Esophageal injuries iatrogenic and others


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

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Esophageal injuries iatrogenic and others

  1. 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. 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. 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
  6. 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. 7. Endoscopic landmarks-distance from incisor teeth 7
  8. 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. 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. 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. 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. 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. 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. 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. 15. Artificial Denture impacted in Esophagus 15
  16. 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. 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. 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. 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. 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. 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. 22. 3 phases of tissue injury from alkali 22
  23. 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. 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. 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. 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. 27. Acute caustic burn 27
  28. 28. Endoscopic Grading & Rx of esophageal and gastric burns 28
  29. 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. 30. Management of caustic injury –acute phase 30
  31. 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. 32. late result of a caustic alkali burn with high oesophageal stricture. 32
  33. 33. Caustic or lye stricture with marked stenosis high in the body of the oesophagus 33
  34. 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. 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. 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. 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. 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. 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. 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. 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. 42. Xray neck- esophageal perforation 42
  43. 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. 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. 45. Esophageal rupture with right pneumothorax with midline shift 45
  46. 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. 47. Barium esophagram of a perforated esophagus. Arrow shows the extravasation of contrast into the left chest 47
  48. 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. 49. CT scan of a perforated esophagus. Note the air and fluid in the mediastinum. 49
  50. 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. 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. 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. 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. 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. 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. 56
  57. 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. 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. 59
  60. 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. 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. 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. 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. 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. 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. 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. 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. 68
  70. 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. 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. 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. 73. .. My Special Thanks to Prof. Dr S.K. Das Sir & Asso. Prof. Dr S.S. Mohanty Sir for their support73