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Surgery_Schwartz. allow precise correlation of the anatomic events, such as opening of the upper esophageal sphincter, with manometric observations, such as sphincter relaxation. Mano-fluorography, although not widely available, is presently the best means available to evaluate complex functional abnormalities.Tests to Detect Increased Exposure to Gastric JuiceTwenty-Four-Hour Ambulatory pH Monitoring. The most direct method of measuring increased esophageal exposure to gas-tric juice is by an indwelling pH electrode, or, more recently, via a radiotelemetric pH monitoring capsule that can be clipped to the esophageal mucosa. The latter consists of an antimony pH elec-trode fitted inside a small, capsule-shaped device accompanied by a battery and electronics that allow 48-hour monitoring and transmission of the pH data via transcutaneous radio telemetry to a waist-mounted data logger. The device can be introduced either transorally or transnasally, and it can be clipped to the esophageal mucosa using


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Surgery_Schwartz. of the pH data via transcutaneous radio telemetry to a waist-mounted data logger. The device can be introduced either transorally or transnasally, and it can be clipped to the esophageal mucosa using endoscopic fastening techniques. It passes sponta-neously within 1 to 2 weeks. Prolonged monitoring of esophageal pH is performed by placing the pH probe or telemetry capsule 5 cm above the manometrically measured upper border of the dis-tal sphincter for 24 hours. It measures the actual time the esopha-geal mucosa is exposed to gastric juice, measures the ability of the esophagus to clear refluxed acid, and correlates esophageal acid exposure with the patient’s symptoms. A 24to 48-hour period is necessary so that measurements can be made over one or two complete circadian cycles. This allows measuring the effect of physiologic activity, such as eating or sleeping, on the reflux of gastric juice into the esophagus (Fig. 25-24).Brunicardi_Ch25_p1009-p1098.indd 102801/03/19 6:03 PM


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Surgery_Schwartz. measuring the effect of physiologic activity, such as eating or sleeping, on the reflux of gastric juice into the esophagus (Fig. 25-24).Brunicardi_Ch25_p1009-p1098.indd 102801/03/19 6:03 PM 1029ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25mpmppH8642mppH8642pH8642sp06:0000:0022:0002:0004:0022:0016:0014:0018:0020:0014:0008:0006:0010:0012:00Figure 25-24. Strip chart display of a 24-hour esophageal pH monitoring study in a patient with increased esophageal acid expo-sure. mp = meal period; sp = supine period. (Reproduced with per-mission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary Tract, 3rd ed. Vol 1. Philadelphia, PA: Elsevier/Saunders; 1991.)BATable 25-2Normal values for esophageal exposure to pH <4 (n = 50)COMPONENTMEANSD95%Total time1.511.364.45Upright time2.342.348.42Supine time0.631.03.45No. of episodes19.0012.7646.90No. >5 min0.841.183.45Longest episode6.747.8519.80SD = standard deviation.Reproduced with permission from Moody FG, Carey LC, Jones RS,


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Surgery_Schwartz. time0.631.03.45No. of episodes19.0012.7646.90No. >5 min0.841.183.45Longest episode6.747.8519.80SD = standard deviation.Reproduced with permission from Moody FG, Carey LC, Jones RS, et al: Surgical Treatment of Digestive Disease. Chicago, IL: Year Book Medical; 1990.Figure 25-23. Esophagograms from a patient with cricopharyngeal achalasia. A. Anteropos-terior film showing retention of the contrast medium at the level of the vallecula and piriform recesses, with no barium passing into the esopha-gus. B. Lateral film, taken opposite the C5–C6 vertebrae, showing posterior indentation of the cricopharyngeus, retention in the hypopharynx, and tracheal aspiration. (Reproduced with per-mission from DeMeester TR, Matthews H: Inter-national Trends in General Thoracic Surgery. Vol 3. Benign Esophageal Disease. St. Louis, Mo: Mosby; 1987.)The 24-hour esophageal pH monitoring should not be con-sidered a test for reflux, but rather a measurement of the esopha-geal exposure to gastric juice. The


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Surgery_Schwartz. Disease. St. Louis, Mo: Mosby; 1987.)The 24-hour esophageal pH monitoring should not be con-sidered a test for reflux, but rather a measurement of the esopha-geal exposure to gastric juice. The measurement is expressed by the time the esophageal pH was below a given threshold during the 24-hour period (Table 25-3). This single assess-ment, although concise, does not reflect how the exposure has occurred; that is, did it occur in a few long episodes or several short episodes? Consequently, two other assessments are neces-sary: the frequency of the reflux episodes and their duration.The units used to express esophageal exposure to gastric juice are: (a) cumulative time the esophageal pH is below a cho-sen threshold, expressed as the percentage of the total, upright, and supine monitored time; (b) frequency of reflux episodes below a chosen threshold, expressed as number of episodes per 24 hours; and (c) duration of the episodes, expressed as the number of episodes >5 minutes per 24


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Surgery_Schwartz. time; (b) frequency of reflux episodes below a chosen threshold, expressed as number of episodes per 24 hours; and (c) duration of the episodes, expressed as the number of episodes >5 minutes per 24 hours, and the time in minutes of the longest episode recorded. Table 25-2 shows the normal values for these components of the 24-hour record at the whole-number pH threshold derived from 50 normal asymptom-atic subjects. The upper limits of normal were established at the 95th percentile. Most centers use pH 4 as the threshold.Based on these studies and extensive clinical experience, 48-hour esophageal pH monitoring is considered to be the gold standard for the diagnosis of GERD.The Bravo pH Capsule (Medtronics, Minneapolis, MN) measures pH levels in the esophagus and transmits continuous Brunicardi_Ch25_p1009-p1098.indd 102901/03/19 6:03 PM 1030SPECIFIC CONSIDERATIONSPART II210:0012:0014:0016:0018:0047pH218:0020:0022:0000:0002:0047202:0004:0006:0008:0010:0047pH probe5 cmabove5


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Surgery_Schwartz. Brunicardi_Ch25_p1009-p1098.indd 102901/03/19 6:03 PM 1030SPECIFIC CONSIDERATIONSPART II210:0012:0014:0016:0018:0047pH218:0020:0022:0000:0002:0047202:0004:0006:0008:0010:0047pH probe5 cmabove5 cmbelowBACombined 24-hourgastric and esophagealpH monitoringFigure 25-25. A. Combined esophageal and gastric pH monitoring showing position of probes in relation to the lower esophageal sphincter. B. Combined ambulatory esophageal (upper tracing) and gastric (lower tracing) pH monitoring showing duodenogastric reflux (arrows) with propagation of the alkaline juice into the esophagus of a patient with complicated Barrett’s esophagus. The gastric tracing (lower) is taken from a probe lying 5 cm below the upper esophageal sphincter. The esophageal tracing (upper) is taken from a probe lying 5 cm above the lower esophageal sphincter. Note that in only a small proportion of time does duodenogastric reflux move the pH of the esophagus above the threshold of 7, causing the iceberg effect.


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Surgery_Schwartz. 5 cm above the lower esophageal sphincter. Note that in only a small proportion of time does duodenogastric reflux move the pH of the esophagus above the threshold of 7, causing the iceberg effect. (Reproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary Tract, 3rd ed. Vol 1. Philadelphia, PA: Elsevier/Saunders; 1991.)Table 25-3Normal composite score for various pH thresholds: upper level of normal valuepH THRESHOLD95TH PERCENTILE<114.2<217.37<314.10<414.72<515.76<612.76>714.90>88.50Reproduced with permission from Moody FG, Carey LC, Jones RS, et al: Surgical Treatment of Digestive Disease. Chicago, IL: Year Book Medical; 1990.esophageal pH readings to a receiver worn on the patient’s belt or waistband (Fig. 25-25). Symptoms that the patient experi-ences are recorded in a diary and/or by pressing buttons on the receiver unit. Generally, 48 hours of pH data are measured with this probe. A recent study has shown that the addition of a second


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Surgery_Schwartz. are recorded in a diary and/or by pressing buttons on the receiver unit. Generally, 48 hours of pH data are measured with this probe. A recent study has shown that the addition of a second day of pH monitoring increased the sensitivity of pH measurement by 22%. The capsule eventually detaches and passes through the digestive tract in 5 to 7 days.Radiographic Detection of Gastroesophageal Reflux. The definition of radiographic gastroesophageal reflux varies depend-ing on whether reflux is spontaneous or induced by various maneu-vers. In only about 40% of patients with classic symptoms of GERD is spontaneous reflux (i.e., reflux of barium from the stom-ach into the esophagus with the patient in the upright position) observed by the radiologist. In most patients who show spon-taneous reflux on radiography, the diagnosis of increased esophageal acid exposure is confirmed by 24-hour esophageal pH monitoring. Therefore, the radiographic demonstration of sponta-neous regurgitation of barium


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Surgery_Schwartz. on radiography, the diagnosis of increased esophageal acid exposure is confirmed by 24-hour esophageal pH monitoring. Therefore, the radiographic demonstration of sponta-neous regurgitation of barium into the esophagus in the upright position is a reliable indicator that reflux is present. However, fail-ure to see this does not indicate the absence of disease, and for this reason this test is rarely used for clinical diagnosis.Tests of Duodenogastric FunctionEsophageal disorders are frequently associated with abnormali-ties of duodenogastric function. Abnormalities of the gastric res-ervoir or increased gastric acid secretion can be responsible for increased esophageal exposure to gastric juice. Reflux of alka-line duodenal juice, including bile salts, pancreatic enzymes, and bicarbonate, is thought to have a role in the pathogenesis of esophagitis and complicated Barrett’s esophagus. Furthermore, functional disorders of the esophagus are often not confined to


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Surgery_Schwartz. and bicarbonate, is thought to have a role in the pathogenesis of esophagitis and complicated Barrett’s esophagus. Furthermore, functional disorders of the esophagus are often not confined to 2Brunicardi_Ch25_p1009-p1098.indd 103001/03/19 6:03 PM 1031ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25the esophagus alone, but are associated with functional disor-ders of the rest of the foregut (i.e., stomach and duodenum). Tests of duodenogastric function that are helpful to investigate esophageal symptoms include gastric emptying studies, gastric acid analysis, and cholescintigraphy (for the diagnosis of patho-logic duodenogastric and/or duodenogastroesophageal reflux).Gastric Emptying Study. Gastric emptying studies are performed with radionuclide-labeled meals. Emptying of solids and liquids can be assessed simultaneously when both phases are marked with different tracers. After ingestion of a labeled standard meal, gamma camera images of the stomach are obtained at 5to 15-minute


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Surgery_Schwartz. liquids can be assessed simultaneously when both phases are marked with different tracers. After ingestion of a labeled standard meal, gamma camera images of the stomach are obtained at 5to 15-minute inter-vals for 2 to 4 hours. After correction for decay, the counts in the gastric area are plotted as the percentage of total counts at the start of the imaging. The resulting emptying curve can be compared with data obtained in normal volunteers. In general, normal subjects will empty 59% of a meal within 90 minutes. Although delayed gas-tric emptying is often associated with gastroesophageal reflux, in general delayed emptying does not correlate with a poorer clinical outcome after antireflux surgery, and it should not be considered a contraindication to surgical treatment.GASTROESOPHAGEAL REFLUX DISEASEGERD was not recognized as a significant clinical problem until the mid-1930s and was not identified as a precipitating cause for esophagitis until after World War II. In the early 21st


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Surgery_Schwartz. REFLUX DISEASEGERD was not recognized as a significant clinical problem until the mid-1930s and was not identified as a precipitating cause for esophagitis until after World War II. In the early 21st century, it has grown to be a very common problem and now accounts for a majority of esophageal pathology. It is recognized as a chronic disease, and when medical therapy is required, it is often lifelong treatment. Recent efforts at the development of various endoscopic antireflux interventions, although innovative, have not been successful in consistently controlling gastroesophageal reflux. Antireflux surgery is an effective and long-term therapy and is the only treatment that is able to restore the gastroesopha-geal barrier. Despite the common prevalence of GERD, it can be one of the most challenging diagnostic and therapeutic problems in clinical medicine. A contributing factor to this is the lack of a universally accepted definition of the disease.The most simplistic approach is to


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Surgery_Schwartz. challenging diagnostic and therapeutic problems in clinical medicine. A contributing factor to this is the lack of a universally accepted definition of the disease.The most simplistic approach is to define the disease by its symptoms. However, symptoms thought to be indicative of GERD, such as heartburn or acid regurgitation, are very com-mon in the general population and many individuals consider them to be normal and do not seek medical attention. Even when excessive, these symptoms are not specific for gastroesophageal reflux. They can be caused by other diseases such as achalasia, DES, esophageal carcinoma, pyloric stenosis, cholelithiasis, gastritis, gastric or duodenal ulcer, and coronary artery disease.A thorough, structured evaluation of the patient’s symptoms is essential before any therapy, particularly any form of esopha-geal surgery. The presence and severity of both typical symp-toms of heartburn, regurgitation, and dysphagia, and atypical symptoms of cough, hoarseness,


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Surgery_Schwartz. any therapy, particularly any form of esopha-geal surgery. The presence and severity of both typical symp-toms of heartburn, regurgitation, and dysphagia, and atypical symptoms of cough, hoarseness, chest pain, asthma, and aspira-tion should be discussed with the patient in detail. Many of these atypical symptoms may not be esophageal related and hence will not improve and may even worsen with antireflux surgery.Heartburn is generally defined as a substernal burning-type discomfort, beginning in the epigastrium and radiating upward. It is often aggravated by meals, spicy or fatty foods, chocolate, alcohol, and coffee and can be worse in the supine position. It is commonly, although not universally, relieved by antacid or antisecretory medications. Epidemiologic studies have shown that heartburn occurs monthly in as many as 40% Table 25-4American Gastroenterologic Association Gallup poll on nighttime gastroesophageal reflux disease symptoms• 50 million Americans have nighttime


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Surgery_Schwartz. that heartburn occurs monthly in as many as 40% Table 25-4American Gastroenterologic Association Gallup poll on nighttime gastroesophageal reflux disease symptoms• 50 million Americans have nighttime heartburn at least 1/wk• 80% of heartburn sufferers had nocturnal symptoms—65% both day & night• 63% report that it affects their ability to sleep and impacts their work the next day• 72% are on prescription medications• Nearly half (45%) report that current remedies do not relieve all symptomsto 50% of the Western population. The occurrence of heartburn at night and its effect on quality of life have recently been high-lighted by a Gallup poll conducted by the American Gastroen-terologic Society (Table 25-4).Regurgitation, the effortless return of acid or bitter gastric contents into the chest, pharynx, or mouth, is highly suggestive of foregut pathology. It is often particularly severe at night when supine or when bending over and can be secondary to either an incompetent or obstructed


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Surgery_Schwartz. pharynx, or mouth, is highly suggestive of foregut pathology. It is often particularly severe at night when supine or when bending over and can be secondary to either an incompetent or obstructed GEJ. With the latter, as in achalasia, the regurgitant is often bland, as if food was put into a blender. When questioned, most patients can distinguish the two. It is the regurgitation of gastric contents that may result in associated pulmonary symptoms, including cough, hoarseness, asthma, and recurrent pneumonia. Bronchospasm can be precipitated by esophageal acidification and cough by either acid stimulation or distention of the esophagus.Dysphagia, or difficulty swallowing, is a relatively non-specific term but arguably the most specific symptom of foregut disease. It can be a sign of underlying malignancy and should be aggressively investigated until a diagnosis is established. Dyspha-gia refers to the sensation of difficulty in the passage of food from the mouth to the stomach and can


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Surgery_Schwartz. malignancy and should be aggressively investigated until a diagnosis is established. Dyspha-gia refers to the sensation of difficulty in the passage of food from the mouth to the stomach and can be divided into oropharyngeal and esophageal etiologies. Oropharyngeal dysphagia is charac-terized by difficulty transferring food out of the mouth into the esophagus, nasal regurgitation, and/or aspiration. Esophageal dys-phagia refers to the sensation of food sticking in the lower chest or epigastrium. This may or may not be accompanied by pain (ody-nophagia) that will be relieved by the passage of the bolus.Chest pain, although commonly and appropriately attrib-uted to cardiac disease, is frequently secondary to esophageal pathology as well. Nearly 50% of patients with severe chest pain, normal cardiac function, and normal coronary arterio-grams have positive 24-hour pH studies, implicating gastro-esophageal reflux as the underlying etiology. Exercise-induced gastroesophageal reflux is well


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Surgery_Schwartz. cardiac function, and normal coronary arterio-grams have positive 24-hour pH studies, implicating gastro-esophageal reflux as the underlying etiology. Exercise-induced gastroesophageal reflux is well known to occur, and may result in exertional chest pain similar to angina. It can be quite diffi-cult, if not impossible, to distinguish between the two etiologies, particularly on clinical grounds alone. Nevens and colleagues evaluated the ability of experienced cardiologists to differentiate pain of cardiac vs. esophageal origin. Of 248 patients initially seen by cardiologists, 185 were thought to have typical angina, and 63 were thought to have atypical chest pain. Forty-eight (26%) of those thought to have classic angina had normal coro-nary angiograms, and 16 of the 63 with atypical pain had abnor-mal angiogram. Thus, the cardiologists’ clinical impression was wrong 25% of the time. Finally, Pope and associates investi-gated the ultimate diagnosis in 10,689 patients presenting to an


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Surgery_Schwartz. had abnor-mal angiogram. Thus, the cardiologists’ clinical impression was wrong 25% of the time. Finally, Pope and associates investi-gated the ultimate diagnosis in 10,689 patients presenting to an Brunicardi_Ch25_p1009-p1098.indd 103101/03/19 6:03 PM 1032SPECIFIC CONSIDERATIONSPART IITable 25-5Normal manometric values of the distal esophageal sphincter, n = 50PARAMETERMEDIAN VALUE2.5TH PERCENTILE97.5TH PERCENTILEPressure (mmHg)135.827.7Overall length (cm)3.62.15.6Abdominal length (cm)20.94.7emergency department with acute chest pain. Approximately 17% were found to have acute ischemia, 6% had stable angina, 21% had other cardiac causes, and 55% had noncardiac causes. The investigators concluded that the majority of people present-ing to the emergency department with chest pain do not have an underlying cardiac etiology for their symptoms. Chest pain pre-cipitated by meals, occurring at night while supine, nonradiat-ing, responsive to antacid medication, or accompanied by other


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Surgery_Schwartz. have an underlying cardiac etiology for their symptoms. Chest pain pre-cipitated by meals, occurring at night while supine, nonradiat-ing, responsive to antacid medication, or accompanied by other symptoms suggesting esophageal disease such as dysphagia or regurgitation should trigger the thought of possible esophageal origin. Furthermore, the distinction between heartburn and chest pain is also difficult and largely dependent upon the individual patient. One person’s heartburn is another’s chest pain.The precise mechanisms accounting for the generation of symptoms secondary to esophageal pathology remain unclear. Considerable insight has been acquired, however. Investiga-tions into the effect of luminal content, esophageal distention and muscular function, neural pathways, and brain localization have provided a basic understanding of the stimuli responsible for symptom generation. It is also clear that the visceroneural pathways of the foregut are complexly intertwined with that of


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Surgery_Schwartz. have provided a basic understanding of the stimuli responsible for symptom generation. It is also clear that the visceroneural pathways of the foregut are complexly intertwined with that of the tracheobronchial tree and heart. This fact accounts for the common overlap of clinical presentations with diverse disease processes in upper GI, cardiac, and pulmonary systems.The Human Antireflux Mechanism and the Pathophysiology of Gastroesophageal Reflux DiseaseThere is a high-pressure zone located at the esophagogastric junc-tion in humans. Although this is typically referred to as the lower esophageal “sphincter,” there are no distinct anatomical land-marks that define its beginning and end. Architecturally speak-ing, there is a specialized thickening in this region that is made up of the collar sling musculature and the clasp fibers. The collar sling is located on the greater curvature side of the junction, and the clasp fibers are located on the lesser curvature side. These muscles


Surgery_Schwartz

Surgery_Schwartz. collar sling musculature and the clasp fibers. The collar sling is located on the greater curvature side of the junction, and the clasp fibers are located on the lesser curvature side. These muscles remain in tonic opposition until the act of swallowing, whereupon receptive relaxation occurs allowing passage of a food bolus into the stomach. In addition, the LES will also open when the gastric fundus is distended with gas and liquid, thus resulting in an unfolding of the valve and enabling venting of gas (a belch). Whether physiologic or pathologic, the common denominator for most episodes of gastroesophageal reflux is the loss of the high-pressure zone and thus a decrease in the resistance it imparts to the retrograde flow of gastric juice into the esophageal body.The Lower Esophageal Sphincter. As defined by esophageal manometry, there are three characteristics of the LES that work in unison to maintain its barrier function. These characteristics include the resting LES pressure,


Surgery_Schwartz

Surgery_Schwartz. Sphincter. As defined by esophageal manometry, there are three characteristics of the LES that work in unison to maintain its barrier function. These characteristics include the resting LES pressure, its overall length, and the intra-abdominal length that is exposed to the positive pressure environment of the abdomen (Table 25-5). The resistance to gastroesophageal reflux is a function of both the resting LES pressure and length over which this pressure is exerted. Thus, as the sphincter becomes shorter, a higher pressure will be required in order to prevent a given amount of reflux (Fig. 25-26). Much like the neck of a balloon as it is inflated, as the stomach fills and distends, sphincter length decreases. Therefore, if the over-all length of the sphincter is permanently short from repeated distention of the fundus secondary to large volume meals, then with minimal episodes of gastric distention and pressure, there will be insufficient sphincter length for the barrier to remain


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Surgery_Schwartz. repeated distention of the fundus secondary to large volume meals, then with minimal episodes of gastric distention and pressure, there will be insufficient sphincter length for the barrier to remain competent, and reflux will occur.LES length (cm)LES pressure (mmHg)60012CompetentIncompetent345121824Figure 25-26. As the esophageal sphincter becomes shorter, increased pressure is necessary to maintain competence. LES = lower esophageal sphincter.A third characteristic of the LES that impacts its ability to prevent reflux is its position about the diaphragm. It is important that a portion of the total length of the LES be exposed to the effects of an intra-abdominal pressure. That is, during periods of elevated intra-abdominal pressure, the resistance of the barrier would be overcome if pressure were not applied equally to both the LES and stomach simultaneously. Thus, in the presence of a hiatal hernia, the sphincter resides entirely within the chest cavity and cannot respond to an


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Surgery_Schwartz. pressure were not applied equally to both the LES and stomach simultaneously. Thus, in the presence of a hiatal hernia, the sphincter resides entirely within the chest cavity and cannot respond to an increase in intra-abdominal pressure because the pinch valve mechanism is lost and gastro-esophageal reflux is more liable to occur.Therefore, a permanently defective sphincter is defined by one or more of the following characteristics: an LES with a mean resting pressure of less than 6 mmHg, an overall sphincter length of <2 cm, and intra-abdominal sphincter length of <1 cm. Compared to normal subjects without GERD these values are below the 2.5 percentile for each parameter. The most com-mon cause of a defective sphincter is an inadequate abdominal length.Once the sphincter is permanently defective, this condi-tion is irreversible, and although esophageal mucosal injury may be healed with antisecretory medication, reflux will continue to occur. Additionally, the presence of a


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Surgery_Schwartz. defective, this condi-tion is irreversible, and although esophageal mucosal injury may be healed with antisecretory medication, reflux will continue to occur. Additionally, the presence of a defective LES may be associated with reduced esophageal body function and thus decrease clearance times of refluxed material. In addition, the progressive loss of effective esophageal clearance may predis-pose the patient to severe mucosal injury, volume regurgitation, aspiration, and pulmonary injury. Reflux may occur in the face of a normal LES resting pressure. This condition is usually due to a functional problem of gastric emptying or excessive air swallowing. These conditions may lead to gastric disten-tion, increased intra-gastric pressure, a resultant shortening or Brunicardi_Ch25_p1009-p1098.indd 103201/03/19 6:03 PM 1033ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Table 25-6Complications of gastroesophageal reflux disease: 150 consecutive cases with proven gastroesophageal reflux


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Surgery_Schwartz. 103201/03/19 6:03 PM 1033ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Table 25-6Complications of gastroesophageal reflux disease: 150 consecutive cases with proven gastroesophageal reflux disease (24-hour esophageal pH monitoring endoscopy, and motility)COMPLICATIONNO.STRUCTURALLY NORMAL SPHINCTER (%)STRUCTURALLY DEFECTIVE SPHINCTER (%)None595842Erosive esophagitis472377aStricture191189Barrett’s esophagus250100Total150 aGrade more severe with defective cardia.Reproduced with permission from Moody FG, Carey LC, Jones RS, et al: Surgical Treatment of Digestive Disease. Chicago, IL: Year Book Medical; 1990.unfolding of the LES, and subsequent reflux. The mechanism by which gastric distention contributes to LES unfolding pro-vides a mechanical explanation for “transient LES relaxation.” It is thought that with repeated gastric distention secondary to large meal volume or chronic air swallowing, there is repeated unfolding of the LES and subsequent attenuation of the collar sling


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Surgery_Schwartz. It is thought that with repeated gastric distention secondary to large meal volume or chronic air swallowing, there is repeated unfolding of the LES and subsequent attenuation of the collar sling musculature. It is at this point that the physiologic and nor-mal mechanism of gastric venting is replaced with pathologic and severe postprandial reflux disease. In addition, patients with GERD will increase the frequency of swallowing in an effort to neutralize the refluxed acid with their saliva (pH 7.0). This phe-nomenon leads to increased air swallowing and further gastric distention, thus compounding the problem. Therefore, GERD may have its origins in the stomach secondary to gastric disten-tion due to overeating/drinking, air swallowing, or consump-tion of carbonated liquids, and this may be further compounded by the ingestion of fatty meals, which result in delayed gastric emptying.Relationship Between Hiatal Hernia and Gastroesopha-geal Reflux Disease. As the collar sling


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Surgery_Schwartz. this may be further compounded by the ingestion of fatty meals, which result in delayed gastric emptying.Relationship Between Hiatal Hernia and Gastroesopha-geal Reflux Disease. As the collar sling musculature and clasp fibers become attenuated with repeated gastric distention, the esophagogastric junction begins to assume an “upside down funnel” appearance, with progressive opening of the acute angle of His. This in turn may result in attenuation and stretching of the phrenoesophageal ligament, with subsequent enlargement of the hiatal opening and axial herniation. There is a high degree of correlation between reflux threshold and the degree of hiatal herniation (Fig. 25-27).Summary. It is believed that GERD has its origins within the stomach. Distention of the fundus occurs because of overeat-ing and delayed gastric emptying secondary to a high-fat diet. The resultant distention causes “unrolling” of the sphincter by the expanding fundus, and this subsequently exposes the squa-mous


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Surgery_Schwartz. and delayed gastric emptying secondary to a high-fat diet. The resultant distention causes “unrolling” of the sphincter by the expanding fundus, and this subsequently exposes the squa-mous epithelium in the region of the distal LES to gastric juice. Repeated exposure results in inflammation and the development of columnar epithelium at the cardia. This is the initial step of the development of carditis and explains why in early disease esophagitis is mild and commonly limited to the very distal aspect of the esophagus. The patient attempts to compensate for Yield pressure (mmHg)04No hernia< 3 cm hernia3 cm hernia81216202428323640Figure 25-27. Yield pressure of the lower esophageal sphincter decreases as hiatal hernia size increases.this by increased swallowing, allowing the saliva to neutralize the refluxed gastric juice and thus, alleviate the discomfort induced by the reflux event. The increased swallowing results in aeropha-gia, bloating, and belching. This in turn creates a


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Surgery_Schwartz. neutralize the refluxed gastric juice and thus, alleviate the discomfort induced by the reflux event. The increased swallowing results in aeropha-gia, bloating, and belching. This in turn creates a vicious cycle of increased gastric distention and thus further exposure and repeti-tive injury to the distal esophagus. The development of carditis explains the complaint of epigastric pain often experienced by patients with early reflux disease. Additionally, this process can lead to a fibrotic mucosal ring located at the squamocolumnar junction, which is termed a “Schatzki ring” and which may result in dysphagia. This inflammatory process may extend into muscu-laris propria and thus result in a progressive loss in the length and pressure of the LES. This explanation for the pathophysiology of GERD is supported by the observation that severe esophagitis is almost always associated with a defective LES.Complications Associated With Gastroesophageal Reflux DiseaseThe complications of


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Surgery_Schwartz. of GERD is supported by the observation that severe esophagitis is almost always associated with a defective LES.Complications Associated With Gastroesophageal Reflux DiseaseThe complications of gastroesophageal reflux disease may result from the direct injurious effects of gastric fluid on the mucosa, larynx, or respiratory epithelium. Complications due to repetitive reflux are esophagitis, stricture, and BE; repetitive aspiration may lead to progressive pulmonary fibrosis. The severity of the complications is directly related to the prevalence of a structurally defective sphincter (Table 25-6). The observation that a structurally defective sphincter occurs in 42% of patients without complications (most of whom have one or two components failed) suggests that disease may be confined to the sphincter due to compensation by a vigorously contracting esophageal body. Eventually, all three components of the sphincter fail, allowing unrestricted reflux of gastric juice into the esophagus


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Surgery_Schwartz. the sphincter due to compensation by a vigorously contracting esophageal body. Eventually, all three components of the sphincter fail, allowing unrestricted reflux of gastric juice into the esophagus and overwhelming its normal clearance mechanisms. This leads to esophageal mucosal injury with progressive deterioration of esophageal contractility, as is commonly seen in patients with strictures and BE. The loss of esophageal clearance increases the potential for regurgitation into the pharynx with aspiration.Brunicardi_Ch25_p1009-p1098.indd 103301/03/19 6:03 PM 1034SPECIFIC CONSIDERATIONSPART II70Prevalence%Gastric reflux(n = 22)Mixed reflux(n = 31)6050403020100A20151050% TimepH<4BpH4–7pH>7Figure 25-29. A. Prevalence of reflux types in 53 patients with gastroesophageal reflux disease. B. Esophageal luminal pH dur-ing bilirubin exposure. (Reproduced with permission from Kauer WK, Peters JH, DeMeester TR, etal: Mixed reflux of gastric and duodenal juices is more harmful to the


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Surgery_Schwartz. B. Esophageal luminal pH dur-ing bilirubin exposure. (Reproduced with permission from Kauer WK, Peters JH, DeMeester TR, etal: Mixed reflux of gastric and duodenal juices is more harmful to the esophagus than gastric juice alone. The need for surgical therapy re-emphasized, Ann Surg. 1995 Oct;222(4):525-531.)350300250200150100500123pH4567891018:00Time06:00Bile acid conc. umol/l0Figure 25-28. Sample bile acid concentration and esophageal pH plotted against time to obtain detailed profiles; in this case showing both significant bile acid (vertical bars) and acid (linear plot) reflux. (Reproduced with permission from Nehra D, Watt P, Pye JK, et al. Automated oesophageal reflux sampler: a new device used to moni-tor bile acid reflux in patients with gastroesophageal reflux disease, J Med Eng Technol. 1997 Jan-Feb;21(1):1-9.)The potential injurious components that reflux into the esophagus include gastric secretions such as acid and pepsin, as well as biliary and pancreatic secretions that


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Surgery_Schwartz. 1997 Jan-Feb;21(1):1-9.)The potential injurious components that reflux into the esophagus include gastric secretions such as acid and pepsin, as well as biliary and pancreatic secretions that regurgitate from the duodenum into the stomach. There is a considerable body of experimental evidence to indicate that maximal epithelial injury occurs during exposure to bile salts combined with acid and pepsin. These studies have shown that while acid alone does minimal damage to the esophageal mucosa, the combination of acid and pepsin is highly deleterious. Similarly, the reflux of duodenal juice alone does little damage to the mucosa, although the combination of duodenal juice and gastric acid is particu-larly noxious.Complications of gastroesophageal reflux such as esopha-gitis, stricture, and Barrett’s metaplasia occur in the presence of two predisposing factors: a mechanically defective LES and an increased esophageal exposure to fluid containing duodenal content that includes bile and


Surgery_Schwartz

Surgery_Schwartz. Barrett’s metaplasia occur in the presence of two predisposing factors: a mechanically defective LES and an increased esophageal exposure to fluid containing duodenal content that includes bile and pancreatic juice. The duodenal origin of esophageal contents in patients with an increased exposure to a pH >7 has previously been confirmed by esopha-geal aspiration studies (Fig. 25-28). Studies have clarified and expanded these observations by measuring esophageal bilirubin exposure over a 24-hour period as a marker for the presence of duodenal juice. Direct measurement of esophageal bilirubin exposure as a marker for duodenal juice has shown that 58% of patients with GERD have increased esophageal exposure to duodenal juice and that this exposure occurs most commonly when the esophageal pH is between 4 and 7 (Fig. 25-29). These earlier studies have been confirmed by other studies that mea-sure volume reflux using impedance technology (Fig. 25-30).If reflux of gastric juice is allowed to


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Surgery_Schwartz. between 4 and 7 (Fig. 25-29). These earlier studies have been confirmed by other studies that mea-sure volume reflux using impedance technology (Fig. 25-30).If reflux of gastric juice is allowed to persist and sustained or repetitive esophageal injury occurs, two sequelae can result. First, a luminal stricture can develop from submucosal and even-tually intramural fibrosis. Second, the tubular esophagus may become replaced with columnar epithelium. The columnar epi-thelium is resistant to acid and is associated with the alleviation of the complaint of heartburn. This columnar epithelium often becomes intestinalized, identified histologically by the presence 100Prevalence of patients with increased bilirubin806040200Normalsubjectsn = 25No mucosalinjuryn = 16Erosiveesophagitisn = 10Barrett’sesophagusn = 27Figure 25-30. Prevalence of abnormal esophageal bilirubin expo-sure in healthy subjects and in patients with gastroesophageal reflux disease with varied degrees of mucosal injury. (*P


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Surgery_Schwartz. = 27Figure 25-30. Prevalence of abnormal esophageal bilirubin expo-sure in healthy subjects and in patients with gastroesophageal reflux disease with varied degrees of mucosal injury. (*P <.03 vs. all other groups; **P <.03 vs. healthy subjects.) (Reproduced with permis-sion from Kauer WK, Peters JH, DeMeester TR, et al: Mixed reflux of gastric and duodenal juices is more harmful to the esophagus than gastric juice alone. The need for surgical therapy re-emphasized, Ann Surg. 1995 Oct;222(4):525-531.)Brunicardi_Ch25_p1009-p1098.indd 103401/03/19 6:03 PM 1035ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25of goblet cells. This specialized IM is currently required for the diagnosis of BE. Endoscopically, BE can be quiescent or associ-ated with complications of esophagitis, stricture, Barrett’s ulcer-ation, and dysplasia. The complications associated with BE may be due to the continuous irritation from refluxed duodenogastric juice. This continued injury is pH dependent and may be


Surgery_Schwartz

Surgery_Schwartz. Barrett’s ulcer-ation, and dysplasia. The complications associated with BE may be due to the continuous irritation from refluxed duodenogastric juice. This continued injury is pH dependent and may be modi-fied by medical therapy. The incidence of metaplastic Barrett’s epithelium becoming dysplastic and progressing to adenocarci-noma is approximately 0.2% to 0.5% per year.An esophageal stricture can be associated with severe esophagitis or BE. In the latter situation, it occurs at the site of maximal inflammatory injury (i.e., the columnar-squamous epi-thelial interface). Patients who have a stricture in the absence of Barrett’s esophagus should have the presence of gastroesopha-geal reflux documented before the presence of the stricture is ascribed to reflux esophagitis. In patients with normal acid exposure and no endoscopic or CT evidence of cancer, the stric-ture may be a result of a drug-induced chemical injury, the latter resulting from the lodgment of a capsule or tablet in the


Surgery_Schwartz

Surgery_Schwartz. normal acid exposure and no endoscopic or CT evidence of cancer, the stric-ture may be a result of a drug-induced chemical injury, the latter resulting from the lodgment of a capsule or tablet in the distal esophagus. In such patients, dilation usually corrects the prob-lem of dysphagia. It is also possible for drug-induced injuries to occur in patients who have underlying esophagitis and a distal esophageal stricture secondary to gastroesophageal reflux. In this situation, a long, string-like stricture progressively devel-ops as a result of repetitive caustic injury from capsule or tablet lodgment on top of an initial reflux stricture. These strictures are often resistant to dilation. The incidence of this problem has lessened since the introduction of proton pump inhibitor medication.Metaplastic (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) ComplicationsThe condition whereby the tubular esophagus is lined with columnar epithelium rather than squamous epithelium was first


Surgery_Schwartz

Surgery_Schwartz. (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) ComplicationsThe condition whereby the tubular esophagus is lined with columnar epithelium rather than squamous epithelium was first described by Norman Barrett in 1950. He incorrectly believed it to be congenital in origin. It is now realized that it is an acquired abnormality, occurs in 10% to 15% of patients with GERD, and represents the end stage of the natural history of this disease. It is also distinctly different from the congenital condition in which islands of gastric fundic epithelium are found in the upper half of the esophagus.The definition of BE has evolved considerably over the past decade. Traditionally, BE was identified by the presence of columnar mucosa extending at least 3 cm into the esophagus. It is now recognized that the specialized, intestinal-type epi-thelium, or intestinal metaplasia (IM) found in the Barrett’s mucosa, is the only tissue predisposed to malignant degenera-tion. Consequently, the


Surgery_Schwartz

Surgery_Schwartz. recognized that the specialized, intestinal-type epi-thelium, or intestinal metaplasia (IM) found in the Barrett’s mucosa, is the only tissue predisposed to malignant degenera-tion. Consequently, the diagnosis of BE is presently made given any length of endoscopically identifiable columnar mucosa that proves, on biopsy, to show IM. Although long segments of columnar mucosa without IM do occur, they are uncommon and might be congenital in origin.The hallmark of IM is the presence of intestinal goblet cells. There is a high prevalence of biopsy-demonstrated IM at the cardia, on the gastric side of the squamocolumnar junction, in the absence of endoscopic evidence of a CLE. Evidence is accumulating that these patches of what appears to be Barrett’s in the cardia have a similar malignant potential as in the longer segments, and are precursors for carcinoma of the cardia.The long-term relief of symptoms remains the primary rea-son for performing antireflux surgery in patients with BE.


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Surgery_Schwartz. potential as in the longer segments, and are precursors for carcinoma of the cardia.The long-term relief of symptoms remains the primary rea-son for performing antireflux surgery in patients with BE. Heal-ing of esophageal mucosal injury and the prevention of disease progression are important secondary goals. In this regard, patients with BE are no different than the broader population of patients with gastroesophageal reflux. They should be con-sidered for antireflux surgery when patient data suggest severe disease or predict the need for long-term medical management. Most patients with BE are symptomatic. Although it has been argued that some patients with BE may not have symptoms, careful history taking will reveal the presence of symptoms in most, if not all, patients.Patients with BE have a spectrum of disease ranging from visually identifiable but short segments, to long segments of classic BE. In general, however, they represent a relatively severe stage of gastroesophageal


Surgery_Schwartz

Surgery_Schwartz. BE have a spectrum of disease ranging from visually identifiable but short segments, to long segments of classic BE. In general, however, they represent a relatively severe stage of gastroesophageal reflux, usually with markedly increased esophageal acid exposure, deficient LES characteris-tics, poor esophageal body function, and a high prevalence of duodenogastroesophageal reflux. Gastric hypersecretion occurs in 44% of patients. Most will require long-term PPI therapy for relief of symptoms and control of coexistent esophageal muco-sal injury. Given such profound deficits in esophageal physi-ology, antireflux surgery is an excellent means of long-term control of reflux symptoms for most patients with BE.The typical complications in BE include ulceration in the columnar-lined segment, stricture formation, and a dysplasia-cancer sequence. Barrett’s ulceration is unlike the erosive ulceration of reflux esophagitis in that it more closely resem-bles peptic ulceration in the stomach or


Surgery_Schwartz

Surgery_Schwartz. formation, and a dysplasia-cancer sequence. Barrett’s ulceration is unlike the erosive ulceration of reflux esophagitis in that it more closely resem-bles peptic ulceration in the stomach or duodenum, and has the same propensity to bleed, penetrate, or perforate. Fortunately, this complication occurs very rarely. The strictures found in BE occur at the squamocolumnar junction, and they are typically higher than peptic strictures in the absence of BE. Ulceration and stricture in association with BE were commonly reported before 1975, but with the advent of potent acid suppression medication, they have become less common. In contrast, the complication of adenocarcinoma developing in Barrett’s mucosa has become more common. Adenocarcinoma developing in Bar-rett’s mucosa was considered a rare tumor before 1975. Today, it occurs at approximately 0.2% to 0.5% per year of follow-up, which represents a risk 40 times that of the general popula-tion. Most, if not all, cases of adenocarcinoma of


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Surgery_Schwartz. tumor before 1975. Today, it occurs at approximately 0.2% to 0.5% per year of follow-up, which represents a risk 40 times that of the general popula-tion. Most, if not all, cases of adenocarcinoma of the esophagus arise in Barrett’s epithelium (Fig. 25-31). About one-third of all patients with BE present with malignancy.The long-term risk of progression to dysplasia and ade-nocarcinoma, although not the driving force behind the deci-sion to perform antireflux surgery, is a significant concern for both patient and physician. Although to date, there have been no prospective randomized studies documenting that antireflux surgery has an effect on the risk of progression to dysplasia and carcinoma, complete control of reflux of gastric juice into the esophagus is clearly a desirable goal.Respiratory ComplicationsA significant proportion of patients with GERD will have associated respiratory symptoms. These patients may have laryngopharyngeal reflux-type symptoms, adult-onset asthma, or


Surgery_Schwartz

Surgery_Schwartz. ComplicationsA significant proportion of patients with GERD will have associated respiratory symptoms. These patients may have laryngopharyngeal reflux-type symptoms, adult-onset asthma, or even idiopathic pulmonary fibrosis. These symptoms and organ injury may occur in isolation or in conjunction with typi-cal reflux symptoms such as heartburn and regurgitation. Sev-eral studies have demonstrated that up to 50% of patients with asthma have either endoscopically evident esophagitis or abnor-mal distal esophageal acid exposure. These findings support a causal relationship between GERD and aerodigestive symptoms and complications in a proportion of patients.3Brunicardi_Ch25_p1009-p1098.indd 103501/03/19 6:03 PM 1036SPECIFIC CONSIDERATIONSPART IIABFigure 25-31. Photomicrographs. A. Barrett’s epithelium with severe dysplasia. (×200.) Note nuclear irregularity, stratification, and loss of polarity. B. Barrett’s epithelium with intramucosal carcinoma. (×66.) Note malignant cells in the


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Surgery_Schwartz. epithelium with severe dysplasia. (×200.) Note nuclear irregularity, stratification, and loss of polarity. B. Barrett’s epithelium with intramucosal carcinoma. (×66.) Note malignant cells in the mucosa (upper arrow), but not invading the muscularis mucosae (bottom arrow). (Reproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary Tract, 3rd ed. Vol 1. Philadelphia, PA: Elsevier/Saunders; 1991.)Etiology of Reflux-Induced Respiratory Symptoms. There are two mechanisms that have been proposed as the cause of reflux-induced respiratory symptoms. The reflux theory sug-gests that these symptoms are the direct result of laryngopha-ryngeal exposure and aspiration of gastric contents. The reflex theory suggests that the vagal-mediated afferent fibers result in bronchoconstriction during episodes of distal esophageal acidification. The evidence supporting a mechanism of direct exposure to the aerodigestive system is based in clinical studies that have


Surgery_Schwartz

Surgery_Schwartz. in bronchoconstriction during episodes of distal esophageal acidification. The evidence supporting a mechanism of direct exposure to the aerodigestive system is based in clinical studies that have documented a strong correlation between idiopathic pulmonary fibrosis and hiatal hernia. In addition, the presence of GERD was demonstrated to be highly associated with several pulmonary diseases in a recent Department of Veteran Affairs multivariate analysis. Next, with ambulatory pH testing, acid exposure within the proximal esophagus is more frequently identified in patients with gastroesophageal reflux and respi-ratory symptoms than in patients who have gastroesophageal reflux symptoms alone. These findings are supported by scinti-graphic studies, which have demonstrated aspiration of ingested radioisotope in patients with both gastroesophageal reflux and pulmonary symptoms. In animal studies, tracheal instillation of acid has been demonstrated to profoundly increase airway resis-tance.


Surgery_Schwartz

Surgery_Schwartz. radioisotope in patients with both gastroesophageal reflux and pulmonary symptoms. In animal studies, tracheal instillation of acid has been demonstrated to profoundly increase airway resis-tance. Finally, in patients who have undergone multichannel intraluminal impedance testing with a catheter configured to detect laryngopharyngeal reflux, a correlation between proxi-mal fluid movement and laryngopharyngeal symptoms, such as cough, can be demonstrated.The reflex mechanism is supported by the bronchocon-striction that occurs with the infusion of acid into the distal esophagus. There is a shared embryologic origin of the tracheo-esophageal tract and vagus nerve, and this reflex is thought to be an afferent fiber–mediated reflex that protects the aerodigestive system from the aspiration of refluxate. In patients with respira-tory symptoms and documented gastroesophageal reflux with-out proximal esophageal acid exposure, pulmonary symptoms will often times significantly improve or


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Surgery_Schwartz. of refluxate. In patients with respira-tory symptoms and documented gastroesophageal reflux with-out proximal esophageal acid exposure, pulmonary symptoms will often times significantly improve or completely resolve after undergoing laparoscopic fundoplication. It is likely that both of the proposed mechanisms work simultaneously to cause these symptoms in the face of GERD.The most difficult clinical challenge in formulating a treat-ment plan for reflux-associated respiratory symptoms resides in establishing the diagnosis. Although the diagnosis may be straightforward in patients with predominately typical reflux symptoms and secondary respiratory complaints, a substan-tial number of patients will have respiratory symptoms that dominate the clinical scenario. Typical gastroesophageal reflux Brunicardi_Ch25_p1009-p1098.indd 103601/03/19 6:03 PM 1037ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25symptoms, such as heartburn and regurgitation, may often be completely absent only to be


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Surgery_Schwartz. Brunicardi_Ch25_p1009-p1098.indd 103601/03/19 6:03 PM 1037ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25symptoms, such as heartburn and regurgitation, may often be completely absent only to be uncovered with objective esopha-geal physiology testing. Traditionally, the diagnosis of reflux-induced respiratory injury is established using ambulatory dual probe pH monitoring, with one probe positioned within the dis-tal esophagus and the other at a proximal location. Proximal probe positioning has included multiple locations such as the trachea, pharynx, and proximal esophagus. Although ambu-latory esophageal pH monitoring allows a direct correlation between esophageal acidification and respiratory symptoms, sensitivity of this testing modality is poor, and the temporal rela-tionship between laryngeal or pulmonary symptoms and reflux events is complex. In addition, as the refluxed gastric fluid trav-els proximally, it may be neutralized by saliva and therefore go undetected with pH


Surgery_Schwartz

Surgery_Schwartz. laryngeal or pulmonary symptoms and reflux events is complex. In addition, as the refluxed gastric fluid trav-els proximally, it may be neutralized by saliva and therefore go undetected with pH monitoring. Impedance testing may also be used to detect the movement of fluid throughout the entire esophageal column regardless of pH content.Treatment. Once the diagnosis is established, treatment may be initiated with either PPI therapy or antireflux surgery. A trial of high-dose PPI therapy may help establish that reflux is partly or completely responsible for the respiratory symptoms. It is important to note that the persistence of symptoms in the face of aggressive PPI treatment does not necessarily rule out reflux as a possible cofactor or sole etiology.Although there is probably some element of a placebo effect, relief of respiratory symptoms can be anticipated in up to 50% of patients with reflux-induced asthma treated with anti-secretory medications. However, when examined


Surgery_Schwartz

Surgery_Schwartz. some element of a placebo effect, relief of respiratory symptoms can be anticipated in up to 50% of patients with reflux-induced asthma treated with anti-secretory medications. However, when examined objectively, <15% of patients can be expected to have improvement in their pulmonary function with medical therapy. In properly selected patients, antireflux surgery improves respiratory symptoms in nearly 90% of children and 70% of adults with asthma and reflux disease. Improvements in pulmonary function can be demonstrated in around 30% of patients. Uncontrolled studies of the two forms of therapy (PPI and surgery) and the evidence from the two randomized controlled trials of medical vs. sur-gical therapy indicate that surgical valve reconstruction is the most effective therapy for reflux-induced asthma. The superi-ority of the surgery over PPI is most noticeable in the supine position, which corresponds with the nadir of PPI blood levels and resultant acid breakthrough and is the time


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Surgery_Schwartz. asthma. The superi-ority of the surgery over PPI is most noticeable in the supine position, which corresponds with the nadir of PPI blood levels and resultant acid breakthrough and is the time in the circadian cycle when asthma symptoms are at their worst.In asthmatic patients with an esophageal motility disorder, performing an antireflux operation will not prevent the regur-gitation and possible aspiration of swallowed liquid or food “upstream” to the valve reconstruction. It is critical that esopha-geal body function be considered prior to surgical intervention in this patient population.Medical Therapy for Gastroesophageal Reflux Disease. With the widespread availability of over-the-counter antisecre-tory medications, most patients with mild or moderate symp-toms will carry self-medication. When initially identified with mild symptoms of uncomplicated GERD, patients can be placed on 12 weeks of simple antacids before diagnostic testing is initi-ated. This approach may successfully


Surgery_Schwartz

Surgery_Schwartz. When initially identified with mild symptoms of uncomplicated GERD, patients can be placed on 12 weeks of simple antacids before diagnostic testing is initi-ated. This approach may successfully and completely resolve the symptoms. Patients should be counseled to elevate the head of the bed; avoid tight-fitting clothing; eat small, frequent meals; avoid eating the nighttime meal immediately prior to bedtime; and avoid alcohol, coffee, chocolate, and peppermint, which are known to reduce resting LES pressure and may aggravate symptoms.Used in combination with simple antacids, alginic acid may augment the relief of symptoms by creating a physical bar-rier to reflux, as well as by acid reduction. Alginic acid reacts with sodium bicarbonate in the presence of saliva to form a highly viscous solution that floats like a raft on the surface of the gastric contents. When reflux occurs, this protective layer is refluxed into the esophagus, and acts as a protective barrier against the noxious


Surgery_Schwartz

Surgery_Schwartz. solution that floats like a raft on the surface of the gastric contents. When reflux occurs, this protective layer is refluxed into the esophagus, and acts as a protective barrier against the noxious gastric contents. Medications to promote gastric emptying, such as metoclopramide or domperidone, are beneficial in early disease but of little value in more severe disease.In patients with persistent symptoms, the mainstay of medical therapy is acid suppression. High-dosage regimens of hydrogen potassium PPIs, such as omeprazole (up to 40 mg/d), can reduce gastric acidity by as much as 80% to 90%. This usu-ally heals mild esophagitis. In severe esophagitis, healing may occur in only one-half of the patients. In patients who reflux a combination of gastric and duodenal juice, acid-suppression therapy may give relief of symptoms, while still allowing mixed reflux to occur. This can allow persistent mucosal damage in an asymptomatic patient. Unfortunately, within 6 months of discontinuation


Surgery_Schwartz

Surgery_Schwartz. therapy may give relief of symptoms, while still allowing mixed reflux to occur. This can allow persistent mucosal damage in an asymptomatic patient. Unfortunately, within 6 months of discontinuation of any form of medical therapy for GERD, 80% of patients have a recurrence of symptoms, and 40% of individuals with daily GERD eventually develop symptoms that “breakthrough” adequately dosed PPIs. Once initiated, most patients with GERD will require lifelong treatment with PPIs, both to relieve symptoms and to control any coexistent esophagitis or stricture. Although control of symptoms has his-torically served as the endpoint of therapy, the wisdom of this approach has recently been questioned, particularly in patients with BE. Evidence suggesting that reflux control may prevent the development of adenocarcinoma and lead to regression of dysplastic and nondysplastic Barrett’s segments has led many to consider control of reflux, and not symptom control, a better therapeutic endpoint.


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Surgery_Schwartz. of adenocarcinoma and lead to regression of dysplastic and nondysplastic Barrett’s segments has led many to consider control of reflux, and not symptom control, a better therapeutic endpoint. However, this hypothesis remains contro-versial. It should be noted that complete control of reflux using PPIs can be difficult, as has been highlighted by studies of acid breakthrough while on PPI therapy and of persistent reflux fol-lowing antireflux surgery. Castell, Triadafilopoulos, and others have shown that 40% to 80% of patients with BE continue to have abnormal esophageal acid exposure despite up to 20 mg twice daily of PPIs. Ablation trials have shown that mean doses of 56 mg of omeprazole were necessary to normalize 24-hour esophageal pH studies. It is likely that antireflux surgery results in more reproducible and reliable elimination of reflux of both acid and duodenal contents, although long-term outcome studies suggest that as many as 25% of postfundoplication patients will have


Surgery_Schwartz

Surgery_Schwartz. in more reproducible and reliable elimination of reflux of both acid and duodenal contents, although long-term outcome studies suggest that as many as 25% of postfundoplication patients will have persistent pathologic esophageal acid exposure confirmed by positive 24-hour pH studies.Suggested Therapeutic Approach. Traditionally a stepwise approach is used for the treatment of GERD. First-line therapy entails antisecretory medication, usually PPIs, in most patients. Failure of medication to adequately control GERD symptoms suggests either that the patient may have relatively severe dis-ease or a non-GERD cause for his or her symptoms. Endoscopic examination at this stage of the patient’s evaluation is recom-mended and will provide the opportunity to assess the degree of mucosal injury and presence of BE. Treatment options for these patients entails either long term PPI use vs. antireflux surgery. Laparoscopic antireflux surgery in these patients achieves long-term control of symptoms


Surgery_Schwartz

Surgery_Schwartz. presence of BE. Treatment options for these patients entails either long term PPI use vs. antireflux surgery. Laparoscopic antireflux surgery in these patients achieves long-term control of symptoms in 85% to 90%. The measurement Brunicardi_Ch25_p1009-p1098.indd 103701/03/19 6:03 PM 1038SPECIFIC CONSIDERATIONSPART IIof esophageal acid exposure via 24-hour pH should be under-taken when patients are considered for surgery. The status of the LES and esophageal body function with esophageal manom-etry should also be performed at this stage. These studies will serve to establish the diagnosis and assess esophageal body dysfunction.Surgical Therapy for Gastroesophageal Reflux DiseaseSelection of Patients for Surgery. Studies of the natural history of GERD indicate that most patients have a relatively benign form of the disease that is responsive to lifestyle changes and dietary and medical therapy and do not need surgical treat-ment. Approximately 25% to 50% of the patients with GERD


Surgery_Schwartz

Surgery_Schwartz. a relatively benign form of the disease that is responsive to lifestyle changes and dietary and medical therapy and do not need surgical treat-ment. Approximately 25% to 50% of the patients with GERD have persistent or progressive disease, and it is this patient pop-ulation that is best suited to surgical therapy. In the past, the presence of esophagitis and a structurally defective LES were the primary indications for surgical treatment, and many inter-nists and surgeons were reluctant to recommend operative pro-cedures in their absence. However, one should not be deterred from considering antireflux surgery in a symptomatic patient with or without esophagitis or a defective sphincter, provided the disease process has been objectively documented by 24-hour pH monitoring. This is particularly true in patients who have become dependent upon therapy with PPIs, or require increasing doses to control their symptoms. It is important to note that a good response to medical therapy in this


Surgery_Schwartz

Surgery_Schwartz. true in patients who have become dependent upon therapy with PPIs, or require increasing doses to control their symptoms. It is important to note that a good response to medical therapy in this group of patients pre-dicts an excellent outcome following antireflux surgery.In general, the key indications for antireflux surgery are (a) objectively proven gastroesophageal reflux disease, and (b) typical symptoms of gastroesophageal reflux disease (heartburn and/or regurgitation) despite adequate medical management, or (c) a younger patient unwilling to take lifelong medication. In addition, a structurally defective LES can also predict which patients are more likely to fail with medical therapy. Patients with normal sphincter pressures tend to remain well controlled with medical therapy, whereas patients with a structurally defec-tive LES may not respond as well to medical therapy, and often develop recurrent symptoms within 1 to 2 years of beginning therapy. Such patients should be


Surgery_Schwartz

Surgery_Schwartz. whereas patients with a structurally defec-tive LES may not respond as well to medical therapy, and often develop recurrent symptoms within 1 to 2 years of beginning therapy. Such patients should be considered for an antireflux operation, regardless of the presence or absence of endoscopic esophagitis.Young patients with documented reflux disease with or without a defective LES are also excellent candidates for anti-reflux surgery. They usually will require long-term medical therapy for control of their symptoms, and some will go on to develop complications of the disease. An analysis of the cost of therapy based on data from the Veterans Administration Coop-erative trial indicates that surgery has a cost advantage over medical therapy in patients <49 years of age.Severe endoscopic esophagitis in a symptomatic patient with a structurally defective LES is also an indication for early surgical therapy. These patients are prone to breakthrough of their symptoms while receiving medical


Surgery_Schwartz

Surgery_Schwartz. in a symptomatic patient with a structurally defective LES is also an indication for early surgical therapy. These patients are prone to breakthrough of their symptoms while receiving medical therapy. Symptoms and mucosal injury can be controlled in such patients, but careful monitoring is required, and increasing dosages of PPIs are nec-essary. In everyday clinical practice, however, such treatment can be both difficult and impractical, and, in such cases, antire-flux surgery can be considered early, especially if PPI therapy is problematic.The development of a stricture in a patient represents a fail-ure of medical therapy, and it is also an indication for a surgical antireflux procedure. In addition, strictures are often associated with a structurally defective sphincter and loss of esophageal contractility. Before proceeding with surgical treatment, malig-nancy and a drug-related etiology of the stricture should be excluded, and the stricture should be progressively dilated up to


Surgery_Schwartz

Surgery_Schwartz. contractility. Before proceeding with surgical treatment, malig-nancy and a drug-related etiology of the stricture should be excluded, and the stricture should be progressively dilated up to a 50 to 60F bougie. When the stricture is fully dilated, the relief of dysphagia is evaluated, and esophageal manometry is performed to determine the adequacy of peristalsis in the distal esophagus. If dysphagia is relieved and the amplitude of esopha-geal contractions is adequate, an antireflux procedure should be performed; if there is a global loss of esophageal contractility, caution should be exercised in performing an antireflux proce-dure with a complete fundoplication, and a partial fundoplica-tion should be considered.Barrett’s CLE is commonly associated with a severe structural defect of the LES and often poor contractility of the esophageal body. Patients with BE are at risk of the development of an adenocarcinoma. Whilst surgeons would like to think that an antireflux procedure can


Surgery_Schwartz

Surgery_Schwartz. the LES and often poor contractility of the esophageal body. Patients with BE are at risk of the development of an adenocarcinoma. Whilst surgeons would like to think that an antireflux procedure can reduce the risk of progression to cancer, the evidence supporting this is relatively weak, and for now Barrett’s esophagus should be considered to be evidence that the patient has gastroesophageal reflux, and progression to antireflux surgery is indicated for the treatment of reflux symptoms, not cancer progression. If, however, high grade dysplasia or intramucosal carcinoma is found on mucosal biopsy specimens, treatment should then be directed at the BE and the lesion, using either evaluation endoscopic ablation, endoscopic resection, or esophageal resection.The majority of patients requiring treatment for reflux have a relatively mild form of disease and will respond to antise-cretory medications. Patients with more severe forms of disease, particularly those who develop persistent or


Surgery_Schwartz

Surgery_Schwartz. treatment for reflux have a relatively mild form of disease and will respond to antise-cretory medications. Patients with more severe forms of disease, particularly those who develop persistent or progressive disease, should be considered for definitive therapy. Laparoscopic fun-doplication will provide a long-term cure in the majority of these patients, with minimal discomfort and an early return to normal activity.Preoperative Evaluation. Before proceeding with an antire-flux operation, several factors should be evaluated. The clinical symptoms should be consistent with the diagnosis of gastro-esophageal reflux. Patients presenting with the typical symp-toms of heartburn and/or regurgitation which have responded, at least partly, to PPI therapy, will generally do well following surgery, whereas patients with atypical symptoms have a less predictable response. Reflux should also be objectively con-firmed by either the presence of ulcerative esophagitis or an abnormal 24-hour pH


Surgery_Schwartz

Surgery_Schwartz. whereas patients with atypical symptoms have a less predictable response. Reflux should also be objectively con-firmed by either the presence of ulcerative esophagitis or an abnormal 24-hour pH study.The propulsive force of the body of the esophagus should be evaluated by esophageal manometry to determine if it has sufficient power to propel a bolus of food through a newly reconstructed valve. Patients with normal peristaltic contrac-tions can be considered for a 360° Nissen fundoplication or a partial fundoplication, depending on patient and surgeon pref-erences. When peristalsis is absent, a partial fundoplication is probably the procedure of choice, but only if achalasia has been ruled out.Hiatal anatomy should also be assessed. In patients with smaller hiatal hernias, endoscopy evaluation usually provides sufficient information. However, when patients present with a very large hiatus hernia or for revision surgery after previous antireflux surgery, contrast radiology provides


Surgery_Schwartz

Surgery_Schwartz. usually provides sufficient information. However, when patients present with a very large hiatus hernia or for revision surgery after previous antireflux surgery, contrast radiology provides better anatomical information. The concept of anatomic shortening of the esoph-agus is controversial, with divergent opinions held about how Brunicardi_Ch25_p1009-p1098.indd 103801/03/19 6:03 PM 1039ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25DistentionFigure 25-32. A graphic illustration of the shortening of the lower esophageal sphincter that occurs as the sphincter is “taken up” by the cardia as the stomach distends.common this problem is. Believers claim that anatomic short-ening of the esophagus compromises the ability of the surgeon to perform an adequate repair without tension and that this can lead to an increased incidence of breakdown or thoracic displace-ment of the repair. Some of those who hold this view claim that esophageal shortening is present when a barium swallow X-ray


Surgery_Schwartz

Surgery_Schwartz. this can lead to an increased incidence of breakdown or thoracic displace-ment of the repair. Some of those who hold this view claim that esophageal shortening is present when a barium swallow X-ray identifies a sliding hiatal hernia that will not reduce in the upright position or that measures more than 5 cm in length at endoscopy. When such identification is made, these surgeons usually add a gastroplasty to the antireflux procedure. Others claim that esoph-ageal shortening is overdiagnosed and rarely seen, and that the morbidity of adding a gastroplasty outweighs any benefits. These surgeons would recommend a standard antireflux procedure in all patients undergoing primary surgery.Principles of Surgical Therapy. The primary goal of anti-reflux surgery is to safely create a new antireflux valve at the gastroesophageal junction, while preserving the patient’s abil-ity to swallow normally and to belch to relieve gaseous disten-tion. Regardless of the choice of the procedure, this goal


Surgery_Schwartz

Surgery_Schwartz. valve at the gastroesophageal junction, while preserving the patient’s abil-ity to swallow normally and to belch to relieve gaseous disten-tion. Regardless of the choice of the procedure, this goal can be achieved if attention is paid to some basic principles when reconstructing the antireflux mechanism. First, the operation should create a flap valve which prevents regurgitation of gas-tric contents into the esophagus. This will result in an increase in the pressure of the distal esophageal sphincter region. Follow-ing a Nissen fundoplication the expected increase is to a level twice the resting gastric pressure (i.e., 12 mmHg for a gastric pressure of 6 mmHg). The extent of the pressure rise is often less following a partial fundoplication, although with all types of fundoplication the length of the reconstructed valve should be at least 3 cm. This not only augments sphincter characteristics in patients in whom they are reduced before surgery but also prevents unfolding of a normal


Surgery_Schwartz

Surgery_Schwartz. length of the reconstructed valve should be at least 3 cm. This not only augments sphincter characteristics in patients in whom they are reduced before surgery but also prevents unfolding of a normal sphincter in response to gastric distention (Fig. 25-32). Preoperative and postoperative esopha-geal manometry measurements have shown that the resting sphincter pressure and the overall sphincter length can be surgi-cally augmented over preoperative values, and that the change in the former is a function of the degree of gastric wrap around the esophagus (Fig. 25-33). However, the aim of any fundopli-cation is to create a loose wrap and to maintain the position of the gastric fundus close to the distal intra-abdominal esophagus, in a flap valve arrangement. The efficacy of this relies on the close relationship between the fundus and the esophagus, not the “tightness” of the wrap.Second, the operation should place an adequate length of the distal esophageal sphincter in the


Surgery_Schwartz

Surgery_Schwartz. relies on the close relationship between the fundus and the esophagus, not the “tightness” of the wrap.Second, the operation should place an adequate length of the distal esophageal sphincter in the positive-pressure 051015˜ P mmHg 20240Degree of wrapY = 4.63 + .023 (x)P < .01BelseyHillN=15NissenN=15N=15360Figure 25-33. The relationship between the augmentation of sphincter pressure over preoperative pressure (ΔP) and the degree of gastric fundic wrap in three different antireflux procedures. (Repro-duced with permission from O’Sullivan GC, DeMeester TR, Joels-son BE, et al: Interaction of lower esophageal sphincter pressure and length of sphincter in the abdomen as determinants of gastro-esophageal competence, Am J Surg. 1982 Jan;143(1):40-47.)environment of the abdomen by a method that ensures its response to changes in intra-abdominal pressure. The permanent restoration of 2 or more cm of abdominal esophagus ensures the preservation of the relationship between the fundus and the


Surgery_Schwartz

Surgery_Schwartz. ensures its response to changes in intra-abdominal pressure. The permanent restoration of 2 or more cm of abdominal esophagus ensures the preservation of the relationship between the fundus and the esophagus. All of the popular antireflux procedures increase the length of the sphincter exposed to abdominal pressure by an average of at least 1 cm.Third, the operation should allow the reconstructed car-dia to relax on deglutition. In normal swallowing, a vagally mediated relaxation of the distal esophageal sphincter and the gastric fundus occurs. The relaxation lasts for approximately 10 seconds and is followed by a rapid recovery to the former tonicity. To ensure relaxation of the sphincter, three factors are important: (a) Only the fundus of the stomach should be used to buttress the sphincter, because it is known to relax in con-cert with the sphincter; (b) the gastric wrap should be properly placed around the sphincter and not incorporate a portion of the stomach or be placed around


Surgery_Schwartz

Surgery_Schwartz. because it is known to relax in con-cert with the sphincter; (b) the gastric wrap should be properly placed around the sphincter and not incorporate a portion of the stomach or be placed around the stomach itself, because the body of the stomach does not relax with swallowing; and (c) damage to the vagal nerves during dissection of the thoracic esophagus should be avoided because it may result in failure of the sphincter to relax.Fourth, the fundoplication should not increase the resis-tance of the relaxed sphincter to a level that exceeds the peri-staltic power of the body of the esophagus. The resistance of the relaxed sphincter depends on the degree, length, and diameter of the gastric fundic wrap, and on the variation in intra-abdominal pressure. A 360° gastric wrap should be no longer than 2 cm and constructed over a large (50 to 60F) bougie. This will ensure that the relaxed sphincter will have an adequate diameter with minimal resistance. A bougie is not necessary when


Surgery_Schwartz

Surgery_Schwartz. no longer than 2 cm and constructed over a large (50 to 60F) bougie. This will ensure that the relaxed sphincter will have an adequate diameter with minimal resistance. A bougie is not necessary when construct-ing a partial wrap.Fifth, the operation should ensure that the fundoplication can be placed in the abdomen without undue tension and main-tained there by approximating the crura of the diaphragm above the repair. Leaving the fundoplication in the thorax converts a sliding hernia into a PEH, with all the complications associ-ated with that condition. Maintaining the repair in the abdomen Brunicardi_Ch25_p1009-p1098.indd 103901/03/19 6:03 PM 1040SPECIFIC CONSIDERATIONSPART IIunder tension predisposes to an increased incidence of recur-rence. How common this problem is encountered is disputed, with some surgeons advocating lengthening the esophagus by gastroplasty and constructing a partial fundoplication, and oth-ers claiming that this issue is now rarely encountered.Procedure


Surgery_Schwartz

Surgery_Schwartz. disputed, with some surgeons advocating lengthening the esophagus by gastroplasty and constructing a partial fundoplication, and oth-ers claiming that this issue is now rarely encountered.Procedure Selection. A laparoscopic approach is now used routinely in all patients undergoing primary antireflux surgery. Some surgeons advocate the use of a single antireflux procedure for all patients, whereas others advocate a tailored approach. Advocates of the laparoscopic Nissen fundoplication as the pro-cedure of choice for a primary antireflux repair would generally apply this procedure in all patients with normal or near normal esophageal motility, and they would reserve a partial fundopli-cation for use in individuals with poor esophageal body motility. Others, based on the good longer-term outcomes now reported following partial fundoplication procedures, advocate the rou-tine application of a partial fundoplication procedure, thereby avoiding any concerns about constructing a


Surgery_Schwartz

Surgery_Schwartz. outcomes now reported following partial fundoplication procedures, advocate the rou-tine application of a partial fundoplication procedure, thereby avoiding any concerns about constructing a fundoplication in individuals with poor esophageal motility.Experience and randomized studies have shown that both the Nissen fundoplication and various partial fundoplication procedures are all effective and durable antireflux repairs that generate an excellent outcome in approximately 90% of patients at longer-term follow-up.Primary Antireflux RepairsNissen Fundoplication. The most common antireflux proce-dure is the Nissen fundoplication. In the past, this procedure has been performed through an open abdominal or a chest incision, but with the development of laparoscopic approaches primary antireflux surgery is now routinely undertaken using the laparo-scope. Rudolph Nissen described this procedure as a 360° fun-doplication around the lower esophagus for a distance of 4 to 5 cm, without


Surgery_Schwartz

Surgery_Schwartz. surgery is now routinely undertaken using the laparo-scope. Rudolph Nissen described this procedure as a 360° fun-doplication around the lower esophagus for a distance of 4 to 5 cm, without division of the short gastric blood vessels. Although this provided good control of reflux, it was associated with a number of side effects that have encouraged modifica-tions of the procedure as originally described. These include using only the gastric fundus to envelop the esophagus in a fash-ion analogous to a Witzel jejunostomy, sizing the fundoplication with a large (50 to 60F) bougie, limiting the length of the fun-doplication to 1 to 2 cm, and dividing the short gastric vessels. The essential elements necessary for the performance of a trans-abdominal fundoplication are common to both the laparoscopic and open procedures and include the following:1. Hiatal dissection and preservation of both vagi along their entire length2. Circumferential esophageal mobilization3. Hiatal closure, usually


Surgery_Schwartz

Surgery_Schwartz. and open procedures and include the following:1. Hiatal dissection and preservation of both vagi along their entire length2. Circumferential esophageal mobilization3. Hiatal closure, usually posterior to the esophagus4. Creation of a short and floppy fundoplication over an esoph-ageal dilatorIn addition, many surgeons also routinely divide the short gastric blood vessels, although this step is not universally applied, and the results of several randomized trials have failed to show that this step yields any benefit.The laparoscopic approach to fundoplication has now replaced the open abdominal Nissen fundoplication as the pro-cedure of choice. Five ports are usually used (Fig. 25-34), and dissection is begun by incising the gastrohepatic omentum above and below the hepatic branch of the anterior vagus nerve, which is usually preserved. The circumference of the diaphragmatic L R Figure 25-34. Patient positioning and trocar placement for lap-aroscopic antireflux surgery. The patient


Surgery_Schwartz

Surgery_Schwartz. anterior vagus nerve, which is usually preserved. The circumference of the diaphragmatic L R Figure 25-34. Patient positioning and trocar placement for lap-aroscopic antireflux surgery. The patient is placed with the head elevated approximately 30° in the modified lithotomy position. The surgeon stands between the patient’s legs, and the procedure is completed using five abdominal access ports.hiatus is dissected and the esophagus is mobilized by careful dis-section of the anterior and posterior soft tissues within the hiatus. The esophagus is held anterior and to the left and the hiatal pillars are approximated with interrupted nonabsorbable sutures, starting posteriorly and working anteriorly. A tension-free fundoplication should be constructed. This can usually be achieved either with or without division of the short gastric blood vessels, accord-ing to surgeon preference. If the vessels are divided, the upper one-third of the greater curvature is mobilized by sequentially


Surgery_Schwartz

Surgery_Schwartz. with or without division of the short gastric blood vessels, accord-ing to surgeon preference. If the vessels are divided, the upper one-third of the greater curvature is mobilized by sequentially dissecting and dividing these vessels, commencing distally and working proximally. Following complete fundal mobilization, the posterior wall of the fundus is brought behind the esophagus to the right side, and the anterior wall of the fundus is brought anterior to the esophagus. The fundic lips are manipulated to allow the fundus to envelop the esophagus without twisting. A 50 to 60F bougie is passed to properly size the fundoplication, and it is sutured using nonabsorbable sutures. Some surgeons use a single U-stitch of 2-0 polypropylene buttressed with felt pledgets (Fig. 25-35), and others use 2-4 interrupted sutures.Brunicardi_Ch25_p1009-p1098.indd 104001/03/19 6:03 PM 1041ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Posterior Partial Fundoplication. Partial fundoplications were


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Surgery_Schwartz. use 2-4 interrupted sutures.Brunicardi_Ch25_p1009-p1098.indd 104001/03/19 6:03 PM 1041ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Posterior Partial Fundoplication. Partial fundoplications were developed as an alternative to the Nissen procedure in an attempt to minimize the risk of postfundoplication side effects, such as dysphagia, inability to belch, and flatulence. The commonest approach has been a posterior partial or Toupet fundoplication. Some surgeons use this type of procedure for all patients present-ing for antireflux surgery, whereas others apply a tailored approach in which a partial fundoplication is constructed in patients with impaired esophageal motility, in which the propulsive force of the esophagus is thought to be insufficient to overcome the outflow obstruction of a complete fundoplication. The Toupet posterior partial fundoplication consists of a 270° gastric fundoplication around the distal 4 cm of esophagus (Fig. 25-36). It is usually stabilized by


Surgery_Schwartz

Surgery_Schwartz. of a complete fundoplication. The Toupet posterior partial fundoplication consists of a 270° gastric fundoplication around the distal 4 cm of esophagus (Fig. 25-36). It is usually stabilized by anchoring the wrap posteriorly to the hiatal rim.Anterior Partial Fundoplication. An alternative approach to partial fundoplication is to construct an anterior partial fundopli-cation. Following posterior hiatal repair, the anterior fundus is rolled over the front of the esophagus and sutured to the hiatal rim and the esophageal wall. Division of the short gastric vessels Figure 25-35. A. Laparoscopic Nissen fundoplication is performed with a five-trocar technique. B. The liver retractor is affixed to a mechani-cal arm to hold it in place throughout the operation. C. After division of the gastrohepatic omentum above the hepatic branch of the vagus (pars flaccida), the surgeon places a blunt atraumatic grasper beneath the phrenoesophageal ligament. D. After completion of the crural closure, an


Surgery_Schwartz

Surgery_Schwartz. omentum above the hepatic branch of the vagus (pars flaccida), the surgeon places a blunt atraumatic grasper beneath the phrenoesophageal ligament. D. After completion of the crural closure, an atraumatic grasper is placed right to left behind the gastroesophageal junction. The grasper is withdrawn, pulling the posterior aspect of the gastric fundus behind the esophagus. E. Once the suture positions are chosen, the first stitch (2-0 silk, 20 cm long) is introduced through the 10-mm trocar, and the needle is passed first through the left limb of the fundus, then the esophagus (2.5 cm above the gastroesophageal junction), then through the right limb of the fundus. F. Final position of the fundoplication.Brunicardi_Ch25_p1009-p1098.indd 104101/03/19 6:03 PM 1042SPECIFIC CONSIDERATIONSPART IIFigure 25-36. Completed laparoscopic posterior partial (Toupet) fundoplication. The fundoplication does not cover the anterior sur-face of the esophagus, and it is stabilized by suturing the


Surgery_Schwartz

Surgery_Schwartz. 25-36. Completed laparoscopic posterior partial (Toupet) fundoplication. The fundoplication does not cover the anterior sur-face of the esophagus, and it is stabilized by suturing the fundus to the side of the esophagus, and posteriorly to the right hiatal pillar.is never needed when constructing this type of fundoplication. Various degrees of anterior partial fundoplication have been described—90°, 120°, 180°. The anterior 180° partial fundopli-cation (Fig. 25-37) provides a more robust fundoplication and achieves an excellent longer-term outcome in approximately 90% of patients at follow-up of at least 10 years. With this procedure, the fundus and esophagus are sutured to the right side of the hiatal rim to create a flap valve at the gastroesophageal junction and to stabilize a 3 to 4 cm length of intra-abdominal esophagus.Collis Gastroplasty. When a shortened esophagus is encoun-tered, many surgeons choose to add an esophageal lengthening procedure before fundoplication, to reduce


Surgery_Schwartz

Surgery_Schwartz. length of intra-abdominal esophagus.Collis Gastroplasty. When a shortened esophagus is encoun-tered, many surgeons choose to add an esophageal lengthening procedure before fundoplication, to reduce the tension on the gastroesophageal junction, believing this will minimize the risk of failure due to postoperative hiatus hernia. The commonest approach to this is the Collis gastroplasty. This entails using a stapler to divide the cardia and upper stomach, parallel to the lesser curvature of Figure 25-37. Completed laparoscopic anterior 180° partial fun-doplication. The fundoplication fully covers the anterior surface of the esophagus, and it is stabilized by suturing the fundus to the right side of the esophagus, and to the right hiatal pillar. Unlike the Nissen procedure, the fundus is not pulled behind the esophagus.the stomach, thereby creating a gastric tube in continuity with the esophagus, and effectively lengthening the esophagus by several centimeters. Laparoscopic techniques for


Surgery_Schwartz

Surgery_Schwartz. behind the esophagus.the stomach, thereby creating a gastric tube in continuity with the esophagus, and effectively lengthening the esophagus by several centimeters. Laparoscopic techniques for Collis gastroplasty have been described (Fig. 25-38). Following gastroplasty a fundoplica-tion is constructed, with the highest suture is placed on the native esophagus when constructing a Nissen fundoplication. Not all sur-geons choose to undertake a Collis procedure, however, as there is controversy about the actual incidence of the shortened esophagus and widely divergent views are held about how often this prob-lem is encountered. In addition, some surgeons have questioned the wisdom of creating an amotile tube of gastric wall, which can secrete acid, and then placing a Nissen fundoplication below this.Outcome After Fundoplication. Studies of long-term outcome following both open and laparoscopic fundoplication document the ability of laparoscopic fundoplication to relieve typical reflux


Surgery_Schwartz

Surgery_Schwartz. below this.Outcome After Fundoplication. Studies of long-term outcome following both open and laparoscopic fundoplication document the ability of laparoscopic fundoplication to relieve typical reflux symptoms (heartburn, regurgitation, and dysphagia) in more than Figure 25-35. (Continued )Brunicardi_Ch25_p1009-p1098.indd 104201/03/19 6:03 PM 1043ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-38. A. After removal of the fat pad and release of tension on the Penrose drain, the gastroesophageal junction (GES) retracts to the level of the hiatus. The interior end of the staple line is marked 2/5 cm below the angle of His. B. The first horizontal firing of the stapler occurs by maximally articulating the stapler to the left, aiming toward the previously marked spot adjacent to the dilator. C. The vertical staple line is created by a single firing of the GIA placed parallel and flush against the 48F dilator. D. The highest Nissen fundoplication suture is placed on the native


Surgery_Schwartz

Surgery_Schwartz. dilator. C. The vertical staple line is created by a single firing of the GIA placed parallel and flush against the 48F dilator. D. The highest Nissen fundoplication suture is placed on the native esophagus, and the second suture tucks in the apex of the staple line.90% of patients at follow-up intervals averaging 2 to 3 years and 80% to 90% of patients 5 years or more following surgery. This includes evidence-based reviews of antireflux surgery, pro-spective randomized trials comparing antireflux surgery to PPI therapy and open to laparoscopic fundoplication and analysis of U.S. national trends in use and outcomes. Postoperative pH stud-ies indicate that more than 90% of patients will normalize their pH tracings. The results of laparoscopic fundoplication compare favorably with those of the “modern” era of open fundoplica-tion. They also indicate the less predictable outcome of atypical reflux symptoms (cough, asthma, laryngitis) after surgery, being relieved in only two-thirds of


Surgery_Schwartz

Surgery_Schwartz. the “modern” era of open fundoplica-tion. They also indicate the less predictable outcome of atypical reflux symptoms (cough, asthma, laryngitis) after surgery, being relieved in only two-thirds of patients.The goal of surgical treatment for GERD is to relieve the symptoms of reflux by reestablishing the gastroesophageal barrier. The challenge is to accomplish this without inducing dysphagia or other untoward side effects. Dysphagia, existing before surgery, usually improves following laparoscopic fun-doplication. Temporary dysphagia is common after surgery and generally resolves within 3 months, but it can take up to 12 months in some individuals, and dysphagia sufficient to require ongoing dietary modification persists in up to 5% of individuals following Nissen fundoplication. Other side effects common to antireflux surgery include the inability to belch and vomit and increased flatulence. Most patients cannot vomit through an intact wrap, though this is rarely clinically


Surgery_Schwartz

Surgery_Schwartz. Other side effects common to antireflux surgery include the inability to belch and vomit and increased flatulence. Most patients cannot vomit through an intact wrap, though this is rarely clinically relevant. Most patients are unable to belch gas from the stomach in the first 3 to 6 months after fundoplication, but 80% to 90% regain the ability to belch normally beyond the first 12 months of fol-low-up. Hyperflatulence is a common and noticeable problem, likely related to increased air swallowing that is present in most patients with reflux disease, aggravated by the inability to belch in some patients.Brunicardi_Ch25_p1009-p1098.indd 104301/03/19 6:03 PM 1044SPECIFIC CONSIDERATIONSPART IIRandomized Controlled Trials Addressing Surgical Technique Division of the Short Gastric Blood Vessels Originally, Nissen’s description of a total fundoplication entailed a 360° fundoplication during which the short gastric blood vessels were left intact. However, with reports of troublesome


Surgery_Schwartz

Surgery_Schwartz. Vessels Originally, Nissen’s description of a total fundoplication entailed a 360° fundoplication during which the short gastric blood vessels were left intact. However, with reports of troublesome postoperative dysphagia, division of these vessels—to achieve full fundal mobilization and thereby ensure a loose fundoplication—was promoted and has entered common practice. The evidence sup-porting dividing these vessels has been based on the outcomes from uncontrolled case series of patients undergoing Nissen fundoplication either with vs. without division of the short gas-tric vessels. However, the results from these studies have been conflicting, with different proponents reporting good results irrespective of whether these vessels have been divided or not. To address this issue, six randomized trials that enrolled a total of 438 patients have been reported. None of these trials demon-strated any differences for the postoperative dysphagia or recur-rent gastro-esophageal reflux.


Surgery_Schwartz

Surgery_Schwartz. randomized trials that enrolled a total of 438 patients have been reported. None of these trials demon-strated any differences for the postoperative dysphagia or recur-rent gastro-esophageal reflux. However, in the three largest of the six trials an increased incidence of flatulence and bloating symptoms, as well as greater difficulty with belching, was seen in patients in whom the short gastric vessels were divided.A recent meta-analysis from Engstrom et al, generated by combining the raw data from Australian and Swedish trials, eval-uated a larger cohort of 201 patients, with 12 years of follow-up in 170, and also confirmed equivalent reflux control but found more abdominal bloating after division of the short gastric ves-sels. Overall, these trials fail to support the belief that dividing the short gastric vessels improves any outcome following Nissen fun-doplication. The trials actually suggest that dividing the vessels increases the complexity of the procedure and leads to a