Spontaneous rupture of esophagus - Boerhaave syndrome

Spontaneous rupture of esophagus - Boerhaave syndrome

    * Introduction
    * Signs and symptoms
    * Diagnosis
    * Treatment
Boerhaave described the spontaneous rupture of the esophagus in 1724. This usually occurs after prolonged and forced emesis. Boerhaave syndrome is transmural perforation of the esophagus. It is different from Mallory-Weiss syndrome, which involves the formation of cracks and ulcers nontransmurale also associated with emesis. Boerhaave syndrome is not spontaneous but the term really help to distinguish it from iatrogenic perforation with over 85-90% of cases of esophageal rupture.
Boerhaave syndrome diagnosis can be difficult because symptoms are usually not present classical and late presentation is common for doctors. Approximately one third of all cases of Boerhaave syndrome are clinically atypical. Early recognition of these potentially fatal conditions is vital to ensure appropriate treatment. Mediastinitis, shock and sepsis are frequently observed in late stages of the disease.
Boerhaave syndrome classic clinical picture usually consists of repeated episodes of vomiting and nausea in people of middle age with the recent change in diet or recent use of alcohol. Atypical clinical presentations prompt diagnosis and appropriate intervention is delayed, with increased mortality and morbidity.
Conservative therapy combined with surgical interventions. It is administered intravenous fluids, broad spectrum antibiotics. Surgery is the standard in most cases. Most doctors indicated surgery in the first 24 hours after rupture. Direct Repair of the rupture and drainage of the mediastinum and right pleural cavity are methods with the best survival rates. Alternatives to primary repair of esophageal esophagus include creating a diversion by using a bowel segment with timing of surgery.
Esophageal rupture can lead to the development of sepsis, pneumomediastinitei, mediastinitei, epansamentelor massive effusion, empyema, or subcutaneous emphysema. Other complications include acute respiratory distress, hydrothorax, pneumothorax. Boerhaave syndrome is rare number 15% of all cases of esophageal rupture. Iatrogenic causes include more than 50-75% of esophageal perforations. Actual incidence depends on the procedure, having a rigid endoscopy perforation rate of 0. 1-0. 4%, while flexible endoscopy 0. 01-0. 06%.
The prognosis is directly related to rapid recognition and appropriate intervention by reconstructive surgery. Boerhaave syndrome diagnosis in the first 24 hours after the rupture has a survival rate of 75%, this drops to 50% if diagnosis is delayed by 24 hours and 10% after 48 hours. Cases of patients who survived without surgery are rare. Mortality is estimated at 30% and is due to secondary infection, mediastinitei, pneumonitis, pericarditis and empyema.
Pathogenesis and causes.
Esophageal rupture in Boerhaave syndrome is thought to be the result of sudden increase in intraluminal esophageal pressure caused by vomiting rrpetate as a result of neuromuscular incoordonarii cricofaringian failure and muscle relaxation. Syndrome is associated with excessive consumption of food or alcohol. The most common anatomical location is the lower third of the posterolateral wall of the esophagus, 2-3 cm proximal to the gastroesophageal junction along the longitudinal wall of the esophagus. The second most common location of rupture is subdiafragmatica area or upper chest.
The esophagus is more vulnerable than the rest of the digestive tract that gives serous lack stability by elastin and collagen fibers. Perforation may follow several mechanisms, including direct puncture of separation along the longitudinal axis, centrifugal forces breaking through necrosis and perforation of the esophageal wall.
Causes and risk factors. Represents an acute injury barogenica by increasing intraluminal pressure against a closed cricofaringian muscle. Perforation typically occurs at the weakest point of the esophagus. Usually subdiafragmatic lower esophagus in adults and in younger patients the right pleural cavity. Alcoholism and hearty meals are the main risk factors. Both can lead to vomiting, which are a major component of the classical presentation. There is no evidence of a genetic predilection.