Medical instrumentation	Percentage risk of iatrogenic oesophageal disruption
Dilatation	0.5
Dilatation for achalasia	2
Endoscopic thermal therapy	1–2
Treatment of variceal bleeding	1–6
Endoscopic laser therapy	1–5
Photodynamic therapy	5
Stent placement	5–25

As a result, in spontaneous perforation, the diagnostic error is high, with only 5% of cases diagnosed at presentation. This leads to diagnostic delay of greater than 12 hours in the majority of cases.⁷ It may be that less than 35% of cases are correctly diagnosed pre-mortem⁸ (Box 19.1). As time passes, the critical condition of the patient further obscures relevant clinical features and the pursuit of incorrect investigations makes the diagnosis even more elusive.

Depending on the aetiology and amount of contamination, pain may be severe, constant, retrosternal or epigastric, distressing, exacerbated by movement and poorly relieved by narcotics or relatively mild. Dysphagia and odynophagia are common. Patients can be tachypnoeic and may sit up to splint their diaphragm. Abdominal pain or tenderness are not uncommon and can lead to a negative laparotomy.⁶ Similarly, subcutaneous emphysema takes time to develop; mediastinal emphysema precedes this and may be visible on a plain chest radiograph. With time the negative intrathoracic pressure draws air, food and fluids into the mediastinum and pleural cavities and a chemical pleuromediastinitis develops. A low-grade pyrexia ensues, and a sympathetic nervous system response develops with pallor, sweating, peripheral circulatory shutdown, tachycardia, tachypnoea and overt haemodynamic shock, which worsens as the systemic inflammatory response gives way to sepsis. Within 24–48 hours cardiopulmonary embarrassment and collapse develop as a consequence of overwhelming bacterial mediastinitis and septic shock. The combination of chest pain and shock may inappropriately, but all too commonly lead to a cardiological referral. Survival is dependent on the evacuation of the contamination, from the mediastinal and pleural cavities at the earliest possible opportunity.⁹ Systemic effects are less common when the cervical oesophagus is damaged, with neck pain, torticollis, dysphonia, cervical dysphagia, hoarseness and subcutaneous emphysema predominating.

Penetrating oesophageal trauma manifests in the same pattern but a high index of suspicion based on the likely tract of the insult is essential for diagnosis. Any deep penetrating transcervical or transmediastinal injury, especially gunshot derived, should be deemed suspect for oesophageal trauma. In contrast, except in the most violent of circumstances, blunt trauma rarely causes oesophageal injury but in high impact events a high index of suspicion should be exercised and injury actively excluded.

Investigations

Plain radiography

The typical findings on plain chest radiography are subtle – dependent on the site and the time interval following the insult. These are documented in Box 19.2 and Fig. 19.1. A plain abdominal radiograph may help to exclude a perforated intra-abdominal viscus.⁷

Box 19.2 Typical chest radiograph findings in spontaneous perforation of the oesophagus

• Pleural effusion

• Pneumomediastinum

• Subcutaneous emphysema

• Hydropneumothorax

• Pneumothorax

• Collapse/consolidation

Figure 19.1 (a,b) Typical chest radiograph findings of intrapleural oesophageal perforation.

Contrast radiography

Oral water-soluble contrast radiography ascertains the site, the degree of containment and the degree of drainage of the perforation (Fig. 19.2). Aqueous agents are rapidly absorbed, do not exacerbate inflammation and have minimal tissue effects. However, false-negative results in 27–66% and the limited applicability to a collapsed, unwell patient have downgraded their usefulness.

Figure 19.2 Contrast swallow demonstrating free extravasation of contrast media after oesophageal perforation during balloon dilatation of achalasia.

Upper gastrointestinal endoscopy

Endoscopic assessment excludes the diagnosis if normal, influences management if underlying pathology is discovered and facilitates the placement of a nasojejunal tube to allow enteral feeding. Risks are minimised using modern, flexible videoscopes together with fluoroscopic guidance, but should only be performed by a highly experienced endoscopist conversant with the consequences of their actions (Figs 19.3 and 19.4). Endoscopy can be performed in the sickest of patients, if necessary ‘on table’, when other injuries or instability of the patient preclude radiological assessment.

Figure 19.3 Endoscopic appearances of full-thickness spontaneous oesophageal perforation.

Figure 19.4 Endoscopic appearances of iatrogenic perforation. (a) Food bolus with false iatrogenic lumen alongside. (b) Appearance after food bolus removed. (c) Contained mediastinal cavity. (d) Six weeks later following conservative management a small pit remains.

In a retrospective review of 55 trauma patients, Horwitz et al. demonstrated 100% sensitivity and 92.4% specificity for upper gastrointestinal endoscopy in confirming oesophageal perforation and although injuries were infrequent (prevalence 3.6%), no injuries were missed and the examination was safe.¹⁰ In a similar study of 31 patients (24 of whom were intubated at the time of the examination), video endoscopy had a sensitivity of 100% and a specificity of 96% with no associated morbidity.¹¹ Video endoscopy has also been used to examine the oesophagogastric anastomosis post-oesophagectomy without additional morbidity.^10–12

Computed tomography (CT)

CT is increasingly useful in patients stable enough to undergo scanning. It is especially helpful in cases of multi-trauma and in critically ill patients with an atypical presentation, but the radiology department remains a dangerous place for an unstable patient. In combination with complex interventional radiology, CT has also revolutionised the management of intrathoracic collections. It plays a significant role post-therapy, be that assessing the patient postoperatively or assessing the adequacy of non-operative management.

In an intubated patient, the sensitivity of CT for spontaneous perforation is increased by placing a nasogastric tube just past the cricopharyngeus to run in a small amount of contrast media ¹³ (Fig. 19.5).

Figure 19.5 CT appearances of spontaneous oesophageal perforation. (a) Left pleural hydropneumothorax. (b) Left basal intercostal chest drain in the same patient as in (a).

Other investigations

Thoracocentesis of frank gastric contents is diagnostic – a pH of less than 6.0, a high amylase or microscopic squamous cells in the fluid can also confirm oesophageal perforation in difficult cases. Swallowed or injected oral/nasogastric dyes, such as methylene blue, may be diagnostically useful if a communicating drain is in situ; however, dye staining can be troublesome in the operative field if surgery is subsequently required.

Management

The rarity and severe consequences of inappropriate treatment have limited the ability to evaluate management options. As a result, published observa- tional case series often span many years, many centres, many surgeons and many techniques. Survival is dependent on controlling mediastinal and pleural contamination so surgery remains mandatory when gross contamination is present and is the mainstay for spontaneous perforation. However, non-operative treatment has become standard for iatrogenic trauma where contamination is more limited and delay in diagnosis is uncommon. Patients require a multidisciplinary approach with input from intensive care, radiology, physiotherapy and rehabilitation services. Hospitals lacking these specialist facilities or the versatile surgical cover necessary to deal with the oesophagus by abdominal or left or right thoracic operative approaches should transfer the patients at the earliest opportunity after stabilisation.

All patients with an oesophageal perforation are critically ill. The immediate priorities are the establishment of a secure and adequate airway, stabilisation of cardiovascular status and relief of pain, often using opiate-based analgesia. Regular reassessment is obligatory as an initially stable patient can rapidly decompensate. An early anaesthetic review is recommended. Box 19.3 documents the initial resuscitation.

Box 19.3 Initial resuscitation in spontaneous oesophageal perforation

• Control of airway and administration of supplementary oxygen

• Early anaesthetic and critical care involvement and support

• Large-bore intravenous access and intravenous fluid resuscitation

• Central venous access and arterial line monitoring with or without inotropic support

• Urethral catheterisation and close monitoring of fluid balance

• Broad-spectrum antibiotic and antifungal agents

• Intravenous proton-pump inhibitors

• Strictly nil by mouth

• Large-bore intercostal chest drainage – possibly bilaterally

• Nasogastric tube (only to be placed under endoscopic vision or radiological guidance)

• Enteral access – nasojejunal tube/formal feeding jejunostomy

• Multidisciplinary approach with low threshold for aggressive/operative intervention

Non-operative management

Non-operative management, endoscopic and minimally invasive operative management have all been shown to be safe and feasible in carefully selected patients who have either been diagnosed with minimal contamination and no mediastinitis or with a contained perforation. It may also be considered in those with a delayed diagnosis who have demonstrated tolerance.⁹

Non-operative treatment comprises observation in intensive care or ward-based high-dependency units with patients kept nil by mouth and fed enterally, if necessary via a feeding jejunostomy. A nasogastric tube should be placed under endoscopic and/or radiological assistance past the perforation to decompress the stomach and to limit refluxate. Contrast radiology, endoscopy and CT are used to monitor the status of the perforation and collections should be drained. The timing of investigations is best guided by the clinical condition of the patient but weekly serial contrast or CT studies are not unreasonable. All patients should be given broad-spectrum intravenous antibiotics, antifungal and antisecretory agents. Non-operative treatment is not ‘conservative’; patients require intensive observation and a low threshold for intervention, with 20% of patients requiring aggressive surgical salvage.

Iatrogenic cervical perforations are usually contained and thus managed non-operatively with percutaneous drainage of collections where necessary. Any resulting oesophagocutaneous fistulas heal rapidly in the absence of distal obstruction. Occasionally, operative prevertebral lavage, primary closure and drainage using a left lateral incision anterior to the sternocleidomastoid are required, and are well tolerated by even critically ill patients.

Criteria have been developed to aid the selection of suitable patients for non-operative management. These are detailed in Box 19.4. Case series applying these criteria demonstrate a mortality rate between zero and 16%, but numbers are small and results are skewed by both selection and publication bias.

Adjuncts to non-operative management

An endoluminal approach can be used to support patients undergoing non-operative management and can replicate some of the principles of open surgery with less associated trauma. This is pertinent in patients where the benefits of surgical exploration are outweighed by the risk and the ultimate outcome (advanced cancer) or in patients in whom the defect is small, clean and easily dealt with at the time of injury. All endoscopic approaches are technically difficult and should not be attempted by inexperienced operators unable to deal with the consequences of their actions.

Closure: clips and sealants: Endoclips are well established in closing small, clean defects after endoscopic mucosal resection or submucosal dissection for early cancer.^14,¹⁵ In the absence of significant contamination, small iatrogenic perforations may be closed immediately using endoclips in addition to supportive non-operative treatment. However, endoclipping ‘en face’ in the oesophagus is extremely challenging and should only be attempted by highly skilled endoscopists. It is also debatable whether this significantly alters the clinical course over a simple non-operative approach.² There is at least one case report of clipping a spontaneous oesophageal perforation but this cannot be recommended in the face of gross contamination.¹⁶

Diversion: stents: Self-expanding stents have been used to seal oesophageal perforations, chronic fistulas and even postoperative anastomotic leaks.17–19 Stents were not designed for use in a normal oesophagus and migration rates approach 30%, and concerns have been raised in terms of extending the defect through pressure necrosis and through the trauma of their subsequent removal.^14,²⁰ Publication bias means that failure and the consequences of failure remain unknown. There is considerable variation in the timing of stent placement and number of stents used. It is evident that the majority of cases also involve aggressive non-operative management.^21–24 It is therefore difficult to attribute successful outcomes to the stent placement alone. For example, one ‘successful’ report documents a patient who had five stents placed over an 8-month period before eventually proceeding to oesophagectomy at a tertiary referral centre.²¹ The one prospective stenting study lists 10 patients with a Boerhaave perforation.²⁵ Stent migration was high (11 out of 33) and there was a 50% complication rate (bleeding/stent fracture/impacted stent) if stents were not removed before 6 weeks.

At present there is insufficient evidence to support the use of oesophageal stents in oesophageal perforations. The authors suggest that their use is highly selective and should always be viewed as a temporary solution. However, in patients whose physical condition precludes more aggressive treatments and those in whom resection is not deemed suitable, stents do offer a serious alternative. If utilised then the stent should be removed within 3 months to avoid long-term complications since the biggest concern is septic erosion into surrounding structures. This horrendous situation does not appear to be represented in the literature (Fig. 19.6).²⁵

Figure 19.6 Endoscopic appearance of septically eroded stent. (a) Bronchoscopic view of carina with proximal stent erosion. (b) J-view of distal stent clearly lying in proximal stomach allowing free reflux into airways.

Drainage: repeated endoscopy: Endoscopic lavage and drainage of contained mediastinal perforations or even endoscopic placement of a vacuum sponge drainage system has been used for liquid contamination. This is certainly a novel approach but labour intensive and not suitable for gross contamination. Success may again simply reflect patients who would have done well with more simple non-operative treatment.^26,²⁷

The authors suggest that the temporary use of covered, self-expanding metal or plastic stents as a primary treatment to seal a spontaneous perforation is limited but that they may have a place to control a postoperative leak and iatrogenic perforation.²⁸ Endoscopic clipping, transoesophageal debridement and mediastinal irrigation should all be viewed as experimental.

Operative management

Open surgery: Surgery is advocated if the patient has overt signs of sepsis, shock, gross contamination, an obstructing pathology, a retained foreign body, a major caustic injury or has failed non-operative management. Virtually all gunshot wounds require surgery. The primary objective of surgical intervention is to restore oesophageal integrity and prevent further soiling. Thorough debridement, drainage, lavage and irrigation are more important for survival than the type of repair.⁹ A feeding jejunostomy should also be fashioned as a routine to facilitate enteral feeding, usually following thoracotomy once the patient can be turned into a supine position. Management of the patients by a multidisciplinary team is again emphasised. Underlying pathology should be dealt with. Spontaneous perforation of the oesophagus carries a considerable mortality risk and a long in-hospital recovery period should the patient survive.

A posterolateral thoracotomy is used to approach the oesophagus, most commonly on the left in the seventh or eighth intercostal space. Solid debris is removed and the pleural cavity thoroughly cleaned. The mediastinal pleura is widely incised to expose the injury, and necrotic, devitalised tissue debrided. A longitudinal myotomy is made (as the mucosal injury is usually longer than the muscular one) and the oesophagus repaired.²⁹

Success with one surgical technique over another probably reflects the expertise and experience of the individual centre rather than a true outcome difference.

Primary repair with or without reinforcement: A simple, single- or two-layered, primary repair can be fashioned using 2/0 or 3/0 interrupted absorbable sutures with or without a small-diameter bougie (40–46 F) in situ (Fig. 19.7). However, primary repair is associated with a significant leak rate (20–50%) and should be reserved for those operated on rapidly with demonstrably healthy tissue and limited soiling.³⁰ There is circumstantial evidence that reinforcing the suture line with an onlay patch of nearby tissues (such as omentum, pleura, lung, pedicled intercostal muscle grafts, gastric fundus, pericardium or diaphragm) may reduce the leak rate.³¹ Regardless, the authors would suggest that all primary repairs will leak and appropriate drains should be placed around the repair (Fig. 19.8).

Figure 19.7 (a) Primary closure and buttressing of suture line. (b) Intercostal muscle flap.

Figure 19.8 Intraoperative photograph of raised intercostal muscle flap.

T-tube repair: The concept of repair over a T-tube is to form a controlled oesophagocutaneous fistula.³² A large-diameter (6–10 mm) T-tube is placed through the tear with the limbs lying beyond the boundaries of the perforation and the oesophageal wall is closed loosely around the tube with fine interrupted, absorbable sutures (Fig. 19.9). The authors suggest anchoring the tube to the diaphragm, as originally described, as aortic erosion due to sepsis and pressure necrosis is possible.³³ The tube is externalised and secured, a further drain is placed down to the repair, and apical and basal intercostal chest drains are sited. Healing is monitored by contrast radiology and CT scans. The T-tube is left until a defined tract is established, with the majority removed around 6 weeks.

Figure 19.9 (a) Diagrammatic representation of T-tube repair of spontaneous oesophageal perforation with T-tube in situ. (b) Operative photograph. (c) Contrast radiological image of the same patient as in (b); note additional intercostal chest drain with small contrast leak directly into this drain.

In view of the high leak rate for primary repairs, the T-tube technique can be recommended for all patients.^6,³³

Resection: Oesophageal resection in the presence of a perforation is a major undertaking with an extremely high mortality. It is to be reserved for damage to a diseased oesophagus or in cases of extensive oesophageal trauma. This has even been performed in this setting as a minimally invasive approach.³⁸ If contamination is minimal then immediate reconstruction would be appropriate but a delayed approach may also be taken with limited differences in outcome.³⁹ The use of non-definitive exclusion and diversion techniques is mostly historical but remains in the armamentarium of an oesophageal surgeon and may occasionally be useful, such as in extensive caustic injuries.

Other approaches:

Minimally invasive surgery: laparoscopic/thoracoscopic: Distal, clean and immediately recognised iatrogenic perforations may be suitable to approach laparoscopically (transperitoneally) to attempt repair and drainage by surgeons used to working at the hiatus. This requires advanced laparoscopic skills in specialist centres with appropriate facilities.³⁴ Equally, selected cases can be managed thoracoscopically.^35,³⁶

Surgical repair over a stent: In view of the high leak rate of primary repair, some authors advocate a surgical repair over a stent (sutured transluminal or externally to prevent migration). This theoretically expedites a return to enteral nutrition.³⁷ However, the problems of stent placement remain in terms of the risks of a foreign body in the site of sepsis.

Management of penetrating injuries

Cervical

Contained cervical perforations may be managed non-operatively irrespective of any delay, but repair should be undertaken when uncontained or in those requiring exploration for another reason, which is likely in any injury where the path traverses platysma or which passes through the mediastinum.

Thoracic

Virtually all transthoracic gunshot wounds will require surgical exploration, and life-threatening cardiovascular, pulmonary and tracheobronchial injuries take precedence. Specialist advice and input should be sought but the majority of the oesophageal injuries will be able to be dealt with using the techniques described previously. The overall mortality of penetrating thoracic oesophageal injuries is hard to ascertain but lies between 15% and 27% (lower for cervical trauma at 1–16%).⁴⁰ The morbidity arises mostly from associated spinal and airway trauma for cervical injuries and from cardiorespiratory damage in thoracic trauma.

Management of underlying pathology

Patients who sustain a perforation of a malignant stricture constitute a difficult group to manage. Those who have known inoperable disease due to metastatic spread or who are unfit for surgery should be managed non-operatively, and in this situation the use of a sealing palliative stent is appropriate. In patients with less clearly defined operability most authors recommend resection with a view to control of contamination and potential cure, but this strategy carries a considerable mortality rate (11–75%).^39,⁴¹

In the presence of oesophageal cancer, the priority is to determine if the lesion was operable before the perforation, as an emergency subtotal oesophagectomy may be performed, although evidence suggests that perforation renders this a palliative resection and associated surgical mortality is high.^41,⁴² Every effort should be made to prevent perforation during staging endoscopic procedures.

Iatrogenic perforation of achalasia is uncommon (1–5%) and usually managed non-operatively or endoscopically as they are usually small, clean, immediately recognised and well contained. Other pathologies such as peptic stricture, infections or treatments can also predispose to perforation, e.g. radio/chemotherapy. Specific operative intervention may be required and, despite reduced contamination, the associated surgical mortality is increased. The indications for operative management are the corollary of those documented in Box 19.4.

Paraoesophageal surgery and procedural injuries

Direct oesophageal trauma is most commonly sustained during antireflux surgery, both open and laparoscopic, but the risk is low, of the order of 0–1.2%.⁴³ The risk increases with an intrathoracic approach, a previous hiatal operation and suturing of the wrap to the oesophagus. The majority of injuries are recognised and repaired immediately with buttressing using the fundoplication wrap. Drainage is advised and it may also be appropriate to form a feeding jejunostomy or to place a nasojejunal tube until the repair is deemed safe by contrast radiology. The mortality of unrecognised and uncontained perforations approaches 20%.

Trauma can also be sustained directly during thoracic and spinal surgery (<0.5% of procedures) or due to endotracheal intubation, nasogastric insertion and surgical tracheostomy. In ventilated patients, the clinical features of an injury may be concealed. Indirect trauma can occur through pressure necrosis or devascularisation, although the rich vascular supply of the thoracic oesophagus makes this extremely uncommmon.

Management algorithm

Diagnostic delay beyond 24 hours is classically associated with a poor outcome, but even when managed promptly and aggressively, perforation of the oesophagus, especially Boerhaave-type disruption, carries a significant mortality rate and reports to the contrary reflect selection bias. A management algorithm based on the therapeutic strategies outlined by the literature is demonstrated in Fig. 19.10. This is for guidance only and cases should be dealt with individually. Personal experience and expertise may well determine the best management.

Figure 19.10 Management algorithm for oesophageal perforation.

Non-perforated spontaneous injuries of the oesophagus

Full-thickness oesophageal perforation contained by the mediastinal pleura is termed ‘intramural rupture’.⁴⁴ This can occur spontaneously or secondary to instrumentation, food impaction or coagulopathies. Non-operative treatments with or without endoscopic adjuncts are usually successful as the perforation is contained, but a minority may require surgical intervention.⁴⁴

‘Black oesophagus syndrome’ or acute oesophageal necrosis is extremely rare. This is circumferential mucosal and submucosal necrosis that ends sharply at the oesophagogastric junction in the absence of a caustic injury, most commonly presenting with upper gastrointestinal bleeding.⁴⁵ The most likely cause is vascular insufficiency from venous thrombosis as part of a ‘two-hit’ traumatic phenomenon associated with systemic hypotension from another cause. It has also been associated with thrombotic disorders. Diagnosis is endoscopic and treatment expectant with a low threshold for surgical resection as the condition can rapidly progress to perforation. Mortality is high, often secondary to the underlying cause.

Caustic injuries

Serious ingestion of a caustic substance is uncommon but devastating. Ingestion by children is more common and almost exclusively accidental whereas, in contrast, ingestion by adults is more often deliberate. Most caustic substances can be grouped into acids or alkalis. Dangerous acids are readily available as toilet cleaners (hydrochloric acid), battery fluid (sulphuric acid) and in metal working (phosphoric and hydrofluoric acids). In addition to local effects, ingestion of hydrofluoric acid leads to effects on metabolic calcium levels through systemic absorption, which can cause refractory cardiac dysrhythmias; specialist poisons advice is recommended and emergency personnel should take precautions, as even dermal exposure is hazardous. Strong alkalis are also readily available as cleaners and bleaches, although most household agents are only mild caustic agents.

There are two important misconceptions about caustic injuries:

Misconception 1: tissue penetration by acids is minimised by coagulative necrosis whereas alkalis more rapidly penetrate transmurally through liquefactive necrosis. Although pathologically correct, this is clinically irrelevant as the ingestion of any strong caustic agent in sufficient quantity will inflict a potentially fatal oesophageal injury. Furthermore, there is evidence to suggest that strong acid ingestion is associated with greater systemic effects, a higher perforation rate and a higher mortality than alkali ingestion.⁴⁶

Misconception 2: acid ingestion causes gastric damage whereas alkali ingestion causes oesophageal injury. Although commonly cited, there is no evidence to support this.^47,⁴⁸

The severity of any caustic injury is related to the corrosive properties, concentration, amount, viscosity and duration of contact between the particular caustic agent and the oesophageal mucosa. Intentional caustic ingestions are associated with larger ingested quantities of agent and so tend to lead to more severe injuries. In contrast, fortunately, the amount ingested accidentally by children is usually small.

Clinical presentation

Presentation can be varied and confusing. In accidental ingestion, symptoms and signs may not have developed due to rapid presentation since clinical features are dependent on the substance and the time since ingestion. Equally, the absence of oral burns or pharyngo-oesophageal symptoms does not exclude more distal injury as the caustic agent may have passed rapidly through the mouth and pharynx. Furthermore, in deliberate ingestion the clinical features may be ‘underplayed’ by the patients. The clinical features of a caustic injury of the oesophagus are documented in Box 19.5. Most patients survive to reach the hospital unless aspiration has occurred. Glossopharyngeal burns cause oedema that may threaten the airway and prevent clearance of secretions with drooling and hypersalivation, and injury to the epiglottis and larynx leads to stridor and a hoarse voice. Dyspnoea is uncommon unless aspiration has occurred. On inspection, oropharyngeal burns can range from mild oedema and superficial erosions to extensive mucosal sloughing and necrosis. Acid burns form a black eschar whereas alkali burns look grey and dull. Oesophageal injury is suggested by dysphagia and odynophagia, and gastric injury by epigastric pain, nausea, anorexia, retching, vomiting and haematemesis. Patients may present shocked or in respiratory distress.

Investigation and management

The immediate priorities are the establishment of a secure airway, the stabilisation of cardiovascular status and the relief of pain. Severe laryngopharyngeal burns or respiratory compromise may require early tracheal intubation and general anaesthesia. Concurrent facial or eye burns should be irrigated and ophthalmology and plastic surgery specialist involvement should be sought. Oral intake is prohibited. Gastric lavage, induced emesis, nasogastric aspiration and the use of neutralising chemicals are contraindicated. Where possible the ingested agent and amount swallowed should be identified and regional poison centres can provide information regarding the properties of specific agents. Endoscopic staging of the burn determines the optimum management, likelihood of subsequent stricture formation and is the only accurate predictor of systemic complications and death ⁴⁶ (Fig. 19.11).

Figure 19.11 Endoscopic appearances of caustic injury to the oesophagus. (a) Acute grade 3a alkali injury. (b) Appearance after 8 weeks with pinhole stricture. (c) A year later and refractory stricture treated by placement of stent.

All patients require admission and flexible video endoscopy of the upper gastrointestinal tract by a skilled practitioner as soon as the patient is stable, preferably within 24 hours of ingestion, to assess the stage of the oesophageal injury. A nasoenteral tube may be placed for early nutritional support – which can also act as a partial stent to prevent strictures.47–49

The severity of the injury is graded using a system similar to that for skin burns (Table 19.2) but differentiation between grades may be difficult, especially between second- and third-degree burns, with implications for management; consequently, some patients will benefit from repeated evaluation (Table 19.3).⁵⁰ There has been interest in the use of oesophageal endosonography to assess depth of necrosis and damage to the muscle layers, but this currently offers no advantage over conventional endoscopic assessment.⁵¹ Equally, a modern CT grading system could be useful but is unlikely to replace an endoscopic assessment, which remains the gold standard.⁵²

Table 19.2

Depth of oesophageal burn

Depth of burn	Degree of burn	Endoscopic findings
Superficial	1	Mucosal oedema and hyperaemia
Transmucosal with or without involvement of the muscularis	2a	Superficial ulcers, bleeding, exudates
	2b	Deep ulcers – focal or circumferential
Full thickness with or without adjacent organ involvement	3a	Full-thickness focal necrosis
	3b	Extensive necrosis

Table 19.3

Endoscopic staging of oesophageal caustic injury

Most caustic injuries are managed non-operatively. The use of steroids and antibiotics during the acute phase remains controversial, with conflicting evidence regarding their benefits.

Steroids form part of the treatment protocol of many units and research continues into their use for the prevention of strictures despite a prospective randomised, controlled trial that clearly demonstrated no benefit from steroids, with the development of oesophageal strictures related only to the severity of the corrosive injury.⁵³

Patients with severe burns who are most at risk of stricture formation also represent the highest perforation risk and steroids may mask clinical symptoms. As such, the authors believe there is no place for steroids in the initial management of a caustic injury.

There are a few interesting animal-based research projects looking at other stricture-preventing medical treatments such as ibuprofen after oesophageal caustic injuries, but these have not yet been tried in a human population.⁵⁵

Asymptomatic patients with unintentional ingestion but no oropharyngeal burns and normal or minor oesophageal findings may be discharged once they are able to take oral fluids. Intravenous fluids, analgesia, nutritional support and antisecretory agents should be given to all other patients. Patients with grade 1 and 2a burns should be admitted and observed for 5–7 days, with diet reintroduced gradually over 24–48 hours, and endoscopy or contrast radiology studies should be arranged for 6–8 weeks after discharge to assess for strictures. Suicidal/intentional injury patients require psychiatric assessment prior to discharge. It is reasonable to observe patients with grade 2b and 3 burns, continuing nasojejunal feeding and if there is no evidence of progression to perforation then clear fluids can be introduced from 48 hours, but be aware that the perforation risk is present for at least 7 days. Those who present with a perforation or deteriorate will require an emergency oesophagogastrectomy as the stomach is almost always injured. The authors do not believe that laparoscopy has a role in assessing gastric viability. Immediate reconstruction with a substernal colonic interposition graft can be performed if there is minimal local contamination but more commonly oesophagostomy and delayed reconstruction 6–8 weeks later is preferred. It is reasonable to consider resection in patients with extensive circumferential mucosal injuries in view of the problem of refractory strictures and the long-term cancer risk. The mortality for these caustic injuries is 13–40%, with the majority of deaths occurring in the adult suicidal group.⁴⁸ Mortality mainly stems from respiratory complications and delay in the aggressive surgical treatment of transmural necrosis. There is no place for ‘conservative’ treatment of a severe caustic oesophageal injury.

Long-term complications and outcomes

Strictures develop in 5–50% of patients, 95% of which are distal and can be graded according to the Marchand classification (Table 19.4).⁵⁶

Table 19.4

The Marchand classification of oesophageal strictures

Most strictures can be managed by serial Savary–Gilliard bougie dilatation.⁵⁷

The procedure-related perforation incidence is less than 1%, but for safety the authors advise allowing approximately 6 weeks after injury before attempting dilatation. Antisecretory medication or even surgery may be required if reflux occurs after dilatation. Young patients with long, grade 3 or 4 strictures are likely to require a lifetime of repeated dilatations with a cumulative risk of iatrogenic perforation and ultimately of cancer, and in these patients other options should be considered. Surgical options are to bypass or resect the obstructive segment or to perform a stricturoplasty. Bypass avoids dissection through mediastinal fibrosis, and a retrosternal or subcutaneous route for the neo-oesophagus may avoid a thoracotomy. However, retaining the damaged oesophagus retains the long-term cancer risk and can lead to problems related to secretions and bacterial overgrowth. Thoracotomy, resection and colonic reconstruction (due to concurrent gastric damage) is therefore preferable. An alternative is an oesophageal stricturoplasty using a vascularised graft of colon, but again this retains the cancer risk. There is increasing interest in the use of removable or absorbable stents for refractory strictures but evidence is limited by numbers. However, these remain an alluring prospect and there is currently a National Institute for Health Research study investigating their use in benign oesophageal strictures.⁵⁸ There is also some evidence for the use of endoscopic triamcinolone acetonide injection into the strictured segment to augment dilatation.⁵⁹

Cancer risk

Squamous malignant transformation of a caustically damaged oesophagus occurs in around 16%, a risk 1000 times that of the general population but with a long latent period for malignant change of between 15 and 40 years. Surveillance may be impractical with such a long latent period and the risk is not proportional to the severity of the injury. Early elective resection before transformation eliminates the risk, with low associated mortality in younger patients. In older patients, simply an awareness of the risk by clinicians and patients should lead to earlier diagnosis and an increase in the number of curative resections where deemed appropriate.

Management algorithm

An algorithm for the management of caustic injuries of the oesophagus is detailed in Fig. 19.12.

Figure 19.12 Management algorithm for caustic oesophageal injuries.

Ingestion of foreign bodies

The oesophagus is the most common site for impaction of ingested foreign bodies within the gastrointestinal tract, accounting for 75% of cases.⁶⁰ By far the majority occur in children under the age of 10 years, with coins, toys, crayons and batteries being the commonest objects swallowed.⁶¹ In adults, food boluses (predominantly meat) or impaction of food-related bone fragments are more common. This is especially the case in edentulous patients due to decreased palatal sensation. Cases also occur in people with mental or psychiatric difficulties, or related to drug and alcohol abuse, and in those seeking secondary gain such as prisoners, and most upper gastrointestinal units are aware of a number of recurrent offenders.

Most foreign bodies impact in the cervical oesophagus, but impaction can occur at any of the physiological narrowings: cricopharyngeus, the aortic arch, the left main bronchus and the gastro-oesophageal junction. Benign pathology accounts for some cases (e.g. Schatzki rings, peptic strictures and eosinophilic oesophagitis); in contrast, malignant strictures are uncommonly associated with impaction due to the long development phase, but there are significant food bolus impaction rates associated with palliative treatments of malignant oesophageal lesions such as self-expanding metal stents.

Clinical presentation

In over 90% there is a clear history of ingestion associated with acute dysphagia at the level of the impaction and thus a rapid diagnosis.⁶² However, in young children and uncooperative adults the diagnosis may not be so clear-cut. Suspicious symptoms in children are refusal of feeds, gagging and choking, but some cases may remain concealed for months or even years and chronic aspiration or reflux may represent long-standing impaction. A high index of suspicion is also required for psychiatric patients with features suggestive of foreign body ingestion. Respiratory symptoms occur in 5–15%, especially in children and in cervical impaction, leading to coughing, wheezing, stridor and dyspnoea. In adults, acute impaction in the cervical oesophagus can cause tracheal obstruction leading to the so-called ‘café coronary’ or ‘steakhouse syndrome’. Typically, sharp object ingestion (e.g. fish bones) can cause a persistent foreign body sensation despite easy passage through the oesophagus without impaction. Physical signs are usually limited unless impaction causes obstruction leading to drooling or perforation leading to neck swelling, erythema, tenderness, subcutaneous emphysema or systemic effects. Long-standing impaction may lead to recurrent aspiration, empyema of the lung, perioesophagitis, oesophageal stenosis or fistulation into the airways or major vessels.

Diagnosis

Plain radiographs may localise both radio-opaque and non-radio-opaque objects and are useful if perforation is suspected (Fig. 19.13). Both anteroposterior and lateral projections should be obtained as objects may not be visible if overlying the vertebrae, and this also helps to distinguish whether objects are in the digestive or tracheobronchial tract. In young children and infants, extensive plain radiography may be required to confirm or refute the diagnosis of a swallowed radio-opaque foreign body. Even in the absence of symptoms or physical signs a potential history of ingestion should prompt the use of radiography, as in one study 17% of asymptomatic children with a history of coin ingestion had an impacted oesophageal coin.⁶³ Water-soluble contrast studies or CT scans may occasionally be required in cases of non-radio-opaque objects such as wood, aluminium, glass and plastics, but the use of hypertonic contrast media and barium should be avoided.

Figure 19.13 (a) Ingested button batteries lying in the gastric antrum. (b) Ingested 50-pence coin.

However, flexible video endoscopy is the investigation of choice. It has been used safely for over 30 years, is associated with a diagnostic sensitivity of 86% and specificity of 63%, and allows for immediate therapeutic intervention in 95%.⁶⁴

Management

In a Western population, the majority of ingested foreign bodies will pass through the gastrointestinal tract uneventfully, with 10–20% requiring endoscopic removal due to impaction and 1% requiring surgical removal.^64,⁶⁵

The indications for urgent intervention are:

1. Airway compromise.

2. Absolute dysphagia with aspiration risk.

3. Oesophageal impaction of sharp object or button battery.

4. Oesophageal impaction of greater than 24 hours duration.

The passage of a foreign body through the oesophagus does not always indicate success as objects over 5–6 cm long or >2 cm in diameter are unlikely to pass through the pylorus or around the duodenal curves and, once impacted, endoscopic removal may be difficult. As such, expeditious retrieval while in the oesophagus is advised. Similarly, although the majority of ingested sharp objects entering the stomach will traverse the gastrointestinal tract without incident, the perforation risk (up to 35%) suggests that retrieval, if safe, should be attempted.

In all other situations, individual management strategies depend on the symptoms, objects and expertise of the receiving speciality, which includes paediatricians, surgeons and psychiatrists.

Observation of up to 24 hours is reasonable in asymptomatic patients with oesophageal coins or similar round, smooth objects as many of these will pass spontaneously.⁶⁶

A number of techniques to dislodge food boluses without recourse to endoscopy have been reported. Proteolytic agents (e.g. papain) that dissolve the food bolus may cause oesophageal trauma and are dangerous if aspirated and they are not recommended. Effervescent agents, such as carbonated drinks and intravenous glucagon, which causes smooth muscle relaxation, were thought to help disimpact the food bolus but there is no good evidence to support their use.⁶⁷ Failure to progress through the gastrointestinal tract or symptomatic deterioration should prompt surgical review. Therapeutic video endoscopy is as successful in object removal as rigid endoscopy but with a significantly lower complication rate (5% vs. 10%) and avoids general anaesthesia in the majority of cases. However, in a minority, the type of object, number of objects or the inability of the patient to cooperate (i.e. young children) may dictate that general anaesthesia is required and rigid endoscopy is still useful for impaction in the pharynx as the view and access are superior, but the authors feel that it should be abandoned for distal obstructions. Patience is important in endoscopic removal but is rewarded with a high success rate (around 95%).⁶⁴ Failure is most likely to occur with long (>10 cm) or complex objects such as dental prostheses.

Smooth objects may be disproportionately difficult to retrieve; a variety of graspers, snares, magnets and baskets may be required and it is useful to practise with the proposed grasper on a duplicate foreign body prior to the actual procedure. Coins should be orientated sideways to aid passage through the cricopharyngeus and sharp or pointed objects may require an overtube or endoscopic hood for safe removal or manipulation to allow ‘blunt end first’ removal.

Food impactions tend to occur in the distal oesophagus and are usually accompanied by underlying pathology. Eosinophilic oesophagitis is of recent interest in this regard as a predisposing factor to acute dysphagia and food impaction. This is especially relevant as the oesophageal mucosa is thin, friable and easily traumatised by instrumentation – as such, dilatation should be avoided. Otherwise, flexible video endoscopy allows relief of the impaction and diagnosis of any underlying pathology with concurrent mucosal biopsying is necessary in all cases. Removal of the food bolus may again be achieved using a variety of techniques and tools. Larger boluses may require piecemeal removal, using an overtube if repeated intubation is required. Once the endoscope has been passed distal to the bolus then the bolus may be gently pushed into the stomach, but this technique should never be performed ‘blindly’. Definitive treatment such as dilatation of a peptic stricture may be performed after successful retrieval.

‘Disc’ or ‘button’ batteries are easily ingested by curious children. Electrical discharge or release of the alkaline contents, once impacted, can lead to local damage, necrosis and perforation. As such, urgent extraction is required if lodged within the oesophagus, and plain radiographs are helpful for localisation. However, if the battery has passed on to the stomach and duodenum then 80–90% will pass without complication. As such, observation with serial radiography is used to monitor progression, reserving endoscopic or surgical intervention if the battery fails to progress out of the stomach within 48 hours, if the patient develops symptoms of intestinal injury or if the battery fragments and there is evidence of mercury toxicity.

Surgery may be necessary when endoscopy fails for large objects, for objects embedded in the oesophageal wall or when there has been an associated or iatrogenic perforation. The surgical approach depends not only on the site and severity of the injury, but also associated inflammation and any underlying oesophageal pathology. Deliberate narcotic packet ingestion is a particularly taxing scenario. The authors suggest that endoscopic removal should not be attempted as successful retrieval is outweighed by the risk of rupture.⁶⁸ Most packets will pass safely through the bowel but urgent surgery is indicated in cases where there is failure to progress, obstruction or rupture, in conjunction with medical support for absorption of relevant contents.