Specialist oesophagogastric emergencies


Introduction

This chapter focuses on the diagnosis and management of injuries to the oesophagus and stomach from a variety of different insults, resulting in a spectrum of damage. It will deal with perforations of the oesophagus as a grouped entity, caustic injuries to the oesophagus and stomach, management of foreign body ingestion, and difficult gastroduodenal perforation. It will not deal with the management of routine gastroduodenal perforations or upper gastrointestinal bleeding. These topics will be covered in the companion series volume Core Topics in General and Emergency Surgery . Management of acute gastric volvulus and paraoesophageal hernia is covered in Chapter 15 in this volume.

Perforation of the oesophagus

Most clinicians gain limited exposure to patients with oesophageal injury due to its rarity. Misdiagnosis, incorrect investigations, and inappropriate and delayed management are common as a result. The difficulty in accessing the oesophagus, its unusual blood supply, the lack of a strong serosal layer, and the proximity of vital structures make clinicians wary. The clinical experience is compounded by a lack of evidence for management, with much of the published literature limited to observational studies. Diagnostic and treatment strategies vary widely. Mortality rates with oesophageal injury have improved but remain high. Management in centres dealing with higher volumes of oesophageal-related problems can improve the chances of a successful outcome.

The management of such injuries is actually straightforward to a clinician who regularly accesses the oesophagus and stomach, and is familiar with the basic principles to minimise morbidity and mortality. Hopefully the outcomes from these injuries will improve with the ongoing reconfiguration of services for patients with upper gastrointestinal disease and the provision of dedicated specialist units.

Partial- and full-thickness perforations of the oesophagus can result from a spectrum of conditions. The underlying aetiology influences the type of disruption and the degree of contamination. Mediastinal and pleural contamination can give rise to a massive systemic inflammatory response and sepsis.

Iatrogenic injuries continue to be the most common aetiology, particularly given the increase in therapeutic endoscopic interventions. The key to diagnosing an oesophageal injury is to have a high index of suspicion following any endoscopic oesophageal procedure and recognise the possibility at the time of the event. It is far better for the patient if the clinician errs on the side of caution and instigates appropriate management if a perforation is suspected. This can always be stepped down if subsequent investigations exclude a full-thickness perforation.

The rare, eponymous Boerhaave’s syndrome of spontaneous perforation of the oesophagus occurs in the absence of pre-existing pathology. Minor differences in management can lead to major outcome improvements. Penetrating and blunt injuries to the oesophagus are similarly uncommon and misdiagnosis often compounds any injury.

Aetiology and pathophysiology

Iatrogenic perforation of the oesophagus

Iatrogenic damage to the oesophagus leading to full-thickness disruption occurs from within in 60–70% of cases, such as during endoscopic instrumentation, or from without, such as during paraoesophageal or thoracic lung surgery. Diagnostic flexible endoscopy remains a safe procedure when performed by appropriately trained individuals. However, the sheer numbers of endoscopies performed have led to an overall increase in perforations. Flexible endoscopy (0.03% perforation risk) has almost totally replaced rigid oesophagoscopy (0.11% perforation risk). There are very few indications to perform a rigid endoscopy and there is no longer a role for food bolus removal with rigid oesophagoscopy given the safer flexible endoscopic techniques.

Intubation of the oesophagus can cause proximal perforation, with the risk increased by hyperextension of the neck and the presence of arthritic cervical osteophytes or an oesophageal diverticulum. However, in 75–90% of diagnostic perforation cases trauma is sustained to the distal oesophagus, often in conjunction with an abnormality.

The majority of oesophageal full-thickness perforation occurs during endoscopic interventions ( Table 16.1 ). Balloon or Savary–Gilliard dilatation of strictures accounts for most perforations. This risk is increased in patients with a malignant stricture, previous radiotherapy, or chemotherapy. The risk from self-expanding metal stents for palliating malignant strictures is lower. Stents placed for other reasons such as attempted treatment of anastomotic disruption or benign strictures can erode through the oesophagus at other sites. Stents not placed for palliation of malignancy should therefore be removed in a timely manner to avoid such situations. Endoscopic mucosal and submucosal resection for dysplastic or intramucosal adenocarcinoma also carries a perforation risk of up to 2%.

Table 16.1
Risk of iatrogenic oesophageal disruption through instrumentation
Medical Instrumentation Percentage Risk of Iatrogenic Oesophageal Disruption
Dilatation
Dilatation for achalasia
Endoscopic mucosal resection
Stent placement
Endoscopic thermal therapy
Treatment of variceal bleeding
Endoscopic laser therapy
Photodynamic therapy
Stent placement
0.5
2
2
2
1–2
1–6
1–5
5
5-25

Treatment for achalasia with pneumatic dilatation has a higher perforation risk than standard balloon dilatation due to the higher pressures and larger balloon size. The risk can be minimised by always starting at the smallest balloon size (30 mm) for the initial dilatation. Per oral endoscopic myotomy (POEM) is a newer treatment for achalasia, with some evidence for its consideration alongside surgical myotomy and pneumatic dilatation. POEM has its own perforation risk.

All other modalities of oesophageal intubation including nasogastric tube placement, transoesophageal echocardiogram, and inadvertent oesophageal placement of an endotracheal tube can result in oesophageal perforation. In contrast to some guidelines advocating blindly pushing through a food bolus, caution should be exercised in performing this manoeuvre unless it is known for certain that the distal lumen is not obstructed by a stricture, either benign or malignant. Pushing a food bolus distally should ideally only be done if the endoscope can pass the bolus and confirm there is no distal obstruction, although often this is not possible.

Mortality rates have improved over the years, but iatrogenic perforation of the oesophagus can still be a life-threatening condition. A case review of 75 patients with iatrogenic perforation reported a not insubstantial mortality rate of 19%. Prevention is the best solution, with continued efforts to increase awareness and training likely to reduce the incidence.

Spontaneous perforation of the oesophagus

Boerhaave’s syndrome is characterised by barogenic trauma in an otherwise normal oesophagus, leading to immediate and gross gastric content contamination of the mediastinum and often of the pleural cavity. The ensuing chemical and septic mediastinitis can precipitate a rapid deterioration in the patient’s condition. The actual degree of damage to the oesophagus and ensuing contamination can vary considerably. The disruption of the oesophageal wall is associated with a sudden increase in intra-abdominal pressure. In most cases this is related to vomiting or retching, although weightlifting, parturition, defecation, the Heimlich manoeuvre, and status epilepticus have all been implicated in the past. The fact that vomiting is common but oesophageal perforation is not suggests as yet unrecognised anatomical or pathological abnormalities may exist. In apparent ‘spontaneous perforation’, an underlying cause such as malignancy, peptic ulceration, or infection is discovered in up to 20% of cases. Eosinophilic oesophagitis can also predispose to oesophageal perforation, spontaneously after vomiting to dislodge an impacted food bolus, or after endoscopic intervention. The mechanism of a spontaneous perforation differs from that of a Mallory–Weiss tear, as the forces resulting in the latter are shearing in nature as opposed to the barogenic force in a perforation.

The most common location for a spontaneous perforation is just above the oesophagogastric junction in the left posterolateral position. The perforation usually occurs in a solitary location, 1–8 cm long, with the disruption longer on the mucosal side than the adventitial side. In cases where the pleura is disrupted, this can occur at the time of the barogenic event or subsequently as a result of gastric acid erosion, exacerbated by intrathoracic pressure.

Penetrating injuries

Penetrating injuries of the oesophagus are rare but associated with significant morbidity and mortality. The overwhelming majority of penetrating injuries to the oesophagus are associated with significant injury to the surrounding tissues and organs. The oesophageal injury can be overlooked at the time of initial presentation when the management of more immediately life-threatening vascular, cardiac, or lung injuries takes precedence. However, a delay in identifying and managing such oesophageal injuries increases the morbidity and mortality from the injury. Injury should be suspected in any gunshot or knife wound to the cervical or mediastinal regions. The degree of disruption is dependent on the type of weapon involved and the velocity of any projectile. High-velocity projectiles will cause far greater damage due to the cavitation effect while lower velocity projectiles might result in more limited injury. The injury severity can be graded according to the American Association for the Surgery of Trauma.

Penetrating injuries from within are much less common, with causes including ingestion of sharp objects, fish or meat bones, and swallowed dentures ( Fig. 16.1 ). The mechanism of penetrating injuries from within more often follows a pattern similar to iatrogenic or spontaneous perforation.

Figure 16.1, Full-thickness oesophageal perforation secondary to swallowed dentures.

Blunt trauma

Blunt trauma that causes significant injury to the oesophagus is rare. The mechanism is almost exclusively high-impact trauma such as road traffic collisions and it is often associated with more immediately life-threatening injuries of the airway, heart, or lungs. The cervical oesophagus is at risk from severe flexion-extension of the neck or from impact of the neck or upper chest on the steering wheel. The fixed points of the oesophagus at the cricoid, carina, and pharyngo-oesophageal junction are most susceptible to rapid deceleration traction laceration. Barogenic damage can occur after a sudden rise in intra-abdominal pressure from compression against a closed glottis. Secondary injury to the oesophagus can occur following interruption of vascular supply.

Blast injuries to the oesophagus are exceedingly rare. There are few reports in the literature.

Clinical presentation

The clinical features depend upon the cause, site, and time from injury. Iatrogenic injuries ought to be recognised at the time of the event or confirmed shortly afterwards with appropriate investigation. The presentation of patients with spontaneous perforation or blunt trauma-related injury can be tenuous. The classical Mackler’s triad in spontaneous perforation of vomiting, chest pain, and subcutaneous emphysema is actually an uncommon presentation. It was present in only 7 of 51 patients (14%) in one large case series. , As a result, the diagnostic error on spontaneous perforation is high, with only 5% of cases diagnosed at presentation. This can lead to diagnostic delays of greater than 12 hours ( Box 16.1 ). As time passes, the critical condition of the patient further obscures relevant clinical features and the pursuit of incorrect investigations can make the diagnosis even more elusive.

Box 16.1
Common misdiagnoses for spontaneous perforation of the oesophagus

Medical

  • Myocardial infarction

  • Pericarditis

  • Spontaneous pneumothorax

  • Pneumonia

  • Oesophageal varices/Mallory-Weiss tear

Surgical

  • Peritonitis

  • Acute pancreatitis

  • Perforated peptic ulcer

  • Renal colic

  • Aortic aneurysm (dissection/leak)

  • Biliary colic

  • Mesenteric ischaemia

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, although this is less likely with computed tomography (CT) imaging. 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 fluid into the mediastinum and pleural cavities. Chemical and microbial pleuromediastinitis develops. Pyrexia ensues, with the sympathetic nervous system response leading to pallor, sweating, peripheral circulatory shutdown, tachycardia, tachypnoea, and overt haemodynamic shock. This 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 cardiology referral. Survival is dependent on treating sepsis, providing organ support as required, and evacuating contamination from the mediastinal and pleural cavities at the earliest possible opportunity.

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 suspicious for oesophageal trauma. In contrast, 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 and dependent on the site and the time interval following the insult. These are documented in Box 16.2 and Fig. 16.2 . A plain abdominal radiograph may help to exclude a perforated intra-abdominal viscus.

Box 16.2
Typical chest radiograph findings in spontaneous perforation of the oesophagus

  • Pleural effusion

  • Pneumomediastinum

  • Subcutaneous emphysema

  • Hydropneumothorax

  • Pneumothorax

  • Collapse/consolidation

Figure 16.2, Typical chest radiograph findings of intrapleural oesophageal perforation.

Computed tomography

Urgent CT is the first-choice imaging modality and should not be delayed when the diagnosis is suspected. With the advent of modern scanners, CT with intravenous contrast should be sensitive enough to identify the site of an oesophageal perforation, although some radiologists still prefer to also administer oral contrast. 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, although in practice this is now rarely performed ( Fig. 16.3 ). It is useful to evaluate images with a radiologist who specialises in (upper) gastrointestinal radiology if at all possible. CT is especially helpful in multi-trauma and critically ill patients with an atypical presentation.

Figure 16.3, Computed tomography appearances of spontaneous oesophageal perforation. (a) Left pleural hydropneumothorax. (b) Left basal intercostal chest drain in the same patient as in (a).

In combination with complex interventional radiology, CT has also revolutionised the management of intrathoracic collections. It plays a vital role in assessing the progress of patients, be that after non-operative or operative management.

Contrast radiography

Oral water-soluble contrast radiography ascertains the site, the degree of containment, and the degree of drainage of the perforation ( Fig. 16.4 ). 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. In assessing healing of a perforation, the author would advocate the use of dilute barium to ascertain the presence or absence of any ongoing leak if water-soluble contrast studies were negative.

Figure 16.4, Contrast swallow demonstrating free extravasation of contrast media after oesophageal perforation during balloon dilatation of achalasia.

Upper gastrointestinal endoscopy

Endoscopic assessment by an experienced endoscopist excludes the diagnosis if normal, influences management if underlying pathology is discovered, and facilitates the placement of a nasojejunal tube to allow enteral feeding ( Figs. 16.5 and 16.6 ). Endoscopy can be performed in the sickest of patients, in the critical care unit, or in theatre, when other injuries or instability of the patient preclude radiological assessment. It is often safest to perform endoscopy in suspected spontaneous perforation under a general anaesthetic with the patient intubated. This can allow for positive-pressure ventilation to reduce the risk of cardiorespiratory embarrassment by air insufflation into the mediastinum and pleural spaces. This risk is minimised by introducing the endoscope without insufflation and using suction to drain fluid from any cavity. It is important to be prepared for rapid chest decompression if chest drains are not already in situ. Otherwise endoscopy should be performed with an anaesthetist present and ready to intubate should the patient become unstable.

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. In a similar study of 31 patients, endoscopy had a sensitivity of 100% and a specificity of 96% with no associated morbidity. Endoscopy has also been used to examine the oesophagogastric anastomosis post-oesophagectomy without additional morbidity.

Figure 16.5, Endoscopic appearance of full-thickness spontaneous oesophageal perforation.

Figure 16.6, Endoscopic appearance of iatrogenic perforation. (a) Food bolus with false iatrogenic lumen alongside. (b) Appearance after food bolus removed. (c) Contained mediastinal cavity. (d) 6 weeks later following conservative management a small pit remains.

Other investigations

Thoracocentesis of 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. Swallowed or injected oral/nasogastric dyes, such as methylene blue, may be diagnostically useful if a communicating drain is in situ. Dye staining can, however, 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. Published observational case series often span many years, many centres, many surgeons, and many techniques. Survival is dependent on managing sepsis and controlling mediastinal and pleural infection, so surgery remains mandatory when gross contamination is present. 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, dieticians, 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 these patients. This should occur at the earliest opportunity after stabilisation, as deterioration can be rapid and unpredictable. , ,

All patients with an oesophageal perforation can be critically ill. The immediate priorities are the establishment of a secure and adequate airway, stabilisation of cardiovascular status, analgesia, broad-spectrum antibiotics, antifungals, and antisecretory medication. Regular reassessment is obligatory, as an initially stable patient can rapidly decompensate. An early anaesthetic review is recommended. Box 16.3 documents the initial resuscitation.

Box 16.3
Initial resuscitation in spontaneous oesophageal perforation

  • Control of airway and supplementary oxygen

  • Large-bore intravenous access and intravenous fluid resuscitation

  • Intravenous broad-spectrum antibiotics and antifungals

  • Intravenous proton pump inhibitors

  • Strictly nil by mouth

  • Urethral catheterisation and fluid balance monitoring

  • Early anaesthetic and critical care involvement

  • Intercostal chest drainage (possibly bilaterally)

  • Nasogastric tube (placed under endoscopic or radiological guidance)

  • Enteral feeding access (nasojejunal tube or feeding jejunostomy)

  • Multidisciplinary approach with low threshold for aggressive/operative intervention

Non-operative management

Non-operative, 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. Non-operative treatment is not ‘conservative’. Patients require intensive observation and a low threshold for intervention, with 20% of patients requiring aggressive surgical salvage.

Non-operative treatment comprises observation in a critical care environment with patients kept nil by mouth and preferably 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, especially in distal oesophageal perforations. Contrast radiology, endoscopy, and CT are used to monitor the status of the perforation. Collections should be drained. The timing of investigations is guided by the clinical condition of the patient, but weekly contrast or CT studies are not unreasonable. All patients should be given broad-spectrum intravenous antibiotics, and antifungal and antisecretory agents.

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. Operative prevertebral lavage, primary closure, and drainage via a left lateral incision anterior to the sternocleidomastoid is occasionally required and is 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 16.4 . Other factors requiring consideration include control of the perforation, excluding underlying oesophageal disease, absence of septic shock, and the ability to change the management strategy promptly if required. Case series applying these criteria demonstrate a mortality rate between 0% and 24%, but numbers are small and results are skewed by both selection and publication bias.

Box 16.4
Criteria for non-operative management of oesophageal perforation

  • Perforation contained by mediastinal pleura

  • No solid food contamination of mediastinal or pleural spaces

  • Drainage of contrast back into the oesophagus on contrast swallow

  • No symptoms or signs of mediastinitis

  • Perforation through an oesophageal malignancy

  • Tolerance to pleural or mediastinal contamination with appropriate drainage

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. This is pertinent in patients where the benefits of surgical exploration are outweighed by the risk and the ultimate outcome (in advanced or perforated cancer, for instance), 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. The mediastinitis, cardiorespiratory compromise, and sepsis accounts for mortality in these patients and not the actual underlying defect. Any endoluminal therapy should not be viewed as the sole definitive solution: ongoing active management is required. In many situations where endoluminal stents or clips have been used, it is apparent that the perforation would have healed with the above non-operative measures and without the endoluminal adjunct. This has to be borne in mind, especially when stents themselves can cause significant complications, including erosion and bleeding.

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