Surgery_Schwartz

Surgery_Schwartz. 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 poorer outcome due to the increase in bloating symptoms.Nissen vs. Posterior Partial Fundoplication Eleven randomized trials have compared Nissen vs. posterior partial fundoplication. Some of the trials contributed little to the pool of evidence, as they are either small or underpowered, and failed to show significant outcome differences. The larger trials, however, have consistently demonstrated equivalent reflux control, but they also show a reduced incidence of wind-related side-effects (flatulence, bloating, and inability to belch) following posterior partial fundoplication procedures, although less dysphagia fol-lowing a posterior fundoplication was only demonstrated in 2 of the 11 trials. Lundell et al reported the outcomes of Nissen vs. Toupet partial fundoplication in a trial that


Surgery_Schwartz

Surgery_Schwartz. less dysphagia fol-lowing a posterior fundoplication was only demonstrated in 2 of the 11 trials. Lundell et al reported the outcomes of Nissen vs. Toupet partial fundoplication in a trial that enrolled 137 patients with reported follow-up to 18 years. Reflux control and dyspha-gia symptoms were similar, but flatulence was commoner after Nissen fundoplication at some medium-term follow-up time points, and revision surgery was more common following Nissen fundoplication, mainly to correct postoperative paraoesophageal herniation. At 18 years follow-up, success rates of more than 80% were reported for both procedures, as well as no significant differences in the incidence of side effects. The data from this trial suggested that the mechanical side effects following Nis-sen fundoplication progressively improve with very long-term follow-up. Strate et al reported 2-year follow-up in a trial that enrolled 200 patients. Approximately 85% of each group was satisfied with the clinical


Surgery_Schwartz

Surgery_Schwartz. progressively improve with very long-term follow-up. Strate et al reported 2-year follow-up in a trial that enrolled 200 patients. Approximately 85% of each group was satisfied with the clinical outcome, but dysphagia was signifi-cantly more common following Nissen fundoplication (19 vs. 8 patients).Other trials (Guérin et al–140 patients, Booth et al–127, Khan et al–121, Shaw et al–100) also report similar reflux control within the first few years of follow-up. Only Booth et al demonstrated less dysphagia following posterior fundoplica-tion. Subgroup analysis in 3 trials (Booth, Shaw, Zornig) did not reveal differences between patients with vs. without poor pre-operative oesophageal motility. Overall these trials suggest that some side-effects, mainly wind-related issues, are less common following posterior partial fundoplication. However, the hypoth-esis that dysphagia is less of a problem following posterior par-tial fundoplication has only been substantiated in 2 of 11


Surgery_Schwartz

Surgery_Schwartz. less common following posterior partial fundoplication. However, the hypoth-esis that dysphagia is less of a problem following posterior par-tial fundoplication has only been substantiated in 2 of 11 trials.Nissen vs. Anterior Fundoplication Six trials have evaluated Nissen vs. anterior partial fundoplication variants. Four have assessed Nissen vs. anterior 180° partial fundoplication (Watson et al–107 patients, Baigrie et al–161, Cao et al–100, Raue et al–64). These trials all demonstrated equivalent reflux control, but less dysphagia and less wind-related side effects after anterior 180° partial fundoplication at up to 5 years follow-up. Only the study from Watson et al has reported follow-up to 10 years, and at late follow-up in their trial there were no significant outcome differences for the two procedures, with equivalent control of reflux, and no differences for side effects due to a progressive decline in dysphagia as follow-up extended beyond 5 years.Two trials compared


Surgery_Schwartz

Surgery_Schwartz. for the two procedures, with equivalent control of reflux, and no differences for side effects due to a progressive decline in dysphagia as follow-up extended beyond 5 years.Two trials compared laparoscopic anterior 90° partial fundoplication vs. Nissen fundoplication (Watson et al–112 patients, Spence et al–79). In both of these trials, side-effects were less common following anterior 90° fundoplication, but this was offset by a slightly higher incidence of recurrent reflux at up to 5 years follow-up. Satisfaction with the overall outcome was similar for both fundoplication variants.Anterior vs. Posterior Partial Fundoplication Two ran-domized trials have directly compared anterior vs. posterior partial fundoplication. Hagedorn et al randomized 95 patients to undergo either Toupet vs. anterior 120° partial fundoplica-tion, and Khan et al enrolled 103 patients to anterior 180° vs. posterior partial fundoplication. Both studies demonstrated bet-ter reflux control, offset by more side


Surgery_Schwartz

Surgery_Schwartz. 120° partial fundoplica-tion, and Khan et al enrolled 103 patients to anterior 180° vs. posterior partial fundoplication. Both studies demonstrated bet-ter reflux control, offset by more side effects following posterior partial fundoplication. The anterior 120° partial fundoplication performed by Hagedorn et al was similar to the anterior 90° vari-ant described above. However, the outcomes following this pro-cedure were much worse in this trial than the outcomes in other studies, with the average exposure time to acid (pH <4%–5.6%) following anterior fundoplication in their study unusually high compared to other studies. Khan et al only reported 6 months follow-up, and longer-term outcomes are awaited before draw-ing firm conclusions. The overall results from all eight trials that included an anterior fundoplication variant suggest that this type of fundoplication achieves satisfactory reflux control, with less dysphagia and other side-effects, yielding a good overall outcome.


Surgery_Schwartz

Surgery_Schwartz. included an anterior fundoplication variant suggest that this type of fundoplication achieves satisfactory reflux control, with less dysphagia and other side-effects, yielding a good overall outcome. However, the reduced incidence of troublesome side-effects is traded off against a higher risk of recurrent reflux.Outcome of Antireflux Surgery in Patients With Barrett’s Esophagus. Few studies have focused on the alleviation of symp-toms after antireflux surgery in patients with BE (Table 25-7). Those that are available document excellent to good results in 72% to 95% of patients at 5 years following surgery. Several nonrandomized studies have compared medical and surgical therapy and report better outcomes after antireflux surgery. Par-rilla and colleagues reported the only randomized trial to evaluate this issue. They enrolled 101 patients over 18 years, and median follow-up was 6 years. Medical therapy consisted of 20 mg of omeprazole (PPI) twice daily since 1992 in all medically


Surgery_Schwartz

Surgery_Schwartz. to evaluate this issue. They enrolled 101 patients over 18 years, and median follow-up was 6 years. Medical therapy consisted of 20 mg of omeprazole (PPI) twice daily since 1992 in all medically treated patients, and surgical therapy consisted of an open Nissen Brunicardi_Ch25_p1009-p1098.indd 104401/03/19 6:03 PM 1045ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Table 25-7Symptomatic outcome of surgical therapy for Barrett’s esophagusAUTHORYEARNO. OF PATIENTS% EXCELLENT TO GOOD RESPONSEMEAN FOLLOW-UP, YEARSStarnes19848752Williamson199037923DeMeester199035773McDonald199611382.26.5Ortiz19963290.65fundoplication. The symptomatic outcome in the two groups was nearly identical, although esophagitis and/or stricture persisted in 20% of the medically treated patients, compared to only 3% to 7% of patients following antireflux surgery. About 15% of patients had abnormal acid exposure after surgery. Although pH data were not routinely collected in patients on PPI therapy, in the subgroup


Surgery_Schwartz

Surgery_Schwartz. 7% of patients following antireflux surgery. About 15% of patients had abnormal acid exposure after surgery. Although pH data were not routinely collected in patients on PPI therapy, in the subgroup of 12 patients that did have 24-hour monitoring on treat-ment, 3 of 12 (25%) had persistently high esophageal acid expo-sure, and most (75%) had persistently high bilirubin exposure.The common belief that Barrett’s epithelium cannot be reversed by antireflux surgery may not be correct. Within the control arm of a randomized trial of ablation vs. surveillance, Bright and associates identified approximately 50% regression in the length of Barrett’s esophagus in 20 patients within the control arm of a randomized trial of ablation vs. surveillance.Current data indicate that patients with BE should remain in an endoscopic surveillance program following antireflux surgery. Biopsy specimens should be reviewed by a patholo-gist with expertise in the field. If low-grade dysplasia is con-firmed,


Surgery_Schwartz

Surgery_Schwartz. remain in an endoscopic surveillance program following antireflux surgery. Biopsy specimens should be reviewed by a patholo-gist with expertise in the field. If low-grade dysplasia is con-firmed, biopsy specimens should be repeated after 12 weeks of high-dose acid suppression therapy. If high-grade dysplasia or intramucosal cancer is evident on more than one biopsy speci-men, then treatment is escalated. Treatment options include endoscopic mucosal resection, endoscopic ablation of the BE, or esophageal resection. Esophageal resection is advisable when an invasive cancer (stage T1b or deeper) is present, or for mul-tifocal long segment BE in younger and fit patients in whom endoscopic treatments are unlikely to be adequate. Endoscopic mucosal resection allows smaller intramucosal tumors to be removed with clear pathology margins, and it can be used as a “big biopsy” to obtain better pathological staging, and even to excise shorter segments of BE in a piecemeal fashion. Ablation,


Surgery_Schwartz

Surgery_Schwartz. to be removed with clear pathology margins, and it can be used as a “big biopsy” to obtain better pathological staging, and even to excise shorter segments of BE in a piecemeal fashion. Ablation, commonly using radiofrequency ablation, has been shown at short-term follow-up in a randomized trial to reduce the rate of progression from high grade dysplasia to invasive cancer by approximately 50%. However, following any endoscopic treatment, patients need to continue with close endoscopic sur-veillance as recurrence can occur and the longer-term outcome following these treatments remains uncertain. Early detection and treatment have been shown to decrease the mortality rate from esophageal cancer in these patients.If the dysplasia is reported as lower grade or indetermi-nant, then inflammatory change that is often confused with dysplasia should be suppressed by a course of acid suppression therapy in high doses for 2 to 3 months, followed by rebiopsy of the Barrett’s segment.Reoperation


Surgery_Schwartz

Surgery_Schwartz. change that is often confused with dysplasia should be suppressed by a course of acid suppression therapy in high doses for 2 to 3 months, followed by rebiopsy of the Barrett’s segment.Reoperation for Failed Antireflux Repairs. Failure of an antireflux procedure occurs when, after the repair, the patient is unable to swallow normally, experiences upper abdominal dis-comfort during and after meals, or has recurrence or persistence of reflux symptoms. The assessment of these symptoms and the selection of patients who need further surgery are challenging problems. Functional assessment of patients who have recur-rent, persistent, or emergent new symptoms following a primary antireflux repair is critical to identifying the cause of the failure. Analysis of patients requiring reoperation after a previous anti-reflux procedure shows that placement of the wrap around the stomach is the most frequent cause for failure after open proce-dures, while herniation of the repair into the chest is


Surgery_Schwartz

Surgery_Schwartz. a previous anti-reflux procedure shows that placement of the wrap around the stomach is the most frequent cause for failure after open proce-dures, while herniation of the repair into the chest is the most frequent cause of failure after a laparoscopic procedure. Partial or complete breakdown of the fundoplication and construction of a too-tight a fundoplication or overnarrowing the esophageal hiatus occurs with both open and closed procedures.Patients who have recurrence of heartburn and regurgitation without dysphagia and have good esophageal motility are most amenable to reoperation, and they can be expected to have an excellent outcome. When dysphagia is the cause of failure, the sit-uation can be more difficult to manage. If the dysphagia occurred immediately following the repair, it is usually due to a technical failure, most commonly a misplaced fundoplication around the upper stomach, or overnarrowing of the esophageal diaphragmatic hiatus and reoperation is usually


Surgery_Schwartz

Surgery_Schwartz. repair, it is usually due to a technical failure, most commonly a misplaced fundoplication around the upper stomach, or overnarrowing of the esophageal diaphragmatic hiatus and reoperation is usually satisfactory. When dysphagia is associated with poor motility and multiple previous repairs, fur-ther revision fundoplication is unlikely to be successful, and in otherwise fit patients it is appropriate to seriously consider esopha-geal resection. With each reoperation, the esophagus is damaged further, and the chance of preserving function is decreased. Also, blood supply is reduced, and ischemic necrosis of the esophagus can occur after several previous mobilizations.GIANT DIAPHRAGMATIC (HIATAL) HERNIASWith the advent of clinical radiology, it became evident that a diaphragmatic hernia was a relatively common abnormality and was not always accompanied by symptoms. Three types of esophageal hiatal hernia were identified: (a) the sliding hernia, type I, characterized by an upward


Surgery_Schwartz

Surgery_Schwartz. was a relatively common abnormality and was not always accompanied by symptoms. Three types of esophageal hiatal hernia were identified: (a) the sliding hernia, type I, characterized by an upward dislocation of the cardia in the posterior mediastinum (Fig. 25-39A); (b) the roll-ing or PEH, type II, characterized by an upward dislocation of the gastric fundus alongside a normally positioned cardia (Fig. 25-39B); and (c) the combined sliding-rolling or mixed hernia, type III, characterized by an upward dislocation of both the cardia and the gastric fundus (Fig. 25-39C). The end stage of type I and type II hernias occurs when the whole stomach migrates up into the chest by rotating 180° around its longitu-dinal axis, with the cardia and pylorus as fixed points. In this situation, the abnormality is usually referred to as an intratho-racic stomach (Fig. 25-39D). In some taxonomies, a type IV hiatal hernia is declared when an additional organ, usually the colon, herniates as well. Types


Surgery_Schwartz

Surgery_Schwartz. is usually referred to as an intratho-racic stomach (Fig. 25-39D). In some taxonomies, a type IV hiatal hernia is declared when an additional organ, usually the colon, herniates as well. Types II–IV hiatal hernias are also referred to as paraesophageal hernia (PEH), as a portion of the stomach is situated adjacent to the esophagus, above the gastroesophageal junction.Incidence and EtiologyThe true incidence of a hiatal hernia is difficult to determine because of the absence of symptoms in a large number of patients who are subsequently shown to have a hernia. When radiographic examinations are done in response to GI symptoms, Brunicardi_Ch25_p1009-p1098.indd 104501/03/19 6:03 PM 1046SPECIFIC CONSIDERATIONSPART IICDBAFigure 25-39. A. Radiogram of a type I (sliding) hiatal hernia. B. Radiogram of a type II (rolling or paraesophageal) hernia. C. Radiogram of a type III (combined sliding-rolling or mixed) hernia. D. Radiogram of an intrathoracic stomach. This is the end stage of a


Surgery_Schwartz

Surgery_Schwartz. Radiogram of a type II (rolling or paraesophageal) hernia. C. Radiogram of a type III (combined sliding-rolling or mixed) hernia. D. Radiogram of an intrathoracic stomach. This is the end stage of a large hiatal hernia regardless of its initial classification. Note that the stomach has rotated 180° around its longitudinal axis, with the cardia and pylorus as fixed points. (Reproduced with permission from Nyhus LM, Condon RE: Hernia, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1989.)Brunicardi_Ch25_p1009-p1098.indd 104601/03/19 6:03 PM 1047ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25the incidence of a sliding hiatal hernia is seven times higher than that of a PEH. The PEH is also known as the giant hiatal hernia. Over time the pressure gradient between the abdomen and chest enlarges the hiatal hernia. In many cases the type 1 sliding hernia will evolve into a type III mixed hernia. Type II hernias are quite rare. The age distribution of patients with PEHs is


Surgery_Schwartz

Surgery_Schwartz. and chest enlarges the hiatal hernia. In many cases the type 1 sliding hernia will evolve into a type III mixed hernia. Type II hernias are quite rare. The age distribution of patients with PEHs is significantly different from that observed in sliding hiatal hernias. The median age of the former is 61 years old; of the latter, 48 years old. PEHs are more likely to occur in women by a ratio of 4:1.Structural deterioration of the phrenoesophageal mem-brane over time may explain the higher incidence of hiatal her-nias in the older age group. These changes involve thinning of the upper fascial layer of the phrenoesophageal membrane (i.e., the supradiaphragmatic continuation of the endothoracic fascia) and loss of elasticity in the lower fascial layer (i.e., the infra-diaphragmatic continuation of the transversalis fascia). Conse-quently, the phrenoesophageal membrane yields to stretching in the cranial direction due to the persistent intra-abdominal pres-sure and the tug of esophageal


Surgery_Schwartz

Surgery_Schwartz. of the transversalis fascia). Conse-quently, the phrenoesophageal membrane yields to stretching in the cranial direction due to the persistent intra-abdominal pres-sure and the tug of esophageal shortening on swallowing. Inter-estingly, the stretching and thinning occurs more anteriorly and posteriorly, with fixation of the left crus of the diaphragm to the stomach at the 3 o’clock position, as viewed from the foot. This creates an anterior and posterior hernia sac, the latter of which is often filled with epiphrenic and retroperitoneal fat. These obser-vations point to the conclusion that the development of a hiatal hernia is an age-related phenomenon secondary to repetitive upward stretching of the phrenoesophageal membrane.Clinical ManifestationsThe clinical presentation of a giant hiatal (paraesophageal) her-nia differs from that of a sliding hernia. There is usually a higher prevalence of symptoms of dysphagia and postprandial fullness with PEHs, but the typical symptoms of


Surgery_Schwartz

Surgery_Schwartz. hiatal (paraesophageal) her-nia differs from that of a sliding hernia. There is usually a higher prevalence of symptoms of dysphagia and postprandial fullness with PEHs, but the typical symptoms of heartburn and regurgi-tation present in sliding hiatal hernias can also occur. Both are caused by gastroesophageal reflux secondary to an underlying mechanical deficiency of the cardia. The symptoms of dysphagia and postprandial fullness in patients with a PEH are explained by the compression of the adjacent esophagus by a distended cardia, or twisting of the GEJ by the torsion of the stomach that occurs as it becomes progressively displaced in the chest. The postprandial fullness or retrosternal chest pain is a thought to be a result of distension of the stomach with gas or food in the hiatal hernia. Many patients with sliding hernias and reflux symptoms will lose the reflux symptoms when the hernia evolves into the paraesophageal variety. This can be explained by the recreation of the


Surgery_Schwartz

Surgery_Schwartz. hernia. Many patients with sliding hernias and reflux symptoms will lose the reflux symptoms when the hernia evolves into the paraesophageal variety. This can be explained by the recreation of the cardiophrenic angle when the stomach herniates along-side the GEJ or becomes twisted in the sac. Repair of the hernia without addressing the reflux can create extremely bothersome heartburn. Respiratory complications are frequently associated with a PEH and consist of dyspnea and recurrent pneumonia from aspiration. New research demonstrates that the cause of dyspnea in the presence of a giant PEH is more likely to be left atrial compression, decreasing cardiac output, than a restrictive pulmonary effect, as has been hypothesized for many years.Approximately one-third of patients with a PEH are found to be anemic, which is due to recurrent bleeding from ulceration of the gastric mucosa in the herniated portion of the stomach, even if ulcerations are not detected at the time of endoscopy. The


Surgery_Schwartz

Surgery_Schwartz. to be anemic, which is due to recurrent bleeding from ulceration of the gastric mucosa in the herniated portion of the stomach, even if ulcerations are not detected at the time of endoscopy. The association of anemia and PEH is best proven by fixing the hernia. Anemia is corrected in >90% of patients with this condition. With time, more and more stomach migrates into the chest and can cause intermittent foregut obstruction due to the rotation that has occurred. In contrast, many patients with PEH are asymptomatic or complain of minor symptoms. However, the presence of a PEH can be life-threatening in that the hernia can lead to sudden catastrophic events, such as excessive bleed-ing or volvulus with acute gastric obstruction or infarction. With mild dilatation of the stomach, the gastric blood supply can be markedly reduced, causing gastric ischemia, ulceration, perfora-tion, and sepsis. The probability of incarceration/strangulation is not well known, although recent studies suggest


Surgery_Schwartz

Surgery_Schwartz. blood supply can be markedly reduced, causing gastric ischemia, ulceration, perfora-tion, and sepsis. The probability of incarceration/strangulation is not well known, although recent studies suggest that the lifetime risk is less than 5%, making this concern an insufficient concern for routine repair of the asymptomatic PEH.The symptoms of sliding hiatal hernias are usually due to functional abnormalities associated with gastroesophageal reflux and include heartburn, regurgitation, and dysphagia. These patients have a mechanically defective LES, giving rise to the reflux of gastric juice into the esophagus and the symp-toms of heartburn and regurgitation. The symptom of dysphagia occurs from the presence of mucosal edema, Schatzki’s ring, stricture, or the inability to organize peristaltic activity in the body of the esophagus as a consequence of the disease.There is a group of patients with sliding hiatal hernias not associated with reflux disease who have dysphagia without any


Surgery_Schwartz

Surgery_Schwartz. activity in the body of the esophagus as a consequence of the disease.There is a group of patients with sliding hiatal hernias not associated with reflux disease who have dysphagia without any obvious endoscopic or manometric explanation. Video barium radiograms have shown that the cause of dysphagia in these patients is an obstruction of the swallowed bolus by diaphrag-matic impingement on the herniated stomach. Manometrically, this is reflected by a double-humped high-pressure zone at the GEJ. The first pressure rise is due to diaphragmatic impinge-ment on the herniated stomach, and the second is due to the true distal esophageal sphincter. These patients usually have a mechanically competent sphincter, but the impingement of the diaphragm on the stomach can result in propelling the contents of the supradiaphragmatic portion of the stomach up into the esophagus and pharynx, resulting in complaints of pharyngeal regurgitation and aspiration. Consequently, this abnormality is often


Surgery_Schwartz

Surgery_Schwartz. of the supradiaphragmatic portion of the stomach up into the esophagus and pharynx, resulting in complaints of pharyngeal regurgitation and aspiration. Consequently, this abnormality is often confused with typical GERD. Surgical reduction of the hernia results in relief of the dysphagia in 91% of patients.DiagnosisA chest X-ray with the patient in the upright position can diag-nose a hiatal hernia if it shows an air-fluid level behind the car-diac shadow. This is usually caused by a PEH or an intrathoracic stomach. The accuracy of the upper GI barium study in detect-ing a paraesophageal hiatal hernia is greater than for a sliding hernia because the latter can often spontaneously reduce. The paraesophageal hiatal hernia is a permanent herniation of the stomach into the thoracic cavity, so a barium swallow provides the diagnosis in virtually every case. Attention should be focused on the position of the GEJ, when seen, to differentiate it from a type II hernia (see Fig. 25-39B and C).


Surgery_Schwartz

Surgery_Schwartz. a barium swallow provides the diagnosis in virtually every case. Attention should be focused on the position of the GEJ, when seen, to differentiate it from a type II hernia (see Fig. 25-39B and C). Fiber-optic esophagos-copy is useful in the diagnosis and classification of a hiatal hernia because the scope can be retroflexed. In this position, a sliding hiatal hernia can be identified by noting a gastric pouch lined with rugal folds extending above the impression caused by the crura of the diaphragm, or measuring at least 2 cm between the crura, identified by having the patient sniff, and the squamoco-lumnar junction on withdrawal of the scope (Fig. 25-40). A PEH is identified on retroversion of the scope by noting a separate orifice adjacent to the GEJ into which gastric rugal folds ascend. A sliding-rolling or mixed hernia can be identified by noting a gastric pouch lined with rugal folds above the diaphragm, with the GEJ entering about midway up the side of the


Surgery_Schwartz

Surgery_Schwartz. rugal folds ascend. A sliding-rolling or mixed hernia can be identified by noting a gastric pouch lined with rugal folds above the diaphragm, with the GEJ entering about midway up the side of the pouch.Brunicardi_Ch25_p1009-p1098.indd 104701/03/19 6:03 PM 1048SPECIFIC CONSIDERATIONSPART IIFigure 25-40. Endoscopic view through a retroflexed fiber-optic gastroscope showing the shaft of the scope (arrow) coming down through a sliding hernia. Note the gastric rugal folds extending above the impression caused by the crura of the diaphragm. (Repro-duced with permission from Nyhus LM, Condon RE: Hernia, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1989.)PathophysiologyPhysiologic testing with 24-hour esophageal pH monitoring has shown increased esophageal exposure to acid gastric juice in 60% of the patients with a paraesophageal hiatal hernia, com-pared with the observed 71% incidence in patients with a sliding hiatal hernia. It is now recognized that paraesophageal hiatal


Surgery_Schwartz

Surgery_Schwartz. juice in 60% of the patients with a paraesophageal hiatal hernia, com-pared with the observed 71% incidence in patients with a sliding hiatal hernia. It is now recognized that paraesophageal hiatal her-nia can be associated with pathologic gastroesophageal reflux.Physiologic studies have also shown that the competency of the cardia depends on an interrelationship between distal esophageal sphincter pressure, the length of the sphincter that is exposed to the positive-pressure environment of the abdomen, and the overall length of the sphincter. A deficiency in any one of these manometric characteristics of the sphincter is associated with incompetency of the cardia regardless of whether a hernia is present. Patients with a PEH who have an incompetent cardia have been shown to have a distal esophageal sphincter with nor-mal pressure, but a shortened overall length and displacement outside the positive-pressure environment of the abdomen. One might expect esophageal body function to be


Surgery_Schwartz

Surgery_Schwartz. esophageal sphincter with nor-mal pressure, but a shortened overall length and displacement outside the positive-pressure environment of the abdomen. One might expect esophageal body function to be diminished with the esophagus “accordioned” up into the chest. Surprisingly, esophageal peristalsis in patients with PEH is normal in 88%.TreatmentThe treatment of paraesophageal hiatal hernia is largely surgi-cal. Controversial aspects include: (a) indications for repair, (b) diaphragmatic repair, (c) role of fundoplication, and (d) exis-tence and treatment of the short esophagus.Indications and Surgical Approach. The presence of a paraesophageal hiatal hernia has traditionally been consid-ered an indication for surgical repair. This recommendation is largely based upon two clinical observations. First, retrospec-tive studies have shown a significant incidence of catastrophic, life-threatening complications of bleeding, infarction, and per-foration in patients being followed with known


Surgery_Schwartz

Surgery_Schwartz. First, retrospec-tive studies have shown a significant incidence of catastrophic, life-threatening complications of bleeding, infarction, and per-foration in patients being followed with known paraesophageal herniation. Second, emergency repair carries a high mortality. In the classic report of Skinner and Belsey, six of 21 patients with a PEH, treated medically because of minimal symptoms, died from the complications of strangulation, perforation, exsangui-nating hemorrhage, or acute dilatation of the herniated intratho-racic stomach. For the most part, these catastrophes occurred without warning. Others have reported similar findings.Recent studies suggest that catastrophic complications may be somewhat less common. Allen and colleagues followed 23 patients for a median of 78 months with only four patients pro-gressively worsening. There was a single mortality secondary to aspiration that occurred during a barium swallow examination to investigate progressive symptoms. Although


Surgery_Schwartz

Surgery_Schwartz. with only four patients pro-gressively worsening. There was a single mortality secondary to aspiration that occurred during a barium swallow examination to investigate progressive symptoms. Although emergency repairs had a median hospital stay of 48 days compared to a stay of 9 days in those having elective repair, there were only three cases of gastric strangulation in 735 patient-years of follow-up.If surgery is delayed and repair is done on an emergency basis, operative mortality is high, compared to <1% for an elec-tive repair. With this in mind, patients with a PEH are generally counseled to have elective repair of their hernia, particularly if they are symptomatic. Watchful waiting of asymptomatic PEHs may be an acceptable option.The surgical approach to repair of a paraesophageal hiatal hernia may be either transabdominal (laparoscopic or open) or transthoracic. Each has its advantages and disadvantages. A transthoracic approach facilitates complete esophageal mobi-lization


Surgery_Schwartz

Surgery_Schwartz. hiatal hernia may be either transabdominal (laparoscopic or open) or transthoracic. Each has its advantages and disadvantages. A transthoracic approach facilitates complete esophageal mobi-lization but is rarely used because the access trauma and postopera-tive pain are significantly greater than a laparoscopic approach.The transabdominal approach facilitates reduction of the volvulus that is often associated with PEHs. Although some degree of esophageal mobilization can be accomplished tran-shiatally, complete mobilization to the aortic arch is difficult or impossible without risk of injury to the vagal nerves.Laparoscopic repair of PEH would appear to have become the standard approach. Laparoscopic repair of a pure type II, or mixed type III PEH is an order of magnitude more difficult than a standard laparoscopic Nissen fundoplication. Most would rec-ommend that these procedures are best avoided until the surgeon has accumulated considerable experience with laparoscopic antireflux


Surgery_Schwartz

Surgery_Schwartz. than a standard laparoscopic Nissen fundoplication. Most would rec-ommend that these procedures are best avoided until the surgeon has accumulated considerable experience with laparoscopic antireflux surgery. There are several reasons for this. First, the vertical and horizontal volvulus of the stomach often associated with PEHs makes identification of the anatomy, in particular the location of the esophagus, difficult. Second, dissection of a large PEH sac may result in significant bleeding if the surgeon deviates from the correct plane of dissection between the peri-toneal sac and the endothoracic fascia. Finally, redundant tissue present at the GEJ following dissection of the sac frustrates the creation of a fundoplication. This tissue, which includes the epi-phrenic fat pad and hernia sac should be removed at the time of PEH repair. Mindful of these difficulties, and given appropriate experience, patients with PEH may be approached laparoscopi-cally, with expectation of success in


Surgery_Schwartz

Surgery_Schwartz. sac should be removed at the time of PEH repair. Mindful of these difficulties, and given appropriate experience, patients with PEH may be approached laparoscopi-cally, with expectation of success in the majority.Diaphragmatic RepairIt has been shown that PEH repair has a relatively high incidence of recurrence (10–40%) when the crura is closed primarily with permanent suture. Techniques to reduce hernia recurrence con-tinue to evolve. Most surgeons believe that recurrence may be reduced with the use of synthetic or biologic mesh to reinforce the standard crural closure. Randomized controlled studies have 4Brunicardi_Ch25_p1009-p1098.indd 104801/03/19 6:04 PM 1049ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25demonstrated a reduction in PEH recurrence rate when mesh was used. Nonabsorbable synthetic mesh must be used carefully and not in a keyhole fashion at the hiatus because of a potential risk of esophagus or gastric erosion and mesh infection. Bio-logic mesh (acellular porcine


Surgery_Schwartz

Surgery_Schwartz. synthetic mesh must be used carefully and not in a keyhole fashion at the hiatus because of a potential risk of esophagus or gastric erosion and mesh infection. Bio-logic mesh (acellular porcine dermis, acellular human dermis, porcine small intestinal submucosa) has become more widely used, but these meshes are significantly more expensive than synthetic mesh, and the only randomized study supporting bio-logic mesh usage failed to demonstrate superiority over suture alone after 5 years of rigorous follow-up.Role of Fundoplication in Giant Hiatal Hernia Repair. Controversy remains as to whether to perform an antireflux procedure at all, in selected cases only, or in all patients. Most advocate the routine addition of an antireflux procedure follow-ing repair of the hernia defect. There are several reasons for this. Physiologic testing with 24-hour esophageal pH monitoring has shown increased esophageal exposure to acid gastric juice in 60% to 70% of patients with a paraesophageal


Surgery_Schwartz

Surgery_Schwartz. are several reasons for this. Physiologic testing with 24-hour esophageal pH monitoring has shown increased esophageal exposure to acid gastric juice in 60% to 70% of patients with a paraesophageal hiatal hernia, nearly identical to the observed 71% incidence in patients with a sliding hiatal hernia. Furthermore, there is no relation between the symptoms experienced by the patient with a PEH and the competency of the cardia. Finally, dissection of the gastro-esophageal esophagus may lead to postoperative reflux despite a negative preoperative pH score.The Short Esophagus and PEHGiant PEH can be associated with a short esophagus in up to 5% to 20% of patients as a result of chronic cephalad displacement of the GEJ. The presence of a short esophagus increases the dif-ficulty of laparoscopic PEH repair. Approximately 10% to 20% of surgical failures with PEH repair is due to the lack of recogni-tion of a short esophagus. Preoperative results of barium swallow and


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Surgery_Schwartz. of laparoscopic PEH repair. Approximately 10% to 20% of surgical failures with PEH repair is due to the lack of recogni-tion of a short esophagus. Preoperative results of barium swallow and esophagogastroduodenoscopy may provide an indication of short esophagus, but no combination of preoperative clinical vari-ables reliably predict the presence of short esophagus, defined as the failure to achieve 2.5 cm of intra-abdominal esophagus with standard mediastinal dissection techniques. Hence, the diagno-sis of this entity continues to be made definitively only in the operating room. Collis gastroplasty achieves esophageal length-ening by creation of a neoesophagus using the gastric cardia. The totally laparoscopic approach to the short esophagus has evolved from a method using an end-to-end anastomosis circular stapler to the current approach that uses a linear stapler creating a sta-pled wedge gastroplasty. Elements of importance in fashioning the fundoplication after Collis gastroplasty


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Surgery_Schwartz. circular stapler to the current approach that uses a linear stapler creating a sta-pled wedge gastroplasty. Elements of importance in fashioning the fundoplication after Collis gastroplasty include placement of the initial suture of the fundoplication on the esophagus, immedi-ately above the GEJ to ensure that acid-secreting (gastric) mucosa does not reside above the fundoplication. A second element that ensures safety and avoids wrap deformation is to place the gastric portion of the staple line against the neoesophagus, such that the tip of the gastric staple line sits adjacent to the middle suture of the fundoplication on the right side of the esophagus.ResultsMost outcome studies report relief of symptoms following sur-gical repair of PEHs in more than 90% of patients. The current literature suggests that laparoscopic repair of a paraesophageal hiatal hernia can be successful. Most authors report symptom-atic improvement in 80% to 90% of patients, and <10% to 15% prevalence of


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Surgery_Schwartz. literature suggests that laparoscopic repair of a paraesophageal hiatal hernia can be successful. Most authors report symptom-atic improvement in 80% to 90% of patients, and <10% to 15% prevalence of recurrent symptomatic hernia. However, the problem of recurrent asymptomatic or minimally symp-tomatic hernia following PEH repair, open or laparoscopic, is Figure 25-41. Barium esophagogram showing Schatzki’s ring (i.e., a thin circumferential ring in the distal esophagus at the squa-mocolumnar junction). Below the ring is a hiatal hernia.becoming increasingly appreciated. Recurrent hiatal hernia is the most common cause of anatomic failure following laparoscopic Nissen fundoplication done for GERD (5–10%), but this risk is compounded for the giant hernia where radiologic recurrence is detected in 25% to 40% of patients. It appears that optimal results with open or laparoscopic giant hiatal hernia repair should include options for mesh buttressing of hiatal closure and selec-tive


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Surgery_Schwartz. detected in 25% to 40% of patients. It appears that optimal results with open or laparoscopic giant hiatal hernia repair should include options for mesh buttressing of hiatal closure and selec-tive esophageal lengthening with one of the many techniques developed for the creation of a Collis gastroplasty. Despite this high incidence of radiologic recurrence, and the surgical pursuit of a remedy, it must be reinforced that asymptomatic recurrent hernias, like primary PEH, do not need to be repaired. The risk of incarceration, strangulation, or obstruction is minimal.SCHATZKI’S RINGSchatzki’s ring is a thin submucosal circumferential ring in the lower esophagus at the squamocolumnar junction, often associ-ated with a hiatal hernia. Its significance and pathogenesis are unclear (Fig. 25-41). The ring was first noted by Templeton, but Schatzki and Gary defined it as a distinct entity in 1953. Its prevalence varies from 0.2% to 14% in the general population, depending on the technique of


Surgery_Schwartz

Surgery_Schwartz. The ring was first noted by Templeton, but Schatzki and Gary defined it as a distinct entity in 1953. Its prevalence varies from 0.2% to 14% in the general population, depending on the technique of diagnosis and the criteria used. Stiennon believed the ring to be a pleat of mucosa formed by infolding of redundant esophageal mucosa due to shortening of the esophagus. Others believe the ring to be congenital, and still others suggest it is an early stricture resulting from inflamma-tion of the esophageal mucosa caused by chronic reflux.Schatzki’s ring is a distinct clinical entity having different symptoms, upper GI function studies, and response to treatment compared with patients with a hiatal hernia, but without a ring. Twenty-four-hour esophageal pH monitoring has shown that patients with a Schatzki’s ring have a lower incidence of reflux than hiatal hernia controls. They also have better LES function. This, together with the presence of a ring, could represent a pro-tective


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Surgery_Schwartz. with a Schatzki’s ring have a lower incidence of reflux than hiatal hernia controls. They also have better LES function. This, together with the presence of a ring, could represent a pro-tective mechanism to prevent gastroesophageal reflux.Brunicardi_Ch25_p1009-p1098.indd 104901/03/19 6:04 PM 1050SPECIFIC CONSIDERATIONSPART IISymptoms associated with Schatzki’s ring are brief epi-sodes of dysphagia during hurried ingestion of solid foods. Its treatment has varied from dilation alone to dilation with antire-flux measures, antireflux procedure alone, incision, and even excision of the ring. Little is known about the natural progres-sion of Schatzki’s rings. Using radiologic techniques, Chen and colleagues showed progressive stenosis of rings in 59% of patients, whereas Schatzki found that the rings decreased in diameter in 29% of patients and remained unchanged in the rest.Symptoms in patients with a ring are caused more by the presence of the ring than by gastroesophageal reflux.


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Surgery_Schwartz. the rings decreased in diameter in 29% of patients and remained unchanged in the rest.Symptoms in patients with a ring are caused more by the presence of the ring than by gastroesophageal reflux. Most patients with a ring but without proven reflux respond to one dilation, while most patients with proven reflux require repeated dilations. In this regard, the majority of Schatzki’s ring patients without proven reflux have a history of ingestion of drugs known to be damaging to the esophageal mucosa. Bonavina and associates have suggested drug-induced injury as the cause of stenosis in patients with a ring, but without a history of reflux. Because rings also occur in patients with proven reflux, it is likely that gastroesophageal reflux also plays a part. This is supported by the fact that there is less drug ingestion in the history of these patients. Schatzki’s ring is prob-ably an acquired lesion that can lead to stenosis from chemical-induced injury by pill lodgment in the distal


Surgery_Schwartz

Surgery_Schwartz. there is less drug ingestion in the history of these patients. Schatzki’s ring is prob-ably an acquired lesion that can lead to stenosis from chemical-induced injury by pill lodgment in the distal esophagus, or from reflux-induced injury to the lower esophageal mucosa.The best form of treatment of a symptomatic Schatzki’s ring in patients who do not have reflux consists of esophageal dilation for relief of the obstructive symptoms. In patients with a ring who have proven reflux and a mechanically defective sphincter, an antireflux procedure is necessary to obtain relief and avoid repeated dilation.SCLERODERMAScleroderma is a systemic disease accompanied by esophageal abnormalities in approximately 80% of patients. In most, the disease follows a prolonged course. Renal involvement occurs in a small percentage of patients and signals a poor prognosis. The onset of the disease is usually in the third or fourth decade of life, occurring twice as frequently in women as in men.Small vessel


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Surgery_Schwartz. a small percentage of patients and signals a poor prognosis. The onset of the disease is usually in the third or fourth decade of life, occurring twice as frequently in women as in men.Small vessel inflammation appears to be an initiating event, with subsequent perivascular deposition of normal col-lagen, which may lead to vascular compromise. In the GI tract, the predominant feature is smooth muscle atrophy. Whether the atrophy in the esophageal musculature is a primary effect or occurs secondary to a neurogenic disorder is unknown. The results of pharmacologic and hormonal manipulation, with agents that act either indirectly via neural mechanisms or directly on the muscle, suggest that scleroderma is a pri-mary neurogenic disorder. Methacholine, which acts directly on smooth muscle receptors, causes a similar increase in LES pressure in normal controls and in patients with scleroderma. Edrophonium, a cholinesterase inhibitor that enhances the effect of acetylcholine when given to


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Surgery_Schwartz. causes a similar increase in LES pressure in normal controls and in patients with scleroderma. Edrophonium, a cholinesterase inhibitor that enhances the effect of acetylcholine when given to patients with sclero-derma, causes an increase in LES pressure that is less marked in these patients than in normal controls, suggesting a neurogenic rather than myogenic etiology. Muscle ischemia due to peri-vascular compression has been suggested as a possible mecha-nism for the motility abnormality in scleroderma. Others have observed that in the early stage of the disease, the manomet-ric abnormalities may be reversed by reserpine, an agent that depletes catecholamines from the adrenergic system. This sug-gests that, in early scleroderma, an adrenergic overactivity may be present that causes a parasympathetic inhibition, supporting SclerodermammHg35 –0Esophagus25 cmEsophagus30 cmEsophagus35 cmSSSS35 –0035 –Figure 25-42. Esophageal motility record in a patient with sclero-derma showing


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Surgery_Schwartz. a parasympathetic inhibition, supporting SclerodermammHg35 –0Esophagus25 cmEsophagus30 cmEsophagus35 cmSSSS35 –0035 –Figure 25-42. Esophageal motility record in a patient with sclero-derma showing aperistalsis in the distal two-thirds of the esopha-geal body with peristalsis in the proximal portion. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)a neurogenic mechanism for the disease. In advanced disease manifested by smooth muscle atrophy and collagen deposition, reserpine no longer produces this reversal. Consequently, from a clinical perspective, the patient can be described as having a poor esophageal pump and a poor valve.The diagnosis of scleroderma can be made manometrically by the observation of normal peristalsis in the proximal striated esophagus, with absent peristalsis in the distal smooth muscle por-tion (Fig. 25-42). The LES pressure is progressively weakened as


Surgery_Schwartz

Surgery_Schwartz. by the observation of normal peristalsis in the proximal striated esophagus, with absent peristalsis in the distal smooth muscle por-tion (Fig. 25-42). The LES pressure is progressively weakened as the disease advances. Because many of the systemic sequelae of the disease may be nondiagnostic, the motility pattern is fre-quently used as a specific diagnostic indicator. Gastroesophageal reflux commonly occurs in patients with scleroderma because they have both hypotensive sphincters and poor esophageal clearance. This combined defect can lead to severe esophagitis and stricture formation. The typical barium swallow shows a dilated, barium-filled esophagus, stomach, and duodenum, or a hiatal hernia with distal esophageal stricture and proximal dilatation (Fig. 25-43).Traditionally, esophageal symptoms have been treated with PPIs, antacids, elevation of the head of the bed, and multiple dilations for strictures, with generally unsatisfac-tory results. The degree of esophagitis is usually


Surgery_Schwartz

Surgery_Schwartz. symptoms have been treated with PPIs, antacids, elevation of the head of the bed, and multiple dilations for strictures, with generally unsatisfac-tory results. The degree of esophagitis is usually severe and may lead to marked esophageal shortening as well as stric-ture. Scleroderma patients have frequently had numerous dilations before they are referred to the surgeon. The surgi-cal management is somewhat controversial, but the major-ity of opinion suggests that a partial fundoplication (anterior or posterior) performed laparoscopically is the procedure of choice. The need for a partial fundoplication is dictated by the likelihood of severe dysphagia if a total fundoplication is performed in the presence of aperistalsis. Esophageal short-ening may require a Collis gastroplasty in combination with a partial fundoplication. Surgery reduces esophageal acid exposure but does not return it to normal because of the poor Brunicardi_Ch25_p1009-p1098.indd 105001/03/19 6:04 PM


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Surgery_Schwartz. in combination with a partial fundoplication. Surgery reduces esophageal acid exposure but does not return it to normal because of the poor Brunicardi_Ch25_p1009-p1098.indd 105001/03/19 6:04 PM 1051ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-43. Barium esophagogram of a patient with sclero-derma and stricture. Note the markedly dilated esophagus and retained food material. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Figure 25-44. The esophagus on the left shows a stacking of rings, demonstrating eosinophilic esophagus. The esophagus on the right is a normal barium swallow.EOSINOPHILIC ESOPHAGITISEosinophilic esophagitis (EE) was first described in 1977, but it has become well known only in the last two decades. The condi-tion is characterized by a constellation of symptoms, endoscopic and radiologic findings, and distinctive pathology. The etiology of


Surgery_Schwartz

Surgery_Schwartz. it has become well known only in the last two decades. The condi-tion is characterized by a constellation of symptoms, endoscopic and radiologic findings, and distinctive pathology. The etiology of eosinophilic esophagitis is not entirely known but its simi-larities, immunologically, to asthma suggest that it is a form of “allergic esophagitis.”SymptomsThe presentation of eosinophilic esophagitis is chest pain (often postprandial) and dysphagia. Dysphagia may occur with liquids or solids, but solid food dysphagia is most common. Because dysphagia and chest pain are characteristic of GERD, EE is often confused with GERD; however, EE does not respond to proton pump inhibitors. The evaluation of the patient with EE and dysphagia and chest pain with esophagram and endoscopy usually reveals the diagnosis.SignsA barium swallow should be the first test obtained in the patient with dysphagia. EE has a characteristic finding often called the “ringed esophagus” or the “feline esophagus,” as the


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Surgery_Schwartz. diagnosis.SignsA barium swallow should be the first test obtained in the patient with dysphagia. EE has a characteristic finding often called the “ringed esophagus” or the “feline esophagus,” as the esophageal rings are felt to look like the stripes on a housecat (Fig. 25-44). The endoscopic appearance of EE is also characteristic, and also appears as a series of rings (Fig. 25-45).PathologyEndoscopic biopsy specimens should be taken when eosin-ophilic esophagus is suspected. To make the diagnosis of EE, the pathologist should see a minimum of 15 eosinophils per high powered field, usually at the base of the epithelium (Fig. 25-46).TreatmentThe treatment of EE is largely symptomatic and includes test-ing for food allergies and elimination of identified items from the diet. Second-line therapy includes inhaled or ingested cor-ticosteroids, as would be used to treat asthma. If dysphagia is not relieved with steroids, it may be necessary to dilate the clearance function of the body of


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Surgery_Schwartz. includes inhaled or ingested cor-ticosteroids, as would be used to treat asthma. If dysphagia is not relieved with steroids, it may be necessary to dilate the clearance function of the body of the esophagus. Only 50% of the patients have a good-to-excellent result. If the esopha-gitis is severe, or there has been a previous failed antireflux procedure and the disease is associated with delayed gastric emptying, a gastric resection with Roux-en-Y gastrojejunos-tomy has proved the best option.Brunicardi_Ch25_p1009-p1098.indd 105101/03/19 6:04 PM 1052SPECIFIC CONSIDERATIONSPART IIFigure 25-46. A cluster of eosinophils are visualized in the esophageal epithelium in a patient with EE.Figure 25-45. The endoscopic appearance of eosinophilic esopha-gitis is characteristically a series of stacked mucosal rings.esophagus. Because of the length of esophageal involvement, rigid dilators (Maloney or Savary) are often used. Great care must be exercised, as the inflamed EE is quite friable. The


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Surgery_Schwartz. mucosal rings.esophagus. Because of the length of esophageal involvement, rigid dilators (Maloney or Savary) are often used. Great care must be exercised, as the inflamed EE is quite friable. The mucosal tears easily, and esophageal perforation (full thickness laceration) has been reported with EE dilation.MOTILITY DISORDERS OF THE PHARYNX AND ESOPHAGUSClinical ManifestationsDysphagia (i.e., difficulty in swallowing) is the primary symp-tom of esophageal motor disorders. Its perception by the patient is a balance between the severity of the underlying abnormality causing the dysphagia and the adjustment made by the patient in altering eating habits. Consequently, any complaint of dyspha-gia must include an assessment of the patient’s dietary history. It must be known whether the patient experiences pain, chokes, or vomits with eating; whether the patient requires liquids with the meal, is the last to finish, or is forced to interrupt or avoid a social meal; and whether he or she has


Surgery_Schwartz

Surgery_Schwartz. experiences pain, chokes, or vomits with eating; whether the patient requires liquids with the meal, is the last to finish, or is forced to interrupt or avoid a social meal; and whether he or she has been admitted to the hos-pital for food impaction. These assessments, plus an evaluation of the patient’s nutritional status, help to determine how severe the dysphagia is and judge the need for surgical intervention, rather than more conservative methods of treating dysphagia.Motility Disorders of the Pharynx and Upper Esophagus—Transit DysphagiaDisorders of the pharyngeal phase of swallowing result from a discoordination of the neuromuscular events involved in chew-ing, initiation of swallowing, and propulsion of the material from the oropharynx into the cervical esophagus. They can be categorized into one or a combination of the following abnor-malities: (a) inadequate oropharyngeal bolus transport; (b) inability to pressurize the pharynx; (c) inability to elevate the larynx; (d)


Surgery_Schwartz

Surgery_Schwartz. categorized into one or a combination of the following abnor-malities: (a) inadequate oropharyngeal bolus transport; (b) inability to pressurize the pharynx; (c) inability to elevate the larynx; (d) discoordination of pharyngeal contraction and cri-copharyngeal relaxation; and (e) decreased compliance of the pharyngoesophageal segment secondary to neuromuscular dis-ease. The latter may result in incomplete relaxation of the crico-pharyngeus and cervical esophagus during swallowing. Taken together, these disorders are termed transit dysphagia by many.Transit dysphagia is usually congenital or results from acquired disease involving the central and peripheral nervous system. This includes cerebrovascular accidents, brain stem tumors, poliomyelitis, multiple sclerosis, Parkinson’s disease, pseudobulbar palsy, peripheral neuropathy, and operative dam-age to the cranial nerves involved in swallowing. Pure muscular diseases such as radiation-induced myopathy, dermatomyositis, myotonic


Surgery_Schwartz

Surgery_Schwartz. pseudobulbar palsy, peripheral neuropathy, and operative dam-age to the cranial nerves involved in swallowing. Pure muscular diseases such as radiation-induced myopathy, dermatomyositis, myotonic dystrophy, and myasthenia gravis are less common causes. Rarely, extrinsic compression of the cervical esophagus by thyromegaly, lymphadenopathy, or hyperostosis of the cervi-cal spine can cause transit dysphagia.Diagnostic Assessment of the Cricopharyngeal SegmentTransit dysphagia difficult to assess with standard manometric techniques because of the rapidity of the oropharyngeal phase of swallowing, the elevation of the larynx, and the asymmetry of the cricopharyngeus. Videoor cineradiography is currently the Brunicardi_Ch25_p1009-p1098.indd 105201/03/19 6:04 PM 1053ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25ABFigure 25-47. A. Zenker’s diverticulum, initially discovered 15 years ago and left untreated. B. Note its marked enlargement and evidence of laryngeal inlet aspiration on recent


Surgery_Schwartz

Surgery_Schwartz. HERNIACHAPTER 25ABFigure 25-47. A. Zenker’s diverticulum, initially discovered 15 years ago and left untreated. B. Note its marked enlargement and evidence of laryngeal inlet aspiration on recent esophagogram. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Time 0Peak pharyngealpressureAtmosphericpressureABBolus pressureinitialMaximum residual(MaxR)contractionB0finalMinimum Residual(MinR)Subatomic pressureFigure 25-48. A. Schematic drawing of a pharyngeal pressure wave indicating the presence of the bolus pressure. B. Schematic drawing of the manometric recording typically seen during crico-pharyngeal sphincter relaxation.most objective test to evaluate oropharyngeal bolus transport, pharyngeal compression, relaxation of the pharyngoesophageal segment, and the dynamics of airway protection during swal-lowing. It readily identifies a diverticulum (Fig. 25-47), stasis of the


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Surgery_Schwartz. pharyngeal compression, relaxation of the pharyngoesophageal segment, and the dynamics of airway protection during swal-lowing. It readily identifies a diverticulum (Fig. 25-47), stasis of the contrast medium in the valleculae, a cricopharyngeal bar, and/or narrowing of the pharyngoesophageal segment. These are anatomic manifestations of neuromuscular disease, and they result from the loss of muscle compliance in portions of the pharynx and esophagus composed of skeletal muscle.Careful analysis of videoor cineradiographic studies com-bined with manometry using specially designed catheters can identify the cause of a pharyngoesophageal dysfunction in most sit-uations (Fig. 25-48). Motility studies may demonstrate inadequate pharyngeal pressurization, insufficient or lack of cricopharyngeal relaxation, marked discoordination of pharyngeal pressurization, cricopharyngeal relaxation and cervical esophageal contraction, or a hypopharyngeal bolus pressure suggesting decreased compli-ance of


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Surgery_Schwartz. relaxation, marked discoordination of pharyngeal pressurization, cricopharyngeal relaxation and cervical esophageal contraction, or a hypopharyngeal bolus pressure suggesting decreased compli-ance of the skeletal portion of the cervical esophagus.In many patients with cricopharyngeal dysfunction, including those with Zenker’s diverticulum, it has been difficult to consistently demonstrate a motility abnormality or discoor-dination of pharyngoesophageal events. The abnormality most apt to be present is a loss of compliance in the pharyngoesopha-geal segment manifested by an increased bolus pressure. Cook and colleagues have demonstrated an increased resistance to the movement of a bolus through what appears on manometry to be a completely relaxed cricopharyngeal sphincter. Using simulta-neous manometry and videofluoroscopy, they showed that, in these patients, the cricopharyngeus is only partially relaxed; that is, the sphincter is relaxed enough to allow a drop of its pressure to


Surgery_Schwartz

Surgery_Schwartz. manometry and videofluoroscopy, they showed that, in these patients, the cricopharyngeus is only partially relaxed; that is, the sphincter is relaxed enough to allow a drop of its pressure to esophageal baseline on manometry, but insufficiently relaxed to allow unimpaired passage of the bolus into the esophagus. This incomplete relaxation is due to a loss of compliance of the muscle in the pharyngoesophageal segment, and may be associ-ated with a cricopharyngeal bar or Zenker’s diverticulum. This decreased compliance of the cricopharyngeal sphincter can be recognized on esophageal manometry by a “shoulder” on the pharyngeal pressure wave, the amplitude of which correlates directly with the degree of outflow obstruction (Fig. 25-49). Increasing the diameter of this noncompliant segment reduces the resistance imposed on the passage of a bolus. Consequently, patients with low pharyngeal pressure (i.e., poor piston function of the pharynx), or patients with increased resistance of the


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Surgery_Schwartz. reduces the resistance imposed on the passage of a bolus. Consequently, patients with low pharyngeal pressure (i.e., poor piston function of the pharynx), or patients with increased resistance of the pha-ryngocervical esophageal segment from loss of skeletal muscle compliance, are improved by a cricopharyngeal myotomy. This enlarges the pharyngoesophageal segment and reduces outflow resistance. Esophageal muscle biopsy specimens from patients with Zenker’s diverticulum have shown histologic evidence of the restrictive myopathy in the cricophayngeous muscle. These findings correlate well with the observation of a decreased com-pliance of the upper esophagus demonstrated by videoradiog-raphy and the findings on detailed manometric studies of the pharynx and cervical esophagus. They suggest that the diver-ticulum develops as a consequence of the outflow resistance to bolus transport through the noncompliant muscle of the pharyn-goesophageal segment.The requirements for a successful


Surgery_Schwartz

Surgery_Schwartz. that the diver-ticulum develops as a consequence of the outflow resistance to bolus transport through the noncompliant muscle of the pharyn-goesophageal segment.The requirements for a successful pharyngoesophageal myotomy are (a) adequate oropharyngeal bolus transport; (b) the presence of an intact swallowing reflex; (c) reasonable coordi-nation of pharyngeal pressurization with cricopharyngeal relax-ation; and (d) a cricopharyngeal bar, Zenker’s diverticulum, or a narrowed pharyngoesophageal segment on videoesophagogram and/or the presence of excessive pharyngoesophageal shoulder pressure on motility study.Zenker’s Diverticulum. In the past, the most common recog-nized sign of cricopharyngeal dysfunction was the presence of a Brunicardi_Ch25_p1009-p1098.indd 105301/03/19 6:04 PM 1054SPECIFIC CONSIDERATIONSPART IIZenker’s diverticulum, originally described by Ludlow in 1769. The eponym resulted from Zenker’s classic clinicopathologic descriptions of 34 cases published in 1878.


Surgery_Schwartz

Surgery_Schwartz. CONSIDERATIONSPART IIZenker’s diverticulum, originally described by Ludlow in 1769. The eponym resulted from Zenker’s classic clinicopathologic descriptions of 34 cases published in 1878. Pharyngoesophageal diverticula have been reported to occur in 1 of 1000 routine barium examinations, and classically occur in elderly, white males. Zenker’s diverticula tend to enlarge progressively with time due to the decreased compliance of the skeletal portion of the cervical esophagus that occurs with aging.Presenting symptoms include dysphagia associated with the spontaneous regurgitation of undigested, bland material, often interrupting eating or drinking. On occasion, the dyspha-gia can be severe enough to cause debilitation and significant weight loss. Chronic aspiration and repetitive respiratory infec-tion are common associated complaints. Once suspected, the diagnosis is established by a barium swallow. Endoscopy is usually difficult in the presence of a cricopharyngeal diverticu-lum, and


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Surgery_Schwartz. infec-tion are common associated complaints. Once suspected, the diagnosis is established by a barium swallow. Endoscopy is usually difficult in the presence of a cricopharyngeal diverticu-lum, and potentially dangerous, owing to obstruction of the true esophageal lumen by the diverticulum and the attendant risk of diverticular perforation.Cricopharyngeal Myotomy. The low morbidity and mor-tality associated with cricopharyngeal and upper esophageal myotomy have encouraged a liberal approach toward its use for almost any problem in the oropharyngeal phase of swallowing. This attitude has resulted in an overall success rate in the relief of symptoms of only 64%. When patients are selected for sur-gery using radiographic or motility markers of disease, a much higher proportion will benefit. Two methods of cricopharyngo-esophageal myotomy are in common use, one using traditional surgical approaches, and one using rigid laryngoscopy and a linear cutting stapler.Open Cricopharyngeal


Surgery_Schwartz

Surgery_Schwartz. Two methods of cricopharyngo-esophageal myotomy are in common use, one using traditional surgical approaches, and one using rigid laryngoscopy and a linear cutting stapler.Open Cricopharyngeal Myotomy, Diverticulopexy, and Diverticulectomy. The myotomy can be performed under local or general anesthesia through an incision along the anterior border of the left sternocleidomastoid muscle. The pharynx and cervi-cal esophagus are exposed by retracting the sternocleidomastoid muscle and carotid sheath laterally and the thyroid, trachea, and larynx medially (Fig. 25-50). When a pharyngoesophageal diverticulum is present, localization of the pharyngoesophageal segment is easy. The diverticulum is carefully freed from the overlying areolar tissue to expose its neck, just below the inferior pharyngeal constrictor and above the cricopharyngeus muscle. It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum. A benefit of local anesthesia is that the patient


Surgery_Schwartz

Surgery_Schwartz. constrictor and above the cricopharyngeus muscle. It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum. A benefit of local anesthesia is that the patient can swallow and demonstrate an area of persistent nar-rowing at the pharyngoesophageal junction. Furthermore, before closing the incision, gelatin can be fed to the patient to ascertain whether the symptoms have been relieved, and to inspect the opening of the previously narrowed pharyngoesophageal seg-ment. Under general anesthesia, and in the absence of a diver-ticulum, the placement of a nasogastric tube to the level of the manometrically determined cricopharyngeal sphincter helps in localization of the structures. The myotomy is extended cephalad by dividing 1 to 2 cm of inferior constrictor muscle of the phar-ynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4 to 5 cm. The cervical wound is closed only when all oozing of blood has ceased


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Surgery_Schwartz. muscle of the phar-ynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4 to 5 cm. The cervical wound is closed only when all oozing of blood has ceased because a hematoma after this procedure is common and is often associated with temporary dysphagia while the hematoma absorbs. Oral ali-mentation is started the day after surgery. The patient is usually discharged on the first or second postoperative day.mm Hg40–0102030400HypopharynxCricopharyngeusFigure 25-50. Cross-section of the neck at the level of the thyroid isthmus that shows the sur-gical approach to the hypopharynx and cervical esophagus. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor dis-orders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Swallow volume010Pharyngeal shoulderpressure mmHgControlsZenker’s2030405101520200150100UES area mm25005101520Zenker’sControlsFigure 25-49. Pharyngeal shoulder pressures and diameter of the


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Surgery_Schwartz. volume010Pharyngeal shoulderpressure mmHgControlsZenker’s2030405101520200150100UES area mm25005101520Zenker’sControlsFigure 25-49. Pharyngeal shoulder pressures and diameter of the pharyngoesophageal segment in controls and patients with Zenker’s diverticulum. UES = upper esophageal sphincter. (Data from Cook IJ, et al. Zenker’s diverticu-lum: evidence for a restrictive cricopharyngeal myopathy. Gastroenterology. 1989;96:A98.)Brunicardi_Ch25_p1009-p1098.indd 105401/03/19 6:04 PM 1055ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Prevertebral fascia MyotomyZenker’sdiverticulumFigure 25-51. Posterior of the anatomy of the pharynx and cervical esophagus showing pharyngoesophageal myotomy and pexing of the diverticulum to the prevertebral fascia.If a diverticulum is present and is large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (i.e., diverticu-lopexy) (Fig. 25-51). If the diverticulum is


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Surgery_Schwartz. large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (i.e., diverticu-lopexy) (Fig. 25-51). If the diverticulum is excessively large so that it would be redundant if suspended, or if its walls are thick-ened, a diverticulectomy should be performed. This is best per-formed under general anesthesia by placing a Maloney dilator (48F) in the esophagus, after controlling the neck of the diver-ticulum and after myotomy. A linear stapler is placed across the neck of the diverticulum, and the diverticulum is excised distal to the staple line. The security of this staple line and effective-ness of the myotomy may be tested before hospital discharge with a water-soluble contrast esophagogram. Postoperative complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner’s syndrome. The incidence of the first two can be reduced by per-forming a


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Surgery_Schwartz. complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner’s syndrome. The incidence of the first two can be reduced by per-forming a diverticulopexy rather than diverticulectomy.Endoscopic Cricopharyngotomy. Endoscopic stapled crico-pharyngotomy and diverticulotomy recently has been described. This procedure is most effective for larger diverticula (>2 cm) and may be impossible to perform for the small diverticulum. The procedure uses a specialized “diverticuloscope” with two retractable valves passed into the hypopharynx. The lips of the diverticuloscope are positioned so that one lip lies in the esopha-geal lumen and the other in the diverticular lumen. The valves of the diverticuloscope are retracted appropriately so as to visu-alize the septum interposed between the diverticulum and the esophagus. An endoscopic linear stapler is introduced into the diverticuloscope and positioned against the common septum with the


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Surgery_Schwartz. to visu-alize the septum interposed between the diverticulum and the esophagus. An endoscopic linear stapler is introduced into the diverticuloscope and positioned against the common septum with the anvil in the diverticulum and the cartridge in the esoph-ageal lumen. Firing of the stapler divides the common septum between the posterior esophageal and the diverticular wall over a length of 30 mm, placing three rows of staples on each side. More than one stapler application may be needed, depending on the size of the diverticulum (Fig. 25-52). The patient is allowed to resume liquid feeds immediately and is usually discharged the day after surgery. Complications are rare and may include perforation at the apex of the diverticulum and failure to relieve dysphagia resulting from incomplete myotomy. The former complication can usually be treated with antibiotics, but it may, rarely, require neck drainage.Recurrence of a Zenker’s diverticulum may occur with long follow-up and is more


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Surgery_Schwartz. myotomy. The former complication can usually be treated with antibiotics, but it may, rarely, require neck drainage.Recurrence of a Zenker’s diverticulum may occur with long follow-up and is more common after diverticulectomy without myotomy, presumably due to persistence of the under-lying loss of compliance of the cervical esophagus when a myot-omy is not performed. After endoscopic cricopharyngotomy Figure 25-52. The technique for transoral cricopharyngotomy and Zenker’s diverticulotomy.lateral residual “pouches” may be seen on radiographs, but they are rarely responsible for residual or recurrent symptoms if the myotomy has been complete.Postoperative motility studies have shown that the peak pharyngeal pressure generated on swallowing is not affected, the resting cricopharyngeal pressure is reduced but not elimi-nated, and the cricopharyngeal sphincter length is shortened. Consequently, after myotomy, there is protection against esoph-agopharyngeal regurgitation.Motility


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Surgery_Schwartz. pressure is reduced but not elimi-nated, and the cricopharyngeal sphincter length is shortened. Consequently, after myotomy, there is protection against esoph-agopharyngeal regurgitation.Motility Disorders of the Esophageal Body and Lower Esophageal SphincterDisorders of the esophageal phase of swallowing result from abnormalities in the propulsive pump action of the esophageal body or the relaxation of the LES. These disorders result from either primary esophageal abnormalities, or from generalized neural, muscular, or collagen vascular disease (Table 25-8). The use of standard and high-resolution esophageal manometry techniques has allowed specific primary esophageal motility disorders to be identified out of a pool of nonspecific motil-ity abnormalities. Primary esophageal motor disorders include achalasia, DES, nutcracker esophagus, and the hypertensive LES. The manometric characteristics of these disorders are shown in Table 25-9.The boundaries between the primary esophageal


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Surgery_Schwartz. include achalasia, DES, nutcracker esophagus, and the hypertensive LES. The manometric characteristics of these disorders are shown in Table 25-9.The boundaries between the primary esophageal motor disorders are vague, and intermediate types exist, some of which may combine more than one type of motility pattern. These findings indicate that esophageal motility disorders should be looked at as a spectrum of abnormalities that reflects various stages of destruction of esophageal motor function.Achalasia. The best known and best understood primary motil-ity disorder of the esophagus is achalasia, with an incidence of six Brunicardi_Ch25_p1009-p1098.indd 105501/03/19 6:04 PM 1056SPECIFIC CONSIDERATIONSPART IITable 25-9Manometric characteristics of the primary esophageal motility disordersAchalasiaIncomplete lower esophageal sphincter (LES) relaxation (<75% relaxation)Aperistalsis in the esophageal bodyElevated LES pressure ≤26 mmHgIncreased intraesophageal baseline pressures relative


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Surgery_Schwartz. lower esophageal sphincter (LES) relaxation (<75% relaxation)Aperistalsis in the esophageal bodyElevated LES pressure ≤26 mmHgIncreased intraesophageal baseline pressures relative to gastric baselineDiffuse esophageal spasm (DES)Simultaneous (nonperistaltic contractions) (>20% of wet swallows)Repetitive and multipeaked contractionsSpontaneous contractionsIntermittent normal peristalsisContractions may be of increased amplitude and durationNutcracker esophagusMean peristaltic amplitude (10 wet swallows) in distal esophagus ≥180 mmHgIncreased mean duration of contractions (>7.0 s)Normal peristaltic sequenceHypertensive lower esophageal sphincterElevated LES pressure (≥26 mmHg)Normal LES relaxationNormal peristalsis in the esophageal bodyIneffective esophageal motility disordersDecreased or absent amplitude of esophageal peristalsis (<30 mmHg)Increased number of nontransmitted contractionsReproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary


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Surgery_Schwartz. absent amplitude of esophageal peristalsis (<30 mmHg)Increased number of nontransmitted contractionsReproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary Tract, 3rd ed. Vol 1. Philadelphia, PA: Elsevier/Saunders; 1991.Simultaneous esophageal waves develop as a result of the increased resistance to esophageal emptying caused by the nonre-laxing LES. This conclusion is supported by experimental studies in which a band placed loosely around the GEJ in experimental models did not change sphincter pressures but resulted in impaired relaxation of the LES and outflow resistance. This led to a mark-edly increased frequency of simultaneous waveforms and a decrease in contraction amplitude. The changes were associated with radiographic dilation of the esophagus and were reversible after removal of the band. Observations in patients with pseudo-achalasia due to tumor infiltration, a tight stricture in the distal esophagus, or an antireflux procedure


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Surgery_Schwartz. and were reversible after removal of the band. Observations in patients with pseudo-achalasia due to tumor infiltration, a tight stricture in the distal esophagus, or an antireflux procedure that is too tight also provide evidence that dysfunction of the esophageal body can be caused by the increased outflow obstruction of a nonrelaxing LES. The observation that esophageal peristalsis can return in patients with classic achalasia following dilation or myotomy provides further support that achalasia is a primary disease of the LES.The pathogenesis of achalasia is presumed to be a neuro-genic degeneration, which is either idiopathic or due to infec-tion. In experimental animals, the disease has been reproduced by destruction of the nucleus ambiguus and the dorsal motor nucleus of the vagus nerve. In patients with the disease, degenerative changes have been shown in the vagus nerve and in the ganglia in the myenteric plexus of the esophagus itself. This degeneration results in


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Surgery_Schwartz. the vagus nerve. In patients with the disease, degenerative changes have been shown in the vagus nerve and in the ganglia in the myenteric plexus of the esophagus itself. This degeneration results in hypertension of the LES, a failure of the sphincter to relax on swallowing, elevation of intraluminal esophageal pres-sure, esophageal dilatation, and a subsequent loss of progressive peristalsis in the body of the esophagus. The esophageal dilatation results from the combination of a nonrelaxing sphincter, which causes a functional retention of ingested material in the esopha-gus, and elevation of intraluminal pressure from repetitive pha-ryngeal air swallowing (Fig. 25-53). With time, the functional disorder results in anatomic alterations seen on radiographic stud-ies, such as a dilated esophagus with a tapering, “bird’s beak”-like narrowing of the distal end (Fig. 25-54). There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which


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Surgery_Schwartz. esophagus with a tapering, “bird’s beak”-like narrowing of the distal end (Fig. 25-54). There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which reflects the degree of resistance imposed by the nonrelaxing sphincter. As the disease progresses, the esophagus becomes massively dilated and tortuous.A subgroup of patients with otherwise typical features of classic achalasia has simultaneous contractions of their esopha-geal body that can be of high amplitude. This manometric pattern has been termed vigorous achalasia, and chest pain episodes are a common finding in these patients. Since the development of high resolution esophageal manometry technology, the term vigorous achalasia has been replaced with Chicago type 3 achalasia. Dif-ferentiation of type 3 achalasia from DES can be difficult. In both diseases, videoradiographic examination may show a cork-screw deformity of the esophagus and diverticulum formation.Diffuse and Segmental


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Surgery_Schwartz. of type 3 achalasia from DES can be difficult. In both diseases, videoradiographic examination may show a cork-screw deformity of the esophagus and diverticulum formation.Diffuse and Segmental Esophageal Spasm. DES is charac-terized by substernal chest pain and/or dysphagia. DES differs from classic achalasia in that it is primarily a disease of the esophageal body, produces a lesser degree of dysphagia, causes more chest pain, and has less effect on the patient’s general con-dition. Nonetheless, it is impossible to differentiate achalasia from DES on the basis of symptoms alone. Esophagogram and esophageal manometry are required to distinguish these two entities. True symptomatic DES is a rare condition, occurring about five times less frequently than achalasia.The causation and neuromuscular pathophysiology of DES are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in Table 25-8Esophageal motility disordersPrimary


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Surgery_Schwartz. pathophysiology of DES are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in Table 25-8Esophageal motility disordersPrimary esophageal motility disordersAchalasia, “vigorous” achalasiaDiffuse and segmental esophageal spasmNutcracker esophagusHypertensive lower esophageal sphincterNonspecific esophageal motility disordersSecondary esophageal motility disordersCollagen vascular diseases: progressive systemic sclerosis, polymyositis and dermatomyositis, mixed connective tissue disease, systemic lupus erythematosus, etc.Chronic idiopathic intestinal pseudoobstructionNeuromuscular diseasesEndocrine and metastatic disordersper 100,000 population per year. Although complete absence of peristalsis in the esophageal body has been proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES. This is based on 24-hour outpatient esophageal motility monitoring, which shows that, even in


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Surgery_Schwartz. proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES. This is based on 24-hour outpatient esophageal motility monitoring, which shows that, even in advanced disease, up to 5% of contractions can be peristaltic. 5Brunicardi_Ch25_p1009-p1098.indd 105601/03/19 6:04 PM 1057ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25A34140120100806050403020100–10–2056*60453525159–5–15–25–3550403020100–10–206040200–20100 mmHg10 mins10 secs100 mmHgB3*4*1501401201008060402001501401201008060402005*1501401201008060402006*1451251051008565455–15MealFigure 25-53. Pressurization of esophagus: ambulatory motility tracing of a patient with achalasia. A. Before esophageal myotomy. B. After esophageal myotomy. The tracings have been compressed to exaggerate the motility spikes and baseline elevations. Note the rise in esophageal baseline pressure during a meal represented by the rise off the baseline to the left of panel A. No such rise occurs postmyotomy


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Surgery_Schwartz. motility spikes and baseline elevations. Note the rise in esophageal baseline pressure during a meal represented by the rise off the baseline to the left of panel A. No such rise occurs postmyotomy (B).Figure 25-54. Barium esophagogram showing a markedly dilated esophagus and characteristic “bird’s beak” in achalasia. (Repro-duced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)the latency gradient. Hypertrophy of the muscular layer of the esophageal wall and degeneration of the esophageal branches of the vagus nerve have been observed in this disease, although these are not constant findings. Manometric abnormalities in DES may be present over the total length of the esophageal body but usually are confined to the distal two-thirds. In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.The classic manometric findings in these


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Surgery_Schwartz. usually are confined to the distal two-thirds. In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.The classic manometric findings in these patients are characterized by the frequent occurrence of simultaneous wave-forms and multipeaked esophageal contractions, which may be of abnormally high amplitude or long duration. Key to the diag-nosis of DES is that there remain some peristaltic waveforms in excess of those seen in achalasia. A criterion of 30% or more peristaltic waveforms out of 10 wet swallows has been used to differentiate DES from vigorous achalasia. However, this figure is arbitrary and often debated.The LES in patients with DES usually shows a normal resting pressure and relaxation on swallowing. A hypertensive sphincter with poor relaxation may also be present. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical and has been termed corkscrew esophagus or


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Surgery_Schwartz. sphincter with poor relaxation may also be present. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical and has been termed corkscrew esophagus or pseudodiverticulosis (Fig. 25-55). Patients with segmental or diffuse esophageal spasm can compartmentalize the esophagus and develop an epiphrenic or midesophageal diverticulum between two areas of high pressure occurring simultaneously (Fig. 25-56).Nutcracker Esophagus. The disorder, termed nutcracker or supersqueezeresophagus, was recognized in the late 1970s. Other terms used to describe this entity are hypertensive peri-stalsis or high-amplitude peristaltic contractions. It is the most common of the primary esophageal motility disorders. By definition the so-called nutcracker esophagus is a manomet-ric abnormality in patients who are characterized by peristal-tic esophageal contractions with peak amplitudes greater than two SDs above the normal values in individual laboratories.


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Surgery_Schwartz. is a manomet-ric abnormality in patients who are characterized by peristal-tic esophageal contractions with peak amplitudes greater than two SDs above the normal values in individual laboratories. Contraction amplitudes in these patients can easily be above 400 mmHg. At the lower end of peak pressure, it is unclear whether nutcracker esophagus causes any symptoms. In fact, chest pain symptoms in nutcracker esophagus patients may be related to GERD rather than intraluminal hypertension. Treatment in these patients should be aimed at the treatment of GERD. At the high end (peak pressures >300 mmHg) chest pain may be the result of the nutcracker physiology, as treatment directed at reducing intraluminal pressure is more effective than when used for those with lower peak pressures.Hypertensive Lower Esophageal Sphincter. Hyperten-sive lower esophageal sphincter (LES) in patients with chest pain or dysphagia was first described as a separate entity by Code and associates. This disorder is


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Surgery_Schwartz. Lower Esophageal Sphincter. Hyperten-sive lower esophageal sphincter (LES) in patients with chest pain or dysphagia was first described as a separate entity by Code and associates. This disorder is characterized by an ele-vated basal pressure of the LES with normal relaxation and Brunicardi_Ch25_p1009-p1098.indd 105701/03/19 6:04 PM 1058SPECIFIC CONSIDERATIONSPART IIFigure 25-56. Barium esophagogram showing a high epiphrenic diverticulum in a patient with diffuse esophageal spasm. (Repro-duced with permission from Castell DO: The Esophagus. Boston, MA: Little, Brown; 1992.)normal propulsion in the esophageal body. About one-half of these patients, however, have associated motility disorders of the esophageal body, particularly hypertensive peristalsis and simultaneous waveforms. In the remainder, the disorder exists as an isolated abnormality. Dysphagia in these patients may be caused by a lack of compliance of the sphincter, even in its relaxed state. Myotomy of the LES may be


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Surgery_Schwartz. the remainder, the disorder exists as an isolated abnormality. Dysphagia in these patients may be caused by a lack of compliance of the sphincter, even in its relaxed state. Myotomy of the LES may be indicated in patients not responding to medical therapy or dilation. When the symp-tom contribution of the hypertensive sphincter is in doubt, it is possible to inject the LES with botulinum toxin, endoscopically. If symptoms are relieved (temporarily) with this technique, then it is likely that myotomy will provide more permanent benefit.Secondary Esophageal Motility Disorders. Connective tissue disease, particularly scleroderma and the CREST syn-drome, exhibits severe esophageal motility disorders. Addi-tionally, patients treated as infants for esophageal atresia will often develop secondary motility disorders manifest later in life. Symptoms of these disorders are heartburn and dysphagia. The latter may be a result of a peptic stricture rather than the esophageal dysmotility. An


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Surgery_Schwartz. motility disorders manifest later in life. Symptoms of these disorders are heartburn and dysphagia. The latter may be a result of a peptic stricture rather than the esophageal dysmotility. An esophageal motility study will usu-ally show severely reduced or absent peristalsis with severely reduced or absent LES pressure. The role of antireflux surgery under these conditions is controversial but, if performed, should be limited to partial fundoplication, as full (Nissen) fundoplica-tion may result in severe dysphagia.Nonspecific Esophageal Motor Disorders and Ineffective Esophageal Motility. Many patients complaining of dys-phagia or chest pain of noncardiac origin demonstrate a vari-ety of wave patterns and contraction amplitudes on esophageal manometry that are clearly out of the normal range, but do not meet the criteria of a primary esophageal motility disor-der. Esophageal motility in these patients frequently shows an increased number of multipeaked or repetitive contractions,


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Surgery_Schwartz. range, but do not meet the criteria of a primary esophageal motility disor-der. Esophageal motility in these patients frequently shows an increased number of multipeaked or repetitive contractions, contractions of prolonged duration, nontransmitted contrac-tions, an interruption of a peristaltic wave at various levels of the esophagus, or contractions of low amplitude. These motility abnormalities have been termed nonspecific esophageal motility disorders. Their significance in the causation of chest pain or dysphagia is still unclear. Surgery plays no role in the treatment of these disorders unless there is an associated diverticulum.A clear distinction between primary esophageal motility disorders and nonspecific esophageal motility disorders is often not possible. Patients diagnosed as having nonspecific esophageal motility abnormalities on repeated studies will occasionally show abnormalities consistent with nutcracker esophagus. Similarly, progression from a nonspecific


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Surgery_Schwartz. as having nonspecific esophageal motility abnormalities on repeated studies will occasionally show abnormalities consistent with nutcracker esophagus. Similarly, progression from a nonspecific esophageal motility disorder to classic DES has been demonstrated. Therefore, the finding of a nonspecific esophageal motility disorder may represent only a manometric marker of an intermittent, more severe esophageal motor abnormality. Combined ambulatory 24-hour esophageal pH and motility monitoring has shown that an increased esopha-geal exposure to gastric juice is common in patients diagnosed as having a nonspecific esophageal motility disorder. In some situ-ations, the motor abnormalities may be induced by the irritation of refluxed gastric juice; in other situations, it may be a primary event unrelated to the presence of reflux. High-amplitude peristal-sis (nutcracker esophagus) and low-amplitude peristalsis (ineffec-tive esophageal motility) are frequently associated with


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Surgery_Schwartz. a primary event unrelated to the presence of reflux. High-amplitude peristal-sis (nutcracker esophagus) and low-amplitude peristalsis (ineffec-tive esophageal motility) are frequently associated with GERD.Diverticula of the Esophageal Body. Diverticula of the esophagus may be characterized by their location in the esoph-agus (proximal, mid-, or distal esophagus), or by the nature of Figure 25-55. Barium esophagogram of patient with diffuse spasm showing the corkscrew deformity.Brunicardi_Ch25_p1009-p1098.indd 105801/03/19 6:04 PM 1059ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-57. Barium esophagogram showing a midesophageal diverticulum. Despite the anatomic distortion, the patient was asymptomatic. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical man-agement, Med Clin North Am. 1981 Nov;65(6):1235-1268.)InflamednodesTraction diverticulumFigure 25-58. Illustration of the pathophysiology of midesopha-geal diverticulum


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Surgery_Schwartz. and their surgical man-agement, Med Clin North Am. 1981 Nov;65(6):1235-1268.)InflamednodesTraction diverticulumFigure 25-58. Illustration of the pathophysiology of midesopha-geal diverticulum showing traction on the esophageal wall from adhesions to inflamed subcarinal lymph nodes.concomitant pathology. Diverticula associated with motor dis-orders are termed pulsion diverticula and those associated with inflammatory conditions are termed traction diverticula. Pulsion diverticula occur most commonly with nonspecific motility disor-ders, but they can occur with all of the primary motility disorders. In the latter situation, the motility disorder is usually diagnosed before the development of the diverticulum. When associated with achalasia, the development of a diverticulum may temporar-ily alleviate the symptom of dysphagia by becoming a receptacle for ingested food and substitute the symptom of dysphagia for postprandial pain and regurgitation of undigested food. If a motil-ity


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Surgery_Schwartz. alleviate the symptom of dysphagia by becoming a receptacle for ingested food and substitute the symptom of dysphagia for postprandial pain and regurgitation of undigested food. If a motil-ity abnormality of the esophageal body or LES cannot be identi-fied, a traction or congenital cause for the diverticulum should be considered.Because development in radiology preceded develop-ment in motility monitoring, diverticula of the esophagus were considered historically to be a primary abnormality, the cause, rather than the consequence, of motility disorders. Conse-quently, earlier texts focused on them as specific entities based upon their location.Epiphrenic diverticula arise from the terminal third of the thoracic esophagus and are usually found adjacent to the diaphragm. They have been associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are “pulsion” diverticula, and they are associated with diffuse spasm,


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Surgery_Schwartz. associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are “pulsion” diverticula, and they are associated with diffuse spasm, achalasia, or nonspecific motor abnormalities in the body of the esophagus.Whether the diverticulum should be surgically resected or suspended depends on its size and proximity to the vertebral body. When diverticula are associated with esophageal motility disorders, esophageal myotomy from the proximal extent of the diverticulum to the stomach should be combined with diverticu-lectomy. If diverticulectomy alone is performed, one can expect a high incidence of suture line rupture due to the same intralu-minal pressure that initially gave rise to the diverticulum. If the diverticulum is suspended to the prevertebral fascia of the tho-racic vertebra, a myotomy is begun at the neck of the diverticu-lum and extended across the LES. If the diverticulum is excised by dividing the neck, the