relevant surgical anatomy in regards to injuries methods of identifying, ivestigating and treating esophageal injuries.

1. Esophageal Injuries-
Iatrogenic and others
Presented By-
Dr Sachin Katyal
PG Student,Department of Gen.Surgery,
M.K.C.G.MCH,Brahmapur
1

2. Aim of the topic
• Understanding the relevant surgical anatomy
of esophagus in regards to injuries.
• Learning the modalities to identify, investigate
and treat esophageal injuries.
2

3. Surgical anatomy
• 25cm mucosa-lined muscular tube that travels
through the neck, chest, and abdomen and rests
in the posterior mediastinum.
• lacks Serosa except abdominal part.
• commences at C6 and terminates in the
abdomen at T11
3

4. COURSE OF ESOPHAGUS
4

5. LAYERS OF ESOPHAGUS
5

6. Surgical anatomy cont’d
• cervical esophagus begins as midline structure.
• deviates to the left of the trachea as it passes through
the neck.
• At the level of the carina, deviates to right to
accommodate the arch of the aorta.
• before entering the abdomen, the esophagus is
pushed anteriorly by the descending thoracic aorta
passes along with it through the diaphragm into the
abdomen separated by the median arcuate ligament.
6

7. Endoscopic landmarks-distance from
incisor teeth
7

8. Modes of injury to esophagus
• 1-Instrumentation /Iatrogenic perforation
the most common.
• 2-Penetrating injury
uncommon, as the oesophagus is a relatively small target
surrounded by other vital organs.
• 3-Foreign bodies
Perforates during removal of a foreign body or due to an
object left in the oesophagus for several days & erodes
through the wall.
• 4-Due to ingestion of corrosives
• 5-Spontaneous Esophageal Rupture
(Boerhaave’s Syndrome)
8

9. Iatrogenic esophageal Injuries
• instrumentation is the most common.
• Perforation related to diagnostic UGI
endoscopy is unusual with an estimated
frequency of 1:4000 examinations.
(Ref. Bailey &love 26th ed.)
• Perforation occur in the pharynx or esophagus,
usually at sites of pathology or when the
endoscope is passed blindly
9

10. Iatrogenic perforation cont’d
• The more common sites are at the normal
anatomic narrowings of the esophagus.
• in the hypopharynx or cervical esophagus
secondary to exertion of force in attempting to pass
endoscope through cricopharynx.
• risk increases during endoscopic therapeutic
manipulations
Perforation of distal esophagus during esophageal
dilatation for esophageal strictures or achalasia.
10

11. Iatrogenic injuries cont’d
• Endoscopic sclerotherapy for esophageal varices
esophageal perforation in 1% to 3% of patients.
• The local necro-inflammatory reaction after
sclerosant injection contributes to the transmural
necrosis of esophageal wall.
• Avoidance of perforation may be achieved by
attempting to control the depth, volume, and
concentration of injection to prevent extensive &
prolonged ischemia to the surrounding tissue
11

12. Few other causes of Iatrogenic perforation
• during transesophageal echocardiography has been
documented.
• rupture of distal esophagus may occur with improper
placement and inflation of the gastric balloon of a
Sengstaken-Blakmore tube to control bleeding
esophageal varices.
• Esophageal intubations-Ryle’s tube placement,
endotracheal tubes, ERCP & endoscopic US-guided
interventions.
12

13. Esophageal injuries during surgical
procedures
• Procedures in close proximity to or directly
involving esophagus.
• Operative procedures include fundoplication,
vagotomy, hiatal hernia repair, lung transplantation,
pneumonectomy, thyroid resection, tracheostomy,
thoracic aortic aneurysm repair, esophageal
leiomyoma enucleation, mediastinoscopy & cervical
spine surgery(Ant. or Antero-lat).
• When injury is recognized intraoperatively, direct
primary repair is successful with minimal morbidity.
13

14. Foreign body ingestion
• ingested foreign objects, by children & individuals
with psychiatric disorders
• common offenders chicken or fish bones, partial
dentures, plastic eating utensils & metal safety pins.
• Objects <2 cm in size traverse normal esophagus
without problems.
• Once in the stomach, most objects can pass through
the rest of GI tract.
• 80% to 90% of ingested foreign bodies pass GIT
spontaneously.
14

15. Artificial Denture impacted in Esophagus
15

16. Foreign body ingestion cont’d
• sharp or jagged foreign bodies lacerate the
wall partially or completely.
• occurs in the normal anatomic narrowings of
the esophagus
• May present with acute airway obstruction
when foreign body impacted near the upper
esophageal sphincter, causing compression of
the trachea.
16

17. An impacted meat bolus at the lower end of the oesophagus-
may be the first presentation of a benign stricture or a malignant tumour.
17

18. Boerhaave’s Syndrome/Barotrauma/spontaneous
perforation
• Hermann Boerhaave ,Prof of medicine,Netherlands,1st
described after autopsy on grand admiral of Dutch fleet Baron
Jan van Wassenaer,Glutton.
• After relieving postprandial discomfort by self-induced
vomiting, the baron died from a distal esophageal perforation .
• recurrent emesis disrupts normal vomiting reflex that enables
sphincter relaxation, resulting in an increase in intrathoracic
esophageal pressure & perforation.
• Barotrauma also reported when one strains against closed
glottis as in blunt thoracic trauma, epileptic seizures,
defecation & childbirth, weight lifting all of which are a/w
increased intra-abdominal pressure.
• A tear in the esophageal mucosa, known as a Mallory-Weiss
tear, also occurs after persistent retching, but is not associated
with perforation.
18

19. Caustic injury
• devastating consequences & the best cure is
prevention.
• Childreningestion accidental &tends to be in
small quantities.
• teenagers & adultsingestion usually deliberate
during suicide attempts & much larger quantities.
• Alkali ingestion more common than acid ingestion
due to lack of immediate symptoms i.e no burning
sensation in the mouth.
• alkali ingestion are much more devastating
significant destruction long-term dysfunction.19

20. Injuries due to ingestion of acid or
alkali
The acute phase is dependent on
• 1- severity and location of the injury.
• 2-type of substance ingested (acid versus alkali),
• 3-form of the substance (liquid versus solid),
• 4-quantity and concentration of the substance
ingested.
• 5-amount of residual food in the stomach.
• 6-duration of tissue contact.
20

21. Chronic phase
• There are several sites that are prone to injury
because of a relative delay in transit through
the esophagus.
These correlate to the anatomic narrowings,
• Result in strictures and disruption of the
swallowing mechanism.
21

22. 3 phases of tissue injury from alkali
22

23. Acid injuries
• causes an immediate burning in the mouth.
• cause coagulative necrosis, forming an eschar
that limits tissue penetration.
• Within 48 hours, the extent to which the acid
will injure the esophagus is already
determined.
• injuries less severe and relatively spare the
esophagus over the stomach.
23

24. Acid burn contd
• Symptoms of respiratory distress, such as
hoarseness, stridor, and dyspnea, suggest upper
airway edema and are usually worse with acid
ingestion.
24

25. Comparison between alkali and acid burns
Alkali burns
More esophageal injury
Liquefactive necrosis->deep
No immediate burning sensation
Larger quantities ingested
Long term that is up till 6 months damages
are predicted.
Acid burns
More gastric injury
Coagulative necrosis->limits penetration
Burning sensation in mouth
Small quantities can be ingested
Within 48 hrs to which extent acid will injure
can be determined
25

26. DIAGNOSIS
• Diagnosis initiated with a physical examination
evaluating mouth, airway, chest, and abdomen.
• Careful inspection of lips, palate, pharynx, and
larynx
• Auscultation of the lungs determine upper airway
involvement.
• abdomen signs of perforation.
• Early endoscopy is recommended 12 to 24 hours
after ingestion to identify the grade of the burn
26

27. Acute caustic burn
27

28. Endoscopic Grading & Rx of esophageal and gastric
burns
28

29. Acute Phase Management
• aimed at limiting and identifying the extent of the injury.
• begins with neutralization of the ingested substance.
• If presents within the first hour of ingestion, neutralization is
attempted.
• Alkalis neutralized with half-strength vinegar or citrus juice.
• Acids neutralized with milk, egg whites, or antacids.
• Emetics and sodium bicarbonate avoided -increase the chance
of perforation.
• Further treatment guided by the extent of injury identified
endoscopically and the patient’s underlying condition.
• Oral nutrition may be resumed when a patient can swallow
saliva painlessly.
29

30. Management of caustic injury –acute phase
30

31. Chronic Phase Treatment
• deals with Mx of strictures,esophageal reconstruction, and fistulas.
• Strictures- prevention is best.
• Early stent placement advocated.
• At 3 weeks, 3 months, and 6 months, barium esophagogram to
evaluate for stricture formation, gastric outlet obstruction, & linitis
plastica appearance.
• endoscopy to determine the extent of reepithelialization.
• After reepithelialization, patients with strictures aggressively
treated with bougie dilations.
• bougie dilation done regardless of symptoms.
• Waiting until symptoms arise results in long-term strictures that
often fail bougie dilatation & ultimately require esophageal
resection.
• Dilatations scheduled daily for 2 to 3 weeks, every other day for 2
to 3 weeks, and then weekly for months.
• If endoscopic dilatation fails to re-establish an adequate lumen (40
Fr), surgical intervention is necessary
31

32. late result of a caustic alkali burn with high
oesophageal
stricture.
32

33. Caustic or lye stricture with marked stenosis high in the
body of the oesophagus
33

34. Reconstruction after caustic injuries
• Restoration of the alimentary tract delayed until 6 to
12 months till scar formation is complete.
• Resection of the damaged organs is recommended as
incidence of esophageal cancer is 1000-fold greater
than in the general population.
• A gastric pull-up is preferred but, if only a portion of
the stomach is viable, the distal portion of the
stomach can be combined with a jejunal
interposition.
• For a long-segment interposition graft, colon is
preferred. 34

35. Clinical presentation
• depends on the cause, location of the injury, size
of the perforation, degree of contamination, length
of time elapsed after injury, and presence of
associated injury.
• signs/symptoms of early esophageal injury -vague
and nonspecific.
• Therefore, a high index of suspicion is critical to
avoid delays in accurate diagnosis.
35

36. Clinical presentation cont’d
• pain most common symptom followed by
fever, dyspnea, and crepitus.
• Dissection of air along the subcutaneous
planes or into the mediastinum is a hallmark
of esophageal perforation.
• Occasionally, a systolic crunching sound, the
―Hammon’s sign”, can be heard over the
cardiac apex and left sternal border.
36

37. Clinical presentation cont’d
• subcutaneous emphysema, chest pain, and
vomiting constitute the Mackler’s triad, a
pathognomonic sign for spontaneous esophageal
rupture .
• Subcutaneous emphysema after thoracic
esophageal perforation is detected by palpation in
30% of patients.
• emphysematous crepitus in the neck after cervical
esophageal perforation is detected by palpation in
60% of patients.
37

38. Cervical esophageal perforation
• neck ache and stiffness are common clinical
findings, but pain is less severe.
• Soilage of oropharyngeal flora through the
retroesophageal space is limited because of
esophageal attachment to the prevertebral
fascia.
38

39. Thoracic esophageal perforation
• retrosternal or chest pain lateralizing to the side of
perforation.
• The initial contamination of the visceral mediastinum is
followed by subsequent perforation of the mediastinal
pleura.
• left pleural space is involved with distal esophageal
perforation.
• right pleural space is commonly violated with proximal
esophageal perforation.
• influx of gastric contents into the mediastinum initiates
intense inflammatory response &cytokine
activationmediastinitis accompanied with fluid
sequestration, hypotension, and sepsis.
39

40. Intra-abdominal esophageal perforation
• With intra-abdominal esophageal perforation, dull
epigastric pain radiating to the backposterior
perforation & communicates with the lesser sac.
• sharp, unrelenting, epigastric pain anterior
perforation with peritoneal contamination.
• early onset of systemic signs such as tachycardia,
tachypnea, and fever.
• Rapid deterioration signs of systemic
inflammatory response such as leukocytosis, sepsis,
and shock within hours of presentation.
40

41. Investigations
• Radiographic studies are invaluable .
• cervical esophageal perforation is suspected, a lateral
neck X-ray demonstrate air in the prevertebral facial
planes before it is detectable by chest radiograph.
• In thoracic or intra-abdominal esophageal perforation,
posterior and lateral chest radiographs, and upright
abdominal series should be obtained.
• Chest radiograph is suggestive in 90% of patients with
esophageal perforation, but may be normal immediately
after the injury
41

42. Xray neck- esophageal perforation
42

43. Investigations-X Rays cont’d
• radiographic evidence of mediastinal emphysema
requires at least 1 hour after the initial injury to
become discernable.
• pleural effusion and mediastinal widening may
take several hours to evolve.
“V sign‖
• reflects localized mediastinal emphysema in the
left lower mediastinum along the aorta and above
the left diaphragm forming the characteristic ―V
sign‖.
43

44. X-RAYS cont’d
radiographic findings include -
• mediastinal air-fluid level
• Hydropneumothorax
• mediastinal widening
• Pleural effusions are located
Right midesophagus perforation .
Left distal perforation.
44

45. Esophageal rupture with right pneumothorax
with midline shift
45

46. CONTRAST ESOPHAGOGRAPHY
• Contrast esophagography is the study of
choice.
• water-soluble contrast agents, such as
gastrograffin (meglumine
sodium)recommended over barium sulfate as
the contrast of choice.
• As extravasation of barium sulfate into the
mediastinum can lead to an intense
inflammatory response,resulting in fibrosing
mediastinitis
46

47. Barium esophagram of a perforated esophagus. Arrow shows
the extravasation of contrast into the left chest
47

48. Role of CT Scan
Thoracic CT imaging is useful to confirm the diagnosis in-
• 1- negative esophagram with a high clinical suspicion.
• 2-critically ill patients unable to undergo esophagography,
• 3-atypical symptoms .
Typical CT findings include-
• mediastinal or extraluminal air
• esophageal thickening
• Pneumomediastinum
• esophagopleural fistula
• pleural effusions
• abscess cavities adjacent to the esophagus
• communication of an air-filled esophagus with an adjacent
mediastinal air-fluid collection.
• extraluminal air -most common CT finding.
48

49. CT scan of a perforated esophagus. Note the air and
fluid in the mediastinum.
49

50. ESOPHAGOSCOPY
• useful in providing a direct visualization of the
perforation.
• a missed perforation hidden in a mucosal fold &
potential to convert a small mucosal or submucosal
tear into a large perforation during air insufflation
argue against the use of esophagoscopy.
50

51. Life saving & life sustaining measures
• Mx in ICU and operating room.
• progress rapidly to hemodynamic instability and shock.
• resuscitation measures with large-bore IV catheters,
urinary catheter, and secured airway are undertaken
before diagnostic testing.
• NPO,IV fluids , blood transfusion, broad-spectrum
antibiotics are started immediately
• nasogastric tube is placed only after management
decisions are made.
• These conservative measures are often lifesaving
and, in patients who do not undergo surgery, are
life-sustaining.
51

52. Four fundamental principles
• 1-elimination of septic focus.
• 2-provision of adequate drainage.
• 3- augmentation of host defenses by antibiotics
• 4- maintenance of adequate nutrition
52

53. Management Options
• Non-operative treatment
• Drainage only-T-tube drainage
• Endoscopic— 1-Esophageal stenting
2-Endoclip application
Open or minimally invasive (Video-assisted thoracoscopic surgery)
• Immediate reconstruction
• Delayed reconstruction
• Exclusion and diversion
• Primary closure
• Primary closure with buttressing of repair
1. Pleural flap
2. Pericardial fat pad
3. Diaphragmatic pedicle graft
4. Omentum onlay graft
5. Rhomboid muscle
6. Latissimus dorsi muscle
7. Intercostal muscle
• Esophagectomy
53

54. Critical determinants of successful
therapy
• cause, location, and severity of the perforation
• time interval between perforation and
intervention.
• The overall health status and physiologic
reserve of the patient
• extent of associated injuries
• underlying esophageal pathologic findings
54

55. Conservative Vs surgical management
Stable
Contained perforation
CONSERVATIVE Mx-
NPO, entral access,
endoluminal stent & repeat
esophagography.
During the course of
conservative
management, if a
patient’s clinical
condition deteriorates or
the perforation is no
longer contained,
surgical intervention is
advised.
Unstable
Free perforation
SURGICAL Mx-
débridement of devitalized
tissue
esophageal diversion /resection
creation of esophagostomy
drainage, placement of
gastrostomy & feeding
jejunostomy
55

56. 56

57. SURGICAL MANAGEMENT
• Cervical esophageal perforation can be treated by
drainage alone.
• Drainage alone is less successful with thoracic or
abdominal perforation because containment of
contamination is difficult.
• Intrathoracic esophageal disruption requires
aggressive mediastinal and pleural drainage.
• parietal pleura opened along the entire length of
the esophagus, & both the mediastinum and
pleural space are debrided, irrigated, and drained
by thoracostomy
57

58. The surgical technique for exposure of the
cervical esophagus
• involves a cervical incision along the anterior
border of left sternocleidomastoid from the level
of the cricoid cartilage to the sternal notch.
• The sternocleidomastoid and carotid sheath
retracted laterally, and trachea and thyroid displaced
medially to expose the esophagus
• Blunt, finger-dissection technique is used to gain
access to the prevertebral space, taking care to
avoid injury to the recurrent larygneal nerve in the
tracheoesophageal groove.
58

59. 59

60. ACCESS IN THORACIC
ESOPHAGEAL PERFORATION
• Access to perforation in the middle third of
the esophagus is through a right thoracotomy
in the fifth or sixth intercostal space.
• perforation in the lower third is best
approached through a left thoracotomy in the
sixth or seventh intercostal space.
60

61. Golden period for primary closure
• most critical variable is the degree of
inflammation surrounding the perforation.
• When patients present within 24 hours of
perforation, inflammation is minimal and primary
surgical repair recommended.
• With time, inflammation progresses and tissues
become friable and no longer ideal for primary
repair.
• The so-called golden period for primary closure
of an esophageal perforation is within the first
24 hours
61

62. Primary repair with/ without buttressing
• treatment of choice in thoracic or abdominal esophageal
perforation.
• Successful outcome requires debridement of necrotic
tissue, full exposure of the mucosal defect after
longitudinal esophagomyotomy & approximation of
mucosal and submucosal edges.
• Muscular layer reapproximated using a running or
interrupted absorbable suture technique.
• A variety of vascularized autogenous tissues, including
pleural flap, diaphragmatic pedicle graft, omentum
onlay graft, rhomboid and latissimus dorsi muscles,
intercostals muscles, and pericardial fat pad have been
used to buttress the primary repair.
• a pedicled intercostal muscle flap is preferred. 62

63. Tips for successful primary repair
• Of paramount significance is the elimination of
obstruction distal to the site of primary repair
commonly seen in strictures and achalasia
• intraoperative dilation attempted for distal
strictures, and esophagomyotomy opposite the
site of perforation accomplished for achalasia
after primary repair of perforation.
• When perforation occurs in presence of severe
gastroesophageal reflux, antireflux procedure can
be considered
63

64. WHEN PRIMARY REPAIR NOT
RECOMMENDED?
• 4 underlying conditions of the esophagus that
affect the treatment of a free perforation of the
esophagus—
• resectable carcinoma
• megaesophagus from end-stage achalasia
• severe peptic strictures
• a history of caustic ingestion.
even in the presence of a healthy tissue bed!!!
64

65. Esophagectomy/Exclusion and
Diversion
• If primary repair not possible due to severe
mediastinitis or underlying esophageal pathologic
findings, surgical options include esophageal
resection with immediate or delayed
reconstruction, or exclusion and diversion.
• Exclusion and diversion techniques employed
in patients with extensive mediastinal
contamination, grossly devitalized esophagus, or
hemodynamic instability unable to tolerate
definitive repair or resection.
65

66. T- Tube
• esophageal injuries that cannot be repaired at the
time of surgery or due to hemodynamic instability
pt. unable to tolerate definitive repair, use of
esophageal T-tube advocated.
• The T-tube creates a controlled esophagocutaneous
fistula, allowing drainage of the esophagus and time
for surrounding tissues to heal.
• Although continued leakage can progress to sepsis
and chronic fistula formation
66

67. Endoluminal stenting and clipping
• Serves as an effective therapeutic maneuver, or
temporary relief of symptoms to allow a more
definitive treatment at a later date.
• Endoscopic clipping(historically used for the control
of gastrointestinal bleeding)has been used for
closing perforations using metallic clips.
• This mode of treatment is suitable only for selected
patients with small (1.5 cm) clean perforation, and
minimal symptoms of infection
67

68. 68

69. MANAGEMENT OF THORACIC AND ABDOMINAL PERFORATIONS
69

70. Minimally Invasive Techniques
Video-Assisted Thoracoscopic Surgery
• preferred in pt. too ill to tolerate radical surgical
debridement and drainage.
• fundamental goals 1-identification of esophageal
perforation, 2-debridement of necrotic debris, 3-control
of leak, 4-wide drainage of mediastinum.
• thoracoscopic approach employs 3or 4trocars positioned
conventionally through the right chest.
• If the defect is 1 cm surrounded by viable tissue, a
primary closure performed with interrupted sutures.
• larger perforation surrounded by inflamed tissue, wide
drainage is advocated with the placement of a T-tube to
control the soilage. 70

71. Take home messages
• 1-Prevention of perforation is better than cure
• 2- Skilled early endoscopy is mandatory for
caustic burns management.
• 3-Recognizing the presentation and
understanding the detailed management of
patients with esophageal perforations is
essential and lifesaving.
71

72. References
• Sabiston 19th ed section IX Esophagus
• Bailey and love 26th ed. Ch 62, The
Oesophagus
• Review Article The Journal of TRAUMA
Injury, Infection, and Critical Care
Esophageal Perforations: New Perspectives
and Treatment Paradigms
James T. Wu, MD, Kenneth L. Mattox, MD, and
Matthew J. Wall Jr, MD
72

73. ..
My Special Thanks to Prof. Dr
S.K. Das Sir & Asso. Prof. Dr
S.S. Mohanty Sir for their support73