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chalasia of the Esophagus: A Surgical Disease
alerie A Williams, MD, Jeffrey H Peters, MD, FACS
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chalasia is a primary esophageal motility disorder of un-lear etiology. As treatment has evolved during the past 10o 15 years, it has become primarily a surgical disease. It isncommon, but not rare, affecting approximately 1 in00,000 individuals per year.1 Occurring equally in mennd women, it is an acquired condition usually diagnosedetween 20 and 50 years of age, but can occur at any age. In672, Sir Thomas William first described the disease ascardiospasm” and treated the problem with dilation usingwhale sponge attached to a whale bone. It was not until927, when A F Hurst determined that the problem washe result of an inability of the lower esophageal sphincterLES) to relax, and named the disease achalasia, a Greekerm meaning failure to relax.2 Normal individuals have aower esophageal high-pressure zone, which completely re-axes with initiation of a swallow. In achalasia, residualressures in the LES remain well above normal after swal-

owing, resulting in a functional outflow obstruction at theastroesophageal junction. In addition, the LES can beypertensive, resulting in higher than normal resting pres-ures, and the esophageal body is aperistaltic, all leading toailure of bolus transport.3 When untreated, intraesopha-eal pressures rise and the esophagus slowly dilates, often tohe point of gross deformity.4

TIOLOGYchalasia can be primary (idiopathic) or secondary. Pri-ary achalasia is thought to result from a complete loss or

elative absence of inhibitory ganglion cells in the myen-eric (Auerbach’s) plexus of the esophagus. This loss createsn imbalance between excitatory and inhibitory neuronsausing failure of the LES to relax.5 Several studies haveocumented diminished numbers of myenteric ganglion iniseased esophageal specimens and demonstrated the pres-nce of lymphocytic infiltrate and collagen depositionithin ganglion.6-8 Given these findings, an infectious

gent, such as a virus, and its subsequent immune response,s thought to be the cause of the ganglion loss, but the exacttiology remains unknown. Neurotransmission and cell

isclosure Information: Nothing to disclose.

eceived March 31, 2008; Revised July 14, 2008; Accepted August 13, 2008.rom the Department of Surgery, University of Rochester Medical Center,ochester, NY.orrespondence address: Jeffrey H Peters, MD, Department of Surgery, Uni-

ersity of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY
c4642. email: [email protected]
1512008 by the American College of Surgeons

ublished by Elsevier Inc.

ignaling as it relates to the distal esophagus and LES inchalasia has been a subject of growing investigation. Nitricxide is thought to be the major inhibitory neurotransmit-er controlling relaxation of esophageal smooth muscle.9,10

t has been suggested that nitronergic inhibitory neuronsre lost in greater proportion than cholinergic neurons dur-ng the achalasia disease process.11

Supporting this thesis, studies in knockout mice lackingitric oxide synthase (NOS) have found high LES restingressures and absent LES relaxation.12 In humans, speci-ens from achalasia patients have shown complete loss ofOS enteric neurons and NOS activity as compared with

onachalasia specimens.13 Bruley des Varannes and col-eagues14 recently reported a study suggesting a serum-orne substance, supporting an immunologic mechanism.astric fundic muscle from normal humans was culturedith serum from achalasia patients, gastroesophageal refluxisease patients, or normal subjects. The normal fundus

ncubated with serum from achalasia patients had a de-rease in NOS neurons as compared with controls. In ad-ition, relaxation of electrically stimulated circular muscleontractions was substantially decreased after incubationith serum from patients with achalasia.The most common secondary cause of achalasia is Cha-

as’ disease15,16 a systemic disease caused by infestation byhe protozoan Trypanosoma cruzi. Chagas is transmitted toumans by the reduviid or “kissing bug” and infects intra-ural neurons, causing autonomic dysfunction. Chagas’

isease is common in South and Central America, andorldwide is considered to be the most common cause of

chalasia.15,16 Pseudoachalasia occurs through infiltrationf the LES by cancer or by iatrogenic condition, such as aight fundoplication or external appliance, such as aand.17,18

RESENTATION AND DIAGNOSISchalasia is a slowly progressive disease. As a consequence,atients often present late in the course of this disease,hen their symptoms and anatomic abnormalities haveecome prominent. Diagnosis earlier in the disease processs possible, given conscientious attention to patients’sophageal reports and a high degree of suspicion. Clinicalymptoms include slowly progressive dysphagia for solidsnd liquids, regurgitation of bland undigested food, chestain, and weight loss. Patients can also have a history sug-estive of aspiration, including recurrent pneumonia or
hronic cough.
ISSN 1072-7515/09/$36.00doi:10.1016/j.jamcollsurg.2008.08.027

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152 Williams and Peters Achalasia of the Esophagus J Am Coll Surg

Of important note, patients with achalasia can presentith heartburn and, as such, mimic the presentation ofastroesophageal reflux disease. Reviewing the symptomsf 67 patients with achalasia, Spechler and colleagues19

ound that 32 (48%) reported heartburn. This fact, cou-led with diagnostic challenges in patients with early acha-

asia, including presence of a normal-caliber esophagus andrtifactual LES relaxation on manometry (caused by rela-ive movement of the catheter and sphincter), likely leadso a small but real number of patients with achalasia erro-eously diagnosed with gastroesophageal reflux disease andndergoing Nissen fundoplication. In fact, it is not un-ommon for patients with achalasia to be treated with pro-on pump inhibitors. The clinician should be aware of thisossibility; a careful review of both the manometric studynd video barium examination will almost always reveal theharacteristics of achalasia. This occurs for several potentialeasons. Physiologically, heartburn has been shown to berecipitated by esophageal distention.20 Different neuraltimuli (luminal acid versus distention) can be interpretedy the brain as the same symptom. It has also been sug-ested that achalasia can develop in the setting of underly-ng gastroesophageal reflux disease. The retrospectiveymptom review referenced here showed that of those witheartburn, 47% (n � 15) had heartburn before develop-ent of dysphagia, which persisted once dysphagia devel-

ped, and an additional 28% (n � 9) had heartburn beforeevelopment of dysphagia, which stopped after onset ofysphagia. Heartburn symptoms developed in the remain-

ng patients (25%) after onset of dysphagia. Interestingly,hose patients reporting heartburn had considerably lessES resting pressures as compared with those withouteartburn symptoms. Both mechanisms are likely at play.A simple chest radiograph can suggest the diagnosis in

dvanced cases by the absence of a gastric bubble and pres-nce of a dilated fluid-filled esophagus, generally seen as aight-sided posterior mediastinal shadow.4 Upper endos-opy should be performed in all patients to exclude ob-truction from tumor or stricture. Findings will commonlynclude retention of saliva and undigested food associatedith a dilated esophagus, but can be normal. A barium

wallow is often diagnostic, showing a dilated aperistalticsophagus, presence of an air-fluid level, or a characteristicbird’s beak” appearance created by a nonrelaxing LES

Abbreviations and Acronyms

HRM � high-resolution manometryLES � lower esophageal sphincterNOS � nitric oxide synthase

Fig. 1).4 Barium studies can be interpreted as “normal,” g

articularly in early achalasia, with the radiologists’ focusn anatomic characteristics, such as dilation and empty-ng.21 Reviewing the symptoms and barium studies of 38atients with confirmed achalasia, Blam and colleagues21

ound a poor correlation between symptoms and bariumtudy findings, which led to a diagnostic delay, particularlyn patients who presented with atypical symptoms (ie,eartburn, weight loss, cough, asthma). Atypical symp-oms were reported in 34% of patients and resulted in aedian delay of 30 months before correct diagnosis, as

ompared with 11 months in those who reported typicalymptoms (dysphagia, chest pain, regurgitation). Carefulxamination of fluoroscopic or video images should be rou-inely done, which will almost always reveal a flaccid non-eristaltic esophagus devoid of the usual “stripping”aves.22,23

The gold standard for diagnosis of achalasia is esopha-

igure 1. Barium esophagogram in a patient with achalasia. Notehe esophageal air-fluid level and characteristic “bird’s beak” nar-owing created by a nonrelaxing lower esophageal sphincter.

eal manometry, which is the most sensitive diagnostic test

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153Vol. 208, No. 1, January 2009 Williams and Peters Achalasia of the Esophagus

vailable.3,17 Manometry is especially helpful in establish-ng the diagnosis in patients who present in an early diseasetate when other diagnostic evaluations appear normal.3

here are four classic manometric characteristics (Table 1):ypertensive LES, present in approximately 50% of pa-ients; nonrelaxing LES; esophageal aperistalsis; and ele-ated lower esophageal baseline pressure. A subset of acha-asia patients can have simultaneous contraction waves ofariable amplitudes, consistent with preserved muscleunction, this is termed vigorous achalasia.3 Examining theanometric tracings of 26 patients with achalasia, Shi and

olleagues24 found residual LES relaxation pressure to behe most accurate diagnostic manometric criteria. Specifi-ally, a residual pressure of �12 mmHg had 92% sensitiv-ty for the diagnosis of achalasia. Coupled with aperistalsis,residual pressure of �10 mmHg had 100% sensitivity

nd 100% positive predictive value for achalasia. Similarly,n a later study by the same group, examination of 58chalasic manometric studies revealed only one variant pa-ient who had a residual pressure after swallow-inducedES relaxation that was �10 (Fig. 2).25

Although traditionally, a nonrelaxing sphincter andomplete aperistalsis were thought to be universally re-uired for diagnosis of achalasia (it is debated which ofhese might be the primary and most important feature), its likely that some heterogeneity exists in the manometricindings in patients with all the clinical characteristics ofchalasia. Hirano and colleagues have recently emphasizedhis fact.25 They carefully analyzed the clinical history andanometric recordings of 58 patients with achalasia and

3 control subjects. Endoscopy, barium swallow, histopa-hology, and response to treatment were used to help estab-ish the diagnosis in patients without classic manometricindings. Although it was uncommon, four manometri-ally distinct variants were seen, ie, high-amplitude non-eristaltic esophageal body contractions, short segments ofperistalsis, retained complete LES relaxation on swallow-ng, and nonswallow transient relaxation. These findingsere seen in only 4 of 58 patients, the vast majority had

lassic manometric findings of achalasia. This study pro-ides a strong argument that variations truly exist. Thelinician should be aware of these possibilities when evalu-ting patients with dysphagia.

The introduction of high-resolution manometryHRM) and multichannel intraluminal impedance (MII)

able 1. Manometric Characteristics of Achalasiaypertensive lower esophageal sphincter resting pressure

ncomplete or nonrelaxing lower esophageal sphincterperistalsis of the esophageal bodysophageal pressurization: elevated lower esophageal baseline pressure

tudies can improve the diagnostic manometric assessment b

f achalasia and assessment of treatment efficacy.26,27 Aperi-talsis is readily evident on HRM and the technique facil-tates assessment of sphincter relaxation, one of the mostifficult aspects of conventional manometry (Fig. 3).RM is made possible by a solid-state catheter with 36

ircumferential sensors spaced at 1-cm intervals. Pressureeasurements obtained from the sensors are plotted in

eference to both space and time. The closely spaced pres-ure transducers and interpolation of the data eliminate theovement artifacts, which confound standard manometric

echniques. Data have shown that, in the absence of previ-us hiatal surgery, failure of the LES high-pressure zone toelax below 15 mmHg is highly specific and sensitive forchalasia.27 The ability of MII to quantitate bolus transportan prove to be useful in the postoperative assessment ofatients with achalasia after laparoscopic myotomy, al-hough few studies to date have investigated its benefit.

REATMENTchalasia is an incurable disease and treatment is focusedn relief of symptoms. The goal of both surgical and non-urgical treatment is to eliminate the outflow obstructionfforded by a nonrelaxing sphincter, relieve dysphagia, andaintain a barrier against gastroesophageal reflux when

ossible. Nonsurgical treatment includes calcium channel

igure 2. Lower esophageal sphincter residual pressure measure-ents of patient controls (n � 43) and achalasics (n � 58). Onlyne achalasia patient had a residual pressure of �10 mmHg.eprinted from: Hirano I, Tatum RP, Shi G, et al. Manometric het-rogeneity in patients with idiopathic achalasia. Gastroenterology001;120:789�798, with permission.

lockers and nitrates, injection of botulinum toxin (Botox;

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llergan) into the LES, and large-caliber (30 to 40 mm)neumatic dilation of the LES. Surgical treatment includesivision of the muscle fibers of the LES and proximal stom-ch. Although pharmacologic treatments such as calciumhannel blockers, nitrates, and sildenafil have been showno have physiologic effects on esophageal function, theyarely result in meaningful clinical improvement. With thedvent of minimally invasive surgery, laparoscopic myot-my has slowly shifted treatment of achalasia toward thereater use of surgical therapy.

harmacologic treatmentharmacologic treatments of achalasia, such as oral nitratesnd calcium channel blockers, act to inhibit intramuraleurons. These drugs attempt to recreate a balance betweentimulatory and inhibitory nerve fibers to decrease the rest-ng and residual pressure of the LES.Their effect is sporadicnd has shown only short-term success.28-30 In light of theiroor outcomes and potentially harmful systemic effects,hese agents are largely unreliable and unrealistic modali-

igure 3. High-resolution manometric study in (A) a normal sub-ect and (B) a patient with achalasia. The lack of propulsive waverogression and the failure of the lower pressure band represent-

ng the lower esophageal sphincter can be clearly seen in (B)ompared with (A).

ies for longterm symptom relief. p

lexible endoscopic treatmentndoscopic injection of Botox into the LES aims to block

elease of acetylcholine from cholinergic neurons in an ef-ort to lower both basal and residual LES pressures.31 Thisreatment is short-lived, rarely results in substantial re-uction in LES pressure, and, although dysphagia can be

mproved, often requires repeat injections for continuedelief. In a prospective randomized controlled trial com-aring Botox injection (n � 40) with laparoscopic my-tomy and partial fundoplication (n � 40), Zaninottond colleagues32 found that although patients in bothroups showed initial improvement in symptoms, 6onths after treatment dysphagia and regurgitation re-

urred in nearly half (45%) of those treated with Botox.n addition, they determined that the probability of be-ng symptom-free at 2 years was considerably higherfter myotomy (87.5%) than after Botox injection34%). It is now recognized that Botox injection creates annflammatory reaction in the distal esophagus with conse-uent submucosal fibrosis, which can make subsequenturgical myotomy more difficult.33 Although commonlyried as a short-term treatment option, the authors believeotox should be reserved for those who are not surgicalandidates or abandoned altogether.

Pneumatic balloon dilation decreases esophageal out-low resistance by forceful “tearing” of the LES muscle fi-ers. Protocols vary among clinicians when performingneumatic dilation. In general, graded balloon dilation isegun using a 30-mm balloon as the initial dilator.34 Thealloon dilator is passed into the esophagus and placed athe gastroesophageal junction by using fluoroscopy or di-ect endoscopic vision. A Gastrografin esophagram fol-owed by a barium swallow is performed after pneumaticilation to exclude esophageal perforation. Repeat balloonilation can be performed using progressively larger dilatorizes to 35 mm and 40 mm. The most common balloonilators in current use are the Rigiflex and Witzel polyeth-lene balloons. Rigiflex is a balloon on a catheter, which islaced using fluoroscopy, and the Witzel balloon is insertedhile attached to the endoscope. Risk of perforation using

he Rigiflex is about 3% and that of the Witzel is 6%.35

Comparing pneumatic balloon dilation with Botox in-ection in a randomized trial, Cleveland Clinic investiga-ors found that 70% (14 of 20) of patients who underwentilation were in symptomatic remission at 1 year as com-ared with 32% (7 of 22) of patients who underwent Botoxreatment.36 In addition, they found that balloon dilationesulted in substantial improvements in LES pressure,sophageal barium column height, and esophageal diame-er, and Botox injection failed to show any change in these
arameters. Similarly, when comparing pneumatic balloon

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ilation with Botox injection in a double-blinded random-zed study, Bansal and colleagues37 found that 89% (16 of8) of patients who underwent balloon dilation had a de-rease in their symptom grade as compared with only 38%6 of 16) of patients who underwent Botox injection. Mostecently, a meta-analysis evaluating pneumatic balloon di-ation and Botox injection for treatment of achalasia re-orted that, although short-term failure rates were similaretween the two techniques, longterm (�6 months) resultshowed considerably less failures after dilation as comparedith Botox.38

In an analysis evaluating the longterm efficacy of pneu-atic dilation for achalasia, Katz and colleagues39 retro-

pectively evaluated 72 patients at a mean of 6.5 years afterilation. Defined as no additional therapy needed for acha-

asia, success was seen in 85% of patients. Four patientsequired additional pneumatic dilation.

More recently, Zerbib and colleagues40 retrospectivelyvaluated longterm remission rates of pneumatic dilationor 150 patients with achalasia, using a fastidious dilationrotocol that included several dilation sessions until devel-pment of remission and close followup with fairly liberalon-demand” repeat dilation sessions, if needed. Theyound initial symptom remission to be 91.3% after a me-ian of 2.6 dilations. Recurrent symptoms developed in5% of patients. At 5 and 10 years, the calculated proba-ility of being in remission was 67% and 50%, respectively.f those patients with recurrent symptoms who required

epeat dilation treatment, 96.4% were in remission at aean of 3.5 years. The probability of being in remission

fter repeat dilation was 96.8% and 93.4% at 5 and 10ears, respectively.40

Although pneumatic dilation has been found to have aore lasting effect on dysphagia than Botox injection, out-

ide of a rigorous dilation protocol, most studies have notemonstrated the longterm outcomes seen after surgicalyotomy. Until recently, the only prospective randomized

rial comparing pneumatic dilation to surgical myotomyas reported by Csendes and colleagues41 from Chile. They

ound that 100% of patients treated with myotomy (n �9) had only mild or no dysphagia at a mean of 3.5 years, asompared with only 61% of those treated with balloonilation (n � 18).41 Very late followup of this trial has alsoeen published.42

Two more recent evaluations are also worth noting. Westnd colleagues43 retrospectively evaluated longterm out-omes of 125 achalasia patients followed prospectively for5 years after pneumatic dilation. In this experience, only

0% of patients had no or occasional (less than once pereek) dysphagia at 5 years, and only 40% at 15 years.
ostec and colleagues44 recently reported a multicenter p
wedish prospective randomized study of 51 patients com-aring pneumatic dilation (n � 26) with laparoscopic my-tomy (n � 25). A predefined dilation protocol was used,eginning with a 30-mm (women) or 35-mm (men) Rigi-lex balloon and progressing as needed to 40 mm in thoseith persistent dysphagia at 7- to 10-day intervals. The lackf such a protocol was one of the major criticisms of thetudy performed by Csendes and colleagues.41 Laparo-copic myotomy was performed by experienced surgeonssing intraoperative endoscopy and Toupet posterioremifundoplication. Outcomes were assessed at 1 year af-er treatment. Failure was defined as incomplete symptomontrol or symptom relapse requiring more than threereatments during the 12-month period, serious complica-ions or side effects, or patient request for alternative treat-ent. Esophageal perforation occurred in two patients in

he dilation group (7.6%). All surgical procedures wereompleted laparoscopically with no substantial periopera-ive morbidity. Treatment failure was significantly moreommon in the dilation group (1 of 25 [4%] versus 6 of 2623%]; p � 0.04). Mean symptom score after operationas 11.3 and after dilation was 17.7 (p � 0.05). The au-

hors concluded that laparoscopic myotomy and partialundoplication was superior to pneumatic dilation inewly diagnosed patients with achalasia.

urgical treatmentsophageal myotomy for achalasia was first described byrnest Heller in 1913.45 In this operation, both the anteriornd posterior lower esophageal sphincter muscle fibersere disrupted. A modified version of this procedure, re-

erred to today as the Heller myotomy, consists of a singlenterior longitudinal myotomy and has become the stan-ard operative technique. Once performed through eitherthoracotomy or laparotomy, esophageal myotomy is nowerformed almost invariably through a laparoscopicpproach.

Outcomes of thoracoscopic myotomy have been showno be inferior to the laparoscopic approach. In a retrospec-ive evaluation of patients undergoing either thoracoscopiceller myotomy (n � 30) or laparoscopic Heller myotomy

n � 30), Patti and colleagues46 found laparoscopic myot-my to be superior with regard to complete dysphagia relief70% versus 77%) and development of postoperative re-lux (60% versus 10%). Similarly, Stewart and colleagues,47

omparing the outcomes of 24 achalasia patients who hadndergone myotomy through a thoracoscopic approachith 63 patients who had a laparoscopic approach, found

hat the laparoscopic approach was not only associatedith decreased operative time, conversion rate, and lengthf stay, but was also better able to relieve dysphagia and
revent heartburn than the thoracoscopic approach. A re-

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ent review of studies evaluating thoracoscopic myotomyrom 1993 to 2003 (n � 10 studies; 204 patients) andaparoscopic myotomy from 1995 to 2002 (n � 15 studies;99 patients) by Abir and colleagues48 found symptomelief to occur in 76% versus 94% of patients, respectively.evelopment of gastroesophageal reflux disease occurred

n 35% of patients after thoracoscopic myotomy and 13%f patients after laparoscopic myotomy.48 The inferiorymptomatic outcomes seen after a thoracoscopic myot-my reflect the difficulty in extending the myotomy ade-uately onto the stomach from the chest and the inabilityo create a fundoplication to counteract development ofeflux disease.46-48

echnique: laparoscopic esophageal myotomy andartial fundoplicationhe patient is placed on the table in the modified lithot-my position with the lower extremities abducted; posi-ioning identical to that of a laparoscopic fundoplication.neumoperitoneum is established and four additionalorts are placed under video laparoscopic control. The dis-ection begins by freeing the upper third of the gastricundus in preparation for later Dor anterior hemifundop-ication. The short gastric vessels are sequentially dissectednd divided with the aid of ultrasonic shears. In contrast toNissen fundoplication for gastroesophageal reflux disease,

he posterior attachments and pancreaticogastric brancheshould not be divided, in an effort to preserve as much ofhe normal posterior gastroesophageal anatomy as possible.f a Toupet posterior hemifundoplication is planned, a pos-erior dissection is necessary. This would be the preferredpproach in the small (4% to 5%) subset of patients whoresent with a concomitant hiatal hernia.The gastroesophageal junction is then exposed by dis-

ecting the gastroesophageal fat pad and retracting it later-lly. The gastroesophageal junction is cleared for 6 to 8 cmn preparation for the myotomy. A vessel loop can be placedround the gastroesophageal junction, including the ante-ior vagus nerve, and brought out through the subxiphoidrocar if necessary. Once the esophagus is mobilized andastroesophageal junction exposed, the myotomy is per-ormed with a combination of scissors and hook-type elec-rocautery (Fig. 4). The extent of the myotomy should beimited proximally by the anterior crural confluence and tohat which can be covered by a fundoplication. It should thene carried down across the gastroesophageal junction, to en-ure that the clasp fibers are divided, and onto the anterior wallf the fundus of the stomach for 2 to 3 cm. The edges of theyotomy are carefully separated from the underlying mucosa

or 40% to 50% of the esophageal circumference. The proce-ure is completed by fashioning an anterior (Dor) or posterior
Toupet) partial fundoplication. r
An anterior partial fundoplication of the Dor type is theost commonly performed antireflux barrier created afteryotomy for achalasia. After fundic mobilization the an-

erior fundus is laid across the myotomy site and the leftundic edge is sewn to the left cut edge of the esophagealyotomy with three or four interrupted sutures of 2-0 silk.he highest stitch is taken through the left crural pillar as

n anchor to prevent torsion of the fundus. The fundus ishen sewn to the right edge of the cut esophageal muscleimilarly; again using three or four interrupted sutures of-0 silk and taking the highest stitch through the rightrural pillar to prevent torsion.49

To create a posterior partial fundoplication (Toupet), thenterior fundus is brought to either side of the myotomy,nd two columns of sutures are placed on either side, leav-ng the myotomy site bare and open.49

ATA SUPPORTING TECHNICAL COMPONENTSxtent of myotomyecent data show that both the proximal and distal extentf esophageal myotomy are important. Chen and col-eagues49 have reported that epiphrenic pseudodiverticu-um developed in as many as 67% of patients followed 7 to6 years post myotomy and fundoplication. This is likelyaused by an absence of coverage by the fundoplicationver the proximal extent of the myotomy. This increasedecognition of the potential for diverticulum formation hased many to limit the proximal extent of the myotomy tohat which can be covered by a fundoplication.

Relief of dysphagia might be better when lengtheninghe distal extent of myotomy. Oelschlager and colleagues51

igure 4. Mobilized esophagus and creation of an esophageal my-tomy by separation of the muscle edges down to esophagealucosa and then proximally onto the esophagus and distally onto

he stomach.

eported better symptomatic improvement and a lower in-

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idence of recurrent dysphagia by increasing the distal ex-ent of myotomy onto the proximal stomach from 1.5 cmo 3 cm. They compared outcomes of 52 patients treatedith a standard myotomy of 1.5 cm onto the proximal

tomach with outcomes of 58 patients treated with an ex-ended myotomy of 3 cm. Postoperative LES pressuresere substantially lower (9.5 mmHg with extended versus5.8 mmHg with standard myotomy) and postoperativeysphagia improved after longer myotomy. Importantly,ostoperative 24-hour pH data showed that extension ofhe distal aspect of the myotomy did not result in a higherrevalence of gastroesophageal reflux.

ddition of fundoplicationlthough myotomy effectively lowers esophageal outflow

esistance and improves esophageal emptying, it also in-reases the propensity for development of gastroesophagealeflux. The importance of the addition of a fundoplicationo the myotomy has, until recently, been debated.

A recent prospective randomized study has put this issueo rest. Richards and colleagues52 reported on 43 achalasiaatients randomized to laparoscopic Heller myotomy withnd without Dor fundoplication. Gastroesophageal reflux,efined by 24-hour distal esophageal acid exposure time4.2%, was present in 47.5% of patients undergoingeller myotomy alone compared with 9.1% of patients

ndergoing Heller myotomy with partial fundoplication.Importantly, there was no substantial difference in post-

perative LES pressures or dysphagia scores between thewo groups. Similarly, a retrospective evaluation of 146atients who underwent laparoscopic Heller myotomyith (n � 88) or without (n � 61) Dor fundoplication byice and colleagues,53 found that pH proved gastroesoph-geal reflux occurred considerably less often after addition

able 2. Outcomes after Laparoscopic Heller Myotomy

irst author Year nFollowup, mo

(range) d

ortale55 2005 248 43 (1�131)onatti56 2005 75 64 (10�131)hajanchee57 2005 121 9 (6�48)rain54 2004 78 24 (6�100)errone58 2004 100 26 (6�72)elschlager50 2003 110 26 (1�85)onahue59 2002 81 45 (1�70)

harp60 2002 100 11 (NA)aninotto61 2002 113 24 (1�83)atti62 1999 133 23 (NA)

Based on postoperative 24-hour pH monitoring.A, not available.

f a partial fundoplication.53 The addition of Dor fundo- t

lication to Heller myotomy did not decrease esophagealmptying when assessed by barium esophagography.

In the presence of an aperistaltic, often dilated and tor-uous esophagus, most agree that a complete fundoplica-ion should be avoided.54 On the other hand, the preciseegree (ie, 180 degrees, 270 degrees) and location (anterior,osterior) of a partial fundoplication is unclear. Currentata suggests a minimal difference between a posterior70-degree (Toupet) fundoplication and an anterior 90- to80-degree (Dor) fundoplication. For example, Arain andolleagues54 found no difference in relief of symptoms, in-luding dysphagia, heartburn, or chest pain, or the need forroton-pump inhibitors when comparing myotomy withor to myotomy with Toupet. Because of the preservation

f natural posterior attachments and its easier technicalonstruction, most centers have migrated toward routinese of a Dor fundoplication.

URGICAL OUTCOMESutcomes of laparoscopic Heller myotomy have now been

tudied for well more than a decade. These data show thaturgical myotomy is more effective than nonsurgical treat-ents at providing longterm relief of dysphagia, regurgita-

ion, and chest pain, while promoting weight gain andatient satisfaction. Many surgeons and gastroenterologistslike believe that surgical myotomy should be recom-ended as primary therapy for virtually all patients with

chalasia.51,55-63

Medium-term outcomes of laparoscopic myotomyave been reported from centers around the worldTable 2).51,55-63 Assessed 2 to 5 years after operation,

90% of patients have either complete relief of, or onlyild persistent, dysphagia. Investigators from Padua,

taly, have provided some of the longest-term data. Por-

lief ofagia (%)

Length of stay,d (range)

Perforations(%)

Reflux(%)

88 5 (3�11) 4 7*84 2 (1�6) 4 1191 1.7 (NA) 6.6 13*77 NA 0 1796 1.2 (1�4) 3 NA90 NA NA 2384 1 (NA) 14 493 1.5 (NA) 8 491 NA NA 689 2 5 17

Reysph

ale and colleagues,56 reported 113 patients who under-

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ent laparoscopic Heller myotomy from 1992 to 1999.ore than 90% (91.2%) were symptom-free at a median

f 2 years followup, with a Kaplan-Meier analysis showing90% probability of remaining asymptomatic at 5 years.ost published results report similar improvement. De-

ree of improvement might not be the same with all symp-oms. Arain and colleagues54 found that the most markedmprovement occurred for the symptom of regurgitation74% complete relief ). Moderate relief was seen for dys-hagia (33% complete relief ) and the least relief was ob-erved for chest pain (18% complete relief ). Difficulty inelieving chest pain has also been reported after pneumaticilation.64

Complications average 10% to 15%, and commonlynclude pneumothorax, wound infection, and esophagealeak.47,55-63 Mortality is uncommon, zero in most large pub-ished series. Inadvertent violation of the esophageal mu-osa occurs in 0 to 14% of procedures and, when recog-ized and repaired, is rarely of clinical consequence.nrecognized mucosal perforation will present as acute

bdominal or chest pain in the early postoperative periodnd has been treated both operatively and nonoperatively.onversion from a laparoscopic operation to open laparot-my is infrequent in experienced laparoscopic centers ands caused by esophageal perforation, uncontrolled hemor-hage, or adhesions.

Postoperative assessment through contrast esophagogra-hy, manometry, and pH monitoring has shown thatsophageal outflow obstruction improves and esophagealiameter decreases, as does resting and residual LES pres-ure. Zaninotto and colleagues,62 reported pH data on 84f 113 patients who underwent postoperative 24-hour pHonitoring. Only 5 of 84 (6%) had tracings consistentith gastroesophageal reflux, three of these reported mildeartburn and one had erosive esophagitis at endoscopy.ongterm followup data from the era of open myotomyuggest that gastroesophageal reflux is a common cause ofecurrent symptoms, with a substantial minority develop-ng progressive regurgitation, heartburn/chest pain, erosivesophagitis, and Barrett’s esophagus. Whether this will alsoe true of the laparoscopic era remains to be determined.Providing the longest followup of surgical myotomy ever

eported, Csendes and colleagues42 published the clinical,ndoscopic, histologic, manometric, and acid reflux studiesf 67 patients enrolled in a prospective randomized studyarried out in the 1970s. Patients were divided into threeroups based on the length of followup; 6 to 10 years, 10 to0 years, and 20 to 30 years. Most patients (73%) had

ong-lasting symptomatic response, although substantialecurrent symptoms were found in 7% of patients �10
ears, 23% of those 10 to 20 years, and 35% of patients g
30 years postmyotomy. Similarly, there was a slowly pro-ressive increase in patients found to have pathologicsophageal acid exposure 15%, 28%, and 53% respectivelyFig. 5). Barrett’s esophagus developed in nine patients andsophageal squamous cell carcinoma developed in three.

utcomes predictorseveral factors have been proposed as predictors of out-omes after treatment for achalasia. Degree of improve-ent in the resting LES pressure has been reported by

everal authors to substantially affect longterm success ofneumatic dilation. Patients in whom the LES pressure waseduced to �10 mmHg had long-lasting (5 years or more)elief of dysphagia, and recurrent dysphagia developedithin the first 12 to 24 months in those with persistentES pressures �20 mmHg (Fig. 6).65 This principle is

ikely as true for surgical myotomy as it is for pneumaticilation, although lowering resting LES pressure to near 10mHg is much more reproducible with myotomy. Young

atients (younger than 40 years) have also been shown toespond less well to pneumatic dilation and are good can-idates for primary myotomy. In a longterm prospectivetudy comparing outcomes of patients who required my-tomy after failed pneumatic dilation with patients whoesponded well to dilation therapy, Gockel and colleagues66

ound that the younger the patient age at diagnosis the

igure 5. Proportion of patients with normal and abnormal esoph-geal acid exposure after myotomy and partial fundoplication forchalasia. Group 1: �10 years, group 2: 10 to 20 years, group 3:30 years followup. Gray bar, normal acid reflux test; black bar,bnormal acid reflux test. Reprinted from: Csendes A, Braghetto I,urdiles P, et al. Very late results of esophagomyotomy for patientsith achalasia; clinical endoscopic, histologic, manometric and acid

eflux studies in 67 patients for a mean follow-up of 190 months.nn Surg 2006;243:196�203, with permission.

reater the probability of needing surgical myotomy for

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ymptomatic relief. Using odds ratios to determine risk forventual myotomy, the authors found that a patient diag-osed with achalasia at age 15 has a 70% probability ofeeding myotomy, a patient diagnosed at age 40 has a 35%robability and a patient at diagnosed at age 70 has an 8%robability (Fig. 7).Several factors have also been suggested to affect out-

omes of laparoscopic myotomy. These include the mag-itude of preoperative LES resting pressure, the degree

igure 8. Correlation between the change in lower esophagealphincter pressure and change in dysphagia score after Helleryotomy. LES, lower esophageal sphincter. Reprinted from: Tor-uati A, Richards WO, Holzman MD, Sharp KW. Laparoscopic myot-my for achalasia: predictors of successful outcome after 200

igure 6. Kaplan-Meier curve demonstrating time to symptom re-urrence after lower esophageal sphincter pneumatic dilation toressures of �10 mmHg, 10 to �20 mmHg, and �20 mmHg.eprinted from: Eckardt VF, Gockel I, Bernhard G. Pneumatic dila-ion for achalasia: late results of a prospective follow up investiga-ion. Gut 2004;53:629�633, with permission .

iases. Ann Surg 2006;243:587�593, with permission.

f preoperative esophageal dilation or tortuosity, oroth, and the presence or absence of earlier nonopera-ive interventions.

Evaluating outcomes of 78 consecutive achalasia pa-ients treated with laparoscopic myotomy, Arain and col-eagues54 found that a high preoperative resting LES pres-ure was an independent predictor of relief of dysphagia.his was confirmed in a recent series of 200 consecutively

reated achalasia patients by investigators at Vanderbiltniversity.67 They found that patients with a preoperativeES resting pressure of �35 mmHg were 21.3 times more

ikely to have relief of their dysphagia than those with pre-perative LES pressures �35 mmHg. These authors alsoeported that the greater the decrease in LES pressure afterperation, the greater the improvement in postoperativeysphagia (Fig. 8).The benefit of surgical myotomy in patients with a di-

ated and tortuous esophagus is unclear. In this setting, inhich the esophagus is not only massively dilated but

igmoid-shaped, bolus flow is impaired by the shape of thesophagus in addition to LES spasm. Even in these circum-tances, patients can perceive benefits. Patti and col-eagues,68 evaluating 66 patients with varying degrees ofilation, found that all 7 patients with esophageal diame-ers of �6 cm and tortuosity had satisfactory outcomes. Inontrast, a case-controlled study by Pechlivanides and col-eagues69 found that esophageal diameter decreased in allatients with esophageal dilation, but only patients with aostoperative diameter of �4 cm experienced excellent re-ults.69 Given this data and the low morbidity and mortal-

igure 7. Relative probability of the need for operation based on theatients age at first diagnosis. Reprinted from: Gockel I, Junginger T,ernhard G, Eckardt VF. Heller myotomy for failed pneumatic dilation

n achalasia: how effective is it? Ann Surg 2004;239:371�377,ith permission.

ty associated with laparoscopic Heller myotomy as com-

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ared with esophagectomy, myotomy is often chosen as theirst line of treatment regardless of the extent of dilation.

Endoscopic interventions performed in achalasia pa-ients before surgical intervention likely influence the suc-ess of surgical myotomy. Smith and colleagues,33 recentlyeported that previously given treatment can effect symp-omatic outcomes. Patients with (n � 154) or withoutn � 55) a history of earlier balloon dilation or Botoxnjection were compared. Defined as persistent or recurrentymptoms or the need for additional treatment, the failureate of those with earlier interventions was found to belmost twice that of those who had no earlier intervention19.5% versus 10.1%). In addition, patients with previousndoscopic therapies were found to have more difficultissection planes, increased mediastinal scarring, which re-ulted in a higher incidence of intraoperative mucosal per-orations, and longer postoperative recovery than thoseithout earlier treatment. These findings support use of

urgical myotomy as the initial treatment method for acha-asia and put forth that endoscopic interventions should beeserved for the rare patient who is not a surgical candidate.

ersistent or recurrent symptomsongterm outcomes data suggest that a properly performed

aparoscopic myotomy and partial fundoplication will behe only therapeutic intervention required in up to 80% ofatients with achalasia.70 Mild to moderate symptoms ofysphagia, regurgitation, heartburn, and chest pain recurith time in as many as 40% to 50% of patients, but few of

hese require additional intervention beyond lifestyle andehavioral changes or proton-pump inhibitor therapy.echanisms of failure include inadequate myotomy, scar-

ing or anatomic distortion of the gastroesophageal junc-ion, complications of gastroesophageal reflux disease, androgressive esophageal dilation or distortion, usually sec-ndary to persistent outflow resistance. Early failures aresually caused by failure to extend the myotomy far enoughnto the stomach or anatomic distortion, or both. Lateailures occur secondary to development of complicatedastroesophageal reflux with stricturing or Barrett’shanges and disease progression. Development of a distalsophageal diverticulum, thought secondary to proximalxtension of the myotomy into the lower posterior medi-stinum, is also an increasingly recognized occurrence. Theredisposing factors and symptomatic importance of thisre as yet unclear.

Recurrent dysphagia after surgical myotomy should benvestigated by upper endoscopy to exclude an obstructingesion, by contrast, esophagography to assess for esophagealilation or tortuosity, and by repeat manometry to assessor high persistent LES resting pressure (�10 to 15
mHg). Management options include pneumatic dilation
r remyotomy for suspected incomplete or scarred myot-my, and esophagectomy for those with end-stage dilationnd tortuosity, stricture, or cancer. Pneumatic dilation,nce believed to be contraindicated after myotomy, can ben attractive option for early persistent dysphagia. In aetrospective analysis of 113 patients treated with myot-my for achalasia, Zaninotto and colleagues62 found that8% of 10 patients with recurrent dysphagia could be ef-ectively treated with pneumatic dilation. They concludedhat pneumatic dilation should be considered as the first-ine treatment for patients with persistent dysphagia andhat reoperation should be reserved for those who do notespond.

Both medical and surgical therapies exist as treatmentptions for patients with achalasia. Administration of phar-acologic agents have had very little clinical effect. Botox

njection has shown symptomatic relief in some, but isften transient, requires multiple treatment sessions, andan make later surgical treatment more difficult. Althoughneumatic dilation has been found to have a more lastingffect on dysphagia than Botox injection, it has not dem-nstrated the longer-lasting outcomes seen with surgicalyotomy. Laparoscopic Heller myotomy has become the

nitial primary treatment and standard surgical approachor patients with achalasia.

Several studies have shown surgical myotomy to provideuperior longterm symptom relief as compared with non-urgical interventions. An extended distal myotomy, alongith a partial fundoplication, has been found to providereater dysphagia relief with minimal development of gas-roesophageal reflux. A high preoperative LES pressureortends better symptomatic outcomes after operation, asoes the absence of earlier nonoperative interventions. Per-istent or recurrent symptoms after surgical myotomy thato not respond to lifestyle changes can be treated effectivelyith pneumatic dilation.

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