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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_832_Библиотеки_им_академика_М_И_Перельмана
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Fig. 11 Completed
posterior fundoplication
A. L. Shada
10 Post-operative Care andComplications
Due to extensive mediastinal dissection, subcutaneous emphysema is commonly
observed. This is rarely of clinical signicance as long as the anesthesiologist has
been attentive to the patient’s PCO2 during the procedure. Another relatively common intra-operative complication is a pleural entry. This is usually managed by
communication with the anesthesiologist and altering the ventilation mode without
the need for any intervention. If the pleural spaces are entered it can be helpful to
extend this pleurotomy widely to avoid tension capnothorax. Routine drain placement is not typical but can be used to evacuate uid and gas within the mediastinum
in the immediate postoperative period. Other peri-operative complications include
atrial brillation, bleeding, deep venous thrombosis, and pneumonia, among others.
Most patients can begin with a liquid meal within the rst 24h of the operation.
Patients rapidly advance to a pureed or soft diet and remain on this diet for about
2weeks. Most patients can be discharged on post-operative day number 1 or 2. A
proportion of patients have delayed gastric emptying after this procedure. This is
more likely in the case of intrathoracic stomach. It is often self limited but if prolonged may require postpyloric feeding for a period of time.
Antiemetics should be used to avoid postoperative nausea and vomiting.
Immediate reherniation of the stomach in the postoperative period is a feared complication and should be suspected if there is dysphagia postoperatively. Routine
postoperative imaging is not typical but can be performed if there is suspicion for
reherniation, or esophageal or stomach injury.
Patients can be taken off of proton pump inhibitors after surgery, though if
esophagitis is present on intraoperative endoscopy this is typically continued for
2weeks postoperatively. Patients with Barrett’s esophagus are advised to consider
continuing proton pump inhibitors.
Radiologic, objective recurrence rates (re-herniation >than 2 cm) have been
reported to occur in approximately 40–60% of patients after laparoscopic repair of
paraesophageal hernia [20, 35], however, most patients with noted recurrences
report no return of symptoms. Despite radiographic evidence of recurrence after a
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large hiatal hernia repair, most patients report enduring and dramatic symptomatic
improvement [27, 31].
Studies report long-term relief of symptoms in 75–87% of patients and a 61–91%
satisfaction rate with the result of the procedure [16, 31, 35].
11 Summary
Paraesophageal hernia has an underlying pathophysiology that is fundamentally different from GERD.Appropriate hiatal repair requires an understanding of the complexity of the anatomy of the herniated stomach. Repair of a symptomatic
paraesophageal hernia can have a profoundly positive impact on patient quality of
life. Elective paraesophageal hernia repair is frequently well tolerated and has a
fairly low morbidity rate, while emergent repair of an incarcerated and/or strangulated hernia has a proportionally higher morbidity and mortality rate [36]. Thus,
elective repair is recommended for patients with symptomatic para-esophageal hiatal hernia and laparoscopic repair is the standard of care. We describe the operative
approach to achieve the critical goals of paraesophageal hernia repair:
1. reduction of the hernia contents
2. excision of the hernia sac,
3. complete esophageal mobilization,
4. crural repair, and
5. antireux operation
References
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2. Haas O, etal. Surgical results of intrathoracic gastric volvulus complicating hiatal hernia. Br
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4. Sihvo EI, etal. Fatal complications of adult paraesophageal hernia: a population-based study.
J Thorac Cardiovasc Surg. 2009;137(2):419–24.
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7. Carrott PW, etal. Iron-deciency anemia is a common presenting issue with giant paraesophageal hernia and resolves following repair. J Gastrointest Surg. 2013;17(5):858–62.
8. Kohn GP, et al. Guidelines for the management of hiatal hernia. Surg Endosc.
2013;27(12):4409–28.
9. Ballian N, etal. A clinical prediction rule for perioperative mortality and major morbidity after
laparoscopic giant paraesophageal hernia repair. J Thorac Cardiovasc Surg. 2013;145(3):721–9.
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10. Wirsching A, etal. Acute vs. elective paraesophageal hernia repair: endoscopic gastric decompression allows semi-elective surgery in a majority of acute patients. J Gastrointest Surg.
2018;22(2):194–202.
11. DeMeester SR.Laparoscopic paraesophageal hernia repair: critical steps and adjunct techniques to minimize recurrence. Surg Laparosc Endosc Percutan Tech. 2013;23(5):429–35.
12. Luketich JD, etal. Outcomes after a decade of laparoscopic giant paraesophageal hernia repair.
J Thorac Cardiovasc Surg. 2010;139(2):395–404, 404.e1.
13. Zehetner J, etal. Laparoscopic versus open repair of paraesophageal hernia: the second decade.
J Am Coll Surg. 2011;212(5):813–20.
14. Cuschieri A, Shimi S, Nathanson LK.Laparoscopic reduction, crural repair, and fundoplication of large hiatal hernia. Am J Surg. 1992;163(4):425–30.
15. Greene CL, etal. Diaphragmatic relaxing incisions during laparoscopic paraesophageal hernia
repair. Surg Endosc. 2013;27(12):4532–8.
16. Oelschlager BK, etal. Biologic prosthesis reduces recurrence after laparoscopic paraesophageal hernia repair: a multicenter, prospective, randomized trial. Ann Surg. 2006;244(4):481–90.
17. Ferri LE, etal. Should laparoscopic paraesophageal hernia repair be abandoned in favor of the
open approach? Surg Endosc. 2005;19(1):4–8.
18. Furnée EJ, etal. Long-term symptomatic outcome and radiologic assessment of laparoscopic
hiatal hernia repair. Am J Surg. 2010;199(5):695–701.
19. Rathore MA, etal. Metaanalysis of recurrence after laparoscopic repair of paraesophageal
hernia. JSLS. 2007;11(4):456–60.
20. Hashemi M, etal. Laparoscopic repair of large type III hiatal hernia: objective followup reveals
high recurrence rate. J Am Coll Surg. 2000;190(5):553–60, discussion 560–1.
21. Berríos-Torres SI, etal. Centers for Disease Control and Prevention guideline for the prevention of surgical site infection, 2017. JAMA Surg. 2017;152(8):784–91.
22. Kim DG, et al. Liver retraction by double-sling suture for laparoscopic gastrectomy. J
Laparoendosc Adv Surg Tech A. 2015;25(2):112–6.
23. Del Castillo Déjardin D, etal. Gastric volvulus after sleeve gastrectomy for morbid obesity.
Surgery. 2013;153(3):431–3.
24. Horvath KD, Swanstrom LL, Jobe BA. The short esophagus: pathophysiology, incidence, presentation, and treatment in the era of laparoscopic antireux surgery. Ann Surg.
2000;232(5):630–40.
25. Mitiek MO, Andrade RS.Giant hiatal hernia. Ann Thorac Surg. 2010;89(6):S2168–73.
26. Granderath FA, et al. Prosthetic closure of the esophageal hiatus in large hiatal hernia repair
and laparoscopic antireux surgery. Surg Endosc. 2006;20(3):367–79.
27. Oelschlager BK, etal. Biologic prosthesis to prevent recurrence after laparoscopic paraesophageal hernia repair: long-term follow-up from a multicenter, prospective, randomized trial. J
Am Coll Surg. 2011;213(4):461–8.
28. Abdelmoaty WF, etal. Combination of surgical technique and bioresorbable mesh reinforcement of the crural repair leads to low early hernia recurrence rates with laparoscopic paraesophageal hernia repair. J Gastrointest Surg. 2020;24(7):1477–81.
29. Aiol A, etal. Medium-term safety and efcacy prole of paraesophageal hernia repair with
Phasix-ST(®) mesh: a single-institution experience. Hernia. 2022;26(1):279–86.
30. Armijo PR, etal. Surgical and clinical outcomes comparison of mesh usage in laparoscopic
hiatal hernia repair. Surg Endosc. 2021;35(6):2724–30.
31. Jones R, etal. Long-term outcomes of radiologic recurrence after paraesophageal hernia repair
with mesh. Surg Endosc. 2015;29(2):425–30.
32. Watson DI, etal. Laparoscopic repair of very large hiatus hernia with sutures versus absorbable
mesh versus nonabsorbable mesh: a randomized controlled trial. Ann Surg. 2015;261(2):282–9.
33. Watson DI, etal. Five year follow-up of a randomized controlled trial of laparoscopic repair of
very large hiatus hernia with sutures versus absorbable versus nonabsorbable mesh. Ann Surg.
2020;272(2):241–7.
A. L. Shada
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34. Stadlhuber RJ, etal. Mesh complications after prosthetic reinforcement of hiatal closure: a
28-case series. Surg Endosc. 2009;23(6):1219–26.
35. Dallemagne B, et al. Laparoscopic repair of paraesophageal hernia. Long-term follow up reveals good clinical outcome despite high radiological recurrence rate. Ann Surg.
2011;253(2):291–6.
36. Kaplan JA, etal. Morbidity and mortality associated with elective or emergency paraesophageal hernia repair. JAMA Surg. 2015;150(11):1094–6.
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Minimally Invasive Treatment ofAchalasia
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KristenA.Wong
1 Introduction
The incidence of achalasia is thought to be around 0.3–1.6 per 100,000 persons per
year [1]. It can present in any age group but peaks between 30 and 60years old and
does not have a predilection for gender or race [2]. Pathophysiology of the disease
involves degeneration of the inhibitory neurons of the myenteric plexus that innervate the lower esophageal sphincter causing increased resting tone and poor relaxation. This functional obstruction causes dilation of the esophagus, and eventually
leads to irreversible aperistalsis and worsening symptoms.
It is not clear what causes achalasia, but an association has been shown with
autoimmune, infectious, and hereditary causes [3]. Pseudoachalasia results from
tumors in the distal esophagus causing inltration or intrinsic compression, which
mimics true achalasia but warrants a different treatment pathway than described here.
2 Presentation
Patients will present with classic achalasia symptoms of dysphagia, chest pain,
regurgitation and unintentional weight loss. Dysphagia is often progressive, rst to
solids then to solids and liquids. Patients will often report waking up at night with a
choking sensation or will regurgitate undigested food especially after laying down.
Heartburn may be present in 27–42% of patients with achalasia; patients are frequently misdiagnosed as having gastroesophageal reux disease (GERD) and
K. A. Wong (*)
Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA
e-mail: kwong@uabmc.edu
Switzerland AG 2024
H. Chen, B. Lindeman (eds.), Illustrative Handbook of General Surgery,
https://doi.org/10.1007/978-3-031-63878-7_16
179© The Author(s), under exclusive license to Springer Nature
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Table 1 Eckardt symptom score for evaluation of achalasia symptom severity
0 1 2 3
Weight loss (kg) None <5 5–10 >10
Dysphagia None Occasional Daily Each Meal
Chest pain None Occasional Daily Each Meal
Regurgitation None Occasional Daily Each Meal
K. A. Wong
treated with proton pump inhibitors [4]. There are several scoring systems that exist
for achalasia symptoms, but the Eckardt Symptom Score is the one most frequently
used to determine severity of disease [5] (Table1). Scores range from 0–12; a score
of 2–3 corresponds to stage I, 4–6 to stage II, and >6 to stage III.
3 Evaluation andDiagnosis
Patients with suspected achalasia should undergo a series of tests beginning with an
esophagogastroduodenoscopy (EGD) to rule out underlying malignancy, strictures,
etc. EGD may reveal a dilated esophagus (41%) with retained food and liquid
(41%), stasis esophagitis (16%), and/or a hypertonic lower esophageal sphincter
(94%) [6]. A timed barium esophagram usually reveals a dilated esophagus with
retained contents, and a smooth tapering at the gastroesophageal junction, i.e. a
classic bird’s beak appearance (Fig.1). Additional X-rays are shot at 1 and 5min
time points after the patient swallows the low density barium suspension, and the
height and width of the column of contrast is measured. The majority of healthy
individuals will empty their esophagus in 1min and all will empty in 5min, whereas
achalasia patients will hold onto the column for 5min. High resolution manometry
(HRM) is the gold standard for diagnosing achalasia (Fig. 2). The Chicago
Classication version 4.0 [7] is the current classication algorithm for interpreting
HRM and identifying primary esophageal motility disorders including achalasia.
Furthermore, it allows determination of the subtype of the disease (Types I-III)
which can inform treatment. All types are characterized by 100% failed peristalsis.
Type I achalasia is “classic” achalasia, without pressurization in the esophageal
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Fig. 1 Classic “bird’s
beak” appearance of the
gastroesophageal junction
on timed barium
esophagram
181
body. Type II, the most common type has ≥20% of swallows with panesophageal
pressurization. Type III is marked by ≥20% premature contractions, with or without
panesophageal pressurization.
Included in the Chicago Classication 4.0 is a new testing modality called
Endoip™ (Functional Lumen Imaging Probe) Impedance Planimetry. A catheterbased balloon device, it evaluates the lower esophageal sphincter by assessing pressure, diameter and real time contraction patterns. The two main objective
measurements are distensibility index and diameter. Not only can EndoFLIP™ be
used in diagnosis, but it is also useful to gauge adequacy of a myotomy if used
intraoperatively.
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K. A. Wong
a
c
b
d
Fig. 2 High resolution manometry (a, c) with impedance measurement (b, d) in a patient with
normal esophageal peristalsis and LES relaxation (a, b) and in a patient with achalasia (c, d). (a)
Shows a normal peristalsis and LES. (b) Shows appropriate clearance of the swallowed bolus. (c)
Shows absent peristalsis at swallow with no LES relaxation. (d) Shows no clearance of the swallowed bolus
4 Treatment ofAchalasia
4.1 Medical Management
Oral pharmacological therapies target relaxation of the smooth muscle of the lower
esophageal sphincter. They include nitrates and calcium channel blockers. Use of
nitrates, such as isosorbide dinitrate, is limited by its poor efcacy and signicant
side effects (hypotension, headache, ushing). Calcium channel blockers are preferred over nitrates, but still only 55–75% effective with 30% of people experiencing adverse effects such as bradycardia and hypotension [8]. Both drugs also induce
tachyphylaxis, and relief can be short lived. For these reasons, treatment with medications is only reserved for those who are not able to undergo or refuse all other
interventions.
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4.2 Endoscopic Therapies
4.2.1 Pneumatic Dilation
Pneumatic Dilation (PD) is aimed at disruption of the circular muscle bers of the
lower esophageal sphincter. It is more effective when compared to medical management, and it is an accepted rst-line therapy for achalasia. Predictors of symptom
relief after dilation include female gender, older age, and type II achalasia [9].
Approximately 70–90% of patients respond with some symptom improvement to
PD initially [10]. However, over one third of these patients will go on to require
repeat or more invasive interventions [11]. PD is performed with a balloon dilator.
The achalasia balloon comes in three sizes (ranging from 30 to 40mm) and is used
with uoroscopic guidance. The most worrisome complications are perforation
(1–3%) [12] and bleeding.
4.2.2 Botulinum Toxin Injection
Botulinum Toxin injection of the lower esophageal sphincter is reserved for patients
who are not candidates for pneumatic dilation or endoscopic/surgical myotomies.
The most commonly used injectable is Botox (botulinum toxin type A, Allergan
Inc., Irvine, California, USA). The injection is done during esophagogastroduodenoscopy. A total of 100units of Botox is injected into four quadrants of the LES.This
results in decreased LES pressure, and the majority of people experience symptom
improvement. There is a reported 80–90% initial response rate [13] that can last up
to 4–6months.
4.2.3 Per Oral Endoscopic Myotomy
The rst endoscopic myotomy for achalasia was performed in 2008in Japan [14].
The procedure in its current form has been shown to be non-inferior to a laparoscopic Heller myotomy in regards to symptom relief [15]. In fact, it is the preferred
approach for type III achalasia because of the ability to perform a longer esophageal
myotomy [16]. Unlike the Heller myotomy, the POEM is not performed in conjunction with an anti-reux procedure. Therefore, there are signicantly higher rates of
pathologic reux with POEM (44% vs. 29%) [16]. However, the majority of patients
with post-POEM reux are successfully managed with proton pump inhibitors.
The procedure begins with a diagnostic esophagogastroduodenoscopy, taking
note of the Z-line location. A distal end cap attachment is placed onto the end of the
scope to assist with unobstructed viewing. A site is then chosen for the mucosotomy
which can be done on the anterior or posterior side of the esophagus, 12cm proximal to the gastroesophageal junction. A submucosal lift with a mixture of methylene blue or indigo carmine diluted with normal saline is performed using an
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K. A. Wong
endoscopic injection needle, followed by a longitudinal 2cm mucosotomy. The
tunnel is entered with the endoscope and extended to approximately 3cm beyond
the high pressure zone of the gastroesophageal junction (Fig.3). The endoscope is
withdrawn and the circular muscle myotomy is performed starting just beyond the
mucosotomy (Fig.4). This is carried distally through the LES and at least 2–3cm
onto the gastric side. The extent of myotomy can be conrmed with the double
endoscope technique using transillumination within the tunnel and a second retroexed pediatric endoscope in the stomach [17]. Once complete, the endoscope is
withdrawn from the tunnel and the mucosotomy is closed using through the scope
hemaclips. Alternatively, it can be endoluminally sutured.
Fig. 3 Per Oral
Endoscopic Myotomy
(POEM): creating the
submucosal tunnel
Fig. 4 Per Oral
Endoscopic Myotomy
(POEM): Performing the
myotomy of the circular
muscle bers, leaving the
longitudinal muscle layer
intact
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