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Diverticula of the esophageal body are protrusions or outpouchings of the esophageal lumen. They are usually classified according to their anatomical relationship with the esophagus and/or mechanism of formation: diverticula originating close to the middle third of the esophagus, 4 to 5 cm from the carina, are defined as midthoracic or parabronchial diverticula; diverticula close to the diaphragm are named epiphrenic diverticula. Midthoracic diverticula have been seen as the consequence of chronic inflammatory processes starting from the mediastinal lymph nodes (usually from granulomatous disease, as in tuberculosis) and involving the esophageal wall; they have also been called traction diverticula, according to Rokitansky. An abnormal esophageal motility, generating high intraluminal pressures in short segments of the gullet, with or without esophageal wall weakness, can lead to mucosal herniation and the development of pulsion diverticula.

Paraesophageal hernias represent approximately 5% of all hiatal hernias. The vast majority of hiatal hernias are type I, or sliding, hiatal hernias, which are characterized by a gastroesophageal junction that migrates through the hiatus. Paraesophageal hernias are commonly classified as type II or type III hiatal hernias. Type II hiatal hernias are true paraesophageal hernias in which the gastroesophageal junction maintains its normal anatomical position, whereas the fundus (and/or another organ) migrates through the hiatus. Type III, or mixed, hiatal hernias represent a combination of types I and II, in which the gastroesophageal junction and the fundus (and/or another organ) both herniate through the hiatal defect.

Hiatal hernias are a common finding in patients undergoing imaging procedures for various abdominal and thoracic complaints. Most hiatal hernias do not cause symptoms per se. Hiatal hernias are categorized as type I to IV, with type I or sliding hernias being the most common type. Type II or true paraesophageal hernias are defined as having the gastroesophageal junction below the diaphragm in a normal anatomic position. Type II hernias are quite rare. In their review of 46,236 patients with hiatal hernia seen at the Mayo Clinic between 19 80 and 1990, Allen and colleagues found only 51 patients with type II hernia defects.

Diaphragmatic eventration is an anomaly defined by the long-lasting or permanent elevation of an entire hemidiaphragm or a portion of it, without defects. The muscular insertions are normal, the normal apertures are sealed, and there is no interruption in pleural or peritoneal layer. These characteristics allow distinction from diaphragmatic hernias. By contrast, the terms eventration and paralysis are often confused: paralysis may be the cause of an abnormal elevation of the diaphragm, whereas pure eventration is not associated with paralysis. A marked decrease in muscular fibers is a characteristic of eventration, whereas in paralysis the diaphragm is still muscular, even if somewhat atrophic. True eventration would be, in the opinion of most authors, the consequence of a congenital defect of one portion or the entire central part of the diaphragm, resulting from an incomplete migration of cervical somites into the pleuro-peritoneal membrane.

Symptoms of unilateral diaphragmatic paralysis can range from sleep-related symptoms to exert ional dyspnea or orthopnea. At times unilateral diaphragm paralysis is found on routine chest radiograph alone when an elevated hemidiaphragm is seen. Ventilatory failure will usually only result if there is bilateral diaphragmatic involvement. When diaphragmatic paralysis is suspected, confirmatory testing is done by inspiratory fluoroscopy (sniff test) and electromyography of the phrenic nerve. To determine if the conduction path of the phrenic nerve is intact from the cervical region to the diaphragm, the key test is fluoroscopic visualization of the diaphragm with transcutaneous stimulation of the phrenic nerve in the neck. If the diaphragm moves during stimulation then the phrenic nerve is intact, but there is a disruption of the signal pathway from the respiratory center in the brain to the phrenic nerve causing the diaphragm not to function.

Since the advent of laparoscopic anti-reflux surgery (LARS) in 1991, this approach rapidly became more acceptable not only for surgeons but also for the medical community. As a consequence the number of referrals for surgery increased considerably. Numerous reports in the literature have shown that minimally invasive surgery for reflux disease offers excellent results in 85% to 95% of patients, with short hospital stay, decreased postoperative discomfort, and early return to regular activities. Over the years the increasing experience gathered with this procedure has made the technique available even for the most technically challenging operations, such as large hiatal hernias. Despite the encouraging low morbidity and mortality rates, the reported rates of anatomical failure have been from 12% to 42%.

Acute traumatic diaphragmatic rupture is diagnosed in 0.8% to 7% of patients following blunt trauma and in as many as 15% of patients following penetrating trauma. However, unrecognized diaphragmatic injuries following laparotomy have also been documented; therefore the actual incidence may be higher than previously reported. Whether to use an abdominal or thoracic exposure to repair the diaphragmatic injury has been debated for years with preference usually for the body cavity containing the most severely injured associated organs. This chapter will review the current literature on the various techniques to diagnose diaphragmatic injuries as well as the optimal choice of exposure for repair.

Surgery has been the standard treatment for benign tracheal stenosis for decades, as it has shown durable results and low morbidity. However, the low incidence of these lesions, the intrinsic technical difficulty of the surgery, and frequent patient comorbidities lead to significant postoperative complications including anastomotic dehiscence and re-stenoses, make stenting an attractive alternative. Most of the experience with stents comes from the palliation of malignant airway strictures, with an estimated 20% to 30 % of patients with lung cancer developing some degree of airway obstruction during the course of their disease. The incidence of benign airway stenoses is unknown.

The goals of major resection of the trachea or carina for malignant invasion by thyroid or esophageal carcinomas should be the opportunity for cure or for the palliation of symptoms related to these secondary tracheal neoplasms. Due to the differences in the natural history of these two distinct malignant processes, airway resection and reconstruction should usually only be considered for tracheal invasion by adjacent thyroid carcinomas. Major airway resection for locally invasive carcinomas of the esophagus is almost never indicated.

Malignant pleural effusions are frequent sequelae of metastatic cancer. Approximately half of all patients with metastatic cancer will develop a pleural effusion, with lung and breast cancer accounting for 75% of cases. The development of a malignant pleural effusion often leads to symptoms, such as dyspnea and cough, which significantly reduce the quality of life. Unfortunately, most malignant effusions do not respond to systemic therapy, thereby necessitating other forms of treatment when symptomatic. Currently the main options for the palliative treatment of symptomatic malignant pleural effusion include repeated thoracenteses, placement of indwelling pleural catheters, and pleurodesis. Repeated thoracenteses and indwelling pleural catheters are reasonable options for patients with very short life expectancies. Over time, repeated thoracenteses are inconvenient and the patient must tolerate recurrent symptoms as the fluid reaccumulates.