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ESOPHAGEAL INJURY
MIRITI.M.D
MASTERS IN CLINICAL MEDICINE: ACCIDENTS AND
EMERGENCY
MCM/2017/73494
FACILITATOR: DR NYAGA
INTRODUCTION
• Traumatic injuries of the esophagus due to
blunt or penetrating mechanisms are rare but
life-threatening. Despite the relative rarity,
clinicians in multiple disciplines, including
general surgery, emergency medicine, thoracic
surgery, trauma surgery, otolaryngology, and
spine surgery, must be knowledgeable
regarding their diagnosis and management.
ESOPHAGEAL ANATOMY
• The esophagus is a fibro muscular tube that extends
from the pharynx to the stomach. It is usually flattened
anteroposteriorly
• The esophagus enters the superior mediastinum
between the trachea and the vertebral column, where
it lies anterior to the bodies of vertebrae T1-T4.
• Initially, the esophagus inclines to the left but is moved
by the aortic arch to the median plane opposite the
root of the left lung.
• The thoracic duct usually lies on the left side of the
esophagus and deep to the aortic arch. Inferior to the
arch, the esophagus inclines to the left as it approaches
and passes through the esophageal hiatus in the
diaphragm.
PREVALENCE
• Perforation of esophagus in the adult is a very
morbid condition with high morbidity and mortality.
• With the increased use of endoscopic procedures,
the incidence of esophageal injury has increased
and iatrogenic perforations during diagnostic or
therapeutic procedures are now responsible for
60% of injuries.
• Traumatic esophageal injuries are rare, with most
large trauma centers treating only one to two cases
per year in the developed countries.
• The incidence of Blunt Esophageal injury is
estimated to be a tenth of the penetrating type.
AETIOLOGY
• Iatrogenic perforation is the leading cause of
esophageal injury about 70%, biggest risk during
Endoscopic procedures.
- Diagnostic endoscopy
- Endoscopic biopsy
- Endoscopic dilatations
- Variceal Sclerotherapy
- Endoscopic laser therapy
- Endoscopic Photodynamic therapy
- Endoscopic Stent Placement
•Nasogastric tube placement
•Endotracheal intubations
•Transesophageal echocardiography
•Minitracheostomy
•Foreign bodies-
Bones, dentures, button batteries
•Trauma
- Blunt
- Penetrating
- Sword/Knife swallowing
•Spontaneous or Boerhaave’s syndrome
•Caustic agents
- Acid and alkali
•Severe Reflux and Mallory-Weiss tear
•Infective causes
- Candida
- Herpes
- Syphilis
- Tuberculosis
- Immunodeficiency status
•Non esophageal surgery -
Mediastinal and cervical –Thyroid, Lung, spine and
mediastinal tumors
•Malignancy of esophagus, Lung and other
mediastinal structures
PATHOPHYSIOLOGY
• Esophageal rupture permits the passage of food, gastric
contents, secretions, and air into the mediastinum.
• The mediastinum can quickly become contaminated,
and mediastinal inflammation is followed by necrosis.
• Perforation of the overlying pleura may then occur.
• Negative intrathoracic pressure causes esophageal
contents to enter the pleural space, causing
contamination of the pleural cavity and pleural
effusion, most commonly on the left. This is explained
by the fact that when perforation occurs proximal to
the gastro esophageal junction, the esophagus lies
adjacent to the left pleura (the middle region bordering
the right pleura).
•Cervical perforations are generally less severe than those
occurring more distally, as mediastinal contamination is
limited by oesophageal attachments to the prevertebral
fascia.
•The time from injury to the initiation of treatment is a crucial
factor in the outcome of these patients.
•Patients who survive have prolonged hospital stays and
develop multiple postoperative complications.
•The most common causes of morbidity are pneumothoraces,
mediastinitis, and pleural effusions. Of these, mediastinitis is
often the most difficult to treat.
•Direct tissue damage due to acidic enteric contents
combined with bacterial contamination of the mediastinal
pleura (which has a very poor blood supply) mean that
therapeutic levels of systemic antibiotics may not be
achieved at the target site.
Clinical features
• Clinical features vary according to the level of
perforation and time interval to presentation.
• Symptoms may be non-specific, mimicking other
diagnoses such as esophagitis, peptic ulcer disease,
myocardial infarction, pneumonia, spontaneous
pneumothorax, acute pancreatitis varices, or aortic
dissection.
• The variety of presenting symptoms highlights the
importance of always considering oesophageal
rupture as a diagnosis in order to avoid any delay in
definitive treatment.
Signs and symptoms
• Initial examination may reveal a range of symptoms and
signs.
• Patients will frequently complain of vomiting,
dysphagia, and pain, dependent on the perforation site.
• On inspection, subcutaneous emphysema may be
obvious, with neck and chest wall swelling, giving a
characteristic crackling sensation on palpation as
trapped air moves within the tissue planes.
• Percussion of the chest wall will be resonant if a
pneumothorax is present, or indeed dull if there is lung
atelectasis.
• Reduced air entry on the affected side is likely upon
auscultation.
•The more frequently occurring cervical perforations present
with subcutaneous emphysema and anterior neck pain,
exacerbated by movement and palpation, accompanied by
dysphonia, dysphagia, or hoarseness.
•Thoracic perforations tend to be more difficult to diagnose.
Pain is present in 70% of full thickness thoracic oesophageal
perforations.
•Other symptoms are non-specific (vomiting, dyspnoea,
dysphagia), explaining the occasional post-mortem diagnosis,
or indeed confusion with oesophagitis, myocardial infarction,
spontaneous pneumothorax, or pneumonia.
•Pneumomediastinum can be heard as a cracking sound upon
auscultation (the Hamman crunch), and Mackler’s Triad,
consisting of thoracic pain, vomiting, and subcutaneous
emphysema, is highly suggestive, but seen in less than one-
third of cases.
DIAGNOSIS
• History & Clinical examinations
• Laboratory- FHG
• Radiology Plain
- Neck X-ray lateral view
- Chest X-ray PA view
- Abdominal X-ray erect
• Radiology Contrast
- Gastrografin study(water soluble contrast)
- Thin barium swallow study
- CT scan of chest and abdomen with oral contrast
• MRI chest and abdomen
• Ventilation perfusion (V/Q) scan
• ECG
Management
• Successful initial resuscitation, rapid diagnosis, and
management in a tertiary referral centre with
experience in the management of oesophageal
injuries improve outcome.
• As overwhelming bacterial mediastinitis may rapidly
cause multiorgan failure, patients with an
oesophageal injury should be considered as being
critically ill and require an aggressive approach to
early resuscitation and management
• The principles of initial management are to treat
infection, prevent continuing septic contamination,
provide nutritional support and restore digestive
tract continuity.
•Individualized i.v. fluid therapy and appropriate
analgesia should be instigated.
•Broad-spectrum prophylactic antibiotics, providing
cover against aerobic gram negative
bacilli and anaerobes, should be given empirically.
•Patients must be kept strictly fasted and a proton
pump inhibitor given. Total parenteral nutrition
should be commenced.
•Factors determining the most appropriate treatment
strategy include the etiology and size of perforation,
and also patient comorbidities and physiological
reserve. Treatment options include medical,
minimally invasive, and surgical management.
Overview of management of Esophageal Perforation
Medical management
• Conservative treatment may be suitable for patients
with limited oesophageal injury and contained
leakage. Such patients include those suffering
endoscopic iatrogenic perforation, as the patient is
likely to be fasted and the diagnosis made promptly.
• They must remain nil by mouth, with appropriate
antibiotic cover, and proton pump inhibitor therapy,
total parenteral nutrition,& continued observation
• Similarly, medical treatment might be suitable for
cases of inoperable malignant stricture, that is,
palliation.
Minimally invasive management
• There is an increasing trend towards endoscopic
stent placement, particularly in cases of contained
iatrogenic perforation with minimal contamination,
and no evidence of sepsis.
• A covered stent is placed over the defect in a
sedated patient using endoscopy and radiological
screening, preventing further contamination while
permitting early resumption of oral intake and
drainage.
• The stent is then usually removed 6–12 weeks later,
once the defect has healed.
Surgical management
• Primary repair is considered the gold standard operative
approach, irrespective of time to diagnosis. It allows for optimal
visualization of the perforation, and assessment of tissue
damage, particularly in patients with extensive mediastinal
contamination and devitalized oesophageal borders, as might
occur in Boerhaave’s syndrome.
• Repair at the cervical level is likely to involve a cervical
incision, with drainage.
• Mid-thoracic perforations may require a left- or right-sided
thoracoscopic or open approach.
• The majority of Boerhaave-type ruptures occur above the
gastro esophageal junction on the left side of the esophagus,
thus determining the approach for these cases.A midline
abdominal incision, or laparoscopic approach, is reserved for
intraabdominal perforations.
•After lavage, and debridement of non-viable mediastinal and
oesophageal tissue, primary repair is undertaken.
•This repair is frequently buttressed with a vascularized pedicle
flap from intercostal, serratus, or latissimus dorsi muscle,
pleura, or omentum in order to reduce fistula formation.
•Surgical technique is best tailored to the individual case, and
may constitute a hybrid approach including aggressive
debridement, drainage, and stent insertion.
•Primary repair is difficult with Boerhaave-type ruptures due to
high failure and leak rates.
•Therefore, if primary repair is deemed unsuitable, closure
might be performed over a T-tube (promoting healing without
contamination as an esophago-cutaneous fistula forms).
•Additionally, placement of drains, anti-reflux procedures, or
oesophageal resection with cervical esophagostomy and distal
feeding tube placement may be performed.
Treatment Options for Esophageal Perforations
PROGNOSIS
• The reported mortality from treated esophageal
injury is 10% to 25%, when therapy is initiated
within 24 hours of perforation and it is 40% to 60%
when the treatment is delayed.
• Major prognostic factors determining mortality are
the cause and location of the injury, the presence of
underlying esophageal pathology, the delay in
diagnosis and the method of treatment.
References
• Bhatia NL, Collins JM, Nguyen CC, Jaroszewski DE,
Vikram HR, Charles JC. Esophageal perforation as a
complication of O.G.D . J Hosp Med 2008; 3: 256–62
• Chirica M, Champault A, Dray X et al. Esophageal
perforations. J Visc Surg 2010; 147: 117–28
• Kuppusamy MK, Hubka M, Felisky CD et al. Evolving
management strategies in esophageal perforation:
surgeons using nonoperative techniques to improve
outcomes. J Am Coll Surg 2011; 213: 164–71

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Basic principles involved in the traditional systems of medicine PDF.pdf
 

Esophageal injury

  • 1. ESOPHAGEAL INJURY MIRITI.M.D MASTERS IN CLINICAL MEDICINE: ACCIDENTS AND EMERGENCY MCM/2017/73494 FACILITATOR: DR NYAGA
  • 2. INTRODUCTION • Traumatic injuries of the esophagus due to blunt or penetrating mechanisms are rare but life-threatening. Despite the relative rarity, clinicians in multiple disciplines, including general surgery, emergency medicine, thoracic surgery, trauma surgery, otolaryngology, and spine surgery, must be knowledgeable regarding their diagnosis and management.
  • 3. ESOPHAGEAL ANATOMY • The esophagus is a fibro muscular tube that extends from the pharynx to the stomach. It is usually flattened anteroposteriorly • The esophagus enters the superior mediastinum between the trachea and the vertebral column, where it lies anterior to the bodies of vertebrae T1-T4. • Initially, the esophagus inclines to the left but is moved by the aortic arch to the median plane opposite the root of the left lung. • The thoracic duct usually lies on the left side of the esophagus and deep to the aortic arch. Inferior to the arch, the esophagus inclines to the left as it approaches and passes through the esophageal hiatus in the diaphragm.
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  • 5. PREVALENCE • Perforation of esophagus in the adult is a very morbid condition with high morbidity and mortality. • With the increased use of endoscopic procedures, the incidence of esophageal injury has increased and iatrogenic perforations during diagnostic or therapeutic procedures are now responsible for 60% of injuries. • Traumatic esophageal injuries are rare, with most large trauma centers treating only one to two cases per year in the developed countries. • The incidence of Blunt Esophageal injury is estimated to be a tenth of the penetrating type.
  • 6. AETIOLOGY • Iatrogenic perforation is the leading cause of esophageal injury about 70%, biggest risk during Endoscopic procedures. - Diagnostic endoscopy - Endoscopic biopsy - Endoscopic dilatations - Variceal Sclerotherapy - Endoscopic laser therapy - Endoscopic Photodynamic therapy - Endoscopic Stent Placement
  • 7. •Nasogastric tube placement •Endotracheal intubations •Transesophageal echocardiography •Minitracheostomy •Foreign bodies- Bones, dentures, button batteries •Trauma - Blunt - Penetrating - Sword/Knife swallowing •Spontaneous or Boerhaave’s syndrome
  • 8. •Caustic agents - Acid and alkali •Severe Reflux and Mallory-Weiss tear •Infective causes - Candida - Herpes - Syphilis - Tuberculosis - Immunodeficiency status •Non esophageal surgery - Mediastinal and cervical –Thyroid, Lung, spine and mediastinal tumors •Malignancy of esophagus, Lung and other mediastinal structures
  • 9. PATHOPHYSIOLOGY • Esophageal rupture permits the passage of food, gastric contents, secretions, and air into the mediastinum. • The mediastinum can quickly become contaminated, and mediastinal inflammation is followed by necrosis. • Perforation of the overlying pleura may then occur. • Negative intrathoracic pressure causes esophageal contents to enter the pleural space, causing contamination of the pleural cavity and pleural effusion, most commonly on the left. This is explained by the fact that when perforation occurs proximal to the gastro esophageal junction, the esophagus lies adjacent to the left pleura (the middle region bordering the right pleura).
  • 10. •Cervical perforations are generally less severe than those occurring more distally, as mediastinal contamination is limited by oesophageal attachments to the prevertebral fascia. •The time from injury to the initiation of treatment is a crucial factor in the outcome of these patients. •Patients who survive have prolonged hospital stays and develop multiple postoperative complications. •The most common causes of morbidity are pneumothoraces, mediastinitis, and pleural effusions. Of these, mediastinitis is often the most difficult to treat. •Direct tissue damage due to acidic enteric contents combined with bacterial contamination of the mediastinal pleura (which has a very poor blood supply) mean that therapeutic levels of systemic antibiotics may not be achieved at the target site.
  • 11. Clinical features • Clinical features vary according to the level of perforation and time interval to presentation. • Symptoms may be non-specific, mimicking other diagnoses such as esophagitis, peptic ulcer disease, myocardial infarction, pneumonia, spontaneous pneumothorax, acute pancreatitis varices, or aortic dissection. • The variety of presenting symptoms highlights the importance of always considering oesophageal rupture as a diagnosis in order to avoid any delay in definitive treatment.
  • 12. Signs and symptoms • Initial examination may reveal a range of symptoms and signs. • Patients will frequently complain of vomiting, dysphagia, and pain, dependent on the perforation site. • On inspection, subcutaneous emphysema may be obvious, with neck and chest wall swelling, giving a characteristic crackling sensation on palpation as trapped air moves within the tissue planes. • Percussion of the chest wall will be resonant if a pneumothorax is present, or indeed dull if there is lung atelectasis. • Reduced air entry on the affected side is likely upon auscultation.
  • 13. •The more frequently occurring cervical perforations present with subcutaneous emphysema and anterior neck pain, exacerbated by movement and palpation, accompanied by dysphonia, dysphagia, or hoarseness. •Thoracic perforations tend to be more difficult to diagnose. Pain is present in 70% of full thickness thoracic oesophageal perforations. •Other symptoms are non-specific (vomiting, dyspnoea, dysphagia), explaining the occasional post-mortem diagnosis, or indeed confusion with oesophagitis, myocardial infarction, spontaneous pneumothorax, or pneumonia. •Pneumomediastinum can be heard as a cracking sound upon auscultation (the Hamman crunch), and Mackler’s Triad, consisting of thoracic pain, vomiting, and subcutaneous emphysema, is highly suggestive, but seen in less than one- third of cases.
  • 14. DIAGNOSIS • History & Clinical examinations • Laboratory- FHG • Radiology Plain - Neck X-ray lateral view - Chest X-ray PA view - Abdominal X-ray erect • Radiology Contrast - Gastrografin study(water soluble contrast) - Thin barium swallow study - CT scan of chest and abdomen with oral contrast • MRI chest and abdomen • Ventilation perfusion (V/Q) scan • ECG
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  • 16. Management • Successful initial resuscitation, rapid diagnosis, and management in a tertiary referral centre with experience in the management of oesophageal injuries improve outcome. • As overwhelming bacterial mediastinitis may rapidly cause multiorgan failure, patients with an oesophageal injury should be considered as being critically ill and require an aggressive approach to early resuscitation and management • The principles of initial management are to treat infection, prevent continuing septic contamination, provide nutritional support and restore digestive tract continuity.
  • 17. •Individualized i.v. fluid therapy and appropriate analgesia should be instigated. •Broad-spectrum prophylactic antibiotics, providing cover against aerobic gram negative bacilli and anaerobes, should be given empirically. •Patients must be kept strictly fasted and a proton pump inhibitor given. Total parenteral nutrition should be commenced. •Factors determining the most appropriate treatment strategy include the etiology and size of perforation, and also patient comorbidities and physiological reserve. Treatment options include medical, minimally invasive, and surgical management.
  • 18. Overview of management of Esophageal Perforation
  • 19. Medical management • Conservative treatment may be suitable for patients with limited oesophageal injury and contained leakage. Such patients include those suffering endoscopic iatrogenic perforation, as the patient is likely to be fasted and the diagnosis made promptly. • They must remain nil by mouth, with appropriate antibiotic cover, and proton pump inhibitor therapy, total parenteral nutrition,& continued observation • Similarly, medical treatment might be suitable for cases of inoperable malignant stricture, that is, palliation.
  • 20. Minimally invasive management • There is an increasing trend towards endoscopic stent placement, particularly in cases of contained iatrogenic perforation with minimal contamination, and no evidence of sepsis. • A covered stent is placed over the defect in a sedated patient using endoscopy and radiological screening, preventing further contamination while permitting early resumption of oral intake and drainage. • The stent is then usually removed 6–12 weeks later, once the defect has healed.
  • 21. Surgical management • Primary repair is considered the gold standard operative approach, irrespective of time to diagnosis. It allows for optimal visualization of the perforation, and assessment of tissue damage, particularly in patients with extensive mediastinal contamination and devitalized oesophageal borders, as might occur in Boerhaave’s syndrome. • Repair at the cervical level is likely to involve a cervical incision, with drainage. • Mid-thoracic perforations may require a left- or right-sided thoracoscopic or open approach. • The majority of Boerhaave-type ruptures occur above the gastro esophageal junction on the left side of the esophagus, thus determining the approach for these cases.A midline abdominal incision, or laparoscopic approach, is reserved for intraabdominal perforations.
  • 22. •After lavage, and debridement of non-viable mediastinal and oesophageal tissue, primary repair is undertaken. •This repair is frequently buttressed with a vascularized pedicle flap from intercostal, serratus, or latissimus dorsi muscle, pleura, or omentum in order to reduce fistula formation. •Surgical technique is best tailored to the individual case, and may constitute a hybrid approach including aggressive debridement, drainage, and stent insertion. •Primary repair is difficult with Boerhaave-type ruptures due to high failure and leak rates. •Therefore, if primary repair is deemed unsuitable, closure might be performed over a T-tube (promoting healing without contamination as an esophago-cutaneous fistula forms). •Additionally, placement of drains, anti-reflux procedures, or oesophageal resection with cervical esophagostomy and distal feeding tube placement may be performed.
  • 23. Treatment Options for Esophageal Perforations
  • 24. PROGNOSIS • The reported mortality from treated esophageal injury is 10% to 25%, when therapy is initiated within 24 hours of perforation and it is 40% to 60% when the treatment is delayed. • Major prognostic factors determining mortality are the cause and location of the injury, the presence of underlying esophageal pathology, the delay in diagnosis and the method of treatment.
  • 25. References • Bhatia NL, Collins JM, Nguyen CC, Jaroszewski DE, Vikram HR, Charles JC. Esophageal perforation as a complication of O.G.D . J Hosp Med 2008; 3: 256–62 • Chirica M, Champault A, Dray X et al. Esophageal perforations. J Visc Surg 2010; 147: 117–28 • Kuppusamy MK, Hubka M, Felisky CD et al. Evolving management strategies in esophageal perforation: surgeons using nonoperative techniques to improve outcomes. J Am Coll Surg 2011; 213: 164–71