moreover, if an EGD is planned, biopsies
of the duodenum usually will make the diagnosis of celiac disease.) If bacterial overgrowth of
the small intestine is being considered, breath hydrogen testing can be considered.
There are many tests to exclude non-functional gastrointestinal diseases. The primary issue,
however, is to decide which tests are reasonable to perform. Since each case is individual,
different tests may be reasonable for different patients. Nevertheless, certain basic tests are often
performed to exclude non-functional gastrointestinal disease. These tests identify anatomic
(structural) and histological (microscopic) diseases of the esophagus, stomach, and intestines.
Both X-rays and endoscopies can identify anatomic diseases. Only endoscopies, however, can
diagnose histological diseases because biopsies (samples of tissue) can be taken during the
procedure. The X-ray tests include:

The esophagram and video-fluoroscopic swallowing study for examining the esophagus
The upper gastrointestinal series for examining the stomach and duodenum

The small bowel series for examining the small intestine

The barium enema for examining the colon and terminal ileum.

The computerized tomography (CT) scan for examining the small intestine

The endoscopic tests include:

Upper gastrointestinal endoscopy (esophago-gastro-duodenoscopy or EGD) to examine

the esophagus, stomach and duodenum
Colonoscopy to examine the colon and terminal ileum
Endoscopy also is available to examine the small intestine, but this type of endoscopy is
complex, not widely available, and of unproven value in dyspepsia.

For examination of the small intestine, there is also a capsule containing a tiny camera and
transmitter that can be swallowed (capsule endoscopy). As the capsule travels through the
intestines, it transmits pictures of the inside of the intestines to an external recorder for later
review. The capsule is not widely available and its value, particularly in dyspepsia, has not yet
been proven.
Newer endoscopes, similar to those used for EGD and colonoscopy are available that allow the
entire small intestine to be examined. Unlike the capsule, however, the endoscope has channels
in it that allow instruments to be passed into the intestine to collect samples of tissue (biopsies)
and to treat abnormal findings such as polyps.
X-rays are easier to perform and less costly than endoscopies. The skills necessary to perform
gastrointestinal X-rays, however, are becoming rare among radiologists because they are doing
them less often. Therefore, the quality of the X-rays often is not as high as it used to be, and, as a
result, CT scans of the small intestine are replacing small intestinal X-rays. As noted previously,
endoscopies have an advantage over X-rays since at the time of endoscopies, biopsies can be
taken to diagnose or exclude histological diseases, something that X-rays cannot do.
Exclusion of acid-related gastrointestinal diseases
Because they are so common, the most important non-functional gastrointestinal diseases to
exclude are acid-related diseases that cause inflammation and ulceration of the esophagus,
stomach, and duodenum. Infection of the stomach with Helicobacter pylori, an infection that is
closely associated with some acid-related diseases, is included in this group. It is not clear,
however, how often Helicobacter pylori causes dyspepsia. Moreover, the only way of excluding
this bacterium as a cause of dyspepsia in a particular patient is by eliminating the infection (if it
is present) with appropriate antibiotics. If dyspepsia is substantially improved by eradication, it is
likely that the bacterium was responsible. Helicobacter pylori infection also can be diagnosed (or
excluded) by blood tests, biopsy of the stomach, urea breath test, or a stool test.
Endoscopy is a good way of diagnosing or excluding acid-related inflammation. If no signs of
inflammation are present, acid-related diseases are unlikely. Nevertheless, some patients without
signs of inflammation respond to potent and prolonged suppression of acid, suggesting that acid
is causing their dyspepsia. Therefore, many physicians will use potent suppression of acid in
dyspepsia as a means to both treat and diagnose. Thus, if dyspepsia improves substantially (more
than 50% to 75%) with suppression of acid, they consider it likely that acid is responsible for the
dyspepsia. For this purpose, it is important to use potent acid suppression with proton pump
inhibitors (PPIs), such as:

omeprazole (Prilosec, Zegerid),

lansoprazole (Prevacid),

rabeprazole (Aciphex),

pantoprazole (Protonix) or

esomeprazole (Nexium).

Treatment often is given at higher than recommended doses for 12 weeks or more before a
decision is made about the effect of treatment on the symptoms. (A short course for just a few
days or weeks is not enough.) If the symptoms of dyspepsia do not improve, it even may be
reasonable to check the amount of acid produced by the stomach (and also the reflux of acid into
the esophagus) by 24 hour ph monitoring to be certain that the acid-suppressing drugs are
effectively suppressing acid. (Up to 10% of patients are resistant to the effects of even the PPIs.)
Exclusion of non-gastrointestinal disease
Patients with dyspepsia often undergo abdominal ultrasonography (US), computerized
tomography (CT or CAT scans), or magnetic resonance imaging (MRI). These tests are used
primarily to diagnose non-intestinal diseases. (Although the tests also are capable of diagnosing
intestinal diseases, their value for this purpose is limited. X-ray and endoscopy are better.) It is
important to realize that US, CT, and MRI are powerful tests and may uncover abnormalities that
are unrelated to dyspepsia. The most common example of this is the finding of gallstones that, in
fact, are causing no symptoms. (Up to 50% of gallstones cause no symptoms.) This can cause a
problem if the gallstones are assumed to be causing the dyspepsia. Surgical removal of the
gallbladder with its gallstones (cholecystectomy) is unlikely to relieve the dyspepsia.
(Cholecystectomy would be expected to relieve only the characteristic symptoms that gallstones
can cause.) Additional tests to exclude non-gastrointestinal diseases may be appropriate in
certain specific situations, although certainly not in most patients.
Exclusion of psychiatric disease
The possibility of psychiatric (psychological or psychosomatic) illness often arises in patients
with dyspepsia because the symptoms are subjective and no objective abnormalities can be
identified. Psychiatric illness may complicate dyspepsia, but it is unclear if psychiatric illness
causes dyspepsia. If there is a possibility of psychiatric illness, a psychiatric evaluation is
appropriate.

Specific tests of gastrointestinal function

Esophageal motility study
Functional disorders of the esophagus can be identified with esophageal motility studies
(manometry). For these studies, a pressure-sensing tube is swallowed and positioned within the
esophagus. Contractions of the esophageal muscle normally cause increases in pressure within
the esophagus that can be monitored by the catheter during and between swallows of water.
Among the abnormalities that can be seen are abnormally high or abnormally low pressures
during swallow-associated contractions and/or during spontaneous contractions unassociated
with swallows.
Gastric emptying study and electrogastrogram
Slow emptying of the stomach is a common functional abnormality that can lead to bloating,
nausea, and vomiting. Rapid emptying of the stomach is relatively uncommon and can lead to

abdominal pain and diarrhea. Both of these abnormalities--slow and rapid emptying--can be
identified by a gastric emptying study.
The most common type of emptying study is a nuclear medicine study. In this test, patients drink
or eat food labeled with radioactive material. A Geiger counter-like device then is placed over the
abdomen and the speed with which the radioactive drink or food empties from the stomach is
monitored.
The electrogastrogram (EGG) is like the electrocardiogram (ECG) for the heart. Electrodes that
are taped to the upper abdomen monitor the electrical activity generated by the muscle of the
stomach. Abnormalities of the electrical rhythm of the stomach frequently are associated with
dyspeptic symptoms, particularly nausea and vomiting. EGGs are not commonly available and
are considered a research tool.
Barostatic study
A barostat is an instrument that is used to measure pressure and determine the compliance
(flexibility) of a gastrointestinal organ. Compliance is a term that describes the effect that
internal stretching has on the organ. The greater the compliance of an organ, the less there is
tension (pressure) generated when the organ is stretched from within.
Compliance is important to the normal function of gastrointestinal organs. For example, as food
fills the stomach during a meal, the muscles of the stomach must relax (comply) to accommodate
the increasing volume of food. If the stomach does not relax properly, the pressure in the
stomach increases abnormally. It is believed that abnormally high pressures within the stomach
(due to reduced compliance) can lead to symptoms such as early satiety (the feeling of
abdominal fullness or pain after only a small amount of food has been ingested).
The barostat includes a balloon that is placed within a gastrointestinal organ through the mouth
or anus. As the balloon is progressively blown up and stretches the organ, the pressure within the
organ is measured by the barostat. In this way, abnormal compliance can be identified. Barostats
can be placed in the esophagus, stomach, small intestine or colon. Barostatic studies, however,
probably should be considered experimental. In fact, barostats and expertise in their use are
available in only a limited number of centers.
Small intestinal transit study
Small intestinal transit studies measure the speed with which food travels through the small
intestine. In the most common type of transit study, a test meal that has been labeled with a
radioactive material is ingested. A Geiger-counter-like device is placed over the abdomen and is
used to follow the radioactive material through the small intestine and into the colon. Rapid
transit is associated with abdominal pain and diarrhea. Slow transit also may be associated with
abdominal pain. Although transit studies are not difficult to conduct, they are not frequently used
because experience with their use is not wide-spread. They probably should be considered
experimental.

Antro-duodenal motility study

Antro-duodenal motility studies measure the pressures that are generated by the contractions of
the muscles of the antrum (outlet) of the stomach and the duodenum. For these studies, a
pressure-sensing tube is swallowed or passed through the nose and positioned in the distal
(outlet) part of the stomach (the antrum) and the first part of the small intestine (the duodenum).
Pressures are measured with the stomach empty and after a test meal. Abnormally high or low
pressures as well as uncoordinated contractions can be identified. These abnormalities are
believed to be associated with symptoms of dyspepsia. Antro-duodenal motility studies and
expertise in their use are not widely available.
Gallbladder emptying studies
Gallbladder emptying studies determine how well the gallbladder empties. Between meals, the
gallbladder stores bile that is produced by the liver. After meals, the muscles of the gallbladder
contract and squeeze out (empty) most of the bile into the intestine. In the intestine, the bile
assists with the digestion of food.
For a gallbladder emptying study, a radioactive material is injected intravenously. The
radioactive material is removed from the blood by the liver and accumulates with the bile in the
gallbladder. The gallbladder then is stimulated to contract with either a meal or an intravenous
injection of a hormone, called cholecystokinin. A Geiger-counter-like device is placed over the
abdomen and the speed with which the radioactivity leaves the gallbladder and enters the
intestine is monitored. Emptying studies of the gallbladder are widely available since this
technology is used for several purposes other than measurement of gallbladder emptying.
It has been suggested that abnormally slow emptying of the gallbladder may be associated with
abdominal pain. Unfortunately, however, the studies that support the association between slow
gallbladder emptying and symptoms are weak. Moreover, many people have abnormally slow
emptying of the gallbladder but no symptoms. For these reasons, abnormal emptying studies of
the gallbladder have not been widely accepted for diagnosing functional disorders of the
gallbladder. The lack of a clear association between dyspepsia and abnormalities of gallbladder
emptying is important since it means that patients with abnormal emptying may not be improved
by removal of their gallbladders.

How is dyspepsia (indigestion) treated?

The treatment of dyspepsia is a difficult and unsatisfying topic because so few drugs have been
studied and have shown to be effective. Moreover, the drugs that have been shown to be useful
have not been substantially effective. This difficult situation exists for many reasons, as follows:

Life-threatening illnesses (for example, cancer, heart disease, and high blood pressure)
are the illnesses that capture the public's interest and, more importantly, research funding.
Dyspepsia is not a life-threatening illness and has received little research funding.
Because of the lack of research, an understanding of the physiologic processes

(mechanisms) that are responsible for dyspepsia has been slow to develop. Effective
drugs cannot be developed until there is an understanding of these mechanisms.
Research in dyspepsia is difficult. Dyspepsia is defined by subjective symptoms (such
as pain) rather than objective signs (for example, the presence of an ulcer). Subjective
symptoms are more unreliable than objective signs in identifying homogenous groups of
patients. As a result, groups of patients with dyspepsia who are undergoing treatment are
likely to contain some patients who do not have dyspepsia, which may dilute (negatively
affect) the results of the treatment. Moreover, the results of treatment must be evaluated
on the basis of subjective responses (such as improvement of pain). In addition to being
more unreliable, subjective responses are more difficult to measure than objective
responses (for example, healing of an ulcer).

Different subtypes of dyspepsia (for example, abdominal pain and abdominal bloating)
are likely to be caused by different physiologic processes (mechanisms). It also is
possible, however, that the same subtype of dyspepsia may be caused by different
mechanisms in different people. What's more, any drug is likely to affect only one
mechanism. Therefore, it is unlikely that any one medication can be effective in all-even
most-patients with dyspepsia, even patients with similar symptoms. This inconsistent
effectiveness makes the testing of drugs particularly difficult. Indeed, it can easily result
in drug trials that demonstrate no efficacy (usefulness) when, in fact, the drug is helping a
subgroup of patients.

Subjective symptoms are particularly prone to responding to placebos (inactive drugs).

In fact, in most studies, 20% to 40% of patients with dyspepsia will improve if they
receive inactive drugs. Now, all clinical trials of drugs for dyspepsia require a placebotreated group for comparison with the drug-treated group. The large placebo response
means that these clinical trials must utilize large numbers of patients to detect meaningful
(significant) differences in improvement between the placebo and drug groups.
Therefore, these trials are expensive to conduct.

The lack of understanding of the physiologic processes (mechanisms) that cause dyspepsia has
meant that treatment usually cannot be directed at the mechanisms. Instead, treatment usually is
directed at the symptoms. For example, nausea is treated with medications that suppress nausea
but do not affect the cause of the nausea. On the other hand, the psychotropic drugs
(antidepressants) and psychological treatments (such as cognitive behavioral therapy) treat
hypothetical causes of dyspepsia (for example, abnormal function of sensory nerves and the
psyche) rather than the symptoms. Treatment for dyspepsia often is similar to that for irritable
bowel syndrome (IBS) even though the causes of IBS and dyspepsia are likely to be different.
Education
It is important to educate patients with dyspepsia about their illness, particularly by reassuring
them that the illness is not a serious threat to their physical health (though it may be to their
emotional health). Patients need to understand the mechanisms (causes) for the symptoms. Most
importantly, they need to understand the medical approach to the problem and the reasons for
each test or treatment. Education prepares patients for a potentially prolonged course of
diagnosis and trials of treatment. Education also may prevent patients from falling prey to the

charlatans who offer unproven and possibly dangerous treatments for dyspepsia. Many
symptoms are tolerable if patients' anxieties about the seriousness of their symptoms can be
relieved. It also helps patients deal with symptoms when they feel that everything that should be
done to diagnose and treat, in fact, is being done. The truth is that psychologically healthy people
can tolerate a good deal of discomfort and continue to lead happy and productive lives.
Diet
Dietary factors have not been well-studied in the treatment of dyspepsia. Nevertheless, patients
often associate their symptoms with specific foods (such as salads and fats). Although specific
foods might worsen the symptoms of dyspepsia, they are not the cause of dyspepsia. (Intolerance
to specific foods, for example, lactose intolerance (milk) and allergies to wheat, eggs, soy, and
milk protein are not considered functional diseases. The common placebo response in functional
disorders such as dyspepsia also may explain the improvement of symptoms in some people with
the elimination of specific foods.
Dietary fiber often is recommended for patients with IBS, but fiber has not been studied in the
treatment of dyspepsia. Nevertheless, it probably is reasonable to treat patients with dyspepsia
with fiber if they also have constipation.
Intolerance to lactose (the sugar in milk) often is blamed for dyspepsia. Since dyspepsia and
lactose intolerance both are common, the two conditions may coexist. In this situation, restricting
lactose will improve the symptoms of lactose intolerance, but will not affect the symptoms of
dyspepsia. Lactose intolerance is easily determined by testing the effects of lactose (hydrogen
breath testing) or trying a strict lactose elimination diet. If lactose is determined to be responsible
for some or all of the symptoms, elimination of lactose-containing foods is appropriate.
Unfortunately, many patients stop drinking milk or eating milk-containing foods without good
evidence that it improves their symptoms. This often is detrimental to their intake of calcium
which may contribute to osteoporosis.
One of the food substances most commonly associated with the symptoms of dyspepsia is fat.
The scientific evidence that fat causes dyspepsia is weak. Most of the support is anecdotal (not
based on carefully done, scientific studies). Nevertheless, fat is one of the most potent influences
on gastrointestinal function. (It tends to slow down the gastrointestinal muscles while it causes
the muscles of the gallbladder to contract.) Therefore, it is possible that fat may worsen
dyspepsia even though it doesn't cause it. Moreover, reducing the ingestion of fat might relieve
symptoms. A strict low fat diet can be accomplished fairly easily and is worth trying.
Additionally, there are other health-related reasons for reducing dietary fat.
Another dietary factor, fructose and fructose-related sugars, has been suggested as a cause of
dyspepsia since many people do not fully digest and absorb them before they reach the distal
intestine. It is diagnosed with a hydrogen breath test using fructose and treated with elimination
of fructose-containing foods from the diet. Unfortunately, fructose and its related sugars are
widespread among fruits and vegetables and are found in high concentrations in many food
products sweetened with corn syrup. Thus, an elimination diet is more difficult to maintain.

Psychotropic drugs
Patients with functional disorders, including dyspepsia, are frequently found to be suffering from
depression and/or anxiety. It is unclear, however, if the depression and anxiety are the cause or
result of the functional disorders or are unrelated to these disorders. (Depression and anxiety are
common and, therefore, their occurrence together with functional disorders may be coincidental.)
Several clinical trials have shown that antidepressants are effective in IBS in relieving abdominal
pain. Antidepressants also have been shown to be effective in unexplained (non-cardiac) chest
pain, a condition thought to represent a dysfunction of the esophagus. Antidepressants have not
been studied adequately in other types of functional disorders, including dyspepsia. It probably is
reasonable to treat patients with dyspepsia with psychotropic drugs if they have moderate or
severe depression or anxiety.
The antidepressants work in dyspepsia and in functional esophageal pain at relatively low doses
that have little or no effect on depression. It is believed, therefore, that these drugs work not by
combating depression, but in different ways (through different mechanisms). For example, these
drugs have been shown to adjust (modulate) the activity of the nerves and to have analgesic
(pain-relieving) effects as well.
Commonly used psychotropic drugs include the tricyclic antidepressants, desipramine
(Norpramine) and trimipramine (Surmontil). Although studies are encouraging, it is not yet clear
whether the newer class of antidepressants, the serotonin-reuptake inhibitors such as fluoxetine
(Prozac), sertraline (Zoloft), and paroxetine (Paxil), are effective in functional disorders,
including dyspepsia.
Psychological treatments
Psychological treatments include cognitive-behavioral therapy, hypnosis, psychodynamic or
interpersonal psychotherapy, and relaxation/stress management. Few studies of psychological
treatments have been conducted in dyspepsia, although more studies have been done in IBS.
Thus, there is little scientific evidence that they are effective in dyspepsia, although there is some
evidence that they are effective in IBS.
Hypnosis has been proposed as an effective treatment for IBS. It is unclear exactly how effective
hypnosis is, or how it works.
Promotility drugs
One of the leading theories for the cause of dyspepsia is abnormalities in the way gastrointestinal
muscles function. The function of muscles may be abnormally increased, abnormally decreased,
or it may by uncoordinated. There are medications, called smooth muscle relaxants, that can
reduce the activity of the muscles and other drugs that can increase the activity of the muscles,
called the promotility drugs.
Many of the symptoms of dyspepsia can be explained on the basis of reduced activity of the
gastrointestinal muscles that results in slowed transport (transit) of food through the stomach and

intestine. (It is clear, as discussed previously, that there are other causes of these symptoms in
addition to slowed transit.) Such symptoms include nausea, vomiting, and abdominal bloating.
When transit is severely affected, abdominal distention (swelling) also may occur and can result
in abdominal pain. (Early satiety is unlikely to be a function of slowed transit because it occurs
too early for slowed transit to have consequences.) Theoretically, drugs that speed up the transit
of food should, in at least some patients, relieve symptoms of dyspepsia that are due to slow
transit.
The number of promotility drugs that are available for use clinically is limited. Studies of their
effectiveness in dyspepsia are even more limited. The most studied drug is cisapride (Propulsid),
a promotility drug that was withdrawn from the market because of serious cardiac side effects.
(Newer drugs that have similar effects but lack the toxicity are being developed.) The few studies
with cisapride for dyspepsia were inconsistent in their results. Some studies demonstrated
benefits whereas others showed no benefit. Cisapride was effective in patients with severe
emptying problems of the stomach (gastroparesis) or severely slowed transit of food through the
small intestine (chronic intestinal pseudo-obstruction). These two diseases may or may not be
related to dyspepsia.
Another promotility drug that is available is erythromycin, an antibiotic that stimulates
gastrointestinal smooth muscle as one of its side effects. Erythromycin is used to stimulate
smooth muscles of the gastrointestinal tract at doses that are lower than those used for treating
infections. There are no studies of erythromycin in dyspepsia, but erythromycin is effective in
gastroparesis and probably also in chronic intestinal pseudo-obstruction.
Metoclopramide (Reglan) is another promotility drug that is available. It has not been studied,
however, in dyspepsia. Moreover, it is associated with some troubling side effects. Therefore, it
may not be a good drug to undergo further testing in dyspepsia.
Domperidone (Motilium) is a promotility drug that is available in the U.S., but requires a special
permit from the US Food and Drug administration. As a result, it is not very commonly
prescribed. It is an effective drug with minimal side effects.
Smooth muscle relaxants
The most widely studied drugs for the treatment of abdominal pain in functional disorders are a
group of drugs called smooth-muscle relaxants.
The gastrointestinal tract is primarily composed of a type of muscle called smooth muscle. (By
contrast, skeletal muscles such as the biceps are composed of a type of muscle called striated
muscle.) Smooth muscle relaxant drugs reduce the strength of contraction of the smooth muscles
but do not affect the contraction of other types of muscles. They are used in functional disorders,
particularly IBS, with the assumption (not proven) that strong or prolonged contractions of
smooth muscles in the intestine-spasms-are the cause of the pain in functional disorders. There
are even smooth muscle relaxants that are placed under the tongue, as is nitroglycerin for angina,
so that they may be absorbed rapidly.

There are not enough studies of smooth muscle relaxants in dyspepsia to conclude that they are
effective at reducing pain. Since their side effects are few, these drugs probably are worth trying.
As with all drugs that are given to control symptoms, patients should carefully evaluate whether
or not the smooth muscle relaxant they are using is effective at controlling the symptoms. If it is
not clearly effective, the option of discontinuing the relaxant should be discussed with a
physician.
Commonly used smooth muscle relaxants are hyoscyamine (Levsin, Anaspaz, Cystospaz,
Donnamar) and methscopolamine (Pamine, Pamine Forte). Other drugs combine smooth muscle
relaxants with a sedative chlordiazepoxide hydrochloride and clidinium bromide (Donnatal,
Librax), but there is no evidence that the addition of sedatives adds to the effectiveness of the
treatment.

What is a reasonable approach to the diagnosis and treatment of dyspepsia

(indigestion)?
The initial approach to dyspepsia, whether it be treatment or testing, depends on the patient's age,
symptoms and the duration of the symptoms. If the patient is younger than 50 years of age and
serious disease, particularly cancer, is not likely, testing is less important. If the symptoms are
typical for dyspepsia and have been present for many years without change, then there is less
need for testing, or at least extensive testing, to exclude other gastrointestinal and nongastrointestinal diseases.
On the other hand, if the symptoms are of recent onset (weeks or months), progressively
worsening, severe, or associated with "warning" signs, then early, more extensive testing is
appropriate. Warning signs include loss of weight, nighttime awakening, blood in the stool or the
material that is vomited (vomitus), and signs of inflammation, such as fever or abdominal
tenderness. Testing also is appropriate if, in addition to symptoms of dyspepsia, there are other
prominent symptoms that are not commonly associated with dyspepsia.
If there are symptoms that suggest conditions other than dyspepsia, tests that are specific for
these diseases should be done first. The reason is that if these other tests disclose other diseases,
it may not be necessary to do additional testing. Examples of such symptoms and possible testing
include:

Vomiting: upper gastrointestinal endoscopy to diagnose inflammatory or obstructing

diseases; gastric emptying studies and/or electrogastrography to diagnose impaired
emptying of the stomach.

Abdominal distention with or without increased flatulence: upper gastrointestinal and

small intestinal x-rays to diagnose obstructing diseases; hydrogen breath testing to
diagnose bacterial overgrowth of the small intestine.

For a patient with typical symptoms of dyspepsia who requires testing to exclude other diseases,
a standard screening panel of blood tests would reasonably be included. These tests might reveal
clues to non-gastrointestinal diseases. Sensitive stool testing (antigen/antibody) for Giardia

lamblia would be reasonable because this parasitic infection is common and can be acute or
chronic. Some physicians do blood testing for celiac disease (sprue), but the value of doing this
is unclear. Moreover, if an EGD is planned, biopsies of the duodenum usually will make the
diagnosis of celiac disease. A plain x-ray of the abdomen might be done during an episode of
abdominal pain (to look for intestinal blockage or obstruction). Testing for lactose intolerance or
a trial of a strict lactose-free diet should be considered. The physician's clinical judgment should
determine the extent to which initial testing is appropriate.
Once testing has been done to an extent that is appropriate for the clinical situation, it is
reasonable to first try a therapeutic trial of stomach acid suppression to see if symptoms improve.
Such a trial probably should involve a PPI (proton pump inhibitor) for 8 to 12 weeks. If there is
no clear response of symptoms, the options then are to discontinue the PPI or confirm its
effectiveness in suppressing acid with 24 hour acid testing. If there is a clear and substantial
decrease in symptoms with the PPI, then decisions need to be made about continuing acid
suppression and which drugs to use.
Another therapeutic approach is to test for Helicobacter pylori infection of the stomach (with
blood, breath or stool tests) and to treat patients with infection to eradicate the infection. It may
be necessary to retest patients after treatment to prove that treatment has effectively eradicated
the infection, particularly if dyspeptic symptoms persist after treatment.
If treatment with a PPI has satisfactorily suppressed acid according to acid testing (or acid
suppression has not been measured) and yet the symptoms have not improved, it is reasonable to
conduct further testing as described above. Esophago-gastro-duodenoscopy, or EGD, (and,
possibly, colonoscopy) would be the next consideration, probably with multiple biopsies of the
stomach and duodenum (and colon if colonoscopy is done). Finally, small intestinal x-rays and
an ultrasound examination of the gallbladder might be done. An abdominal ultrasound
examination, CT scan, or MRI scan can exclude non-gastrointestinal diseases. Once appropriate
testing has been completed, empiric trials of other drugs (for example, smooth muscle relaxants,
psychotropic drugs, and promotility drugs) can be done. (An empiric trial of a drug is a trial that
is not based on an understanding of the exact cause of the symptoms)
If all of the appropriate testing reveals no disease that could be causing the symptoms and the
dyspeptic symptoms have not responded to empiric treatments, other, more specialized tests
should be considered. These tests include hydrogen breath testing to diagnose bacterial
overgrowth of the small intestine, gastric emptying studies, EGG, small intestinal transit studies,
and antro-duodenal motility and barostatic studies. These specialized studies probably should be
done at centers that have experience and expertise in diagnosing and treating functional diseases.

What is in the future for dyspepsia (indigestion)?

The future of dyspepsia will depend on our increasing knowledge of the processes (mechanisms)
that cause dyspepsia. Acquiring this knowledge, in turn, depends on research funding. Because
of the difficulties in conducting research in dyspepsia, this knowledge will not come quickly.
Until we have an understanding of the mechanisms of dyspepsia, newer treatments will be based
on our developing a better understanding of the normal control of gastrointestinal function,

which is proceeding more rapidly. Specifically, there is intense interest in intestinal

neurotransmitters, which are chemicals that the nerves of the intestine use to communicate with
each other. The interactions of these neurotransmitters are responsible for adjusting (modulating)
the functions of the intestines, such as contraction of muscles and secretion of fluid and mucus.
5-hydroxytriptamine (5-HT or serotonin) is a neurotransmitter that stimulates several different
receptors on nerves in the intestine. Examples of experimental drugs for intestinal
neurotransmission are sumatriptan (Imitrex) and buspirone (Buspar). These drugs are believed to
reduce the responsiveness (sensitivity) of the sensory nerves to what's happening in the intestine
by attaching to a particular 5-HT receptor, the 5-HT1 receptor. The 5-HT1 receptor drugs,
however, have received only minimal study so far and their role in the treatment of dyspepsia, if
any, is unknown.
Promotility drugs similar to cisapride, as previously discussed, are being pursued actively.

Dyspepsia (Indigestion) At A Glance

Dyspepsia is a functional disease in which the gastrointestinal organs, primarily the

stomach and first part of the small intestine, function abnormally. It is a chronic disease
in which the symptoms fluctuate in frequency and intensity.
Theories of the cause of dyspepsia include abnormal input from intestinal sensory nerves,
abnormal processing of input from the sensory nerves, and abnormal stimulation of the
intestines by motor nerves.

The primary symptoms of dyspepsia are upper abdominal pain, belching, nausea,
vomiting, abdominal bloating, early satiety, and abdominal distention (swelling). The
symptoms most often are provoked by eating.

Dyspepsia is diagnosed on the basis of typical symptoms and the absence of other
gastrointestinal diseases, particularly acid-related diseases and non-gastrointestinal
diseases that might give rise to the symptoms.

Testing in dyspepsia is directed primarily at excluding the presence of other

gastrointestinal diseases and non-gastrointestinal diseases. Some patients may require
specific testing of certain gastrointestinal functions.

Treatment in dyspepsia is primarily with education as well as smooth muscle relaxant and
promotility drugs. There also may be a role for anti-depressant drugs and dietary changes.

Future advances in the treatment of dyspepsia depend on a clearer understanding of its

cause(s).