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Laparoscopic large hiatus hernia repair

ALEX NAGLE, GEOFFREY S. CHOW AND NATHANIEL J. SOPER

INTRODUCTION

The diaphragm is both a muscular and tendinous tissue that begins to bear mechanical pressure from the abdominal viscera during the tenth week of life. Abnormal diaphragmatic development can lead to large congenital diaphragmatic hernias present at birth, while other smaller areas of diaphragmatic weakness can enlarge over time and become apparent later in life. Hiatal hernias result from a widening of the diaphragmatic crura and a weakening of the phrenoesophageal membrane. This results in a protrusion of a hernia sac containing intra-abdominal organs through the diaphragmatic hiatus and into the mediastinum. The prevalence of large hiatal hernias increases with age, suggesting that environmental and tissue-aging factors are involved in the pathophysiology. In addition, there is a positive association between the presence of hiatal and inguinal hernias, suggesting either a genetic predisposition affecting tissue integrity or some other common factor, such as increased intra-abdominal pressure.

A large hiatal hernia can result in a wide range of symptoms and potentially lead to gastric incarceration and strangulation, a life-threatening emergency. For this reason, hernia repair is generally indicated for most patients with symptomatic hernias. The technical aspects of such operations have undergone significant evolution in the last century and laparoscopy is now considered the preferred approach. When compared with laparotomy or thoracotomy, laparoscopy offers reductions in pain, convalescence, hospital length of stay, and morbidity. However, many controversies still remain, including whether to reinforce the crural closure with mesh, how frequently an esophageal lengthening procedure is necessary, and the role of a concomitant antireflux procedure. This chapter will address the work-up and preoperative evaluation of patients with a large hiatal hernia, describe the technical aspects of a laparoscopic repair as we perform it, and review the literature regarding the unresolved debates over optimal technique.

HERNIA CLASSIFICATION

Hiatal hernias are subclassified into four types (see Table 39.1). In a type I hiatal hernia, the esophagogastric junction (EGJ) migrates cephalad to the crura, resulting in a portion of intrathoracic stomach. As the EGJ forms the leadpoint of herniation between the abdomen and mediastinum, type I hiatal hernias are also termed “sliding hernias.” Type I hernias are by far the most common form of hiatal hernia, making up 95% of the total prevalence. Type II, III, and IV hernias are together termed “paraesophageal hernias” (PEHs) and combined account for the remaining 5% of hiatal hernias. Type II anatomy consists of a hernia in which a portion of the stomach (usually the fundus) has migrated through the hiatus and into mediastinum, but with an EGJ that remains below the diaphragm. A true type II hiatal hernia is rare. In a type III hernia, the EGJ is above the diaphragm and a portion of the stomach is additionally present within the chest and alongside the esophagus. Type III hernias are typically caused by a large crural separation, which can result in a large portion, or the entirety, of the stomach lying intrathoracically. For this reason, type III hernias are often referred to as “giant” PEHs. A type III hiatal hernia is the most common type of PEH. Type IV is defined as any hiatal hernia in which an intra-abdominal organ other than the stomach has also migrated through the crura. Common examples are the omentum, small bowel, transverse colon, spleen, and/or pancreas.

PRESENTING SYMPTOMS

Patients with PEHs commonly present with symptoms due to either intermittent obstruction or gastroesophageal reflux. Obstruction is caused by a kinking of the esophagus and/or stomach, and results in episodes of dysphagia, early satiety, regurgitation, nausea, vomiting, and/or chest pain. The anatomic distortion of PEHs often leads to an incompetence of normal EGJ function. This in turn causes gastroesophageal reflux, with its characteristic symptom of intermittent retrosternal heartburn, which is often postprandial and exacerbated when supine. PEHs can also result in erosions of the gastric mucosa, termed “Cameron ulcers.” These ulcers can cause anemia from chronic bleeding and their exact etiology has not been conclusively determined. Friction from repeated passage of the stomach through the hiatus, increased acid exposure from stasis of gastric juices, and ischemia have all been proposed as causal mechanisms. Larger type III and IV hernias can additionally cause respiratory and cardiac impairment via direct compression of the lungs and left atrium of the heart.

The symptoms discussed so far are usually subacute, and patients can suffer for prolonged periods of time while being evaluated, and often incorrectly treated, for more common conditions such as non-hernia-related gastroesophageal reflux, peptic ulcer disease, angina, and biliary colic. This scenario of clinical manifestation is distinct from patients who present acutely with an incarcerated PEH. Acute PEH incarceration is a life-threatening surgical emergency, as it can lead to gastric ischemia and, if not alleviated, necrosis. The classic presenting symptoms and signs of an acute incarceration are together known as “Borchardt’s triad”: chest pain, the urge but inability to vomit, and failure of nasogastric tube passage below the diaphragm. Immediate reduction of the hernia is required to restore blood flow to the stomach, and a laparotomy or thoracotomy is often necessary to achieve this. The remainder of this chapter will address only the evaluation and management of patients with PEH in an elective setting.

INDICATIONS FOR SURGERY

Based on the potential for gastric incarceration, it was a long accepted surgical principle that PEHs should be repaired on an elective basis when discovered, regardless of the patient’s symptoms. This traditional assumption was challenged by a landmark study by Stylopoulos and colleagues in 2002. The authors constructed a Markov Monte Carlo analytic model using pooled outcomes data to estimate quality of life years for patients with asymptomatic PEH treated with either laparoscopic repair or watchful waiting. This analysis showed that watchful waiting resulted in a yearly acute incarceration rate of only 1.1%, and was superior to surgery for 83% of patients. Based on these findings, expectant management is now considered a reasonable option in patients with truly asymptomatic PEH. On the other hand, the presence of any symptoms related to a PEH is considered an indication for laparoscopic repair, as long as the patient is of reasonable operative risk.

PREOPERATIVE EVALUATION

In addition to a thorough history and physical examination, several tests are indicated preoperatively to secure the diagnosis of PEH and help define the anatomy and physiology of the esophagus and stomach. Contrast esophagram, or an “upper GI (gastrointestinal) study,” forms the basis for diagnosis of a PEH and description of its anatomy (see Figure 39.1). The location of the esophagus, EGJ, stomach, and pylorus can all be assessed. This secures the diagnosis and subclassification within hiatal hernia type, and allows the surgeon to approximate the size of the hernia sac and width of the crural defect. The distance between the EGJ and hiatus can also be measured, which, if greater than 5 cm, serves as a predictor that an esophageal lengthening procedure may be required. The use of fluoroscopy to obtain multiple images over time allows for an assessment of esophageal function. Pooling of a contrast column within the esophagus and a delay in contrast transit through the EGJ indicate a functional obstruction as a result of the hernia. Conversely, reflux of contrast material from the stomach back into the esophagus is indicative of an incompetent EGJ, resulting in gastroesophageal reflux.

Upper endoscopy is mandatory in the preoperative evaluation of patients prior to planned PEH repair (refer to Chapter 27, “Endoscopy”). The primary purpose is to rule out a malignancy near the EGJ, which can present with the same obstructive symptoms as a PEH. It is also important to check for the presence of esophagitis or gastritis, Barrett esophagus, Cameron ulcers, and/or peptic ulcer disease.

Although not universally adopted, we routinely perform an esophageal manometry study on patients being evaluated for PEH. This study is often technically difficult to perform in these patients and it is often easiest to place the manometry catheter during endoscopy. Patients with a PEH often have abnormal esophageal motility, and these impairments can improve after surgery. However, in patients with complete aperistalsis on preoperative manometry, or those who have weak peristalsis and dysphagia that cannot be explained by the anatomy seen on esophagram, we will tailor our operation to include a partial, rather than complete 360-degree, fundoplication.

A 24-hour pH monitoring study is not necessary, as the results will not change the need for surgery or alter the surgical approach.

OPERATIVE TECHNIQUE

Patient positioning and set-up

Laparoscopic PEH repair is performed under general anesthesia with endotracheal intubation and full paralysis. Patients are positioned supine with legs abducted. We tuck the right arm and abduct the left arm, and use a vacuum beanbag mattress to support the patient’s sides and perineum. This positioning provides stability when the table is shifted into a steep reverse Trendelenburg position and helps to prevent neuropathy during what may be a lengthy operation. Pneumatic compression stockings and a urinary catheter are placed, and patients receive appropriate antibiotic prophylaxis prior to the initial incision.

Trocar placement

Five trocars are utilized: one for the laparoscope, two for the operating surgeon, one for the assistant, and one for a liver retractor (see Figure 39.2). We begin by placing a 10 mm trocar slightly to the left of midline and superior to the umbilicus, approximately 12-15 cm from the xiphoid process. This is typically done using a Veress technique in patients without prior upper abdominal surgery, but an open Hasson technique may be used as well. Once this trocar is inserted and the abdomen insufflated, a 30or 45-degree laparoscope is inserted and an initial diagnostic laparoscopy is performed. Use of an angled laparoscope during PEH repair is essential so that unobstructed views can be obtained when working in the confined space of the hiatus and mediastinum.

A 5 mm trocar for the liver retractor is then placed just below the right costal margin, approximately 15 cm from the xiphoid. We use a self-retaining retractor to elevate the left lateral segment of the liver and expose the hiatus. A 5 mm port for the assistant’s instrument is then placed in the right upper abdomen, approximately midway between the liver retractor and laparoscope ports. A common alternative is to place the assistant’s trocar in a lateral position below the left costal margin.

The two trocars for the operating surgeon’s instruments are then placed. The positioning of these ports is intended to create a triangulation effect, in which the two instruments enter the operative field at a 30to 60-degree angle from either side of the laparoscopic image. The esophagus enters the abdomen through the hiatus at a right-to-left angle, so the surgeon’s two working trocars are also arranged “off center” toward the patient’s left side. For the surgeon’s right hand, a 10 mm trocar (to accommodate a curved needle) is inserted just inferior to the left costal margin, approximately 10 cm from the xiphoid process. We lastly place the surgeon’s left-hand 5 mm trocar slightly inferior and to the right of the xiphoid process. Depending on the size and anatomy of the liver, this trocar may need to be placed more inferiorly on the abdominal wall. For this reason, once the liver retractor has been secured, we test potential locations for this trocar by first passing a Veress needle through the abdominal wall to ensure that the working instrument will have a clear path to the hiatus.

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