Transcript Boerhaave Syndrome

Boerhaave Syndrome
Preethi Yeturu and Erik Mikaitis
MS IV
Background
Transmural perforation of the esophagus
Distinguished from Mallory-Weiss
syndrome (non-transmural tear)
Diagnosis is difficult because often no
classic symptoms are present
History
First described in 1724 by Hermann Boerhaave
His patient, Baron van Wassenaer, would eat
large meals and induce vomiting by ingesting
ipecac so that he could immediately have
another large meal
After vomiting, he began having severe chest
pain & dyspnea and died 18 hours later
At autopsy, Boerhaave found olive oil and roast
duck in the left pleural cavity.
Pathophysiology
Rupture is caused by a sudden rise in
intraluminal esophageal pressure produced
during vomiting.
Neuromuscular incoordination results in failure
of the cricopharyngeus muscle to relax.
Most common location of the tear is the left
posterolateral wall of the lower third of the
esophagus.
(2nd most common is subdiaphragmatic or upper
thoracic area)
Causes
Commonly associated with:
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Alcoholism
Bulimia
Overindulgence in food and drink
Epidemiology
Rare but most lethal perforation of the GI
tract
Most studies report a 100% mortality
within 7 days without surgery
Only a 70% overall survival with surgery
However, the syndrome is very rare:
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Only 16 cases reported from 1958-1973
A 1980 review cited only 300 cases in
literature worldwide
Epidemiology
Accounts for 15% of all traumatic ruptures
or perforations of the esophagus
Other 85% of ruptures are from iatrogenic
perforation (Not Boerhaave’s syndrome)
Mortality and Morbidity
The overall mortality of 30% is due to:
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Subsequent infection
Mediastinitis
Pneumonitis
Pericarditis
Empyema
Epidemiology
There is equal distribution of Boerhaave’s
throughout all races
Male-to-female ratio ranges from 2:1 to 5:1
Most frequently seen in patients aged 5070 years
80% of patients are middle aged men
Diagnosis
Clinical History
Repeated episodes of retching and
vomiting
Sudden onset of chest pain in lower thorax
and upper abdomen
Pain may radiate to the back or to the left
shoulder
Swallowing can aggravate the pain
Clinical History
Hematemesis is not seen after rupture
(which helps distinguish from MalloryWeiss)
Swallowing may precipitate cough
SOB is common due to pleuritic pain or
pleural effusion
Physical Exam
Mackler triad is the classic presentation,
including:
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Vomiting
Lower thoracic pain
Subcutaneous emphysema
Presentation may depend on:
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Location of tear
Cervical tear may have neck of upper chest pain
Mid to lower esophagus tear may have interscapular or
epigastric pain.
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Cause of the injury
Time since the perforation
Physical Exam
Pleural effusion is common
Subcutaneous emphysema is very helpful
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It is seen in 28-66% of patients
Typically found later
Tachypnea and abdominal rigidity are other
classic findings
Pneumomediastinum is an important finding
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May cause crackling on chest auscultation (Hamman
crunch)
Heard coincident with each heartbeat (can be
mistaken for pericarial friction rub)
Found in 20% of cases
Later stages of Illness
Can manifest as signs of infection and
sepsis
Symptoms may include fever,
hemodynamic instability, progressive
obtundation
Diagnosis at later stages is more difficult
as septic complications begin to dominate
the clinical picture
Workup
Laboratory Studies
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Findings are non-specific
May present with leukocytosis with left shift
50% of patients have hematocrit over 50%.
Thought to be due to fluid loss into pleural
spaces and tissues
Thoracentesis
If patient presents with pleural effusion:
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Pleural fluid can aid in diagnosis
May find undigested food particles and gastric
juices
If no gross particles are found, cytology can
confirm its presence
pH of the fluid will be less than 6 and amylase
will be elevated
Squamous cells from saliva may be found
Imaging Studies
Upright Chest X-ray
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90% of patients have an abnormality after perforation
Most common finding is a left unilateral effusion
May have:
Pneumothorax
Hydropneumothorax
Pneumomediastinum
Subcutaneous emphysema
Mediastinal widening
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V-sign of Naclerio
Streaks of air that dissect the planes behind the heart and form a
‘V’.
Fairly specific, but very insensitive
Found of 20% of patients
Imaging Studies
Esophagram
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Helps confirm the diagnosis
Shows extravasation of contrast
Outlines the length of the perforation and its location
(aids in decision of surgical approach, thoracic vs.
abdominal)
Initially use water soluble contrast (Gastrografin)
which has 90% sensitivity
Barium is associated with severe medistinitis
If study is negative but suspicion remains high, try left
and right lateral decubitus images
Imaging Studies
CT Scan
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Can reveal decisive criteria for diagnosis
Helpful in patients too ill to tolerate
esophagrams
Shows localized collections of fluid
Visualizes adjacent structures to help narrow
the differential diagnoses.
Can demonstrate periesophageal air tracks
It may not precisely localize the site of
perforation
Procedures
Endoscopy
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Not commonly used
Carries a risk of increasing the size and
extent of the perforation as well as pushing
more air through the perforation
More useful in thoracic esophagus
May be useful when perforation is suspected
but not proven
Treatment
Medical care
Therapy includes:
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IV volume resuscitation
Broad-spectrum aantibiotics
Prompt surgical intervention
Conservative vs aggressive treatment
depends on:
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Time delay
Extent of perforation
Overall medical condition
Medical management
Conservative management may be
appropriate if:
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The disruption is well contained within the
mediastinum
The cavity should be drained back into the
esophagus
Few symptoms
Clinical sepsis should be minimal
Conservative Management
Consists of the following:
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IVF
Antibiotics (Primaxin)
NGT on suction
Keep patient NPO
Drainage with tube thoracostomy
Early us of nutritional supplements (via
jejunostomy tube)
Surgical Care
First successful surgical repair in 1947
Goals in surgery:
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Direct repair of the rupture
Adequate drainage of the mediastinum and pleural
cavity
Left thoracotomy is the preferred approach
Omental flap may be used to support the
primary closure
Grastrostomy and jejunostomy tubes are placed
for drainage and nutrition respectively
Surgical Care
Alternatives to primary repair:
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Creation of an esophageal diversion through
the use of a loop or end-cervical
esophagostomy
T-tubes result in the formation of a controlled
fistula and cause a drainage of esophageal
secretions and refluxed gastric materials
Primary repair can be considered for
perforations as old as 72 hours
Surgical Care
Late complications
Empyema
Esophagotrachael fistula
esophagobronchial fistula
Consultations
Thoracic or general surgery as soon as
diagnosis is suspected
Infectious disease for antimicrobial therapy
Complications
Esophageal rupture which may lead to:
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Septicemia
Pneumomediastinum
Medistinitis
Pleural effusion
Empyema
Subcutaneous emphysema
Other complications
A rupture extending into the pleura will
cause a hydropneumothorax
ARDS
Prognosis
Directly related to early recognition and
appropriate intervention
Early intervention allows for prompt
surgical repair
Patients who undergo repair within 24
hours have a 70-75% survival.
Repair at 24-48 hours, survival drops to
35-50%
At more than 48 hours, survival is 10%
Questions?