spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure
combined with negative intrathoracic pressure
most commonly results from severe retching or vomiting
most patients have a normal underlying esophagus
Pathogenesis
usually involves a longitudinal tear of the posterolateral aspect of the distal esophagus
mediastinum becomes contaminated with gastric contents, resulting in a chemical mediastinitis
left untreated, bacterial infection and mediastinal necrosis will supervene
rupture of the mediastinal pleura contaminates the pleural cavity
Clinical Manifestations
classic presentation is severe retrosternal chest pain following an episode of vomiting or retching
within several hours of perforation, patients develop tachycardia, fever, dyspnea, and hypotension
some patients will have crepitus of the chest wall
Diagnosis
Chest X-ray
suggestive findings include a left pleural effusion, mediastinal air, or subcutaneous emphysema
Esophagram
should be done initially with gastrograffin, but if this study is negative and suspicion is high,
then a barium esophagram can be performed
accurately demonstrates the site and extent of perforation in 90% of cases
CT Scan
useful study when an esophagram cannot be done (uncooperative or unstable patient)
suggestive findings include esophageal wall thickening and edema, periesophageal fluid, or mediastinal air
does not accurately localize the site of perforation
Initial Management
all patients will require fluid resuscitation and broad-spectrum antibiotics in preparation for
definitive management
Definitive Management
Endoscopic Stenting
in cases of spontaneous perforation, endoscopic stenting should be limited to patients who
are unlikely to tolerate surgery because of significant comorbidities
additional measures include drainage of fluid collections, PPIs, TPN
clinical deterioration will require surgery
Primary Surgical Repair
the distal esophagus is best approached through a left thoracotomy at the 7th or 8th intercostal space
debride all necrotic tissue
incise the muscle to expose the entire extent of the mucosal injury
close the defect in 2 layers
an intercostal muscle flap or pleural flap can be used to buttress the repair
the repair and mediastinum are widely drained with 2 chest tubes
consider a jejunostomy tube in malnourished patients
Damage Control Procedures
for delayed presentations of perforation > 24 hours, mediastinal inflammation or necrosis
may preclude safe primary repair
cervical esophagostomy, gastrostomy tube, wide chest tube drainage, and a feeding jejunostomy
should control drainage above and below the perforation and allow for postop alimentation
another option would be to place a large t-tube into the perforation and widely drain the mediastinum
Iatrogenic Esophageal Perforation
Etiology
most esophageal perforations occur after therapeutic upper endoscopy: pneumatic dilation for strictures
or achalasia, stent placement, sclerotherapy for varices
iatrogenic perforations may occur in the neck, thorax, or abdomen
Clinical manifestations
need a high index of suspicion to make an early diagnosis
cervical perforations may present with a neck ache, swelling, or crepitation
abdominal perforations may present with an acute abdomen
thoracic perforations may present like spontaneous perforations
some patients will have tachypnea, tachycardia, low-grade fever, but no other overt signs of perforation
Diagnosis
esophagram with water-soluble contrast usually reveals the perforation
chest CT may show mediastinal air and fluid at the site of perforation
made by endoscopy, bronchoscopy, barium esophagram
size of the fistula and location with respect to the carina, vocal cords, UES, LES should be noted
Treatment
Preventing Further Lung Contamination
NPO
HOB elevated to 45 degrees
frequent pulmonary suctioning
feeding tube placement
IV antibiotics, PPIs
Malignant TEFs
treated palliatively since life expectancy is minimal
for lesions in the proximal to mid esophagus,
combined tracheal and esophageal stenting should be done since an esophageal stent alone can cause airway compromise
more distal esophageal fistulas usually just require an esophageal stent since airway compromise is less likely
in this location
Nonmalignant TEFs
use of biologic glues or endoscopic clips has been used for small tracts with some success
larger tracts will require surgical closure
fistula tract is exposed and divided through a cervical or thoracic incision
the esophagus and trachea are primarily repaired
segmental resection of the trachea may reduce the incidence of tracheal stenosis
intercostal or strap muscle flap must be placed between the trachea and esophagus
quick extubation should be the goal since positive pressure mechanical ventilation may lead to wound dehiscence
and fistula recurrence
Caustic Injury in Adults
Etiology
in children ingestion is by accident, and is usually of low volume
in teenagers and adults, ingestion is usually deliberate (suicide attempt)
alkali ingestion is more serious and results in significant destruction of the esophagus
Alkali Ingestion
most common agents are drain cleaners, other household cleaning products, and disc batteries
does not cause immediate symptoms such as a burning sensation in the mouth
dissolves tissues by liquefaction necrosis
phase 1: acute necrotic phase lasts 1 – 4 days
phase 2: ulceration and granulation phase follows and lasts 3 – 12 days (esophagus is weakest during
this phase)
phase 3: scar tissue formation leads to stricture formation
Acid Ingestion
hard to ingest large quantities because acids cause an immediate burning sensation in the mouth
coagulative necrosis causes eschar formation that limits tissue penetration
overall, acid ingestion is less severe than alkali (lye) ingestion
Symptoms
acute symptoms include oral and substernal pain, hypersalivation, odynophagia, dysphagia, hematemesis, vomiting,
fever
hoarseness, stridor, dyspnea indicates respiratory injury, and are usually worse with acid ingestion
back and chest pain may indicate mediastinal perforation
abdominal pain may indicate abdominal perforation
Diagnosis
inspect the lips, mouth, palate, pharynx, larynx
auscultate the lungs to assess degree of airway injury
palpate the abdomen for evidence of perforation
Endoscopy
used to identify the grade of the injury and guide treatment (similar to burns)
should only be done in patients with no emergency indication for surgery
first degree: mucosal hyperemia, edema
second degree: exudates, ulceration, pseudomembrane formation
third degree: mucosal sloughing, deep ulcerations, hemorrhage, luminal obstruction, charring
fourth degree: perforation
Treatment
Acute Phase
Neutralization
many authors recommend against this because it can worsen the injury
other experts suggest neutralization can be attempted if the patient presents within an hour
of ingestion
alkalis (lye) are neutralized with half-strength vinegar or citrus juice
acids are neutralized with milk, egg whites, or antacids
emetics (cause retching) or sodium bicarbonate (releases heat) should be avoided because they increase
the chance of perforation
no evidence that corticosteroids are beneficial in adults
No Evidence of Injury
if the physical exam is negative, the patient is asymptomatic, and the ingestion volume was low,
then oral nutrition can be started once the patient can swallow saliva painlessly
endoscopy is not necessary
most patients can be safely discharged from the ER
First-Degree Injury
48 hours of observation indicated
acid suppression with PPIs
oral nutrition can be resumed once patient can swallow saliva painlessly
will need outpatient monitoring for stricture formation (most strictures will have developed by
8 months)
Second- and Third-Degree Injuries
Resuscitation
massive fluid shifts, renal failure, sepsis can occur rapidly
aggressive fluid resuscitation in the ICU
IV antibiotics
proton pump inhibitor
aerosolized steroids can reduce airway obstruction
fiberoptic intubation may be required
use of steroids to reduce stricture formation is controversial – may mask symptoms or peritonitis
Esophagus Management
more than one acceptable approach
if the stomach and esophagus are viable, then a jejunostomy tube for feeding and an esophageal stent
can be placed, with oral intake resuming when the patient can swallow painlessly
laparoscopy, thoracoscopy may be necessary to fully evaluate the viability of the esophagus and stomach
if the viability of the esophagus and stomach are questionable, then a second look procedure should be
performed in 36 hours
if full-thickness necrosis or perforation is present, then all the necrotic stomach and esophagus must be
resected and an end-cervical esophagostomy is performed, along with a feeding j-tube
if necrosis is limited to the stomach, then a total gastrectomy can be performed with preservation of
the esophagus
esophagectomy with preservation of the stomach is rarely possible or indicated
Chronic Phase
Strictures
some authors recommend esophageal stenting and prophylactic bougienage to prevent stricture formation,
although there are only case series to support this practice
scheduled esophagrams and endoscopy are used to screen for stricture formation
any stricture, even if asymptomatic, is treated with frequent bougie dilation
esophageal resection will be necessary for strictures that do not respond to dilation
Reconstruction
delayed until 6 – 12 months
if the damaged esophagus has been left in situ, it must be resected (1000X risk of esophageal cancer in
patients with a caustic injury)
gastric conduit is preferred if available
other possible conduits include a colon interposition or jejunal interposition
site of anastomosis is dependent on the extent of injury (chest versus neck)
Screening for Esophageal Cancer
up to 30% of patients with caustic injuries develop esophageal squamous cell cancer, with a mean latency
period of 41 years
overall, these cancers have a better prognosis than other esophageal squamous cell cancers
recommended screening protocol is endoscopy every 2 – 3 years beginning 10 – 20 years after the caustic ingestion
Other Rare Complications
upper GI bleeding occurs in 3% of patients, usually 2 – 4 weeks after ingestion
tracheoesophageal fistulas occur in 3% of patients
aortoenteric fistulas are vary rare but are associated with a high mortality rate
References
Sabiston, 19th ed., pgs 1040 – 1047
Cameron, 11th ed., pgs 64 – 68
UpToDate. Boerhaave Syndrome: Effort Rupture of the Esophagus. Triadafilopoulos md, George. Feb 21, 2018. Pgs 1 – 21
UpToDate. Surgical Management of Esophageal Perforation. Raymond MD, Daniel. May 30, 2018. Pgs 1 – 47
UpToDate. UpToDate. Tracheo- and Broncho-Esophageal Fistula in Adults. Majid MD, Adnan. May 15, 2018. Pgs 1 – 24
UpToDate. Caustic Esophageal Injury in Adults. Triadafilopoulos MD, George. Jan 09, 2019. Pgs 1 – 31