Significant bleeding during surgery is uncommon and usually is easily controlled laparoscopically. It mainly occurs during short gastric division, when mobilizing the fundus of the stomach. Splenic injuries may occur during this dissection, but the need for incidental splenectomy is rare and dropped from 10 % during open surgery to less than 1 % for laparoscopic surgery [14]. This fortunate decrease is probably related to the improved exposure and vision provided by laparoscopy together with the dramatic change in energy instrumentation that allows a more straightforward technique to complete this step of the operation.

Dysphagia is a common side effect of fundoplication. Usually self-limiting, post-operative dysphagia is reported by 10–90 % of patients to varying degrees [15, 16]. Post-operative tightening of the gastroesophageal junction due to edema: with consequent slower emptying is normal due to local edema and esophageal trauma. In fact, dysphagia should probably be considered a normal consequence of the fundoplication, and can typically last up to 6 weeks. It is usually well managed by dietary advice with a soft food diet being mandated by most surgeons for the first month or so. Severe dysphagia with important weight loss or dysphagia during this period should be investigated.

We believe that a water soluble upper X-ray study should be performed in every patient on post-operative day one to confirm the position of the fundoplication and assess the passage of the contrast into the stomach. If the exam shows contrast passing into the stomach, albeit slowly, and a correct sub-diaphragmatic position of the antireflux valve and stomach, a conservative approach can be followed even if the patient has significant dysphagia, and swallowing will usually improve over the ensuing few days (Fig. 17.3). Steroids are often effective for early dysphagia due to edema and can often relieve the obstruction and accelerate recovery. However, if absolutely no contrast passes into the stomach, early endoscopy and/or laparoscopic exploration is recommended to rule out technical flaws; such as too tight a crural repair, too tight or twisted a fundoplication, or too long a valve. In addition, other possible causes of dysphagia such as a malposition or a displacement of the valve (slippage) can only be ruled out by re-exploration.

The choice of early endoscopic dilatation in this setting is controversial. Severe acute dysphagia is not tremendously likely to respond to conservative treatments like dilatation, but it is a well tolerated, a benign intervention, helpful in the identification of the underlying problem, and occasionally works.

Pneumothorax, or more precisely capnothorax, is not to be considered a complication but rather a side effect of a complex mediastinal dissection. During such dissections, it is not unusual to tear one or both pleura when mobilizing the intrathoracic esophagus especially in patients with severe periesophagitis, large hiatal hernia, and previous operations. The consequences are negligible because the CO₂ is easily controlled with positive pressure ventilation and is quickly resorbed. In most patients pneumothorax is asymptomatic and does not compromise patients’ hemodynamic and ventilatory status. Certain patients with poor pulmonary function or hemodynamic problems may represent more problematic management problems. Disciplined cooperation between anesthesiologists and surgeons is needed to ensure proper intra-operative management. PEEP modification can be used to manage the vast majority of cases of pneumothorax [16, 17]. Passage of CO₂ into the pleura after injury is facilitated due to the existence of a pressure gradient; intra-abdominal pressure > intrapleural end-expiratory pressure. Application of PEEP decreases or reverses the gradient which prevents further CO₂ build up. Being highly diffusible, the existing CO₂ in the pleura is rapidly removed by the circulating blood. Also, re-expansion of the lung with PEEP mechanically seals the surgically induced tear in the parietal pleura. An index of suspicion, close clinical observation of airway pressure and end-tidal CO₂, periodic auscultations of chest, and communication with the surgeon are needed to detect the rare occurrence of a tension pneumothorax which is potentially life threatening and needs prompt management with decompression by chest tube insertion or widening the pleural defect laparoscopically. Any attempt to seal a pleural tear should be avoided in order to prevent an iatrogenic tension pneumothorax.