April 19, 2001
America's Center
St. Louis, Missouri
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Program Chairman |
Bruce D. Schirmer, M.D. |
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Course Director |
Michael Holzman, M.D. |
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SAGES President |
Nathaniel J. Soper, M.D. |
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SAGES Executive Director |
Sallie Liesmann Matthews |
1. Persistent Symptoms after Fundoplication: The Gastroenterologist's Perspective
Professor of Medicine and Psychiatry, Division of Gastroenterology, Washington University School of Medicine
Anti-reflux surgery establishes or restores the anti-reflux barrier and corrects other abnormalities that may be conducive to reflux events. An adequate procedure reduces esophageal acid exposure time, but does not necessarily eliminate symptoms. The explanation for persistent or new symptoms after surgery can usually be classified into one of four categories, although establishing the precise explanation is not always straightforward. These categories are: (1) inadequate correction of gastroesophageal reflux, (2) persistence of a functional esophageal syndrome, (3) development of symptoms related to the anti-reflux procedure itself, and (4) persistence of symptoms that were unrelated to reflux disease or esophageal dysfunction from the beginning. As a general rule, the best outcome can be predicted if pathological reflux can be demonstrated on amublatory pH studies, the primary symptom is typical of GERD, and a good clinical response occurs with acid suppression therapy (1). When any of these criteria are absent, the likelihood of postoperative symptoms climbs.
The first of the four stated mechanisms is the simplest to determine, because ambulatory pH monitoring can reliably establish the degree of esophageal acid exposure and reveal the adequacy or inadequacy of the anti-reflux operation. Technical problems with pH monitoring, correct positioning of the pH probe, and patient discomfort are the most important factors in the utilization of these methods. Failure to adequately control reflux occurs in as many as 20% of patients and is more likely at one year after a partial wrap than a complete Nissen procedure (2,3). Persistently abnormal esophageal acid exposure time remains the most common reason overall for re-operation (4). Consequently, this explanation for failure must be considered in all patients with persistent post-operative symptoms.
The presence of a functional esophageal syndrome is more difficult to establish pre-operatively but is a common explanation for persistent symptoms. Functional esophageal syndromes often complicate reflux disease, as acid reflux events are considered important provoking factors in the pathophysiology of these disorders. At present, both motility abnormalities and visceral sensitivity are thought to participate in these syndromes. Spastic motor disorders and increased sensitivity to intra-esophageal balloon distention are important markers, but no physiological measurement is sufficiently sensitive nor specific to be uniformly clinically useful. The best clinical indicator is the persistence of symptoms following adequate medical treatment, and refractory symptoms, unresponsive to medical treatment, are recognized as predictors of poorer outcome from anti-reflux surgery.
Symptoms related to the surgical procedure itself may mimic some of the presenting symptoms, as the repertoire of esophageal symptoms is quite limited. For example, dysphagia from reflux disease, e.g., the non-obstructive dysphagia reported by some patients, may be replaced by dysphagia from a fundoplication. The two may not be differentiable by the patient. Painful swallowing resulting from an obstructing fundoplication may resemble chest pain related to reflux preceding the operation. Objective data are often more important in the post-operative setting for correct attribution of symptom origin.
Finally, some symptoms are unrelated to reflux disease, were thought to be a part of the reflux syndrome, and fail to respond to anti-reflux surgery. The most typical example is the group of "atypical" reflux symptoms, such as ENT or pulmonary manifestations. It is difficult to fully establish a direct relationship of such atypical symptoms in the preoperative setting, and response to medical management is also difficult to interpret in these situations [although response to medical therapy remains one of the best predictors of response to surgery even for atypical symptoms (6)]. Chronic cough has a notoriously poor relationship to reflux events on ambulatory pH studies, even when the symptom is directly related to GERD [but a good preoperative association remains a predictor of good surgical outcome (7)]. Only after successful anti-reflux surgery, when acid exposure time is markedly reduced and other, non-acid reflux events are eliminated, can the relationship of reflux to the symptoms be fully appreciated - and then the therapeutic trial may prove a failure. Data continue to accumulate demonstrating the benefits of anti-reflux surgery on atypical symptoms or unusual symptoms that may be clustered with heartburn and regurgitation (such as nausea), but the best indicator of success continues to be excessive reflux on an ambulatory pH study and a statistically significant association of the symptom with reflux events.
Heartburn is the most specific of the esophageal symptoms for GERD, yet it is insensitive and has only modest predictive value (2). Why? Because the limited symptom profile from reflux disease, other esophageal disorders, and other visceral chest disorders contaminates the value of this symptom. Cardiac pain can be reported as heartburn, and even the most sophisticated of patients may not be able to differentiate angina from GERD. Heartburn after anti-reflux surgery is the most useful symptom for evaluating the success of the operation, but it still is of limited accuracy. The positive predictive value of this symptom for surgical failure is no more than 43%, but the negative predictive value for surgical success is higher (2). Thus, the reporting of persistent heartburn following fundoplication requires investigation before a conclusion is drawn that the operation was ineffective in normalizing esophageal acid exposure time. As mentioned above, acid reflux can induce in some patients a tendency toward functional symptoms that are less associated with reflux events. Acid sensitizes esophageal mucosal chemoreceptors. The sensitization extends to other receptors, including stretch receptors, in some patients. Eliminating reflux may not rapidly reduce this sensitization, and symptoms may persist. This is a mechanistic hypothesis behind functional GI symptoms in general. Proof that the surgery was effective in eliminating acid reflux is sufficient, and ambulatory pH monitoring is typically the best diagnostic tool.
Diagnosis. An effective anti-reflux procedure dramatically reduces esophageal acid exposure time. Heartburn related to GERD should be eliminated. Ambulatory pH studies are recommended over therapeutic trials with acid suppressant medications in the patient with persistent heartburn to document the adequacy of the operation, and more than half with persistent heartburn will be have normal acid exposure (2). The objective adequacy of surgery does not improve over time, so you might as well evaluate early in the patient with persistent heartburn. Listen carefully to the history to make certain that a non-esophageal source is not suggested. Rarely, motor disorders such as achalasia can produce heartburn-like symptoms, but these disorders should have been excluded in the pre-operative evaluation.
Treatment. Once the adequacy of the operation is determined and alternative explanations for the symptom are excluded, functional heartburn can be assumed. This process can be managed like many functional GI disorders with a graduated approach depending on the severity of the symptom. Transient acid suppression can be employed, but the limitations and short-term need for these agents should be apparent from the findings on ambulatory pH monitoring. We use low-dose tricyclic antidepressant regimens frequently in these patients, as these agents can eliminate residual symptoms and presumably correct some of the neurological pathophysiology resposible for perpetuation of symptoms (8).
Episodic chest pain should always be considered an atypical manifestation of GERD. The symptom reflects not only the occurrence of reflux events but also an atypical response by the host. This response may be influenced by transient factors that heighten autonomic reactivity, including stress and other psychological/psychiatric factors. Chest pain, even more than heartburn, is suggestive that the neurological mechanisms relevant to the functional GI syndromes are active. The approach is virtually identical to that for persistent heartburn, but the need to suppress symptoms is more pressing. Chest pain induces heightened concern in doctors as well as patients.
Diagnosis. Rely on ambulatory pH monitoring to determine the adequacy of the anti-reflux procedure. If inadequate and pain persists with the addition of anti-secretory medications, repeat pH monitoring while the patient is on medications. A quality of life assessment in addition to esophageal symptom rating is useful (5), as disparity between these reports is recognized in functional disorders (symptoms are highly rated, but quality of life may be good).
Treatment. We introduce low-dose tricyclic antidepressant regimens earlier in the treatment plan when chest pain is the dominant or persistent symptom. At least 70-80% have a very good or excellent response if reflux disease has been controlled. A similar percentage will have long-term remission (8,9). These agents can be discontinued 6-24 months after successful symptom control in the majority of patients. Other psychopharmacological agents can be beneficial, but their use requires a careful consideration of the potential mechanisms of action.
Dysphagia is the dreaded symptom after anti-reflux surgery and occurs in at least 15% of patients. Severe dysphagia with regurgitation and poor nutrition is indicative of esophageal obstruction. Presence of a reliable preoperative physiological predictor of this complication remains debated, as most cases can be attributed directly to an excessively tight or long fundoplication. Liberal criteria for hypomotility of the esophageal body (e.g., mean wave amplitude <30 mm Hg or >30% failed swallows) are probably not very predictive, whether a complete or partial fundoplication is performed (3). However, more severe degrees of hypomotility likely increase the potential for complete esophageal failure above the fundoplication, an achalasia-like picture, and significant to severe symptoms. Preoperative presence of dysphagia also has some predictive value for persistence of this symptom (10). And, of course, a poorly performed surgery with a wrap of excessive length, a slipped fundoplication, or a paraesophageal hernia can produce the symptoms that will only respond to reoperation (11). Without sounding like a broken record, I must also point out that functional symptoms can also present with dysphagia as a part of the symptom picture. If such are suspected, all of the above comments for heartburn and chest pain would apply.
Diagnosis. A transit study with barium or radionuclide can show evidence of retention, a finding that usually indicates the fundoplication is on the obstructive side. Endoscopy can help clarify the picture but is usually employed once therapeutic intervention is deemed appropriate. It is difficult to provide a highly useful post-operative endoscopic evaluation unless the endoscopist is experienced in this specific situation. When the explanation is not conspicuous from endoscopic and radiological evaluation, we use a high-resolution manometric system that provides a semi-anatomical representation of pressures in the esophageal body and through the lower sphincter region (12). With this system we can readily evaluate the degree of trans-sphincteric pressure gradient, the manometric length of the fundoplication, and the esophageal response to the obstruction. This technique has been helpful in understanding the mechanisms behind dysphagia following anti-reflux surgery and can help detect abnormalities that may be difficult to interpret by endoscopy or imaging (12,13). In the typical community setting, a combination of radiological (barium) and endoscopic data will be required. Good transit implies that the patient is too sensitive to the obstructive physiology. Poor transit means the obstruction is probably too extreme and needs modification.
Treatment. Empiric dilation at the time of endoscopy is acceptable, but only simple dilation to 20 mm should be performed unless evidence of poor transit is available. Very poor transit, with significant obstruction symptoms is an indication for aggressive dilation, but not within the first 3 months following surgery if possible. Gradual improvement occurs with nothing more than periodic bougiennage in most patients during this early post-operative period. Perforation rates for dilation with dilators in excess of 20mm diameter are higher than for achalasia, for example, but dilation is still preferred over re-operation in the average case. If transit is acceptable and the patient only has dysphagia without regurgitation, "desensitization" with tricyclic antidepressants may also be effective. Over time, dysphagia may improve and the medications may be discontinued. Serial barium swallows may be required, however, to confirm that the esophagus is not dilating in response to chronic obstruction. Re-operation may be needed if evidence of a poorly constructed wrap is apparent during the evaluation.
1. Campos GM, Peters JH, DeMeester TR, Oberg S, Crookes PJ, Tan S, DeMeester SR, Hagen JA, Bremner CG. Multivariate analysis of factors predicting outcome after laparoscopic Nissen fundoplication. J Gastrointest Surg 1999;3:292-300.
2. Eubanks TR, Omelanczuk P, Richards C, Pohl D, Pellegrini CA. Outcomes of laparoscopic antireflux procedures. Am J Surg 2000, 179:391-5.
3. Farrell TM, Archer SB, Galloway KD, Branum GD, Smith CD, Hunter JG. Heartburn is more likely to recur after Toupet fundoplication than Nissen fundoplication. Am Surgeon 2000;66:229-36.
4. Pointner R, Bamner T, Then P, Kamolz T. Laparoscopic refundoplication after failed antireflux surgery. Am J Surg 1999;178:541-4.
5. Kamolz T, Bammer T, Wykypiel H Jr, Pasiut M, Pointner R. Quality of life and surgical outcome ater laparoscopic Nissen and Toupet fundoplication. Endoscopy 2000;32:363-8.
6. Floch NR. Surgical therapy for atypical symptoms of GERD: patient selection and preoperative evaluation. J Clin Gastroenterol 2000;30(suppl 3):S45-S47.
7. Patti MG, Arcerito M, Tamburini A, Diener U, Feo CV, Safadi B, Fisichella P, Way LW. Effect of laparoscopic fundoplication on gastroesophageal reflux disease-induced respiratory symptoms. J Gastrointest Surg 2000;4:143-9.
8. Clouse RE. Antidepressants for functional gastrointestinal syndromes. Dig Dis Sci 1994;39:2352-63.
9. Prakash C, Clouse RE. Long-term outcome of tricyclic antidepressant treatment of functional chest pain. Dig Dis Sci 1999;44:2373-9.
10. Herron DM, Swanstrom LL, Ramzi N, Hansen PD. Factors predictive of dysphagia after laparoscopic Nissen fundoplication. Surg Endoscopy 1999;13:1180-3.
11. Seelig MH, Hinder RA, Klinger PJ, Floch NR, Branton SA, Smith SL. Paraesophageal herniation as a complication following laparoscopic antireflux surgery. J Gastrointest Surg 1999;3:95-99.
12. Clouse RE, Prakash C. Topographic esophageal manometry: an emerging clinical and investigative approach. Digestive Diseases 2000;18:64-74.
13. Prakash C, Soper NJ, Clouse RE. Topographic manometry in the evaluation of symptomatic patients following fundoplication. Gastroenterology (abstract) 2001 (in press).
1. Hogan WJ, Shaker R. Life after antireflux surgery. Am J Med 2000;108(suppl 4a):181S-191S.
2. Rice TW. Why antireflux surgery fails. Dig Dis 2000;18:43-7.
3. Hinder RA. Surgical therapy for GERD: selection of procedures, short-, and long-term results. J Clin Gastroenterol 2000;30(suppl 3):S48-S50.
4. Waring JP. Postfundoplication complications. Prevention and management. Gastroenterol Clin North Am 1999;28:1007-19.
2. Postoperative Dysphagia: Evaluation and
Management
Director of Surgical Laparoscopy and Endoscopy, Hospital ING, Goiania, Brazil
Laparoscopic antireflux surgery has evolved to be a safe, reliable and a highly effective operation when applied to an unselected gastroesophageal reflux disease (GERD) patient population. It has been demonstrated that the technique of open surgery could be reproduced with lower morbidity and mortality rates, shorter hospital stay and quicker resumption of daily activities [1,2]. Although we still lack long-term results, laparoscopic fundoplication will probably offer a long lasting control of GERD in the great majority of patients.
Both open and laparoscopic fundoplication may be accompanied by postoperative adverse side effects, which includes dysphagia, odynophagia, inability to belch, epigastric pain, bloating and increased flatulence. These symptoms have been reported in a frequency that varies from institution to institution and may be dependent on a variety of factors [3,4,5].
Some transitory and mild dysphagia occurs in most patients immediately after a laparoscopic fundoplication, especially following a circumferential or Nissen wrap, but this settles in the great majority of patients by the sixth postoperative week. The incidence of persistent dysphagia after open Nissen fundoplication has ranged from 1 to 43% [4,5,6,7] and from 2% to 24% [8,9,10,11,12,13] following the laparoscopic fundoplication. As in the open literature, these differences are largely related to patient population, to different methods of definition and valuation of dysphagia and to operative techniques. Evaluation of postoperative dysphagia following a laparoscopic fundoplication includes graduation of this symptom according to severity and frequency (dysphagia score), an upper digestive endoscopy, barium meal and esophageal manometry.
The causes of persistent postoperative dysphagia include inappropriate selection of patients to fundoplication, lack of adequate objective preoperative evaluation, type of antireflux operation and technical problem or Surgeon-depending factor.
Inappropriate selection of patients to fundoplication: These would include patients with achalasia, diffuse esophageal spasm, scleroderma, malignancy at the esophagogastric junction, global loss of esophageal motility, short esophagus and strictures. The routine use of preoperative, objective evaluation of GERD is likely to prevent these patients to be operated or submitted to an inappropriate surgical procedure. Frequently a revision surgery is needed when the cause of persistent postoperative dysphagia is related to an inadequate indication [14]. Extra-care must be taken in patients with preoperative dysphagia. Patti et al. [15] showed that about one-third of GERD patients without strictures experienced dysphagia; and dysphagia resolved in about 90% of such patients following a laparoscopic fundoplication. Ritter et al. [16] suggested that preoperative dysphagia in patients with advanced GERD and short esophagus should be considered for primary esophagectomy. Peters and DeMeester [17] have emphasized that the short esophagus may be the most important factor causing failure of surgery. Dysphagia is usually the main postoperative complaint in this setting. Despite controversies about its incidence, short esophagus has contributed to lower the success rate of laparoscopic fundoplication. It can be difficult to diagnose both pre and intraoperatively. Hill and Mercer [18] stated that "have yet to encounter the so called short esophagus". Testart [18] suggested this finding when 0.3 kg traction could not achieve 2 cm of intra-abdominal esophagus below the frontal edge of the hiatus. Gastal et al. [19] suspected of short esophagus preoperatively in patients with a hiatal hernia of 5 cm or larger, a nonreducible hiatal hernia, or an esophageal stricture. Awad et al. [20] combined an endoscopic and laparoscopic intraoperative evaluation for a more accurate diagnosis, and finally Henderson [21] stated that there is no absolute preoperative test of esophageal length. The overall surgical importance of short esophagus associated to GERD is also controversial. A laparoscopic Collis-gastroplasty followed by a total or partial fundoplication for this specific subgroup of patients is our current approach [22]. Stenosis not properly dilated to 45 Fr., requiring multiple and regular sessions of dilatations or not amenable to endoscopic dilatation, especially in the set of previous antireflux operations and/or poor esophageal body motility, represents a major risk to postoperative dysphagia. There is clear evidence that the proportion of patients presenting with reflux stricture that necessitates a Collis gastroplasty or resection is diminishing with earlier referral and more powerful antisecretory drugs [23].
Lack of adequate objective preoperative evaluation: The non-use of anatomic and functional evaluation tests of GERD quite frequently leads to misjudgment of surgical indication and the type of procedure. Peters and DeMeester [24] mentioned that preoperative esophageal manometry is important as it excludes patients with a lower esophageal sphincter manometrically normal, as well as evaluates the esophageal motor function. They emphasized that fundoplication in patients with normal LES must be performed cautiously as these patients are usually upright refluxers and do not do well after antireflux surgery. The determination of the propulsive force of the body of the esophagus evaluates whether the bolus will be able to overcome the resistance created by the valve and therefore the convenience of performing a total fundoplication [25]. Patients with normal peristalsis usually do well after a Nissen fundoplication. Gill et al. [26] and Escandell et al. [27] have demonstrated recovery of esophageal contractility following antireflux operation. Stein et al. [28] observed that despite the improvement of esophageal contractility, the amplitude of contractions as well as the prevalence of simultaneous and interrupted contractions remained unchanged following a Nissen fundoplication. Patients with severely impaired contractility like those with stenosis and Barrett did not present any improvement at all. On the other hand, Mughal et al. [29] found that an unsatisfactory result was not more likely in those with upright reflux, with an esophageal motility disorder or with a competent cardia as defined by preoperative manometry. Rydberg et al. [30] found no relationship at all between the clinical outcome and preoperative manometric findings, with similar results in the two fundoplications groups (Nissen-Rossetti and Toupet). These groups were submitted to a randomized clinical study with long-term follow-up and were allocated irrespective of the preoperative manometric findings.
Type of antireflux operation: Our comparative study of 190 cases of total and 103 cases of partial laparoscopic fundoplication have showed a 2.8 % incidence of persistent dysphagia after total fundoplication and 2.1 % after partial. Patti et al. [31] also made a comparison of laparoscopic total and partial fundoplication. Total fundoplication was performed in patients with normal esophageal peristalsis and partial fundoplication in patients with severe abnormalities of esophageal peristalsis. The same percentage of patients has resolution of heartburn (93%) and regurgitation (97%) after partial as compared to total fundoplication. Dysphagia developed in four patients (8%) after total fundoplication (one patient required dilatation) and in no patients after partial fundoplication. Both operations produced similar changes in lower esophageal sphincter function, but only partial fundoplication was associated with improvement in esophageal dysfunction. Hunter et al. [32] demonstrated a 2% rate of moderate and severe dysphagia to solids after a laparoscopic Nissen and Toupet fundoplication and 11% after Nissen-Rossetti fundoplication. However, Lundell et al. [33] in a prospective and randomized study followed over several years between an open Nissen-Rossetti and Toupet type fundoplication found that the only long-term difference between these two procedures was significantly more complaints of flatulence after the total fundoplication.
Technical problem or Surgeon-depending factor: The performance of a too-long or too-tight wrap is more likely to determine postoperative dysphagia. DeMeester et al. [4] demonstrated that a Nissen fundoplication when performed over a 60 Fr. bougie inside the esophagus reduced the temporary incidence of swallowing discomfort from 83% to 39%, and by decreasing the size of the valve from 4 to 1 cm, also determined a reduction from 21% to 3% of postoperative persistent dysphagia. Failure to close or too loose the closure of the crura can result in a paraesophageal hernia, which is a cause of postoperative dysphagia. If overly tight crural closure is the cause of dysphagia, endoscopic dilation is usually unsuccessful. Same remarks can be made for a too tight or too long wrap. Reoperation is usually necessary. Watson et al. [34] in a prospective and randomized study of laparoscopic Nissen fundoplication with vs. without division of the short gastric vessels failed to demonstrate a reduction in the likelihood of dysphagia. The importance of the construction of the wrap using both the posterior and anterior wall of the fundus, avoiding the corkscrew-like image of the wrap, must be highlighted in order to minimize adverse postoperative side effects. Jamieson et al. [35] have demonstrated that patients with more severe dysphagia after a Nissen fundoplication were less able to relax their newly constructed LES and had a higher residual relaxation pressure. The importance of the experience of the surgeon has to be recognized and also the impact of the learning curve on the occurrence of intra and postoperative complications, despite the fact that at this moment, as a large number of surgeons have already passed the learning curve of laparoscopic fundoplication, the reasons for failure or postoperative side effects directly related to technical problems are probably less frequent.
Management of postoperative dysphagia following a laparoscopic fundoplication is certainly dependent on the cause of this symptom. Siewert et al. emphasized that nearly 90% of the patients operated on via an open approach with postoperative dysphagia or a combination of dysphagia and reflux symptoms will require reoperation [36]. This seems to be the same in the laparoscopic era.
1. Hinder RA, Filipi CJ, Wetscher G, et al. (1994) Laparoscopic Nissen fundoplication is an effective treatment for gastroesophageal reflux disease. Ann Surg 220:472 - 483
2. Trus TL, Laycock, WS, Branum G, Waring JP, Mauren S, Hunter JG (1996). Intermediate Follow-up of Laparoscopic Antireflux Surgery. Am J Surg 171:32-35
3. Donahue PE, Samuelson S, Nyhus LM, Bombeck TC. The floppy Nissen fundoplication. Arch Surg 1985;120:663-668
4. DeMeester TR, Bonavina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease. Evaluation of primary repair in 100 consecutive cases. Ann Surg 1986;204:9-20
5. Negre JB. Post-fundoplication symptoms. Do they restrict the success of Nissen fundoplication? Ann Surg 1983;198:869-700
6.Luostarinen M. Nissen Fundoplication for Reflux Esophagitis. Ann Surg 1993:217;329-337
7.Shirazi, SS, Schulze, K, Soper RT: Long-term follow-up for treatment of complicated chronic reflux esophagitis. Arch. Surg. 1987;122:548.
8.Cuschieri A, Hunter J, Wolfe B, Swanstrom LL, Hutson W. Multicenter prospective evaluation of laparoscopic antireflux surgery. Preliminary report. Surg Endosc 1993;7:505-510
9. Bittner HB, Meyers WC, Brazer SR, Pappas TN. Laparoscopic Nissen fundoplication: operative results and short-term follow-up. Am J Surg 1994;167:193-198
10. Cadiere GB, Houben JJ, Bruyns J, Himpens J, Panzer JM, Gelin M. Laparoscopic Nissen fundoplication: technique and preliminary results. Br J Surg 1994;81:400-403
11. Jamieson CG, Watson DI, Britten-Jones R, Mitchell PC, Anvari M. Lapaorscopic Nissen fundoplication. Ann Surg 1994;220:137-145
12. Bittner HB, Meyers WC, Brazer SR, Pappas TN. Laparoscopic Nissen Fundoplication:operative results and short-term follow-up. Am J Surg 1994;167:193-200
13. Peters JH and DeMeester TR. Indications, Principles of Procedure Selection, and Technique of Laparoscopic Nissen Fundoplication. Seminars in Laparoscopic Surgery 1995;2:27-44
14. DePaula, AL, Hashiba K, Bafutto, M, Machado CA. Laparoscopic reoperations after failed and complicated antireflux operations. Surg Endosc 1995;9:681-686.
15. Patti MG, Feo CV, De Pinto M, et al. Results of laparoscopic antireflux surgery for dysphagia and gastroesophageal reflux disease.Am J Surg 1998 Dec;176(6):564-8
16. Ritter, MP, Peters JH, DeMeester TR, Gadenstatter, M, Oberg S, Fein M, Hagen JA, Crookes PF, Bremner CG. Treatment of advanced gastroesophageal Reflux Disease with Collis Gastroplasty and Belsey Partial Fundoplication. Arch Surg 1998;133:523-528
17. Peters JH, DeMeester TR. The lessons of failed antireflux repairs. In: Peters JH, DeMeester TR, eds. Minimally Invasive Surgery of Foregut. St Louis, Mo: Quality Medical Publishers Inc. 1994; 188-196.
18. Testart J. What is definition of brachyesophagus? In Giulli R, Tytgat GNJ, DeMeester TR, Galmiche JP (eds). The Esophageal Mucosa. Elsevier Science B.V., Amsterdam, 1994;533-535.
19. Gastal OL, Hagen JA, Peters JH, Campos GM, Hashemi M, Theisen J, Bremner CG,
DeMeester TR. Short esophagus: analysis of predictors and clinical implications.
Arch Surg 1999;134:633-638.
20. Awad ZT, Dickason TJ, Filipi CJ, Shiino Y, Marsh RE, Tomonaga T, Tasset MR, Mittal S. A combined laparoscopic-endoscopic method of assessment to prevent the complications of short esophagus. Surg Endosc 1999;13:626-627
21. Henderson RD. How can a conservative procedure be considred in view of a stenosis on an irreducible cardia? In: Giuli R, McCallum RW (eds) Benign Lesions of Esophagus and Cancer. Berlin: Springer Verlag, 1988;459-462.
22. DePaula AL, Hashiba K, Bafutto M, Machado C. Laparoscopic Collis gastroplasty with total and partial fundoplications. Surg Endosc 1996;10: 228
23. Watson A. Reflux stricture of the esophagus. Br J Surg 1987;74:443-448.
24.Peters JH, DeMeester TR. Indications, Principles of Procedure Selection, and Technique of Laparoscopic Nissen Fundoplication. Seminars in Laparoscopic Surgery 1995;2:27-44
25.Kahrilas PJ, Dodds, WJ, Hogan WJ: Effect of peristaltic dysfunction on esophageal volume clearance. Gastroenterology 1988;94:73-80
26.Gill RC, Bones KL, Murphy PD, Chingman YJ. Esophageal motor abnormalities in gastroesophageal reflux and the effects of fundoplication. Gastroenterology 1986;91-364-369
27.Escandell AL, DeHaro LFM, Paricio PP et al. Surgery improves defective oesophageal peristalsis in patients with gastroesophageal reflux. Br J Surg 1991;78:1095-1097
28.Stein HJ, Eypasch EP, DeMEester TR, et al: Circadian esophageal motor function in patients with gastroesophageal reflux disease. Surgery 1990;108:769-773
29.Mughal MM, Banciewicz J, Marples M. Oesophageal manometry and pH recording does not predict the bad results of Nissen fundoplication. Br J Surg 1990;77:43-45
30. Rydberg L, Ruth M, Lundell L. Should the antireflux procedure be Atailored@ based on the preoperative manometric findings? Results of a randomised, clinical study. Abstr OESO 1996
31. Patti MG, De Pinto M. de Bellis M. et al. Comparison of laparoscopic total and partial fundoplication for gastroesophageal reflux disease. Gastroenterology 1996;110:A1409.
32.Hunter JG, Swanstrom L, Waring JP: Dysphagia after laparoscopic antireflux surgery. Ann Surg 1996;224:51-57
33.Lundell L, Abrahamsson H. Ruth M. et al. Long-term results of a prospective randomized comparison ot total fundic wrap (Nissen-Rossetti) or semifundoplication (Toupet) for gastroesophageal reflux. Br J Surg 1996;83:830-835
34.Watson DI, Pike GK, Mathew G, et al.: Prospective double blind randomised trial of laparoscopic Nissen fundoplication with vs without division of short gastric vessels. Abstract book, Sixth World Congress of the International Society for diseases of the esophagus
35.Jamieson GG, Tew S, Holloway RH. How can the pressure profile along the wrap be determined? Is there a correlation with dysphagia? Does it correlate with the opening diameter of the lower esophageal sphincter? In: Giuli R, Galmiche JP, Jamieson GG, Scarpignato C. (eds). The Esophagogastric Junction. John Libbey Eurotext, 1988;791-794.
36. Stein HJ, Feussner H, Siewert JR. Causes of failure of antireflux surgery and management strategies. Am J Surg 1996;171:36-41
3. Gas bloat and diarrhea: Evaluation and Management
Gas bloat syndrome refers to patients that have bloating, abdominal distention, early satiety, or other mild symptoms of fullness after eating. Gas bloat syndrome was a common complication during the era in which surgeons would perform a long, tight Nissen fundoplication often consisting of six or seven sutures over a 42-French Bougie. This long, tight Nissen would completely stop reflux of acid into the esophagus but also would consistently prevent the patient from vomiting or belching. In the eighties surgeons refined techniques for performing Nissen Fundoplication to reduce the incidence and severity of gas bloat syndrome. Currently a loose, floppy Nissen is the standard of care for open or laparoscopic Nissen fundoplication. It is rare to see a patient who is unable to vomit or has such severe gas bloat syndrome that they pass a nasogastric tube for relief of symptoms. The development of the loose, floppy Nissen fundoplication was a direct result of surgeons who developed operative techniques to prevent the severe symptoms of gas bloat seen after the long, tight Nissen fundoplications.
A. Pathophysiology
As shown in Figure 1, the degree of wrap directly correlates with the change in LES pressure
after fundoplication. Thus, the Hill repair develops the lowest pressure, while the 360?
Nissen fundoplication develops the highest pressure. There is a direct correlation between the
degree of wrap and the augmentation of LES pressure.
The pressure required to overcome valve resistance to gastroesophageal reflux is directly
correlated to the length of the wrap as shown in Figure 2. There is virtually no resistance to the
240 gastric wrap created by the Belsey Mark IV. However, there is quite significant pressure
developed by the valve mechanism by the 360 Nissen. This resistance exists at all levels but
also increases with the length of the gastric wrap. The dramatic increase in valve resistance at
any length of fundoplication is quite significant and explains the patient's impaired ability to belch in
the postoperative period. This is most significant in the early postoperative period when there is an
acute dramatic change from the preoperative condition.
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B. Incidence of Gas Bloat
Gas bloat has been a fairly common early postoperative symptom. While patients almost always retain the ability to burp after a properly constructed loose, floppy Nissen fundoplication, they invariably note that it is more difficult for them to burp and that they experience some bloating in the early postoperative period. Some of this can be attributed to the increase in valve resistance with a 360 fundoplication. Moreover, many patients with severe gastroesophageal reflux, particularly that which has lasted for a long period of time, swallow many times per day, unconsciously pushing esophageal acid back into the stomach with alkalinizing saliva as well as air.1 This unconscious reflex continues even after anti-reflux surgery. As can be seen previously, the Nissen fundoplication consistently elevates the resistance to reflux of acid and air into the esophagus and therefore impairs the ability to belch. It is not surprising then that a great number of patients after even a loose, floppy Nissen fundoplication exhibit mild symptoms of early satiety, bloating, and increased flatulence.
At Vanderbilt we have used several questionnaires to assess patients before and after fundoplication. One questionnaire uses a Likert scale from 0 to 100 to assess bloating with 100 being constant, disabling bloating and 0 being no symptoms. Six weeks after laparoscopic Nissen patients rated their bloating as mild occurring 1-2 times per week. While surprising that patients had so many bloating symptoms a examination of their symptoms reveals that bloating is more severe preop than it is postop (Figure 3).
This illustrates that patients with GERD commonly have aerophagia and bloating preoperatively and that patient education is very important to alleviate concerns that patients may have in the early postop period. Gas bloat symptoms are exacerbated in the first several weeks after Nissen but by the end of 6 weeks patients on average have less gas bloat because they have unlearned aerophagia because they no longer have as many reflux episodes. Thus for most patients education and tincture of time resolves their symptoms.
C. Diagnosis
If preoperative gastroparesis can cause excessive gas bloat symptoms then injury to the vagal trunks with resulting gastroparesis may be responsible for a small number of patients with gas bloat syndrome that is severe in nature or prolonged in duration. In a review of patients undergoing laparoscopic anti-reflux surgery performed at the Virginia Mason Medical Center in Seattle there were nine patients referred for evaluation of severe gas-bloat syndrome(3). Eight of the nine patients had their surgical procedure performed outside the Virginia Mason Clinic and were referred for evaluation. Typically, patients with severe gas bloat present very early after surgery with symptoms. Intractable gas bloat symptoms were present in five patients. Four out of the five had vagal nerve injury diagnosed through the use of Congo red staining, pentagastrin stimulation test, or by a solid-phase gastric emptying study. They concluded that bilateral truncal nerve injury could lead to severe solid food gastroparesis with associated severe intractable gas bloat syndrome. The single best test for identification of this problem is a Technetium 99 solid-phase scrambled egg gastric emptying study, which will identify significant gastroparesis. After excluding the mechanical gastric outlet obstruction then the appropriate treatment can be carried out.
D. Treatment.
Most gas bloat symptoms will improve with time and by six weeks
it is rare to see a patient still troubled with bloating. The early symptoms
can be treated with chewable Mylicon tablets or with charcoal caps. I
instruct patients not to drink liquids with a straw or to ingest carbonated
beverages. Frequently I find that mere reassurance that this will pass
with time is enough to buoy the patient's spirits. In addition, the surgeon
should discuss with the patient their likely predisposition to unconsciously
swallow air that was induced by years of significant gastroesophageal
reflux. Most patients can unlearn their aerophagia and reduce the amount
of symptoms that they have.
A much more significant problem with gas bloat syndrome is indicated if
the patient is unable to belch or vomit. Additional workup is indicated
in these patents early in their course. If nuclear medicine Tc-99 scrambled
egg gastric emptying study demonstrates significant gastroparesis the
surgeon should consider performing a pyloroplasty. Laparoscopic pyloromyotomy
or pyloroplasty is adequate to enhance gastric emptying and alleviate
the symptoms of intractable gas bloat in these patients. Takedown of the
Nissen fundoplication would re-establish GERD, which may even be worse
than preoperatively because of the gastroparesis. I would advise not taking
in the fundoplication until pyloroplasty has had a time to improve symptoms
of gas bloat.
Prevention of vagal injury is key in preventing significant gas bloat
syndrome. Visual identification of both the anterior and posterior vagal
trunks with careful preservation of vagal nerves will prevent this problem
in the first place.
A. Pathophysiology of diarrhea.
The etiology of severe post fundoplication diarrhea is thought to be on the basis of vagal nerve injury. The anterior vagal truck splits off a hepatic branch as well as splitting to the anterior nerve of Latarjet. The posterior vagal trunk splits off into the posterior nerve of Latarjet and to the Celiac branch supplying parasympathetic innervation to the small intestine, ascending and transverse colon. Injury or division of the anterior vagus denervates the gallbladder and liver, which induces the development of gallstones. Injury to the Celiac plexus of the posterior vagus denervates the pancreas, small intestine, and large intestine. Adverse effects include decreased secretion of amylase, lipase, pancreatic juice and decreased response to secretin. In the small intestine vagotomy reduces fat absorption and motility which both combine to cause diarrhea. Increased amounts of bile salts reach the colon which have also been associated with episodic diarrhea.
Sawyers and colleagues4 performed a prospective randomized study comparing truncal to selective gastric vagotomy in patients undergoing open antiulcer procedures. Selective gastric vagotomy denervates the body and antrum of the stomach while preserving the hepatic branch of the anterior vagus and the celiac branch of the posterior vagus. Thus, if the vagus can be implicated in causing diarrhea, a selective gastric vagotomy should reduce the incidence of postvagotomy diarrhea. Patients undergoing selective gastric vagotomy had the amount of diarrhea than patients undergoing truncal vagotomy thus confirming that posterior vagal injury induces diarrhea.
It should also be noted that frequently patients who have irritable bowel syndrome have a heightened perception of gastrointestinal symptoms. Thus, we note that patients with IBS experience symptoms of GERD more frequently and more severely both pre-and postoperatively. Thus, the heightened visceral sensation that IBS patients have may lead to less than ideal results after Nissen fundoplication. My own experience suggests that patients with IBS symptomatology do not experience as good a relief of their GERD symptoms after Nissen fundoplication.
Physicians underestimate the amount of gas bloat and diarrhea that exists in the population preoperatively. Standardized questionnaires are helpful in identifying gastrointestinal symptoms preoperatively. Gas bloat as mentioned previously is fairly common in patients with GERD. Our patients had a gas bloat score of 37 +/- 5 preoperatively that decreased to 31 +/- 5 six-week postoperatively. Thus, while they still had a significant amount of symptoms of gas bloat at the six-week follow up; this was improved from their preoperative symptoms. Likewise diarrhea stayed unchanged pre-and postoperatively. In a larger follow up of our patients undergoing laparoscopic anti-reflux procedures in which questionnaires were filled out by 113 patients we noted that 19 out of the 113 patients noted moderate to severe diarrhea. While this seems to be excessive it should be tempered with the note that approximately twenty percent of our patients are diagnosed with some level of IBS preoperatively, thus, the true incidence of diarrhea post Nissen fundoplication may not be all that different from the preoperative status.
Once patients report significant diarrhea post Nissen fundoplication workup can be helpful to pinpoint a specific diagnosis. Presumably patients that present with more diarrhea have a localized injury to the posterior vagal trunk or to specifically the celiac branch of the posterior vagus. It is thus much more difficult to absolutely diagnose this as any of the pentagastrin stimulation studies, sham-feeding and gastric analysis, or solid-phase gastric emptying may lead to normal results because of the lack of injury to the anterior vagal trunk or to the posterior nerve of Latarjet. In the early postoperative period intractable diarrhea should be worked up to exclude Clostridium-Difficile colitis with a stool specimen sent for the C-Diff toxin. Diarrhea can also occur in the presence of gastrinoma and with the cessation of PPI therapy in the early postoperative period. This may unmask a previously undiagnosed gastrinoma. A fasting serum gastrin will be helpful in the determination of this type of problem.
When faced with the patient that does not have any of these acute problems but has persistent diarrhea after laparoscopic Nissen fundoplication, workup should first start with simple qualitative fecal fat determination. This has a high degree of sensitivity and specificity for the diagnosis of malabsorption. Another simple test to diagnose the cause of diarrhea is to fast the patient and determine whether or not they continue with diarrhea. Patients with mild, watery diarrheas that decrease significantly while fasting are typically patients with IBS, food allergies, post vagotomy diarrhea, microscopic collagenous colitis, or carbohydrate malabsorption. If the patient continues to have secretory-type, watery diarrhea while fasting, then the more esoteric types of diarrheas such as VIPoma need to be ruled out.
B. Treatment.
Treatment of specific, supposedly post vagotomy-induced, diarrheas can be instituted with cholestyramine. Cholestyramine is thought to be specifically helpful for post-vagotomy diarrhea because vagotomy induces changes in transit through the small intestine which increases bile acid concentrations in the colon. Thus, cholestyramine which binds bile acids and reduces colonic levels has been promoted for post-vagotomy diarrhea. Alternately, drugs such as Loperamide have proven to be very helpful. The advantage of Loperamide is that it does not have any anti-cholinergic effect and therefore does not have the significant cardiac effects, as does Lomotil. Typically, I will give Loperamide one tablet for every loose bowel movement up to eight per day. This appears to be adequate for the majority of patients.5
Katzka, D., Dimarion, A., Jr. Pathophysiology of Gastroesophageal Reflux Disease: LES Incompetence in the Esophageal Clearance, N. Castell, DO, Editor: The Esophagus Boston, Little Brown, 1992, Pages 449-455.
Lundell, L.R., Myers, J.C., Jamieson, G.G. Delayed Gastric Emptying and its Relationship to Symptoms of Gas Float After Anti-Reflux Surgery, European Journal of Surgery, 1994, Vol. 160, Pages 161-166.
Kozarekra; Lowde; Raltz, S.L. Complications Associated with Laparoscopic Anti-Reflux Surgery: One Multispecialty Clinic's Experience. Gastrointestinal Endoscopy, Vol. 46, No. 6, December 1997, Pages Kozarekra's and colleagues' note 3 Patients Presented with Intractable Diarrhea.
Sawyers, J.L.; Scott, H.W., Jr.; Edwards, W.H.; Shull, H.J.; Law, D.H. Comparative Studies of the Clinical Effects of Truncal and Selective Gastric Vagotomy, American Journal of Surgery, 1968, Pages 115, 165-172. Taken from book chapter Selective Gastric Vagotomy, John L. Sawyers in Surgery of the Stomach, Duodenum, and Small Intestine, H. William Scott, John L. Sawyers, Editors, Second Edition, Pages 503-509.
Swanstrom, L.; Wayne, Robert Spectrum of Gastrointestinal Symptoms after Laparoscopic Fundoplication, The American Journal of Surgery, Vol. 167, May 1994, Pages 538-541.
J. Patrick Waring Post-Fundoplication Complications in Gastroesophageal Reflux Disease in Gastroenterology Clinics, Vol. 28, No. 4., Pages 1007-1020.
Bremner, DeMeester, Crooks, et. al.The Effect of Symptoms in Non-Specific Motility Abnormalities on Outcomes of Surgical Therapy for Gastroesophageal Reflux Disease, , The Journal of Thoracic and Cardiovascular Surgery, May 1994, Page 1244-1250.
4. Persistent Nausea
Nausea is a centrally mediated, subjective sensation of dyspepsia. It can be either a low-grade dysphoria or, may induce a physical reaction of retching or vomiting to the point of pain. The cause of nausea can be from central stimulation, from exogenous sources or as a result of mechanical causes. Frequently it is idiopathic. Table 1
Table 1
Causes of nausea
|
Central |
increased intracraneal pressure -brain tumor -cerebral bleed -OTHER pain or stress reaction psychologic |
|
exogenous |
medication side effect Infectious -viral -bacterial |
|
mechanical |
gastroparesis duodenal gastric reflux gastric outlet obstruction small bowel obstruction |
|
Idiopathic |
|
Since gastroesophageal reflux (GER) is a functional disorder of gastric origin (without a stomach there is no GER!) It is not surprising that there is a strong correlation with nausea among the reflux population. As many as 38% of GER patients complain of nausea as a major component of their symptomatology. Well GER does not cause nausea, for the most part; nausea can certainly be expressed as GER with hyperemesis leading to heartburn, esophagitis, strictures and abnormal 24-hour pH testing.
Anti reflux surgery (ARS) can be a disaster in cases of nausea/vomiting which present before surgery and therefore, all such patients presenting with these symptoms must be cautiously and thoroughly assessed before proceeding with surgery.
ARS in the face of severe nausea/vomiting can be either an absolute disaster or a cure. Hui, et al. found that there was a 79% reduction in the number of patients complaining of nausea following laparoscopic fundoplication. It is essential that the surgeon determine who will benefit from ARS (i.e., those whose nausea is secondary to GER) from those who have other reasons for nausea/vomiting. Considering the classic difficulty that anti reflux surgery poses to vomiting and the known damage of wrap disruption or herniation with postoperative emesis it is imperative that patients who present with nausea as a predominant symptom should be thoroughly worked up and counseled before surgery:
In spite of all preoperative evaluations and exclusions there will always be cases following ARS who will have significant postoperative nausea. In our experience this represents 15 percent of postoperative patients. In the majority of these patients this problem is mild and self-limited - with only five percent having nausea past 13 months. Mild cases of nausea can usually be managed by anti emetics, prokinetic (reglan, propulcid, erythromycin), anti gas medication (simethacon), dietary management (small meals, low-fat non-dairy diets and avoidance of trigger foods) and time. This always represents a trying period for both patients and surgeon and it is probably worth evaluating the patient for underlying, correctable causes if the problem persists for more than a few weeks. Postoperative evaluation of severe nausea should include both an EGD and a gastric emptying study. If these tests are negative and nausea persists a CT scan of the head and a small bowel follow-through series should be performed. In 0.3 percent of patients who have an antireflux surgery, profound intractable nausea will develop. These patients may require admission to the hospital for IV fluids, IV anti-emetics and even total parenteral nutrition. They also represent a high, medical- legal risk group and should be treated carefully with all manoevours carefully documented.
If postoperative testing reveals a mechanical obstruction it will probably require surgical correction as it will be unlikely to improve on its own. If the problem appears functional, medical treatment should be tried. Standard anti-emetic medications (phenothiazine derivatives or odansterone), prokinetic agents and, in our experience, sucrulfate can help to some extent. Patients should be counseled to avoid gas producing foods, high fats and dairy products. If bile gastritis is suspected, particularly if the patient has had a cholecystectomy, cholestyramine may help. Psycologic consultation may help to identify an obscure eating or behavior problem, but, for those with an idiopathic reaction to ARS, reassurance and waiting is the main treatment. Surgeons should avoid early aggressive reintervention (such as taking the wrap down) unless a definite problem is identified on post operative testing, as reoperation will seldom help, may create complications and leaves the patient with their original problem, reflux. For the truly refractory, end stage cases there are prototype gastric stimulator devices that hold promis.
Nausea goes hand-in-hand with GERD, as both are functional GI diseases. It is critical for surgeons to avoid those patients with non-reflux related nausea and vomiting, as operative outcomes will be poor. Recognition of these patients depends on a thorough GI history and comprehensive preoperative evaluation. For the small percentage of patients with intractable postoperative nausea; mechanical and technical problems beg a surgical solution. Idiopathic problems are less curable and should be treated with encouragement or conservative measures.
1. Kozarek RA, Low DE, Raltz SL. Complications associated with laparoscopic anti-reflux surgery: one multispecialty clinic's experience. Gastrointest Endosc 1997; 46:527-531.
2. Hui TT, Fass SM, Giurgiu DI, Iida A, Takagi S, Phillips EH. Gastroesophageal disease and Nausea: Does fundoplication help or hurt? Arch Surg 2000; 135:545-549.
3. Swanstrom L, Wayne R. Spectrum of gastrointestinal symptoms after laparoscopic fundoplications. Am J Surg 1994; 167:538-541.
4. Brzna RJ, Koch KL. Gasroesophageal reflux disease presenting with intractable nausea. Ann Intern Med 1997; 126: 704-707.
5. Management of Atypical Symptoms
Associate Professor of Surgery, Department of Surgery
University of California, San Francisco
533 Parnassus Avenue, U-122; San Francisco, CA 94143-0788
Fax: (415) 476-8694; E-mail: pattim@surgery.ucsf.edu
Gastroesophageal reflux disease (GERD) can produce typical symptoms such as heartburn and regurgitation and atypical symptoms such as cough and chest pain. While it is well known that laparoscopic fundoplication controls very well heartburn and regurgitation, the effects on respiratory symptoms and chest pain are less clear. Confusion stems from difficulty preoperatively in determining whether cough or chest pain are actually caused by reflux when reflux is present on pH monitoring.
The diagnosis of GERD-induced respiratory symptoms is not always easy, as some patients may not experience heartburn or have visible signs of esophagitis on endoscopy. In addition, the pathogenesis of GERD-induced respiratory symptoms is multifactorial. They may be due to (1) activation by refluxed material of a vagal reflex with consequent bronchoconstriction or (2) microaspiration of gastric contents. Although the former mechanism would only require reflux from the stomach into the distal esophagus, the latter would require reflux into the proximal esophagus and spillage into the tracheobronchial tree. In order to distinguish between these 2 mechanisms and determine the upward extent of reflux, we use a pH probe with 2 sensors, which are located 5 and 20 cm above the lower esophageal sphincter. We determined that the results of pH monitoring help identifying which patients with respiratory symptoms are more likely to benefit from antireflux surgery. Cough, in fact, resolved in 83% of patients when a correlation between cough and reflux was detected during pH monitoring, but only in 57% of patients when this correlation was not seen. Furthermore, cough resolved in 77% of patients who had a correlation between cough and acid in the distal esophagus, but it resolved in 90% of patients when the cough was associated with acid in the proximal as well as the distal esophagus.
Approximately 20-30% of patients with chest pain undergoing cardiac catheterization have normal coronary arteries and are classified as having "non-cardiac chest pain". GERD is the most common cause of "non-cardiac chest pain". However, is not easy to determine preoperatively whether the chest pain is actually caused by reflux. As for respiratory symptoms, we found that pH monitoring is the most important test. We recently studied 165 patients with GERD and chest pain. Based on the relationship between pain and reflux during pH monitoring, these patients were divided in 3 groups:
In summary, during the last 10 years major progress has been made in understanding the pathophysiology of GERD-induced respiratory symptoms and chest pain. Prolonged pH monitoring has emerged as the key test to establish this correlation and is useful in predicting the outcome of therapy.
SESSION II
6. Recurrent Heartburn
Chief of Surgery
Presbyterian Medical Center
University of Pennsylvania
39th and Market Streets
Philadelphia, PA 19104
Antireflux surgery enjoys a high success rate, with symptom relief approaching 90% or higher. Most patients present for surgery with a primary complaint of heartburn; among those who have a different primary complaint, at least half will list heartburn as the second most bothersome symptom. Thus recurrence or persistence of heartburn after an antireflux operation represents a failure to satisfactorily address the primary problem.
Classic heartburn, as described in Castell's text book The Esophagus, is "a substernal burning sensation with a tendency to radiate toward the mouth." It may be associated with a bitter or acid taste in the mouth, often occurs within 30 minutes to 2 hours of eating, and is made worse by lying down or bending over. It may awaken sufferers from sleep. It is precipitated by large meals and by certain dietary habits such as fat intake, chocolate, coffee, or alcohol consumption. Although classic heartburn is certainly strongly suggestion of acid reflux, other conditions may cause the same or similar symptoms. This confusion needs to be held clearly in mind when evaluating the patient with recurrent heartburn.
Several studies have shown that the symptom of heartburn does not correlate perfectly with reflux. Katzka et al in Philadelphia have demonstrated both that patients who are completely acid suppressed may experience a symptom that they describe as heartburn, and, conversely, that patients with severe reflux may not perceive any symptoms of heartburn at all. Trimble has demonstrated nicely that there is a group of patients who have normal or physiologic levels of acid reflux who have characteristic symptoms of heartburn. Some of these patients have a very high symptom index, indicating that they have a highly sensitive or irritable esophagus. This condition, like it's cousin irritable bowel syndrome, is unlikely to improve with surgery. Heartburn in the post-operative patient has been shown by Eubanks et al to have only a 43% positive predictive value; of 22 patients complaining of post-operative heartburn, only 9 had abnormal esophageal acid exposure by 24 h pH.
Several authors have addressed the issue of failed fundoplications. Patients may complain of new symptoms or persistence of old symptoms. Some degree of mild symptomatology may be normal or at least expected in the early postoperative period, and it is reasonable to treat these complaints with reassurance, medical management, and tincture of time. An early barium swallow can serve to reassure both the patient and the surgeon that there are no gross anatomic flaws with the wrap. Waring asserts that if both a barium swallow and an EGD demonstrate an intact fundoplication, both early heartburn and dysphagia will usually resolve. Symptoms persisting for more than 6-12 weeks, or symptoms that are very debilitating to the patient, need to be pursued more vigorously.
This pursuit can be divided into three categories: one, was the initial diagnosis correct; two, was the ideal procedure performed; and three, is the wrap itself anatomically and geometrically proper.
The original presenting complaints of the patient should be reviewed, and copies of the work-up evaluated. Review of the pre-operative 24h pH may reveal poor symptom correlation, which would steer evaluation away from a technically poor wrap and more towards a functional or hypersensitivity disorder of the esophagus. Conversely, good symptom correlation of a classic symptom such as heartburn implies that the existing wrap may not be adequate. Careful review of the video or films of the pre-operative barium swallow may reveal stricture, suspicion of Barrett's, or hiatal hernia, any of which might suggest a shortened esophagus resulting in inadequate intraabdominal length. Review of the pre-operative manometry studies may reveal esophageal dysmotility, and the post-operative symptom of heartburn may be related to failure of esophageal clearance.
If the pre-operative studies reveal risk factors for a short esophagus (large or fixed hiatal hernia, stricture, or Barrett's), was a lengthening procedure done as part of the first operation? Although not always necessary, failure to do a lengthening procedure on a short esophagus can lead to post-operative herniation of the fundoplication, with resultant incompetence of the valve and heartburn.
Was a partial wrap or a Toupet performed? These patients are more likely than those who undergo a Nissen or full wrap to develop heartburn a year or more after surgery. If motility is adequate, revision to a full wrap may be helpful. Alternatively, if a full wrap was performed in the face of pre-operative deranged motility, the solution to post-operative heartburn may be conversion to a partial wrap.
Operative reports should be obtained to look for technical details. Failure to divide the short gastrics may predispose to a twisted or angulated wrap. Failure to close the crura increases the risk of intrathoracic migration of the GE junction, with or without the wrap.
Regardless of the results of the pre-operative evaluation, a new evaluation to assess the current situation is in order. In addition to a detailed history, objective evaluation needs to be undertaken. A barium swallow as the initial study can provide a tremendous amount of information. First and foremost, it tells us the location and integrity of the wrap, providing information about wrap migration, paraesophageal hernia, and rarely, disintegration of the wrap. It may suggest disordered motility or food stasis in the presence of an intact wrap. It provides a road map for further evaluation.
Upper GI endoscopy should be undertaken for all patients with a complaint of post-operative heartburn. Mild esophagits may be identified. The GE junction should be evaluated for intraabdominal location, and the presence of a twisted or low-lying wrap. A low-lying wrap, in which the fundus is wrapped to the greater curve of the stomach, can be identified endoscopically as a double-compartment stomach, with the fundus of the stomach seen above the wrap.
A 24 h pH must be performed in all post-operative patents to confirm the presence of pathologic acid exposure as well as good (greater than 50%) symptom correlation.
Finally, if re-operation is being considered, a repeat esophageal manometry is warranted to be sure that esophageal motility remains adequate to tolerate a full wrap.
Management of recurrent heartburn will depend upon the results of the above studies. In the good risk patient with heartburn and pathologic acid exposure on 24 h pH, re-operation is reasonable. This can be approached laparoscopically, and the details of the procedure will vary according to the first operation. We always take down the wrap, revisit the short gastrics to be sure they are all divided (even when this has been described in the operative report, we commonly find high short gastrics still intact), close the crura more snugly around a 60 F bougie, and revise the wrap as a short, floppy fundoplication. Success with this approach is reportedly as low as 85% and as high as 95% if heartburn is the only post-operative complaint.
If the 24 h pH does not show pathologic acid exposure, another solution must be sought. The esophagus is a primitive organ, and does not tell us clearly what it is experiencing. Patients complaining of heartburn may be suffering from peptic disease of the stomach or duodenum, gastric distension from diabetic gastroparesis, aerophagia, or vagal injury, or from things farther afield such as gallstones. Acid suppression for the first, prokinetics for the 2nd, and cholecystectomy for the 3rd may help ameliorate symptoms. An experienced speech pathologist may be able to minimize aerophagia and improve symptoms.
Finally the hypersensitive esophagus or patient may benefit from antidepressants, but will almost certainly not benefit from further surgery.
Castell DO and Richter JE, ed. The Esophagus, 3rd edition, Lippincott Williams & Wilkins, Philadelphia, PA: 1999
Eubanks TR, Omelanczuk P, Richards C et al. Outcomes of Laparoscopic Antireflux Procedures. The Am J Surg. 2000;179(5):391-395.
Katzka DA, Castell DO. Successful elimination of reflux symptoms does not insure adequate control of acid reflux in patients with Barrett=s esophagus. Am J Gastroenterol 1999; 89(7)989-91.
Katzka DA, Paoletti V, Leite L, et al. Prolonged ambulatory pH monitoring in patients with persistent gastroesophageal reflux disease symptoms: testing while on therapy identifies the need for more aggressive anti-reflux therapy. Am J Gastroenterol. 1996;91:2110-2113.
Law YKL, Hagen JA, KauerWKH, et al. Reoperation for Failed Antireflux Procedures. In: Modern Approach to Benign Esophageal Disease. Bremner, DeMeester, Peracchia, ed. Quality Medical Publishing, St. Louis, MO: 1995
Horgan S, Pohl D, Bogetti D et al. Failed antireflux surgery: what have we learned from reoperations? Arch Surg. 1999;134(8):809-817.
Hunter JG, Smith CD, Branum GD et al. Laparoscopic fundoplication failures. Patterns of failure and response to fundoplication revision. Ann Surg. 1999;230(4):595-606.
Trimble KC, Pryde A, Heading RC. Lowered oesophageal sensory thresholds in patients with symptomatic but not excess gastro-oesophageal reflux: evidence for a spectrum of visceral sensitivity in GORD. Gut. 1995;37(1):7-12.
Waring JP. Management of postfundoplication complications. Seminars in Gastrointestinal Disease. 1999;10(3):121-9.
Watson DI, Chan AS, Myers JC et al. Illness behavior influences the outcome of laparoscopic antireflux surgery. J Am Coll Surg.. 1997;184(1):44-8.
7. Reoperative Fundoplication
and The Short Esophagus
Emory University Hospital
1364 Clifton Road, NE (H-122)
Atlanta, Georgia 30322
john_hunter@emory.org
As with open surgery, the most popular laparoscopic operations for GERD are total fundoplication (Nissen) and partial (270 degree) esophagogastric fundoplication. When performed through a laparotomy or thoracotomy somewhere between 9 and 30% of patients develop recurrent symptoms or new troublesome symptoms that result as a side effect of fundoplication.1-3 Reported failure rates with laparoscopic fundoplication range from 2 to 17% depending upon how failure is defined.4-8 That these failure rates are indeed lower than those reported for open fundoplication probably reflects the fact that laparoscopic fundoplication is relatively new, not that laparoscopic fundoplication is intrinsically better.
The anatomy of failure includes four common types of fundoplication failure previously described with open surgery. These are: 1) slipped or misplaced fundoplication, 2) the disrupted fundoplication, 3) the herniated fundoplication, and 4) the fundoplication that is too tight or too long.9 To this list of four can be added two new anatomical problems, the "two compartment stomach" and the twisted fundoplication.10
Early postoperative symptoms.
The most common postoperative symptom is solid food dysphagia. Because distal esophageal edema (with or without hematoma) and transient esophageal dysmotility are common sequelae of fundoplication, it is no wonder that the majority of individuals have difficulty swallowing solid foods after a loose, floppy fundoplication is performed. We generally recommend that the patient stay on a full liquid diet for a week after surgery, and then maintain a soft diet for the next three weeks following operation. This protocol has reduced dramatically the incidence of post-operative food impaction, nausea, and vomiting seen when a regular diet is started too soon after operation. When a patient complains of postoperative dysphagia, we urge them to return to a liquid diet until swallowing is easy, and then advance to a soft diet. If a patient cannot advance from the full liquid diet, a barium swallow is performed. If fundoplication herniation or foregut obstruction is found, reoperation is indicated. If not, options for early intervention include esophageal dilation and/or feeding tube placement. We have utilized nasal enteric tubes and gastrostomy tubes when early postoperative dysphagia or nausea becomes so severe as to cause weight loss and dehydration. Some surgeons have advocated early reoperation for patients with severe dysphagia, but when the fundoplication is anatomically intact, our conservative approach has rarely failed.
Recurrent GERD symptoms.
When recurrent or new symptoms develop in the late postoperative period (greater than three months) investigation is warranted. For an individual who returns with symptoms identical to those for which they underwent their operation, a diagnostic trial of antireflux medication is appropriate. In addition, we generally order a barium swallow, as we have determined that at least 90% of all fundoplication abnormalities can be seen with this study.10 If the barium swallow is normal (i.e. the fundoplication is intact), it is unusual for patients to respond to proton pump inhibitor therapy. In this case, the most frequent explanation for the occurrence of recurrent symptoms is that the symptom reported is a result of a problem distinct from gastroesophageal reflux. Because respiratory symptoms and atypical gastroesophageal reflux symptoms are so often intertwined, it may take the performance of a fundoplication to determine which superesophageal symptoms are related to reflux and which are not. The best predictors of superesophageal symptom relief after a fundoplication are the response of the symptom to proton pump inhibition, and/or the correlation of superesophageal symptoms with reflux events on a 24-hour pH study.
If preliminary evaluation with a postoperative barium swallow does not reveal any abnormalities, and a trial of medical therapy fails, further investigation is unlikely to bear fruit, but should be done nevertheless. In 10% of our patients referred for postoperative GERD symptoms, an EGD revealed an anatomic problem missed by barium swallow.10 The most common anatomic problem discovered on EGD when the barium swallow looked normal was a slipped or misplaced Nissen fundoplication. While the gastroesophageal junction may be hard to define on barium swallow, an EGD demonstrating the presence of gastric folds above a fundoplication indicates a Nissen valve that has been misplaced or slipped onto the stomach. Additionally, a partially disrupted fundoplication will be visible on EGD in the retroflexed position, demonstrated by a gastroesophageal junction that is patulous (does not hug the scope), but this finding may be missed on barium swallow. When the EGD is normal and the barium swallow is normal, the 24-hour pH study (the fourth test) is almost always normal, as well.
Persistent postoperative dysphagia.
In contradistinction to the patient with recurrent GERD symptoms, the patient with new onset dysphagia represents a different problem. The management of the patient with early dysphagia is discussed above. In the patient with dysphagia that persists past three months, we confirm that an anatomic abnormality exists by performing a video barium swallow with a 12.5 mm barium pill. If the pill passes the gastroesophageal junction readily, one must suspect that the dysphagia is a result of a subtle esophageal motility disturbance or is of psychogenic nature. Thus, the normal barium swallow is followed with an esophageal motility study in patients with significant dysphagia. If the barium swallow demonstrates an anatomic fundoplication abnormality, a motility study is necessary, but only in preparation for "redo" operation. The decision to reoperate must be individualized based on the patient's nutritional status and the severity of the dysphagia. A patient who is still confined to liquids, three months postoperatively, or a patient who is losing weight because of dysphagia should be offered early elective reoperation. If the solid food dysphagia is mild or moderate, dietary restrictions are few, and weight loss is not present, we prefer a conservative course of management for the first year postoperatively. If, at that time, the barium tablet still hangs in the distal esophagus and the patient is bothered by the dietary restrictions necessary, a second operation is offered. While esophageal dilation may be beneficial for early postoperative dysphagia, it rarely helps for late dysphagia.
Fundoplication herniation.
The most frequent anatomic problem we have encountered in our patients following laparoscopic fundoplication has been the herniation of the fundoplication across the diaphragm.10 This has occurred in four settings. The first setting is the patient who strains, or retches in the early postoperative period. Pain immediately folows the herniation event, but may subside with time. This is a surgical emergency and should be confirmed with a water soluble contrast radiograph, followed by rapid return to the operating room for a laparoscopic or open reduction of the herniated stomach.
The second setting is the patient who has a single or repetitive events creating increased intraabdominal pressure (e.g. straining, coughing, lifting, retching), remote from the time of surgery. While these patients may develop severe acute pain after herniating their fundoplication, it is more usual for the event to be followed by heartburn, the new onset of dysphagia, or the development of postoperative chest pain resulting from gas or food distending the mediastinal portion of the herniated fundoplication. These patients should be evaluated with a barium swallow and esophagogastroscopy. Elective reoperation is offered.
The third scenario is more insidious yet. This is the patient who develops the slow onset of recurrent or new symptoms (chest pain, dysphagia, heartburn) in the absence of a precipitating event. Reflection on the preoperative status of these patients usually demonstrates that they had a paraesophageal hernia, an esophageal stricture, or Barrett's esophagus before their first operation. These patients have herniated because esophageal foreshortening was not detected and adequately treated at the first operation. Elective re-repair should include a Collis gastroplasty when esophageal foreshortening is found intraoperatively, repair of the esophageal hiatus, and redo fundoplication.
The fourth group of patients who herniate their fundoplication are asymptomatic. Patients who have undergone their first operation for a paraesophageal hiatal hernia are most commonly found in this group.11 If a patient is truly asymptomatic, not anemic, and has no evidence of ulceration in their herniated fundoplication, we will not recommend a reoperation, usually.
Slipped Nissen fundoplication.
Patients with a "slipped Nissen" represent a different challenge. Those with a gastric pouch above the fundoplication that is either long or bulbous will suffer the most severe symptoms of reflux and regurgitation. Not only is food trapped in this pouch during swallowing, it serves as a trap for acid rich refluxate immediately below an incompetent sphincter. Reoperation on patients with a misplaced fundoplication often reveals a virgin segment of mediastinal esophagus just above the gastroesophageal junction, evidence that the esophagus was never adequately mobilized at the first operation and the fundoplication was placed around the stomach. These patients are extremely grateful when their fundoplication is placed in the right spot on the esophagus.
Disrupted, twisted fundoplication and two compartment stomach.
The disrupted fundoplication is perhaps the easiest to diagnose and repair. The preoperative evaluation of these patients will often include a 24-hour pH study as well as esophageal motility, barium swallow, and EGD. In the absence of erosive esophagitis or Barrett's esophagus, it is important to document gastroesophageal reflux with a pH study before reoperating on a patient with a disrupted fundoplication.
The new defects, unique to laparoscopic surgery, are the twisted fundoplication and the two-compartment stomach. The twisted fundoplication results from failure to mobilize the greater curvature of the stomach from the spleen and diaphragm (Rosetti- Nissen). A portion of the anterior wall of the stomach is pulled from the left around the esophagus to the right and sutured in this position. This creates tension at the gastroesophageal junction which can result in rotation of the distal esophagus and a spiral type deformity seen in retroflection of the endoscope. This deformity usually presents with symptoms of dysphagia and severe postoperative gas bloat. This defect is very resistant to esophageal dilation and requires reoperation to correct it. Occasionally individuals who undergo this Rosetti modification of the Nissen fundoplication will have an additional problem, the two compartment stomach. This occurs when a point on the greater curvature too far from the fundus is pulled up to the gastroesophageal junction to form the fundoplication. These patients are extremely uncomfortable and require urgent reoperation once the diagnosis is made. Barium swallow and upper endoscopy usually reveal the septated nature of the stomach, and the diagnosis is not difficult.
Bloating, nausea, and epigastric pain.
A small subset of patients who undergo laparoscopic Nissen will be plagued by persistent bloating, nausea, and epigastric pain postoperatively. These patients fall into two groups: those with functional problems, and those with delays in gastric emptying which may be a result of inadvertent vagal injury. In the early postoperative period, treatment with antiemetics is the best therapy. When nausea persists beyond the usual three-month postoperative period, however, investigation is warranted. If an EGD and gastric emptying study are normal, it is usually sufficient to treat these patients with antiemetic medications, including ondanasetron, promethazine, and the prokinetic agent, metaclopromide. On the contrary, when the EGD demonstrates food in the stomach, one must postulate that gastoparesis has occurred postoperatively or was overlooked on the preoperative evaluation. Significant food in the stomach is strong evidence of gastroparesis. There is probably little need for a gastric emptying study in these patients, but we generally perform this study to quantify the amount of gastric retention. If gastric emptying cannot be normalized on prokinetic agents (and it rarely is), we will recommend the performance of pyloroplasty, and, if the patient is losing weight, a feeding jejunostomy. Following these two procedures, we prefer to wait for a year to determine whether gastric emptying will return. If there is no appreciable improvement in gastric emptying after a 12-month followup period, subtotal gastrectomy with Roux-en-Y gastrojejunostomy is appropriate.
In addition to our study, mentioned earlier, there have been a number of other studies that have looked at "redo" laparoscopic fundoplication.12-15 Some surgeons attempt to perform all redo fundoplications laparoscopically, some surgeons will perform all redo fundoplications through a thoracotomy, and some surgeons perform all redo fundoplications through a laparotomy. We generally tailor our redo operation to the method used for the previous operations(s). That is, when the first operation was performed through a thorocotomy or a laparoscopy, our preferred approach is a laparoscopic approach. When the first operation was performed with a laparotomy, our preferred operative approach is through a laparotomy. When we have approached this latter group through a thorocotomy, the intra-abdominal adhesions make redo surgery difficult. When we have performed the redo operation following laparotomy with laparoscopic access, we have found that intra-abdominal adhesions made the laparoscopic procedure quite lengthy. Whether the redo operation is performed laparoscopically or through laparotomy, the principles are the same.
Exposure for Laparoscopic "Redo" Fundoplication.
We use the same five-trocar technique that was used for the primary operation. Because there will frequently be adhesions between the fundoplication and the liver, it may be necessary to adjust the liver retractor several times as the adhesions are taken down. Dissection then proceeds by identifying the diaphragmatic crura. This is generally easiest on the left side of the fundoplication. If the short gastrics have been previously mobilized, it is easy to follow the left hemidiaphragm down to its base. The right diaphragm is best approached by identifying the caudate lobe of the liver and proceeding superiorly and to the left until the right crus is encountered. If the hepatic branch of the vagus has not been divided on the first operation, it is usually necessary to do so on the second operation to better facilitate dissection and repair. If the short gastric vessels have not been not been taken down during the first operation, this is performed. Three hundred sixty degree dissection of the diaphragmatic crura allows a Penrose drain to be placed behind the esophagus. The Penrose is held in place with clips or with an endoloop. The surgeon should note that if the fundoplication has herniated, this Penrose drain will be around the stomach and not around the esophagus. Inferior traction on the drain allows the surgeon to reduce the herniated fundoplication back into the abdomen. Again, dissection stays close to the stomach to avoid developing a pneumothorax. If a pneumothorax does occur, generally the intra-abdominal pressure is decreased to 8 to 10 mm of Hg, and dissection proceeds without physiologic difficulty. Once the fundoplication has been reduced from the chest, the next step is to take the old fundoplication apart. This is performed with sharp dissection by identifying the stitches on the anterior portion of the fundoplication and dividing them sharply. The fundus of the stomach is then peeled to the left and to the right from the midposition to take down the fundoplication circumferentially. Again, sharp dissection without the use of electrosurgery or harmonic scalpel is preferred to insure that the vagal nerves do not suffer themal injury in the course of this dissection. Generally, the vagal trunks will be found within the prior fundoplication. The posterior vagus can usually be preserved if it was previously left inside the fundoplication, but is more difficult to preserve if it was left outside the fundoplication. The anterior vagus nerve should be and can be preserved if it has not been encased in scar at the level of the diaphragm. Once the fundoplication has been entirely taken down, an assessment of intra-abdominal length is performed by pulling the crura together with a grasper and letting go of the drain. If two centimeters of tension-free esophagus exist in the abdomen, the esophagus is not foreshortened and a Collis procedure need not be done. If the gastroesophageal junction lies within two centimeters of the closed hiatus, a Collis gastoplasty is performed.
Collis gastroplasty.
The acquired short esophagus can - to a certain extent - be predicted preoperatively. These predictors have been well described and include a large hiatal hernia, esophageal stricture, Barrett's esophagus, reoperative surgery, and a manometrically defined lower esophageal sphincter above 35 cm from the incisors. These findings are present in approximately 20% of individuals undergoing laparoscopic antireflux surgery. Of the individuals with these criteria, one in five will have esophageal foreshortening as defined in the previous paragraph. Thus, 4% of all individuals undergoing reoperative surgery will have esophageal foreshortening. Swanstrom has looked carefully at the criteria for esophageal foreshortening and determined, as did we, that 8 - 10% of patients with Barrett's esophagus meet the intraoperative criteria.
There are several approaches one can take to performance of esophageal lengthening. Certain surgeons will exclude the 20% of patients with risk factors for esophageal foreshortening from their laparoscopic practice. These patients will either be referred or will undergo an open procedure. This is a very reasonable approach.
For the advanced laparoscopic surgeon who wishes to tackle these complex cases laparoscopically, there are two general approaches that can be utilized: a totally laparoscopic approach and a laparoscopic and thoracoscopic approach. We have popularized the totally laparoscopic approach. The technique that we originally utilized was a variation of the technique used for vertical banded gastroplasty. A transgastric hole is placed adjacent to a 48 French dilator along a lesser curvature, 4 cm down from the Angle of His. This hole is created with a 21 mm EEA stapler that is introduced through a small perixiphoid stab incision. After this hole is made, a linear cutting stapler is introduced through the low epigastric trocar and is placed through the hole in the stomach, then fired parallel and snug to the dilator to create a neoesophagus. Occasionally, a second or third firing of the GIA will be necessary to create a gastric tube. A small "hammerhead deformity" above the circular staple line is then usually amputated with a second firing of the linear cutting stapler. Upon completion of these steps, the stomach is wrapped around the esophagus, and a Nissen fundoplication is performed. For this procedure to be successful, it is critical that a tight gastric tube be made adjacent to the 48 French dilator, and that the first stitch of the Nissen fundoplication is placed on the native esophagus and not on the neoesophagus. If a portion of stomach resides above the fundoplication, a slipped Nissen has been created, and the patients are quite miserable.
A novel way of performing a laparoscopic Collis gastroplasty has come from the bariatric surgery field. In this variation we use an angulated, roticulating GIA-type linear cutting stapler which we introduce through the left subcostal port. The 48 French dilator is then placed. A point adjacent to this dilator, 4 cm down from the Angle of His, is marked. The gastric fundus is reduced as inferiorly as possible, and a GIA stapler, maximally flexed, is brought in from the greater curvature side and fired until this point is reached. Occasionally two or three firings of the stapler will be necessary to reach the dilator. Once this transverse staple line has been completed, a vertical staple line is created by roticulating the stapler in a different direction and firing flush to the dilator in a cephalad direction. While this procedure removes a small portion of the stomach, the amount of stomach sacrificed is quite small, and no greater than that sacrificed in the previously described operation. Our clinical success with both of these techniques has been superb, and there are no discernible differences in symptomatic outcome in patients who have and have not had a Collis gastroplasty. Most importantly, we have seen no herniated fundoplications in these patients.
The other method for performing minimally invasive Collis gastroplasy utilizes a right thoracoscopic approach and was popularized by Swanstrom et al. When it is clear intraoperatively that esophageal shortening exists, a small incision is made in the midaxillary line of the 4th or 5th interspace. A low pressure pneumothorax is obtained to collapse the right lung and a zero degree telescope is passed to the gastroesophageal junction inferiorly. Transillumination of the phrenoesophageal ligament allows the surgeon to locate the laparoscopic image. The laparoscope is then removed and a linear cutting stapler is introduced through the thoracoport and brought down into the abdomen. Again, a 48 transdilor is placed and 4 cm tube is stapled adjacent to the dilator with a linear cutting stapler. In general, the blue (3.5 mm) staples are used as they are more hemostatic than the thick tissue (4.8 mm) green staples. Nonetheless, for thick stomachs the green staples should be used. Upon completing the Collis tube, the port is removed and the lung is blown up to a water seal. The tube is removed before the patient leaves the operating room with a fully expanded lung.
I am often asked whether a pyloroplasty is indicated when neither vagal trunk can be identified because of one or two previous operations. We generally do not recommend this, as most vagotomized stomachs will empty reasonably normally, and pyloroplasty can then be used for those patients who develop difficulties with poor gastric emptying post-operatively. It has been extremely rare that we have found the need to return at a later date for pyloroplasty. Lastly, the topic of second and third time revisional operations frequently arises. We have reported that the results of redo fundoplication deteriorate with each successive operation.10 Whereas success for the first operation runs between 90 and 95%, second operations are successful between 80 and 90% of the time, and third operations are successful between 50 and 66% of the time. Because fourth time operations are rarely successful at all, many individuals suggest that esophageal resection be performed after three failed fundoplications. This is generally our policy, when all other conservative measures have failed.
In conclusion, the revolution in laparoscopic antireflux surgery has created a huge new area for thought and investigation, the failed laparoscopic Nissen. With careful and thorough preoperative evaluation, most of these patients may be re-repaired with meticulous laparoscopic technique.
1. DeMeester TR, Bonivina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease: evaluation of primary repair in 100 consecutive patients. Ann Surg 1896; 204(1):9-20.
2. Hiebert CA, O'Mara CS. The Belsey operation for hiatal hernia: a twenty-year experience. Am J Surg 1979; 137:532.
3. Shirazzi SS, Schulze K, Soper RT. Long-term follow-up for treatment of complicated chronic reflux oesophagitis. Arch Surg 1987; 122:548-552.
4. Hinder RA, Filipi CJ, Wetscher G, Neary P, DeMeester TR, Perdikis G. Laparoscopic Nissen fundoplication is an effective treatment for gastroesophageal reflux disease. Ann Surg 1994; 220:472-483.
5. Hunter JG, Trus TL, Branum,GD, Waring JP, Wood WC. A physiologic approach to laparoscopic fundoplication for gastroesophageal reflux disease. Ann Surg 1996; 223:673-687.
6. Peters JH, Heimbucher J, Kauer WK, Incarbone R, Bremner CG, DeMeester TR. Clinical and physiologic comparison of laparoscopic and open Nissen fundoplication. J Am Coll Surg 1995; 180:385-393.
7. Jamieson GG, Watson DI, Britten-Jones R, Mitchell PC, Anvari M. Laparoscopic Nissen fundoplication. Ann Surg 1994; 220:137-145.
8. Cushieri A, Hunter JG, Wolfe B, Swanstrom LL, Hutson W. Multicenter prospective evaluation of laparoscopic antireflux surgery. Surg Endosc 1995; 7:505-510.
9. Hinder RA, Kingler PJ, Perdikis G, Smith SL. Management of the failed antireflux operation. Surg Clin North Am 1997; 77(5):1083-1098.
10. Hunter JG, Smith CD, Branum GD, Waring JP, Trus TL, Cornwell M, Galloway K. Laparoscopic Fundoplication Failures: Patterns of Failure and Response to Fundoplication Revision. Ann Surg 1999; 230:595-606.
11. Watson DI, Jamieson GG, Devitt PG, Mitchell PC, Game PA. Paraesophageal hiatus hernia: an important complication of laparoscopic Nissen fundoplication. Br J Surg 1995; 82:521-523.
12. Soper NJ, Dunnegan D. Anatomic fundoplication failure after laparoscopic antireflux surgery. Ann Surg 1999; 229:669-677.
13. Curet MJ, Josloff RK, Schoeb O, Zucker KA. Laparoscopic Reoperation for Failed Antireflux Procedures. Arch Surg 1999; 134(5); 559-563.
14. Pointner R, Bammer T, Then P, Kamolz T. Laparoscopic Refundoplications after Failed Antireflux Surgery. Am J Surg 1999; 178(6); 541-544.
8. Open Management of Failed Antireflux Surgery; Rationale and Techniques.
Professor of Surgery, University of Southern California. Los Angeles
Achieving consistently successful outcomes is difficult with any form of therapy and laparoscopic fundoplication is no exception. Failure rates as high as 15-20 % have been reported following primary Nissen fundoplication [1-5], and as high as 50%, 3 years following laparoscopic partial fundoplication [6,7].
An antireflux procedure is considered a failure when the patient is unable to swallow normally, experiences upper abdominal discomfort 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 remains a challenge. Functional assessment of patients who have recurrent, persistent, or new symptoms following a primary antireflux repair is critical in identifying the cause of failure. The reasons for failure must be identified prior to the remedial procedure, but can be overlooked in the enthusiasm to relieve the patient's symptoms. It also provides an opportunity to identify those operative principles that are crucial to performing a successful primary antireflux procedure.
Successful treatment of failed antireflux procedures requires careful attention to:
1) the primary symptoms responsible for failure
2) the anatomic and functional reasons for failure
3) the selection and optimal performance of a remedial antireflux procedure tailored to the
individual patient.
Persistent dysphagia and heartburn are the symptoms responsible for failure in the vast majority of patients [8-12]. Dysphagia tends to occur early after the failed procedure usually due to faulty construction of the repair such as a "slipped" or misplaced, too tight or too long of a fundoplication. Less commonly, dysphagia is due to lack of appreciation of a preexisting esophageal motor abnormality or underlying reflux induced stricture. Patients with dysphagia as the primary symptom often have a poorer outcome than patients re-operated for recurrence of heartburn. Heartburn is the second most common reason for failure in patients following failed antireflux surgery. It generally occurs later and is due to partial or complete disruption of the previous repair. The outcome of patients with heartburn as the primary symptom is predictably more favorable.
The two most common causes of technical failure are the low placement of the fundoplication (ie `slipped' Nissen) and herniation of the fundoplication into the chest [13-17] These complications are likely to occur when the esophagus is short, or when mobilization is inadequate. Esophageal shortening occurs most commonly in patients with advanced reflux disease due to acid related inflammatory changes in the muscular wall of the esophagus which on healing result in contracture. While severe degrees of esophageal shortening are obvious on a contrast esophagogram, subtler degrees of acquired shortening are difficult to detect. As a result, acquired esophageal shortening remains a potential cause of treatment failure with the laparoscopic approach.
Several authors have analyzed the most common reason for failure following laparoscopic Nissen fundoplication [13-16]. Recurrent hernia of an intact or partially disrupted wrap has emerged as the most common anatomic reason for failure (Table I). Why this is the case is unclear, but it may be related to the selection of laparoscopic access in patients with a shortened esophagus, lack of, or breakdown of the crural closure, less extensive esophageal mobilization, and perhaps, a reduced tendency for adhesion formation after laparoscopic compared to open surgery.
Hunter has compared the reasons for failure in 71 patients following laparoscopic Nissen fundoplication to 29 patients following an open procedure [13]. The reasons for failure were significantly different (II). Failures following laparoscopic fundoplication were largely due to recurrent hernia, while failures following open fundoplication were due to wrap disruption/slippage or too long or tight a fundoplication. Soper likewise found recurrent hernia to be the most common cause of "anatomic" fundoplication failure [14]. Dallemagne suggested that technical quality of the operation was responsible for the majority of the failures (22/26), most of which were secondary to the use of a Nissen-Rosetti fundoplication (no short gastric division) and consequent dysphagia [15]. Horgan and Pellegrini have concluded that the most important technical factors preventing recurrence were effective crural closure, transhiatal esophageal mobilization, attention to the geometry of the fundoplication and anchoring the wrap to the esophagus and surrounding tissues (Table) [16].
One area that has received scant attention is the influence of body habitus on the outcome of laparoscopic fundoplication. A recent study identified obesity as a major factor in the failure of antireflux surgery [17]. Perez et al. evaluated 224 patients after antireflux surgery, laparoscopic Nissen fundoplication in 187 and open transthoracic Belsey repair in 37. At a mean follow-up time of 37 months, 12% of patients had objective evidence of recurrence. Patients with a body mass index exceeding 30 had a significantly higher recurrence rate (27%) than either those with a body mass index <25 (5%) or those with a body mass index between 25 and 29 (8%).
The data show that technical errors account for the majority of failed antireflux repairs. These include a misplaced fundoplication, breakdown of the repair, herniation of the repair into the chest, too long or too tight fundoplication, and operative damage to the lower esophagus. An underlying primary motor disorder, an error in diagnosis or an intact but ineffective repair are responsible for the remainder. In the era of open fundoplication the most common technical error was placement of a Nissen fundoplication around the stomach instead of the lower esophagus. Historically this has been referred to as a "slipped" Nissen. A gastric wrap is most often misplaced because poor exposure leads to insufficient visualization of the hiatal area, especially in obese patients, or because the esophagus is insufficiently reduced into to the abdomen in the presence of a short esophagus. A short esophagus should be suspected if a hiatal hernia does not reduce on an upright barium swallow, or the distance between the crura and the gastroesophageal junction on endoscopy is in excess of 5 cm. In these situations a thoracic approach is preferred to permit mobilization of the esophagus from the diaphragm to the aortic arch, to allow for the possibility of a lengthening procedure, and to ensure placement of a properly positioned fundoplication below the diaphragm without undue tension.
Breakdown of the fundoplication is the second most common cause of failure. Inadequate mobilization of the fundus is the usual reason which was confirmed by intraoperative findings including no evidence of a crural dissection or division of the short gastric vessels. The repair may herniate into the chest if it is placed under too much tension, the crura are not adequately approximated or the crural closure is disrupted. The crural sutures should incorporate the peritoneum covering the crura and not just the muscular tissue. The tendinous portion of the diaphragm at the apex of the right crus should be avoided. The temptation not to close the crura during laparoscopic fundoplication should be avoided.
Less common causes for failure include a fundoplication which is too tight or too long or esophageal damage. A wrap limited to 1-2 cm is an effective antireflux barrier as a longer wrap and reduces the potential for permanent dysphagia in the late postoperative course. Calibrating the diameter of the wrap with a 60 French intraluminal bougie prevents making it too tight and reduces the incidence of immediate postoperative dysphagia. Gentleness in handling tissues is one of the cornerstones of esophageal surgery and prevents damage to the esophageal muscle resulting in poor motility of that portion of the esophagus after the surgery.
Patients who present with dysphagia and a severe motility disorder, weak or interrupted contractions, a stricture that cannot be dilated, a history of multiple previous unsuccessful repairs, and patients in whom fibrosis of the esophageal muscular layer is found intraoperatively have irreversible functional esophageal damage. An esophageal resection and colon interposition is, in our experience, the best way to restore alimentary function in these patients [19].
The preferred surgical approach to a patient who has had a previously failed antireflux procedure is an open thoracotomy. The diaphragm is divided via a peripheral circumferential incision to permit simultaneous exposure of the upper abdomen and dissection of the previous repair.
Four factors should be taken into account in choosing a remedial procedure: the patient's symptoms, the number of previous repairs, the results of esophageal functional tests, and the operative findings (Table 4). A 360 Nissen fundoplication should be performed in patients with positive 24 hour pH studies, who complain primarily of heartburn and who have normal esophageal length and motility. A Belsey partial fundoplication is performed in patients who complain of heartburn and have a positive 24 hour pH study, normal esophageal length, but abnormal esophageal motility (i.e., a contraction amplitude of < 15 mm Hg) or patients who complain of dysphagia and had a normal 24 hour pH tracing but abnormal esophageal motility.21,22 In these patients, a gastroplasty can be added if the esophagus is shortened. A myotomy of the esophageal body plus a Belsey procedure should be performed in patients who have >20% simultaneous waves and complete lower esophageal sphincter relaxation on swallowing. A myotomy of the sphincter plus a Belsey procedure is appropriate for patients whose initial wrap was properly placed around the sphincter but motility studies show incomplete relaxation of the lower esophageal sphincter on swallowing with adequate esophageal peristalsis. An esophageal resection is often required for patients with dysphagia, who have a history of two or more previous repairs with absent or severely depressed esophageal body contractility, or a stenosis resistant to dilatation.
Esophageal body function is an important criterion to determine the optimal procedure in patients with a history of failed antireflux surgery. We found that patients with a normal esophageal body motility have a significantly higher success rate following reoperation, while those with poor motility are less likely to experience symptom relief.
The best approach to failed antireflux surgery is to prevent it. Detailed physiologic evaluation prior to surgery and attention to technical details during the primary operation will avoid failure in the vast majority of patients. There is no single remedial operation to correct a previously failed antireflux procedure. Rather, the operation must be tailored to each patient on the basis of the presenting symptoms, number of previous repairs, the results of esophageal function tests, and the operative findings. In patients who present with heartburn and increased esophageal acid exposure secondary to a mechanically defective sphincter, a remedial antireflux procedure is generally sufficient. The choice of the procedure depends primarily on the motility study. If good lower esophageal sphincter relaxation and contraction amplitude of the esophageal body are present, a Nissen fundoplication can be used. A transthoracic, transdiaphragmatic approach is helpful to free the esophagus and stomach from adjacent structures and allow takedown of the previous repair. If esophageal body contractility is poor, a Belsey partial fundoplication should be done to minimize outflow resistance. A gastroplasty can be added to a Belsey repair if the esophagus has shortened and the repair is under tension. Patients who present with nonobstructive dysphagia are best managed with a Belsey repair combined with a myotomy when a primary esophageal motor disorder or incomplete relaxation of the sphincter are present. If esophageal body function is adequate and the cause of dysphagia is a too tight or too long of a fundoplication, an appropriate-sized Nissen fundoplication can be reconstructed.
Table I
Causes of Failure in Open and Laparoscopic Fundoplication
|
Cause of Failure |
Open Fundoplication (N=29) |
Lap Fundoplication Emory (N=31) |
Lap Fundoplication Referred (N=40) |
p Value |
|
Re-herniation |
22% |
84% |
25% |
<0.01 |
|
Disruption |
39% |
3% |
0 |
<0.01 |
|
Slipped/misplaced |
22% |
3% |
30% |
<0.05 |
|
Too long or tight |
13% |
3% |
5% |
NS |
|
Twisted |
0 |
6% |
30% |
<0.01 |
|
Achalasia |
4% |
0 |
10% |
NS |
Hunter JG et al. Ann Surg 1999; 230; 595-606
Table II
Most Common Reasons for Failed Fundoplication Following Open Repair
|
Reason for Failure |
Number of Patients (N=105) |
|
Recurrent heartburn |
|
|
Wrap Disruption |
48 |
|
Postop dysphagia or dysphagia & heartburn |
|
|
Displaced repair |
24 |
|
Too Long or too tight |
11 |
|
Esophageal motor disorder |
10 |
|
Re-Herniation |
6 |
|
Gastric symptoms |
|
|
Delayed gastric emptying |
6 |
Stein HJ et al. Am J Surg 1996; 171:36-40
Table III
Intraoperative findings in 46 patients with failed fundoplication
Reason for failure Number of patients Percent
Recurrent hernia 31 ---------
Sliding 18 39%
Paraesophageal 13 28%
Wrap disruption 20 43%
Slipped fundoplication 9 20%
Wrap too tight 5 11%
Missed achalasia 2 4%
Modified from Floch NR, Hinder RA, Klingler PJ et al. Arch Surg 1999;134:733-737.
Table IV
Technical factors important in preventing recurrence following laparoscopic fundoplication
Effective crural closure
Transhiatal esophageal mobilization
Attention to the geometry of the fundoplication
Anchoring the fundoplication to the esophagus and surrounding tissues
1. Hunter JG, Trus TL, Branum GDet al. A physiologic approach to laparoscopic fundoplication for gastroesophageal reflux disease. Ann Surg 1996;223:673-85.
2. Hinder RA, Filipi CJ, Wetscher G et al. Laparoscopic Nissen fundoplication is an effective treatment for gastroesophageal reflux disease. Ann Surg 1994;220:472-81.
3. Peters JH, DeMeester TR, Crookes P et al. The treatment of gastroesophageal reflux disease with laparoscopic Nissen fundoplication. Prospective evaluation of 100 patients with "typical" symptoms. Ann Surg 1998;228:40-50.
4. Jamieson GG, Watson DI, Britten Jones R, Mitchell PC, Anvari M. Laparoscopic Nissen fundoplication. World J Surg 1994;16:335-6.
5. Pearson FG. Hiatus hernia and gastroesophageal reflux: indications for surgery and selection of operation. Seminars in Thoracic & Cardiovascular Surgery. 1997;9:163-68
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13. Hunter JG, Smith D, Branum GD, Waring JP, Trus TL, Cornwell M, Gailloway K. Laparoscopic fundoplication failures. Patterns of failure and response to fundoplication revision. Ann Surg 1999; 230:595-606.
14. Soper NJ, Dunnegan D. Anatomic fundoplication failure after laparoscopic antireflux surgery. Ann Surg 1999;229:669-677.
15. Dallemagne B, Weerts JM, Jehaes C et al. Causes of failure of laparoscopic antireflux operations. Surg Endosc 1996;10:305-310.
16. Horgan S, Pohl D, Bogetti D et al. Failed antireflux surgery: what have learned from reoperations? Arch Surg 1999;134:809-817.
17. Perez AR, Moncure AC, Rattner DW. Obesity is a major cause of failure for both transabdominal and transthoracic antireflux operations. Gastroenterology 1999;116:A1343.
18. Godenstatter M, Hagen J, DeMeester TR, Ritter MP, Peters JH, Mason, RJ, CG Crookes PF. Esophagectomy for failed antireflux surgery. J Thorac Cardiovasc Surg, 1998, 115:296-302.
prevalence of failure lap
reasons for failure open
reasons for failure lap
benefits of complete mobilization
need for collis
results of 2nd & third procedures
lap redo results
symptoms
outcome of open redo's
