Introduction Oesophageal perforation is a potentially life-threatening clinical situation with a high morbidity Forskolin research buy and a mortality. The clinical symptoms and signs are non-specific.

The relative paucity of experience at any given center makes the diagnosis difficult and often delayed. There are no randomized studies, no class I evidence for diagnostic and management precepts. However, multiple series reported in the literature allow some strong recommendations. Review of literature Oesophageal perforation is slightly more common in males [1–7] in their sixties. Iatrogenic perforation is the most common cause of injury. The incidence is small, less than 0.5%, when all the procedures on the Enzalutamide in vivo oesophagus are considered. Sclerotherapy of oesophageal varices, nasogastric tubes and improperly selleck chemicals placed Sengstaken- Blakemore tubes have been known to produce oesophageal perforation. Oesophageal “stents”, temperature probes, repeated attempts at endotracheal intubation, impacted foreign bodies, both sharp and blunt, may all cause oesophageal injury. Blast injury and spontaneous rupture of the oesophagus are secondary to a sudden rise in intraluminal pressure and occur usually at the lower end

of the oesophagus. Oesophageal trauma has been reported as a complication following anti-reflux procedures, pneumonectomy, truncal vagotomy (an incidence of 0.5%) and rarely, during anterior

cervical spinal fusion Blunt oesophageal injury is exceedingly rare and often is missed. The predominant site of rupture is in the cervical and upper thoracic location (82.3%), and associated tracheooesophageal fistulas were noted in 28 patients in one series. Penetrating objects, usually GSW, injure the oesophagus more commonly than does blunt mechanism. It is not a very frequent injury. In a large multi-center study from the AAST, Asensio [3] collected 405 patients from 34 trauma centers over 10.5 years. Ingestion injury to the oesophagus may occur with caustic liquids [8], especially in children by cleaners, battery liquids and solutions used in industrial operations. Acids cause coagulative tissue necrosis with a lower risk of penetration while alkalis tend to be more palatable and those cause liquefactive necrosis that rapidly becomes transmural. The amount, viscosity and concentration of the agent and the duration of contact between the caustic agent and the oesophageal mucosa determine the depth and extent of the injury. Diagnosis The clinical symptomatology is non-specific early after perforation. Radiologic clues are subtle and may easily be missed. Consequently, delayed diagnosis of oesophageal perforation is extremely frequent. This is especially true in non-endoscopic iatrogenic trauma and after spontaneous perforation.