Esophageal Procedures - Clinical Tree

Introduction

Esophageal surgery in adults is associated with a high perioperative morbidity (52%) and mortality (12%). Postoperative complications are mainly pulmonary with an incidence of up to 52%, which significantly reduces the short- and long-term survival of patients. Although patient-specific risk factors (comorbidities, age, gender, nutritional status, etc.) are difficult to influence, perioperative management and medical care research is increasingly focusing on the optimization of procedural risk factors. Minimally invasive surgical techniques with consecutive reduction of both the duration of the operation and the amount of blood loss, are being investigated. Perioperative anesthesiologic management should focus on the anesthesia procedure (general anesthesia with or without neuraxial anesthesia), the intraoperative ventilation, and hemodynamic management strategy.

In addition to the anatomic and disease-specific basics, this chapter is intended to provide practical support for the surgical procedure and illustrate concrete recommendations to ensure patient safety.

Core Chapter

Anatomy (and Physiology)

The adult esophagus is a muscular tube, 25 to 28 cm long and approximately 2 cm in diameter, which serves as a duct for the passage of fluid and solid substances from the pharynx to the stomach ( Fig. 44.1 ). Length is affected by age, sex, gender, and physiologic condition. In general, the esophagus is divided into three anatomic parts, the cervical (sixth cervical vertebra to first thoracic vertebra), the thoracic (first to 11th vertebra), and the abdominal esophagus (11th vertebra). The esophagus originates at the cricoid cartilage at the sixth cervical vertebra (C6) where it emerges from the pars laryngea of the pharynx. This is the location of the narrowest point of the esophagus at the upper esophageal sphincter (15–16 cm after maxillary central incisor teeth), at the point of the transition of the hypopharynx to the cervical esophagus. Descending through the superior mediastinum, the esophagus crosses behind the trachea, the aortic arch, a typical narrowing corresponding to the fourth and fifth thoracic vertebrae (23–25 cm after maxillary central incisor teeth), and the left recurrent laryngeal nerve. Subsequently, the esophagus passes the posterior mediastinum behind the tracheal bifurcation where the anatomic relation to the left mainstem bronchus results in a further narrow section (27.5 cm after maxillary central incisor teeth). Continuing caudal passing, the esophagus is located behind the left atrium. In front of the descending thoracic aorta, the esophagus joins the stomach at the level of the 11th thoracic vertebra. Here is the location of the last narrowing, thelower esophageal sphincter (LES, 40 cm after maxillary central incisor teeth), defined by functional aspects rather than an exact anatomic correlate, partly built by the esophageal hiatus in the diaphragm (see Fig. 44.1 ).

The relation of the esophagus with the surrounding structures ( Table. 44.1 ) and its emerging narrowing points result in important pathophysiologic and clinical consequences. Because of the partial coverage of the cervical esophagus by the trachea on the left side, this open margin provides natural surgical access for cervical esophagectomy. However, the relationship of the cervical esophagus to the left recurrent laryngeal nerve, crossing under the aortic arch at the ligamentum arteriosum and ascending in a groove at the junction of the trachea and the esophagus (tracheoesophageal sulcus), leads to the potential risk of harm during surgery. A unilateral injury of this nerve typically results in swallowing difficulties or hoarseness, in contrast a bilateral injury causes complete vocal fold paresis. Stridor, respiratory distress, and aphonia occurs because of the closure of the glottic aperture necessitating immediate intervention.

Table44.1

Relation of the Esophagus to the Surrounding Structures

Relative Position to the Esophagus Related Structures
Anterior	Trachea, aortic arch, right pulmonary artery, left main bronchus, plexus of esophagus, left atrium, anterior vagus nerve
Posterior	Vertebral column, longus coli muscle, posterior intercostal arteries, azygos vein, hemiazygos vein, anterior wall of descending aorta, posterior vagal nerve, thoracic duct, pleura
Left	Aortic arch, left subclavian artery, left inferior laryngeal nerve, left vagus nerve, thoracic ductus, and the thoracic part of aorta, carotid artery
Right	Azygos vein, pleura, right main bronchus, right vagus nerve

The proximity of the upper thoracic esophagus to the thoracic duct endangers this structure during surgical procedures. The proximity of the thoracic esophagus to the heart, especially to the left atrium, allows the anesthetist to examine the heart by the transesophageal echocardiography (TEE), revolutionizing cardiac anesthesia and perioperative hemodynamic management. Also the narrow points of the esophagus represent important landmarks with clinical implications. Typically, they build predilection sites for damage during esophageal instrumentation. For example, the first narrowing in the hypopharynx is the classical zone of esophageal perforation through TEE, a rare but severe complication. The vulnerable areas in the esophagus, beneath the cricoid muscle and on the left side close to the diaphragmatic hiatus, predispose for diverticula (Zenker’s diverticulum or epiphrenic diverticulum) or spontaneous rupture.

The esophagus consists of four histologic layers: mucosa, submucosa, muscularis propria, and adventitia. Because no serosa is found on the esophagus, contrary to the rest of the gastrointestinal tract, infections and tumors can spread easily. The esophageal lumen is covered by nonkeratinized stratified squamous epithelium. The transition between the cells of the esophagus and the simple columnar epithelium in cardia of the stomach is called the line or squamocolumnar junction. A displacement of the squamocolumnar junction into the distal esophagus is a sign of the Barrett esophagus.

The arterial supply of the cervical esophagus is mainly achieved by branches of the inferior thyroid arteries. Blood circulation for the thoracic segments is generated by the bronchial arteries, from esophageal branches of the aorta and right intercostal arteries. The abdominal portion receives blood from the left gastric artery, short gastric arteries, and descending branch of left phrenic artery.

The venous drainage of the esophagus is more variable than the arterial supply. Cervical portions empty into inferior thyroid veins, whereas thoracic segment’s venous drainage empties mainly into the azygos and right brachiocephalic vein. Venous drainage of the abdominal esophagus empties primarily into left gastric veins, additional venous drainage ensues over short gastric veins, splenic vein, and left gastroepiploic vein, all tributary of the portal vein. Therefore lower esophageal veins communicate with caval venous and portal venous systems. Impairment of portal venous blood flow, for instance because of hepatic cirrhosis, could lead to retrograde flow through this shunt system, causing venous dilatation and varices, which may result in fatal bleeding.

Esophageal peristalsis is a complex interplay of straited muscle in the upper third and smooth muscle in the remaining parts of the esophagus, behaving as a single functional unit, producing peristalsis at will (primary peristalsis) in contrast to the intestine. Beside primary peristalsis, local stimulation by distension at any point in the body of the esophagus will elicit peristaltic wave (secondary peristalsis). The neuronal control of esophageal peristalsis takes place in the central nervous system, especially in the brain stem, as well as in local nerves, modified by autonomic reflexes, and sympathetic and parasympathetic systems. In selected procedures like esophageal anastomosis, suppression of secondary peristalsis is needed. Therefore perioperative administration of hyoscine butylbromide is required.

Esophageal sphincters: For adequate function of the esophagus, coordinated activity of the UES and LES is essential. The UES is a high-pressure zone, relaxing in precise intervals, owing to distraction and preventing the passage of air into the stomach. The LES builds a pressure barrier, ranging between 15 and 35 mm Hg, at the gastroesophageal junction, to prevent gastroesophageal reflux. However, accurately timed relaxation during swallowing is crucial for ingestion. Regulation of LES tone and its relaxation is controlled by parasympathetic and sympathetic nerve fibers and modulated by a variety of neurohormonal influences. Furthermore, transient lower esophageal sphincter relaxations (TLESRs) account for physiologic gastroesophageal reflux, provoked by gastric distension. Dysfunction of the LES leads to gastroesophageal reflux or esophageal achalasia, and muscarinic receptor agonists or α-adrenergic agonist could increase LES tone, β-adrenergic agonists, nitric oxide donors, or inhibitors of phosphodiesterase-5 could reduce LES contraction. Opioids and tricyclic antidepressant medications could decrease LES pressure, whereas metoclopramide or metoprolol could increase LES tone.

Esophageal Pathologies andSurgical Therapies

Benign Disease of the Esophagus

Esophageal Diverticula (Pharyngoesophageal Diverticulum, Epiphrenic Diverticulum)

Esophageal diverticula are a rare disease of the esophagus, which is divided into the rarer true diverticula, a protrusion of all layers of the esophageal wall by traction, typically in the middle third of the thoracic esophagus, and the more common false or pseudodiverticula, a bulge without muscular covering, located in muscularly weak regions, such as the hypopharynx (Zenker’s diverticula) or the distal esophagus (epiphrenic diverticula), because of an emulsion caused by increased intraluminal pressure, which causes herniation. The prevalence of esophageal diverticula is between 0.015% and 3%, whereas Zenker’s diverticula is the most common form of esophageal diverticula, accounting for 70%. Genuine diverticula, which are usually caused by mediastinal disease, such as tuberculous lymphadenitis or sarcoidosis, are caused by motility disorders. Zenker’s diverticula in particular are mainly caused by insufficient relaxation of the UES. However, some studies show abnormal esophageal motility even in true esophageal diverticula, although it is unclear whether the motility abnormality is primarily or secondarily resulting from the presence of the diverticulum. Achalasia is also associated with epiphrenic esophageal diverticula followed by diffuse esophageal spasms.

In general, dysphagia, regurgitation of undigested food, bad breath, and a history of silent aspiration with recurrent pneumonia are typical symptoms of esophageal diverticula. However, patients with small diverticula are often asymptomatic until the pouch becomes enlarged. In rare cases, patients with long-lasting dysphagia caused by esophageal diverticula experience weight loss and malnutrition. Large Zenker’s diverticula can lead to a complete obstruction of the esophagus because the retained contents press anteriorly. In addition, patients with Zenker’s diverticula are often associated with hiatal hernia and gastroesophageal reflux disease (GERD; 72%).

The diagnosis is confirmed by radiologic imaging, such as barium esophagography, endoscopy, and esophageal manometry. In addition, transcutaneous sonography may be an alternative method for diagnosing Zenker’s diverticulum in experienced hands.

Despite an improvement in surgical therapy, mortality from esophageal diverticulum surgery is still 1% to 5%. Surgical therapy is usually indicated in patients with esophageal diverticulum, but some authors recommend surgery only in symptomatic patients. The Zenker’s diverticulum could be resected through an open left cervical or transoral access with rigid or flexible endoscopy. Diverticulectomy or diverticulopexy could be performed, including myotomy of the cricopharyngeal muscle to treat UES dysfunction. Diverticula located in the middle of the esophagus require a transthoracic approach. The operation can usually be performed by thoracoscopy or thoracotomy from the left side. An additional myotomy may also be necessary. For diverticula of the lower esophagus, especially epiphrenic diverticula, transabdominal laparoscopic surgery with transhiatal access is recommended. Diverticulectomy and additional myotomy/cardiomyotomy imply the need for antireflux procedures, such as partial fundoplication. In some patients, dilatation of the inferior esophageal sphincter may be an alternative to myotomy and the required antireflux procedure, but the clinical evidence is not conclusive.

Esophageal Fistula (Tracheo- and Bronchoesophageal Fistula) (see Chapter 45 )

A fistula from the airways to the upper gastrointestinal tract bypasses the normal protection provided by intact laryngeal reflexes and could lead to significant morbidity and mortality. There are connections between the esophagus and the trachea or large bronchi, all of which are grouped together as tracheoesophageal fistula (TEF). In adults, most acquired TEFs are associated with malignant diseases, such as esophageal or lung cancer, and surgical procedures, such as esophagectomy, radiotherapy, or chemotherapy. ^, TEFs rarely occur because of benign diseases, such as prolonged endotracheal intubation, dilatation tracheotomy, endoscopic procedures (e.g., endobronchial laser or cryotherapy, esophageal stenting), infectious diseases, or trauma. Particularly in anesthesia and intensive care units (ICUs), injury mechanisms, such as traumatic intubation, suction of the airways, and vascular compression of the tracheal wall, which is caused by prolonged overinflation of the endotracheal cuff leading to ischemia and subsequent ulceration. Most congenital TEFs are typically associated with esophageal atresia (90% with esophageal atresia have an esophageal fistula).

Symptoms when spontaneously breathing include postprandial coughing, recurrent pneumonia, hoarseness, and dysphagia. The Ohno sign, postprandial cough with fluid intake, is pathognomonic. Acquired TEF should be considered in any ventilated patient with recurrent chest infections and recurrent weaning disorders and weight loss.

Radiologic imaging, such as chest x-rays enhanced by barium swallowing, thoracic computed tomography (CT) with oral contrast agent, or magnetic resonance imaging, facilitates the localization of TEFs and the identification of their likely etiology. Bronchoscopy or gastrointestinal endoscopy should be performed to confirm TEFs, whereas oral instillation of methylene blue helps to identify even small TEFs.

The therapy of TEFs depends on the etiology and localization of the fistula. Spontaneous closure of TEFs is rare, and surgical therapy is therefore necessary. In the majority of patients with acquired, nonmalignant TEFs, successful closure could be safely achieved by a single repair of the esophagus and trachea supported by tissue flaps. Surgical access is via a cervical incision or thoracotomy, depending on the location of the TEF. Esophageal stenting is the dominant treatment of TEFs in malignant or critically ill patients with a high perioperative mortality rate. Stenting of the esophagus, trachea, or both (double stenting) may be necessary to achieve closure of the fistula. A congenital fistula, especially in combination with esophageal atresia, usually requires neonatal surgery, which is performed as a thoracotomy or thoracoscopy with comparable complications and a total mortality rate of 3.2%. The outcome in patients with benign TEF who are successfully operated on is usually good; in patients with malignant TEF, the treatment may reduce dysphagia, repeated episodes of pneumonia, and improvement of palliative care.

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