Oesophageal rupture from a pneumatic blast injury: an unusual mechanism of blunt oesophageal trauma

Abstract

Oesophageal perforation is a serious condition associated with significant morbidity and mortality. Clinical suspicion of oesophageal injury in patients sustaining neck or torso trauma is essential as early diagnosis and management are associated with better outcomes. Oesophageal perforation resulting from blunt trauma is uncommon, and traumatic oesophageal perforation following blast injury is exceedingly rare. We present two cases of patients developing oesophageal perforation from this rare mechanism, review basic principles of management, and key learning points.

Background

Oesophageal perforation in the setting of trauma is a rare but serious and potentially life-threatening condition that necessitates early recognition and management.¹ The majority of cases of traumatic oesophageal perforation result from penetrating mechanisms such as gun shots or stab wounds.^2–4 Injury from blunt mechanisms is less common.^5–8 An even rarer mechanism of oesophageal perforation is external pneumatic blast, where a high pressure of compressed air is released into the oesophagus through the victim’s nasopharynx (figure 1). The incidence of this mechanism causing oesophageal perforation is estimated to be ~0.004%–0.01% in case series including patients with oesophageal perforations.^{9 10}

Figure 1.

Illustration of mechanism of pneumatic blast injury causing oesophageal perforation. A closed lower oesophageal sphincter contributes to the pressure building up in the oesophagus, propagating the perforation.

We report two cases of oesophageal perforation following pneumatic blast injury, highlight the importance of early diagnosis, and review key management principles.

Case 1

A previously healthy man in his mid-20s was working with air-conditioning piping when a compressed air canister exploded near his face. He was alert and oriented at the scene, but developed rapidly worsening facial and cervical swelling. On assessment at a local hospital, he had extensive subcutaneous emphysema and was intubated for concern of impending airway compromise. A right-sided chest tube was inserted for a large pneumothorax. He underwent CT scans that demonstrated bilateral pneumothoraces, pneumomediastinum and pneumopericardium. A bronchoscopy to rule out a tracheobronchial injury was negative. An upper endoscopy identified two lacerations in the thoracic oesophagus, and at this point he was transferred to a tertiary care centre for further management.

On examination, he was haemodynamically stable and was sedated and mechanically ventilated. His abdomen was soft and non-distended. Pelvis was stable. Focused Assessment with Sonography for Trauma (FAST) was positive for intra-abdominal fluid but there was no evidence of pericardial fluid. There was no evidence of burn injuries to the face, eyes or neck, and no identified injuries to the extremities. He had a right-sided chest tube in place.

A chest X-ray revealed evidence of bilateral hydropneumothoraces. A CT scan of the chest, abdomen and pelvis was performed. In the abdomen, there was evidence of pneumoperitoneum and small volume of abdominal free fluid of unclear origin. In the chest, there was a moderate left-sided haemothorax with bilateral pneumothoraces as well as significant pneumomediastinum and evidence of free fluid within the mediastinum (figure 2A).

Figure 2.

(A, B) Chest CT in axial view for first and second patient (respectively) showing subcutaneous emphysema (red arrow), bilateral pneumathoraces (blue arrows) and pneumomediastinum (green arrow). (C) Coronal view of CT of second patient showing pneumoperitoneum around gastro-oesophageal junction (yellow arrows).

A left-sided chest tube was inserted, which returned approximately 700 mL of bloody fluid. A central venous catheter was placed and he received intravenous antibiotics. He was transferred to the operating room in conjunction with the thoracic surgery service for urgent repair of his oesophageal perforation.

In the operating room, the upper endoscopy was repeated and this demonstrated a left-sided 10 cm long full-thickness oesophageal tear (figure 3A). A right-sided postero-lateral thoracotomy was made, and after a washout, a two-layer repair of the ruptured oesophagus was performed (figure 3B), covered by an intercostal muscle buttress over the repair (figure 3C). An intraoperative pneumatic leak test was performed with a gastroscope, which was negative. Following this, he underwent a laparotomy that ruled out a hollow-viscous injury, and a feeding jejunostomy was created.

Figure 3.

Intraoperative pictures of surgical repair of full-thickness oesophageal perforation. (A) Full-thickness tear evident, nasogastric tube (green arrow) seen travelling in oesophageal lumen, intercostal muscle buttress seen prepared away from site of perforation for use at end of repair (red arrow). (B) Two-layer sutured repair. (C) Intercostal muscle buttress (red arrow) over repair.

Postoperatively, he recovered in the intensive care unit and then on the ward. His only major issue was a loculated fluid collection in the left pleural cavity that was drained with tube thoracostomy and tissue plasminogen activator. An oral contrast oesophagram performed 1 week postoperatively demonstrated no leak, and he began tolerating an oral diet. He was discharged home in stable condition 17 days after admission.

Case 2

A previously healthy man in his 20s was adjusting a pressurised air canister on a truck when it accidentally released its pressurised contents onto his face, neck and chest. He had no reported loss of consciousness at the scene and was haemodynamically stable at the local hospital he was initially taken to. He had findings of subcutaneous emphysema but no visible injuries otherwise. A chest X-ray at the referring hospital revealed bilateral pneumothoraces, and he had bilateral chest tubes placed. Given the severe mechanism of his trauma, he was transferred to a tertiary care centre for complete assessment.

On arrival to the trauma bay, he had a patent and protected airway and was in no respiratory distress. His blood pressure was normal but he was mildly tachycardic at 105–110 bpm. His oxygen saturation was normal on 2 L of oxygen. A FAST was negative for abdominal free fluid. He had mild diffuse crepitus over his chest wall, neck and face. There was no evidence of bruising or burn injuries on his skin, and no extremity injuries.

A chest X-ray in the trauma bay found that the pneumothoraces had resolved. He had a CT scan of the chest, abdomen and pelvis that demonstrated bilateral pneumothoraces and trace pleural effusions, as well as pneumomediastinum and trace pleural dehiscence (figure 2B, C). There was evidence of mild gas tracking along the oesophagus down to the gastro-oesophageal junction, but otherwise there were no acute abdominal or pelvic abnormalities.

Over the next 48 hours following his admission, he developed persistent tachycardia and ongoing air leaks from his chest tubes. He was transferred to the intensive care unit and a CT scan with oral contrast was attempted to identify an oesophageal perforation. The patient was unable to tolerate the oral contrast or the prone positioning for the CT, so the scan provided minimal additional information. At this time, he became increasingly tachypneic and tachycardic and was intubated for ventilatory support. An urgent upper endoscopy was performed and found evidence of a full-thickness oesophageal perforation in the mid-oesophagus. The patient was then taken to the operating room in conjunction with the thoracic surgery service for exploration.

The patient underwent a postero-lateral right-sided thoracotomy and lung decortication that allowed the identification of two distinct 5 cm long tears on the right and left sides of the mid-oesophagus. These were both repaired primarily in two layers from the right side. In addition, a laparotomy for feeding jejunostomy creation was performed. Given concerns for inability to tolerate single-lung ventilation for an extended period of time, a left-sided thoracotomy for decortication and washout was deferred.

Postoperatively, the patient remained intubated and was transferred to the intensive care unit. Two days later, he developed Staphylococcus aureus bacteremia and persistent sepsis. Leak from the oesophageal repair was suspected, and the patient was taken back to the operating room for a left-sided thoracotomy and decortication. The leak was confirmed intraoperatively and on endoscopy. After formal decortication was performed, two overlapping oesophageal stents were placed to cover the repaired perforation sites for concerns of poor tissue healing. He had a tracheostomy for prolonged ventilatory needs, but following this began to improve and he was transferred out of the intensive care unit. He had bilateral empyema tubes that were slowly retracted then removed, and his oesophageal stents were removed approximately 80 days after his initial operation. A barium swallow demonstrated no leakage from his oesophagus, and he was discharged home in stable condition approximately 10 weeks following his initial admission date. He was on an oral diet but had some issues with dysphagia for which he required ongoing nutritional supplementation via his jejunostomy tube.

Outcomes and follow-up

In both cases, the patients had positive outcomes and were able to resume normal life functions. The patient in case 1 was seen in follow-up clinic twice in the 8 weeks following his operation and was doing well. His feeding tube was removed and he had no issues returning to his normal life. The patient in case 2 was discharged home with supplemental jejunostomy feeds, but his feeding tube was removed approximately 6 weeks after discharge when his dysphagia resolved. He also developed a superficial wound infection at the site of his right thoracotomy incision, and this was managed with a negative pressure dressing and wound care.

Discussion

Oesophageal perforation is a serious and potentially life-threatening condition. Mechanisms of oesophageal injury vary, with the most common being iatrogenic due to oesophageal instrumentation, followed by spontaneous rupture and Boerhaave’s syndrome, foreign body ingestion and penetrating trauma.^{11 12} External blunt trauma causing oesophageal perforation is rare, and traumatic oesophageal perforation resulting from high pressure and rapid decompression of compressed air into a victim’s mouth is exceedingly rare. Only case reports of this mechanism are available in the literature,9 10 13–20 with the estimated incidence of pneumatic blast trauma as the cause of oesophageal rupture being <0.01%.¹⁸

Mortality following oesophageal perforation ranges from 10% to 20%,²¹ and delays in treatment have been associated with worse outcomes.²² Delays in diagnosis of oesophageal perforation can occur as the signs and symptoms in the early stages of oesophageal injury can be non-specific.² Because of this, a high degree of suspicion for potential oesophageal injury is necessary in the evaluation of patients following high-energy trauma to neck and/or torso. The most common presenting symptoms are pain, fever, dyspnoea and subcutaneous emphysema.²³ Cervical oesophageal injuries are associated with neck ache and stiffness, while perforations of the thoracic oesophagus have a higher likelihood of contamination of surrounding mediastinal spaces leading to sharp retrosternal pain and tachycardia.² External blunt trauma is more likely to cause injury to the thoracic oesophagus.²⁴

Diagnosis of oesophageal perforation is heavily influenced by radiographic imaging. Cervical oesophageal injuries may be visualised on lateral neck X-rays,² but thoracic oesophageal injuries caused by blunt trauma are better visualised with chest X-rays or CT scans. Chest X-rays may be normal initially, but within a few hours after the onset of injury can demonstrate pneumomediastinum, pleural effusion and hydropneumothorax.^{2 25} Chest CT scans are more sensitive and can demonstrate pneumomediastinum, extra-luminal air, pleural effusions and air-fluid collections near the oesophagus.² Oral contrast studies can be useful in diagnosing suspected oesophageal perforation, but there is a high false-negative rate, up to 10%.²⁶ In case of a negative contrast study, if clinical suspicion remains high the study can be repeated a few hours later.²

Endoscopy as a diagnostic modality for oesophageal perforation is controversial. While it has high sensitivity and specificity of identifying oesophageal perforation,²⁷ it has the potential of converting a small mucosal or submucosal tear into a large perforation due to pneumatic insufflation.² As such, it is useful in resolving diagnostic uncertainty in a clinically unwell patient,²¹ as it can visualise and localise the perforation with plans for more definite management to follow.

Once diagnosed and localised, the basic principles of management of oesophageal perforation are haemodynamic resuscitation, broad-spectrum antimicrobial coverage, source control of leaked contents, primary repair of the oesophageal defect when possible and maintaining adequate nutrition. Non-operative management may be considered in cases of contained perforation in stable patients with minimal mediastinal contamination,2 13 19 24 but surgical therapy is necessary for definitive management in the majority of patients. Operative intervention was the mainstay of treatment in the majority of the case reports reviewed.9 10 15 17–20 Conservative management was successful in cases where the perforation was contained and appeared to have sealed spontaneously, likely due to the small size of the oesophageal defect and lack of extensive mediastinal contamination.^{13 14 16}

The technical details of surgical intervention are beyond the scope of this review, but the basic principles are ensuring adequate mediastinal washout and primarily repairing the perforation when possible, with a pedicled intercostal muscle flap can be sewn over the oesophageal repair to buttress the repair.²⁸ Consideration can also be given to diversion and delayed reconstruction options in cases of extensive contamination.² Ongoing leakage beyond the primary repair can be addressed with endoscopically placed oesophageal covered stents, in conjunction with thoracoscopic decortication.²⁸

Our two cases demonstrate the diagnostic uncertainty of early oesophageal perforation from the rare mechanism of blunt pneumatic injury, as well as the importance of early recognition and management of traumatic oesophageal perforation. Both cases shared the same traumatic mechanism, had comparable imaging findings and had similar extent of oesophageal injury. The patient in the first case had a more dramatic presentation with extensive subcutaneous emphysema that led to early endoscopy and diagnosis of the oesophageal defect, while the patient in the second case had less specific signs and symptoms and was diagnosed later. This delay in diagnosis likely contributed to his longer and more complicated postoperative course due to the sepsis and bacterial contamination from the leak. In both cases, the management principles of contamination control and sepsis management were followed. Operative repair was required in both cases, and despite the differences in their time to diagnosis and postoperative courses, both ultimately had a positive outcome following a potentially life-threatening injury. These two cases highlight the point that unexplained traumatic subcutaneous emphysema and pneumomediastinum warrants work-up to rule out airway and/or oesophageal injury.

Learning points.

• Oesophageal perforation is a serious and potentially life-threatening condition that necessitates early diagnosis and management.

• Blunt trauma from pneumatic decompression of compressed air is a rare mechanism of trauma, and oesophageal injury must be suspected in the setting of such trauma to the face, neck or torso.

• Unexplained traumatic subcutaneous emphysema and pneumomediastinum warrant work-up to rule out airway and/or oesophageal injury.

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