esophagus Flashcards
dysphagia becomes more common with aging and
affects up to
15% of persons age 65 or older
inability to propel
a food bolus successfully from the hypopharyngeal area through
the upper esophageal sphincter (UES) into the esophageal body is
called
oropharyngeal or transfer dysphagia.
Dysphagia
that occurs immediately or within one second of swallowing suggests
an oropharyngeal abnormality
Swallowing associated
with a gurgling noise may be described by patients with
Zenker diverticulum
Most patients with esophageal dysphagia localize their symptoms
to the
lower sternum or, at times, the epigastric region. A smaller
number of patients describe a sensation in the suprasternal notch
or higher even though the bolus stops in the lower esophagus
Esophageal dysphagia can frequently be relieved by various
maneuvers like
repeated swallowing, raising the arms over the
head, throwing the shoulders back, and using the Valsalva maneuver.
Causes of Oropharyngeal Dysphagia
NEUROMUSCULAR* Amyotrophic lateral sclerosis (ALS, Lou Gehrig disease) CNS tumors (benign or malignant) Idiopathic UES dysfunction Manometric dysfunction of the UES or pharynx† Multiple sclerosis Muscular dystrophy Myasthenia gravis Parkinson disease Polymyositis or dermatomyositis Postpolio syndrome Stroke Thyroid dysfunction
STRUCTURAL Carcinoma Infections of pharynx or neck Osteophytes and other spinal disorders Prior surgery or radiation therapy Proximal esophageal web Thyromegaly Zenker diverticulum
Common Causes of Esophageal Dysphagia
NEUROMUSCULAR (MOTILITY) DISORDERS Primary Achalasia Distal esophageal spasm Hypercontractile (jackhammer) esophagus Hypertensive LES Nutcracker (high-pressure) esophagus Other peristaltic abnormalities* Secondary Chagas disease Reflux-related dysmotility Scleroderma and other rheumatologic disorders
STRUCTURAL (MECHANICAL) DISORDERS Intrinsic Carcinoma and benign tumors Diverticula Eosinophilic esophagitis Esophageal rings and webs (other than Schatzki ring) Foreign body Lower esophageal (Schatzki) ring Medication-induced stricture Peptic stricture Extrinsic Mediastinal mass Spinal osteophytes Vascular compression
Patients who report dysphagia with solids and liquids are more
likely to have an esophageal motility disorder than mechanical
obstruction.
Achalasia is the prototypical esophageal motility
disorder;
Episodic and nonprogressive dysphagia without weight loss
is characteristic of an
esophageal web or a distal esophageal
(Schatzki) ring
True dysphagia may be seen in patients with pill, caustic,
or viral esophagitis, but the predominant complaint of patients
with these acute esophageal injuries is usually
odynophagia
Causes of Odynophagia
CAUSTIC INGESTION Acid Alkali PILL-INDUCED INJURY Alendronate and other bisphosphonates Aspirin and other NSAIDs Emepronium bromide Iron preparations Potassium chloride (especially slow-release form) Quinidine Tetracycline and its derivatives Zidovudine INFECTIOUS ESOPHAGITIS Viral CMV EBV HIV HSV Bacterial Mycobacteria (tuberculosis or Mycobacterium avium complex) Fungal Candida albicans Histoplasmosis Protozoan Cryptosporidiosis Pneumocystis jiroveci SEVERE REFLUX ESOPHAGITIS ESOPHAGEAL CARCINOMA
is a feeling of a lump or tightness in the throat,
unrelated to swallowing
Globus sensation
Globus
sensation is present between meals and swallowing of solids or
large liquid boluses may give temporary relief. Frequent dry
swallowing and emotional stress may worsen this symptom.
Globus
sensation should not be diagnosed in the presence of dysphagia
or odynophagia.
The symptom of hiccups (hiccoughs, singultus) is caused by a
combination of
diaphragmatic contraction and glottic closure.
Most
cases of hiccups are idiopathic, but the symptom has been associated
with many conditions (trauma, masses, infections, uremia)
that affect the central nervous system, thorax, or abdomen.
chlorpromazine, nifedipine, haloperidol, phenytoin, metoclopramide,
baclofen, and gabapentin
Esophageal chest pain is usually described as a
squeezing or
burning substernal sensation that radiates to the back, neck, jaw,
or arms.
day trial
of an oral PPI taken twice daily has been shown to be sensitive
and specific for the diagnosis of esophageal chest pain when compared
with ambulatory intraesophageal pH testing
A 10- to 14-
If a patient fails this trial, the next practical approach may
be a trial of agents such as imipramine or trazodone that raise the
pain threshold
Extraesophageal Manifestations of GERD
Asthma Chronic cough Excess mucus or phlegm Globus sensation Hoarseness Laryngitis Pulmonary fibrosis Sore throat
Dyspepsia is derived from the Greek words “δυς-” (dys-) and
“πέψη” (pepse) and literally means
“difficult digestion.” In current
medical terminology, dyspepsia refers to a heterogeneous group of
symptoms in the upper abdomen.
Only 4 symptoms
are now considered to be specifically of gastroduodenal origin
(postprandial fullness,
early satiation, and epigastric pain or epigastric burning)
refers to dyspeptic symptoms in persons in whom diagnostic
investigations have not yet been performed and in whom a specific
diagnosis that explains the dyspeptic symptoms has not been
determined.
uninvestigated dyspepsia
The risk of esophageal cancer is increased in
men,
smokers, persons with high alcohol consumption, and those with
long-standing heartburn
Diagnostic criteria* for
functional dyspepsia†
1. One or more of the following: Bothersome postprandial fullness Bothersome early satiation Bothersome epigastric pain Bothersome epigastric burning AND 2. No evidence of structural disease (including at EGD) that is likely to explain the symptoms
Criteria fulfilled for the previous 3 months with symptom onset at least 6 months prior to diagnosis
Diagnostic criteria* for
postprandial distress
syndrome (PDS)
Must include one or both of the following at least 3 days a week:
1. Bothersome postprandial fullness (i.e., severe enough to impact usual activities)
2. Bothersome early satiation (i.e., severe enough to prevent finishing a regular-sized meal)
3. No evidence of organic, systemic, or metabolic disease that is likely to explain the symptoms on routine investigations
(including at EGD)
Supportive Criteria
1. Postprandial epigastric pain or burning, epigastric bloating, excessive belching, and nausea can also be present
2. Vomiting warrants consideration of another disorder
3. Heartburn is not a symptom of dyspepsia but often may coexist with PDS
4. Symptoms that are relieved by evacuation of feces or gas should generally not be considered part of the
dyspepsia symptom complex
5. Other individual digestive symptoms or groups of symptoms (e.g., from GERD or IBS) may coexist with PDS
Diagnostic criteria* for epigastric pain syndrome (EPS)
Must include one or both of the following symptoms at least 1 day a week:
1. Bothersome epigastric pain (i.e., severe enough to impact on usual activities)
2. Bothersome epigastric burning (i.e., severe enough to impact usual activities)
No evidence of organic, systemic, or metabolic disease that is likely to explain the symptoms on routine investigations
(including at EGD).
Supportive Criteria
1. Pain may be induced by ingestion of a meal, relieved by ingestion of a meal, or may occur while fasting
2. Postprandial epigastric bloating, belching, and nausea can also be present
3. Persistent vomiting likely suggests another disorder
4. Heartburn is not a symptom of dyspepsia but may often coexist with EPS
5. The pain does not fulfill criteria for biliary pain
6. Symptoms that are relieved by evacuation of feces or gas generally should not be considered part of the
dyspepsia symptom complex
7. Other digestive symptoms (such as GERD and IBS) may coexist with EPS
, defined as abnormally enhanced perception
of visceral stimuli, is considered one of the major pathophysiologic
mechanisms in functional GI disorders
Visceral hypersensitivity
In a
population with a high prevalence (>20%) of Hp infection, the
test-and-treat approach remains attractive because patients with
PUD will be cured.
The tests of choice are the urea breath test
or the fecal antigen test.
constructed as an 18- to 26-cm long hollow
muscular tube with an inner “skin-like” lining of stratified squamous
epithelium
The esophagus
Between swallows the esophagus is
collapsed, but the lumen distends up to 2 cm anteroposteriorly and
3 cm laterally to accommodate a swallowed bolus. Structurally, the
esophageal wall is composed of
4 layers: innermost mucosa, submucosa,
muscularis propria, and outermost adventitia; unlike the
remainder of the GI tract, the esophagus has no serosa
The muscularis propria is responsible for carrying out the organ’s
motor function.
The upper 5% to 33% is composed exclusively of
skeletal muscle, and the distal 50% is composed of smooth muscle.
Proximally, the esophagus
begins where the inferior pharyngeal constrictor merges with
the cricopharyngeus, an area of skeletal muscle known functionally
as the
upper esophageal sphincter (UES)
The UES
is contracted at rest and, hence, creates a high-pressure zone that
prevents inspired air from entering the esophagus. Below the UES,
the esophageal wall is composed of inner circular and outer longitudinal
layers of muscle
The esophageal body
lies within the posterior mediastinum behind the
trachea and left mainstem bronchus and swings leftward to pass behind the heart
and in front of the aorta.1
At the T10 vertebral level the esophageal
body leaves the thorax through a hiatus located within the right
crus of the diaphragm (see Fig. 43.1).
Within the diaphragmatic
hiatus the esophageal body ends in a 2- to 4-cm length of asymmetrically
thickened circular smooth muscle known as the lower
esophageal sphincter (LES
The venous
drainage of the upper esophagus is through the superior vena
cava,
the midesophagus through the azygos veins, and the distal esophagus through the portal vein by means of the left and short gastric veins.
The submucosal venous anastomotic network of the
distal esophagus is important because it is where esophageal varices emerge in patients with portal hypertension
The lymphatic system of the esophagus is also segmental; the
upper esophagus drains to the deep cervical nodes,
the midesophagus
to the mediastinal nodes, and the distal esophagus to the celiac
and gastric nodes
multilayered epithelium consists of 3 functionally distinct layers: stratum corneum, stratum spinosum, and stratum germinativum
The upper esophagus is supplied by branches of the superior
and inferior thyroid arteries, the midesophagus by branches of
the bronchial and right intercostal arteries and descending aorta,
and the distal esophagus by branches of the left gastric, left inferior
phrenic, and splenic arteries
In the most common TEF, the trachea communicates with the distal
segment of the atretic esophagus (B).
The next most common type is
the H-type TEF, in which the trachea communicates with an otherwise
normal esophagus
Esophageal atresia occurs as an isolated anomaly in only 7%
of cases; the rest are accompanied by a form of tracheoesophageal
fistula, most often (89%) a distal-type fistula (see Fig. 43.7B) and
rarely (3%) the H-type fistula
Dysphagia lusoria is the term given for symptoms arising from
vascular compression of the esophagus by an aberrant right subclavian
artery
A, Interface between lumen and mucosa; B, mucosa; C, submucosa; D, muscularis propria; E, adventitia.) Note that
A, C, and E are hyperechoic, and
B and D are hypoechoic.
The distal esophagus may contain 2 “rings,” the A and B (Schatzki)
ring, that demarcate anatomically the proximal and distal borders
of the esophageal vestibule.
The A (muscular) ring is located at the proximal border (see Fig. 43.3). It is a broad (4 to 5 mm) symmetrical band of hypertrophied muscle that constricts the tubular esophageal lumen at its junction with the vestibule
In this location the A
ring, which is covered by squamous epithelium, corresponds to the
upper end of the LES.55 The A ring is rare,
Symptomatic A rings can be treated by
passage of
a large-caliber mercury-weighted esophageal dilator, injection of
botulinum toxin, or by peroral endoscopic myotomy
The B ring, otherwise known as the mucosal or Schatzki ring,
is very common, and found in 6% to 14% of subjects having a
routine upper GI series
On
barium study it is always found in association with a hiatal hernia
and is recognized as a thin (2-mm) membrane that constricts
the esophageal lumen at the junction of the vestibule and gastric
cardia
The Schatzki ring has squamous epithelium
on its upper surface and columnar epithelium on its lower surface
and so demarcates the squamocolumnar junction.
The ring itself
is composed of only mucosa and submucosa; there is no muscularis
propria. Schatzki rings can be congenital or acquired, and a
relationship to GERD is likely
Most B rings are asymptomatic, yet when the diameter of the
esophageal lumen is narrowed to
13 mm or less, rings commonly are
the cause of intermittent dysphagia for solids or unheralded acute
solid-food impactions
are developmental anomalies characterized by
1 or more thin horizontal membranes of stratified squamous epithelium
within the upper (cervical) esophagus and midesophagus
Esophageal webs
Unlike rings, these anomalies rarely encircle the lumen but
instead protrude from the anterior wall, extending laterally but
not to the posterior wall
Webs are
fragile membranes and so respond well to esophageal bougienage
with mercury-weighted dilators.
refers to the appearance on endoscopy of a small
(0.5 to 2 cm) distinctive, velvety red island of heterotopic gastric
mucosa amid a lighter pink squamous mucosa, generally localized
immediately below the UES
inlet patch
In rare instances, an inlet patch is found in association
with an esophageal web or stricture74 or ulcer, the latter
resulting in bleeding or perforation.69
Adenocarcinoma arising
in an inlet patch is a rare complication, although there is a statistically
significant association between inlet patches and proximal
esophageal adenocarcinomas
Diverticula are outpouchings from tubular structures. True diverticula
involve all layers of the intestinal wall, whereas
false diverticula
are due to herniation of mucosa and submucosa through
the muscular wall
True diverticula are often assumed to
be congenital lesions, and false diverticula are assumed to be
acquired, but this is not always the case. Some authors reserve the
terms false diverticula or pseudodiverticula for diverticula caused by
an inflammatory process.
The prevalence of Zenker diverticula has been estimated to
be between 0.1% and 0.01%.
Patients generally present in the
seventh or eighth decade of life. Twice as many men as women
develop Zenker diverticula
Zenker diverticula are acquired. They develop when abnormally
high pressures occur during swallowing, leading to mucosa
that protrudes through an area of anatomic weakness in the pharynx
known as
Killian triangle (`
Killian triangle is
located posteriorly where the
transverse fibers of the cricopharyngeus
muscle of the upper esophageal sphincter (UES) intersect
with the oblique fibers of the inferior pharyngeal constrictor
muscle.
With a Zenker diverticulum, opening of the UES is impaired,
generating high pressures with swallowing
are seen just below the
cricopharyngeus and have a similar presentation to Zenker
diverticula.
Killian-Jamieson diverticula
, a palpable nodule or swelling on the left anterior
neck that may gurgle on palpation, can be found
Boyce sign
Zenker diverticulum can be suspected from a careful history.
Barium swallow is the most useful diagnostic study
Barium swallow in the lateral
view using video fluoroscopy is helpful for detecting small
diverticula
During endoscopy, Zenker diverticulum should be
suspected if, on entering the pharynx, the UES cannot be located.
In such cases, the endoscopy should be stopped, and the patient
sent for a barium study.
Presenting Symptoms in Patients with a Zenker
Diverticulum
Aspiration Choking Dysphagia Halitosis Regurgitation Voice changes Weight loss
Squamous cell cancer may develop in Zenker diverticula;
the estimated
incidence is 0.4% to 1.5%.
Zenker diverticula may be treated by open surgical procedures
or by transoral endoscopic techniques using rigid or flexible
endoscopes
Open surgery for Zenker diverticula is typically performed
through the left neck in patients with large (>5 cm) diverticula
that extend into the thorax
Large diverticula can be resected, inverted, or suspended (diverticulopexy).
Cricopharyngeal myotomy is performed to treat
the hypertonic cricopharyngeus muscle, and is the key aspect to
treating this disorder; the hypertonic cricopharyngeus muscle
must be divided to relieve distal obstruction.
If diverticula are
resected without myotomy,
there is an increased risk of postoperative
leaks and an increased frequency of recurrence.
Complications
of open surgery include anastomotic leaks, mediastinitis,
esophagocutaneous fistula, and vocal cord paralysis from injury to
the recurrent laryngeal nerve, which runs in the tracheoesophageal
groove.
Endoscopic treatment of Zenker diverticulum can be performed
using a rigid endoscope or flexible endoscope, with
division of the fibrotic septum between the esophagus and the
diverticulum
Endoscopic
techniques are suitable for patients with medium-sized
diverticula (2 to 5 cm).
This septum is composed of
the posterior wall of the esophagus and the anterior wall of the
diverticulum and includes the UES.
The muscular layers of this
septum (and UES) are incised, restorating a single lumen.
Traction diverticula are related to an inflammatory,
fibrotic, or neoplastic process outside of the esophagus.
Traction
diverticula are often related to mediastinal inflammation associated
with tuberculosis or histoplasmosis
Pulsion diverticula are typically caused by motility
disorders.
The most common type of pulsion diverticula is an epiphrenic
diverticula, which is located near the diaphragmatic hiatus (
About 80% of epiphrenic diverticula are associated with esophageal motility disorders such as achalasia or distal esophageal
spasm,
Epiphrenic
diverticula have been reported as a complication of band-based
obesity surgery,
due to obstruction of the esophagus and upper
stomach by the band
Squamous cell carcinoma has been reported in epiphrenic diverticula.
44,45
As with Zenker diverticula, accumulation of radioactive
iodine tracer in esophageal diverticula has been mistaken for metastatic thyroid cancer
To prevent gastroesophageal
reflux after myotomy, a partial posterior (Toupet) or
anterior (Dor) fundoplication may be performed.
EIP most commonly in their sixth or seventh decades. The condition
is slightly more common in men than in women.54
EIP are abnormally dilated ducts of submucosal glands. They
are thought to be acquired and are often associated with conditions
that cause chronic esophageal inflammation.
A hernia is a protrusion of an organ or structure into an opening
or pouch. Abdominal wall hernias protrude through the muscular
and fascial walls of the abdomen and have 2 parts:
(1) the orifice or defect in the aponeurotic wall of the abdomen, and (2) the hernia sac, which consists of peritoneum and abdominal, contents.
Abdominal wall hernias are external if the sac protrudes
through the abdominal wall or interparietal if the sac is contained
within the abdominal wall.
Internal hernias are contained within
the abdominal cavity and do not always have a hernia sac
Hernias are reducible when the protruding contents can be
returned to the abdomen and irreducible or incarcerated when
they cannot.
A hernia is strangulated when the vascular supply
of the protruding organ is compromised,
where only one side of the bowel (most often the antimesenteric
side) protrudes through the hernia orifice.
Richter hernia,
3 main types of diaphragmatic hernias:
hiatal and paraesophageal
hernias (both involve the hiatus), congenital hernias,
and traumatic hernias
most common diaphragmatic hernias are sliding hernias
of the stomach through the esophageal hiatus hiatal and paraesophageal hernias.
Sliding hiatal hernias (type I) occur when the gastroesophageal
junction and some portion of the stomach are displaced above the
diaphragm, but the orientation of the stomach axis is unchanged.
The frequency of sliding hiatal hernias increases with age. The
phrenoesophageal membrane anchors the gastroesophageal junction
to the diaphragm
Hiatal hernias
may be caused by age-related deterioration of this membrane,
combined with normal positive intra-abdominal pressure and
traction of the esophagus on the stomach as the esophagus shortens
during swallowing
Paraesophageal hernias (type II) occur when the stomach protrudes through the esophageal hiatus alongside the esophagus (Fig. 27.1A).
The gastroesophageal junction remains in a normal position
at the level of the diaphragm, because there is preservation
of the posterior phrenoesophageal ligament and normal anchoring
of the gastroesophageal junction, and only the stomach moves
proximally
Most paraesophageal hernias contain a sliding hiatal component
in addition to the paraesophageal component and are thus
mixed diaphragmatic hernias (type III
other intra-abdominal structures (e.g.,
omentum, colon, spleen) may also herniate
(type IV
cross
sectional imaging with CT scan will be the test of choice to document
a type IV defect, as the barium study may not reveal adjacent
colon or pancreas through the hiatus.
Does the gastroesophageal junction lie at or
above the hiatus? (2) Does the stomach or any other visceral structure
lie above the gastroesophageal junction?
For example, if the
gastroesophageal junction is above the hiatus and there is stomach
above it, the patient has a type III (mixed) hernia
14% to 84% of patients examined, depending on the
patient population, method of diagnosis, and symptoms present.
In general, hiatal hernias are more frequent in patients
with GERD.
About 90% to 95% of hiatal hernias found by
radiograph are sliding (type I) hernias; the remainder are paraesophageal hernias.
With chest radiography, a hiatal
hernia may be noted as a soft tissue density or an air-fluid level in
the retrocardiac area
Hiatal hernias are sometimes diagnosed on
UGI barium studies.
Cameron lesions or linear erosions may develop in patients
with sliding hiatal hernias, particularly large hernias
These mucosal lesions are usually found on the lesser curve
of the stomach at the level of the diaphragmatic hiatus
This is the location of the rigid anterior margin of the
hiatus formed by the central tendon of the diaphragm
Cameron lesions may cause acute or chronic UGI bleeding with a
poor response to acid suppression therapy.14 Iron deficiency anemia
due to chronic bleeding is seen in 30% to 40% of patients
with paraesophageal hernia
Gastric volvulus is a life-threatening complication of paraesophageal
hernia.
Symptoms include acute abdominal pain and
retching, and it can progress rapidly to a surgical emergency (
Simple sliding hiatal hernias do not require treatment, unless
symptomatic from reflux (see Chapter 46). Patients with symptomatic
giant sliding hiatal hernias, paraesophageal, or mixed
hernias should be offered surgery.
When closely questioned, most
patients with type II, III, or IV hernias will have symptoms
motility disorders, the surgeon may elect to perform
a loose anterior wrap
(Dor fundoplication) or use a gastrostomy
tube or gastropexy to fix the stomach intra-abdominally
The principles of surgery for repair of hiatal or paraesophageal
hernias include 4 main elements:
(1) reduction of the hernia
from the mediastinum or chest, with excision of the hernia
sac; (2) reconstruction of the diaphragmatic hiatus, with simple
posterior closure with or without bolstering with prosthetic
mesh; (3) providing bulk at the hiatus to prevent prolapse into
the chest with a fundoplication, which can lessen postoperative
reflux; and (4) addition of a gastropexy or gastrostomy tube to
provide an additional tacking mechanism for the stomach intraabdominally.
Patients with sliding hiatal or paraesophageal hernias may have
shortening of the esophagus. This makes it difficult to restore the
gastroesophageal junction below the diaphragm without tension,
a key factor in decreasing recurrence.
In such cases, an extra length
of neoesophagus can be constructed from the proximal stomach
(Collis-Nissen procedure
Recurrence is higher in obese patients and many will favor a
Roux-en-Y gastric bypass (RYGB) procedure in those that have a
BMI greater than 35kg/m2
Hernias manifesting in neonates are most often
Bochdalek
The key finding is a posterior
chest mass, as the defect of Bochdalek is posterior
Morgagni hernias are anterior,
are ingested materials (food or
other materials) that accumulate in a normal or abnormal stomach.
Bezoars
The most common patient group that unintentionally ingests
foreign bodies is children, particularly those between
ages 6 months and 3 year
Children account for 80% of true foreign body ingestions
Coins are the most common objects swallowed by children, but
other frequently swallowed objects include marbles, small toys,
crayons, nails, and pins
The most common groups that intentionally ingest foreign
bodies are
psychiatric patients and prisoners,21 in whom ingestion
is often done for secondary gain
The vast majority (75% to 100%) of patients with
an esophageal food impaction have an underlying predisposing
esophageal pathology,25,26 most often peptic strictures, Schatzki
rings, and increasingly eosinophilic esophagitis (EoE
Food impactions most commonly occur in adults in their
fourth or fifth decade of life but are becoming more prevalent
in young adults because of the rising incidence of eosinophilic
esophagitis
The majority (≈ 80% to 90%) of GIFBs pass through the GI tract without any clinical sequelae and cause no harm to the patient.1,35
The remaining 10% to 20% of GIFBs will require endoscopic
intervention, and 1% of GIFBs may require operative therapy.
The pharynx is the first area where foreign bodies
may become entrapped and cause complications.
In the hypopharynx,
short sharp objects like fish bones and toothpicks may
lacerate the mucosa or become lodged
Once in the esophagus, there are 4 areas of narrowing where
food boluses and foreign bodies become lodged:
upper esophageal
sphincter, level of the aortic arch, level of the mainstem
bronchus, and esophagogastric junction
These areas all have
luminal narrowing to 23 mm or less.4
Foreign body and food impaction in the esophagus
have the highest incidence of overall adverse events, with the
complication rate directly proportional to how long the object is
lodged in the esophagus.
Esophageal foreign bodies in children
have a significantly lower spontaneous passage rate, as low as 12%
compared with other GIFBs
Large objects (>2.5 cm [1 inch] in diameter) may not be able to pass through the pylorus.
Long objects (>5 cm [2 inches]) such
as pens, pencils, and eating utensils may not negotiate around the
duodenal sweep or through the pylorus
Inserted rectal objects are often tenaciously retained because
of anal sphincter spasm and edema, making spontaneous passage
of the object difficult.
The angulation and valves of Houston may
also impede passage of objects through the rectum.
Diagnostic upper endoscopy for foreign bodies is relatively
contraindicated when there are clinical or radiographic signs
of perforation. Once an ingested foreign object has passed the
ligament of Treitz, endoscopy is generally not indicated, because
these objects will typically pass unimpeded with notable exceptions
(see later).
Similarly, most small (<2.5 cm) blunt objects in
an adult patient’s stomach do not require endoscopic retrieval;
most will pass without complication
80% to 90% of GIFBs will spontaneously pass through
the GI tract without complication
smooth muscle relaxant glucagon is the most widely used and
studied drug for the treatment of esophageal food and foreign
object impactions. Glucagon, given in intravenous doses of 0.5 to
2 mg, can produce relaxation of the lower esophageal sphincter
Nifedipine and nitroglycerin are not recommended because of
hypotension-related side effects and questionable efficacy.
Ideally, no object should be left in the esophagus
longer than
24 hours.
Objects longer than 5 cm and round objects wider
than 2.5 cm also may not be passed and should be removed from
the stomach with an endoscope at presentation or if they have
not progressed in 3 to 5 days.
More than 75% of patients with food impactions have associated
esophageal pathology,5,26 and about half of patients with food bolus impactions have abnormal 24-hour esophageal pH
studies and/or esophageal manometry.
If an esophageal stricture
or Schatzki ring is present after the food bolus is cleared, it can
be safely and effectively dilated concurrently if circumstances
allow. More often, mucosal abrasions or erythema from the food
dwelling in the esophagus for an extended period exists, and dilation
is delayed for 2 to 4 weeks, during which patients should
be prescribed proton pump inhibitor therapy
Sharp and pointed objects may cause a perforation in up to
15% to 35% of patients and account for one third of all perforations
from GI foreign bodies, with a 2.5-fold greater risk of
complications compared to other GIFB
Sharp and pointed objects retained in the esophagus are considered
a medical emergency and should be removed within 6 to 12 hours.
Ingested objects longer than 5 cm (2 inches), especially those
longer than 10 cm (4 inches), have difficulty passing through
the pylorus and duodenal sweep and can get hung up, causing
obstruction or perforation at these locations
Long objects should be grasped at one end
and oriented longitudinally to permit removal. For extraction of
long objects, use of the 60-cm overtube endoscope assembly, as
described earlier, should be considered
In adults, the pylorus will allow passage of most blunt
objects up to 25 mm in diameter, which includes all coins except
half-dollars (30 mm) and silver dollars (38 mm
once
in the stomach, a regular diet is appropriate, with radiographic
monitoring every 1 to 2 weeks to confirm progression or elimination.
If after 3 to 4 weeks a blunt object has not passed, endoscopic
removal should be performed.
Half of patients with disc batteries in the stomach have
mucosal damage and thus gastric batteries should also be removed
via the endoscope.127 Once in the small intestine, disc batteries
rarely cause clinical problems and can be observed radiographically,
with 85% passing through the GI tract within 72 hours
Body stuffers
are drug users or traffickers who quickly ingest small amounts
of drugs, but in poorly wrapped or contained packages that are
prone to leakage. Body packers are “mules” used by drug smugglers
for drug transport; they ingest large quantities of carefully
prepared packages intended to withstand GI transit
Bezoars are collections of indigestible material that accumulate in
the GI tract, most frequently in the stomach.
The 3 most common
types of bezoars encountered are phytobezoars, composed
of vegetable matter; trichobezoars, made up of hair or hair-like
fibers; and medication bezoars (pharmacobezoars)
Phytobezoars are the most common type of bezoar. Offending
fruits and vegetables include celery, pumpkin, prunes, raisins,
leeks, beets, and persimmon
is a term
used to describe trichobezoars located primarily in the stomach
that extend past the pylorus and into the duodenum, causing
bowel obstruction or even jaundice or pancreatitis because of
obstruction at the level of the ampulla of Vater.
Rapunzel syndrome
Alkaline ingestion causes a liquefactive necrosis that very rapidly
extends through the mucosa, submucosa, muscularis of the
esophagus, and stomach
Vascular thrombosis occurs following
the necrosis.
Acidic agents cause a coagulative necrosis, with thromboses of
mucosal blood vessels and a more limited superficial necrosis.
Acidic agents are more apt to damage the stomach, particularly the antrum, more than the esophagus
With alkali ingestion, the esophagus is most
affected; neutralization by gastric acid limits damage in the stomach.
Acidic agents tend to be ingested in smaller quantities because of their offensive
taste and immediate pain, so they are associated with less overall damage than alkali agents.
TABLE 28.1 Endoscopic Grades of Caustic Injury
Grade Endoscopic Findings
Grades
I and IIA burns, which correspond to first- and second-degree burns, will usually heal without sequelae.
I Edema and erythema
IIA Hemorrhage, erosions, blisters, ulcers with exudate
IIB Circumferential ulceration
III Multiple deep ulcers with brown, black, or gray discoloration
IV Perforation
strictures will develop in 70% to 100% of patients with grade IIB injury, which causes circumferential ulceration, and grade III injury with
associated necrosis.
Grade IV injury with perforation carries a
mortality rate of up to 65% and requires urgent surgery
Up to one third of caustic ingestion patients will develop esophageal
stricture after initial recovery (see Fig. 28.13)
Stricture formation presents most commonly at 2 months after injury but can occur at any time from 2 weeks to many years after the initial injury.
Perforation
24-72 hours
Endoscopic injection of triamcinolone into the stricture or use of topical mitomycin has been reported to be beneficial in treating caustic strictures
