Esophageal perforation constitutes a surgical emergency. Despite its gravity, no single strategy has been described as sufficient to deal with most situations to date. The aim of this study was to assess the etiology, management, and outcome of esophageal perforation over a 28-year period, to characterize optimal treatment options in this severe disease. A retrospective clinical review of all patients treated for esophageal perforation at Ramón y Cajal Hospital between January 1987 and December 2015 was performed (n = 57). Iatrogenic injury was the most frequent cause of esophageal perforation (n = 32). Abdominal esophagus was the main location (23 patients; 40.4%). Eight patients (14%) were managed with antibiotics and parenteral nutrition. In seven patients (12.3%), an endoscopic stent was implanted. Surgical therapy was performed in 38 patients (66.7%). Morbidity and 90-day mortality rates were 61.4 and 28 per cent, respectively. Five patients were reoperated (8.8%). Median hospital stay was 23.5 days. The mortality rate was higher among patients with spontaneous and tumoral perforation (54.5 and 100%; P = 0.009), delayed diagnosis (>24 hours; P = 0.0001), and abdominal/thoracic location (37.5%; P = 0.05). No statistical differences were found between surgical and conservative/endoscopic management (31% vs 20%; P = 0.205) although hospital staying was longer in surgical group (36.30 days vs 15.63 days; P = 0.029). Esophageal perforation was associated with high morbidity and mortality rates. Global outcomes depend on etiology, site of perforation, and delay in diagnosis. An individualized approach for each patient should be chosen to prevent septic complications of this potentially fatal disease.

This study evaluates the contact system, coagulation inhibitors and fibrinolysis in 23 full-term newborns with sepsis (8 with septic shock). The results were compared with a group of 20 healthy newborns. Blood samples were obtained at the time of clinical diagnosis and 3 days after the antibiotic therapy was started. The results showed that: severe infection was associated with activation of the contact system, depletion of anticoagulant proteins and elevation of C4b-binding protein levels. There was a shift in protein S to the complexed inactive form, and the thrombin-antithrombin complexes increased. These changes occurred in parallel to both activation and inhibition of fibrinolysis. These changes were more pronounced in the septic shock patients than in nonshock neonates. After therapy, this procoagulant state decreased among survivor patients while in those who died, the abnormalities in coagulation did not improve. Our study suggests that neonatal sepsis induces a hypercoagulable state that persists in nonsurvivor neonates despite a correct treatment.

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Tc-99m-antigranulocyte monoclonal antibody fragment Fab'2 scintigraphy seems to be a useful method in the diagnosis of osteoarticular infection.

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