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54
ab
I. Braghetto and O. Korn
However, once again, the question arises of how the measurement was made and
how meticulous the intra-mediastinal dissection to adequately mobilize the esophagus was. [10].
When these three methods of evaluation are jointly used for the diagnosis of the
supposed short esophagus, the specicity is 100% but the sensitivity is only 28%. [10].
Intraoperative Measurement
Despite all the preoperative diagnostic considerations, the denitive diagnosis of a
short esophagus is conrmed during a surgical procedure after extended esophageal
mediastinal dissection. In some cases, identication of EGJ can be difcult even
with intraoperative endoscopy in patients with hiatal hernia or Barrett’s esophagus.
Mattioli etal. have conducted a very elegant method for measuring the length of the
intraabdominal segment of esophagus after a 6–8cm dissection of the mediastinal
esophagus. The distance between EGJ and the apex of the hiatus was determined.
When the sub-diaphragmatic segment of esophagus is less than 1.5cm, it was categorized as a short esophagus. [11] In this study, after preoperative barium swallow,
short esophagus was found in 1.2%, while during surgery, 37% presented an intraabdominal esophagus shorter than 1.5 cm. Collis gastroplasty was performed in
14.5% and Collis-Nissen procedure in 3.8%. These results are very inconsistent. In
our experience, after esophageal dissection, we always obtained the intra- abdominal
segment of distal esophagus more than 2–3cm, even in patients with hiatal hernia
or complicated Barrett’s esophagus (Fig.6.6).
Fig. 6.6 Intraoperative measurement of mediastinal dissection of distal esophagus (a) and intra-
abdominal esophageal segment after dissection (b)
6 Short Esophagus: Its Relationship with Fundoplication Failure and Postoperative…
55
Reported Incidence
The precise incidence of the truly shortened esophagus is unknown. In a review of
the open and laparoscopic literature, the frequency of esophageal shortening
ranges widely from the 60% reported by Pearson and Todd to 0% reported by Hill
and some laparoscopic series [12–14]. In the laparoscopic literature, the incidences of esophageal shortening requiring a Collis gastroplasty are 3–5%. This
enormous variation is due, in part, to the magnitude and type of intra-medastinic
dissection of the esophagus. An extensive review carried out by Herbella [14]
establishes that the true existence depends on the extension of the esophageal dissection of the surgical approach and of the basic pathology. These criteria are
fundamental to determining the exact incidence of the existence of a true short
esophagus. According to Dallemagne, the esophagus should be mobilized up to
5–7cm above the hiatus, and Swanstrom suggested continuing dissection to the
level of the lower pulmonary vein. This high mobilization of the esophagus
enables the reconstruction of a sufciently long abdominal esophageal segment
which is possible to obtain in a high proportion of cases. For us, in agreement with
the majority of authors, a true short esophagus is very rare. For Hinder, the true
short esophagus is less than 1% [12–15].
In Table6.1, we show a summary of the reported incidence of a short esophagus.
In our surgical experience, after 40years of work in esophageal surgery, we have
only seen three cases of short esophagus in difcult dissection situations, in which,
when attempting to descend, there was a transversal tear in a scar area that forced
esophageal resuturing and gastroplasty repair.
Post-fundoplication Failure: Technical Failure or Short Esophagus?
In a study by Swanstrom’s group, it was clearly established that a good intramediastinal dissection reduces the failure rate of Nissen fundoplication without
the need for a Collis gastroplasty, which otherwise does not guarantee good
Table 6.1 Reported
incidence of short esophagus
Patients with GERD 1.53%
Laparotomy approach 0.08%
Laparoscopic approach 0.84%
Thoracotomic approach 57.4%
Thoracoscopic approach 5.4%
Paraesophageal hernia 11.9%
Barrett’s esophagus 0.95%
Reoperation after fundoplication 2.9%
Incidence Short
Esophagus
56
results, aside from its complexity as a process. Poor results have been described
with a high rate of postoperative complications, persistence of abnormal acid
reflux in more than 50% of cases determined by 24h pH monitoring, and poor
long-term results such as dysphagia, esophageal peristalsis, and recurrence.
Therefore, a good intra- mediastinal mobilization of the esophagus, of at least
7cm (Type II intra- mediastinal dissection), should be chosen, which results in
an adequate length of the abdominal esophagus to perform a fundoplication
[16–17].
I. Braghetto and O. Korn
Recurrence ofPostoperative Hiatal Hernia: Is theShort
Esophagus theCause? Failure intheDissection oftheSac
andMobilization oftheEsophagus?
It is widely accepted that in order to avoid a post-repair recurrence of a hiatal
hernia, a fundoplication should be performed on the free abdominal esophagus,
for which at least 2–3cm of the intra-abdominal esophagus should be obtained.
If this is not obtained, one could think of the existence of a short esophagus. It
has been perceived by those who recognize it that a short esophagus contributes to a recurrence in 15–35% of the patients, but as we have already mentioned, with a wide dissection of the intra-mediastinal hernia sac, sectioning all
the fibrous tracts that keep traction toward proximal hernia content and good
dissection (Type II), it is possible to obtain an optimal length of intra-abdominal esophagus, which has been corroborated in many reported experience
[10–17].
Collis Gastroplasty: When toIndicate?
Therefore, given the low incidence of the true short esophagus and accepting
that there are exceptional situations, the question is when to perform a Collis
Nissen gastroplasty and how often should it be performed? Here, there is great
bias due to the partiality with which patients are handled. In some centers prone
to accepting the existence of a short esophagus, the Collis gastroplasty or CollisNissen technique is more openly performed. For some, the short esophagus simply does not exist and they have never performed a Collis gastroplasty [14–16],
and others have performed it in up to 14% of the patients operated on for GERD
[17–22].
Figure 6.7 shows the algorithm for the treatment of GERD suggested more
recently; however, it has not been accepted at all [23].
6 Short Esophagus: Its Relationship with Fundoplication Failure and Postoperative…
Symptomatic GERD
with + 24 hour pH
monitoring
57
Normal esophageal
Hiatal Hernia ≤ 3cm
Sphincter
augmentation
body function
Early Progressive
Normal LES*
Hiatal Hernia
> 3cm
Nissen
Fundoplication
Disease
*...or a LES with one or
occasionally two
destroyed components
Abnormal
Esophageal body
function
Partial
Fundoplication
Normal esophageal
Adequate
Esophageal Length
Nissen
body function
Advanced Disease
Permanently failed
Short Esophageal
Length
Collis/Nissen
LES
Esophageal Length
Fundoplication
Adequate
Partial
Abnormal
Esophageal body
function
Short Esopahgeal
Length
Collis/ Partial
Fundoplication
Fig. 6.7 Algorithm for treatment of gastroesophageal reux disease according to the preoperative
evaluation and intraoperative ndings
References
1. Stephens HB.The problem of the acquired short esophagus. Calif Med. 1949;71:385–90.
2. Paterson WG, Kolyn DM.Esophageal shortening induced by short term intraluminal acid per-
fusion in opossum: a cause for hiatus hernia. Gastroenterology. 1994;107:1736–40.
3. Puri V, Jacobsen K, Bell JM, Crabtree TD, Kreisel D, Krupnick AS, Patterson GA, Meyers
BF. Hiatal hernia repair with or without esophageal lengthening: is there a difference.
Innovations. 2013;8:341–7.
4. Yano F, Stadlhuber RJ, Tsuboi K, Garg N, FilipiCh J, Mittal SK.Preoperative predictability of
the short esophagus: endoscopic criteria. Surg Endosc. 2009;23:1308–12.
5. Heitmann P, Csendes A, Strauszer T.The myth of short esophagus. Dig Dis. 1971;16:307–20.
6. Korn O, Csendes A, Burdiles P, etal. Length of the esophagus in patients with gastroesopha-
geal reux disease and Barrett’s esophagus compared to controls. Surgery. 2003;133:358–63.
7. Peters JH, Kauer WKH, DeMeester TR. Tailored antireux surgery. In: Bremner CG,
DeMeester TR, Peracchia A, editors. Modern approach to benign esophageal disease. St Louis,
MO: Quality Medical Publishing, Inc; 1995. p.57–68.
8. Gastal OL, Hagen JA, Peters JH, etal. Short esophagus: analysis of predictors and clinical
implications. Arch Surg. 1999;134:633–6.. [discussion: 637–8]
9. Kunio NR, Dolan JP, Hunter JG.Short Esophagus. Surg Clin N Am. 2015;95:641–52.
10. Awad ZT, Mittal SK, Roth TA, et al. Esophageal shortening during the era of laparoscopic
surgery. Worl J Surg. 2001;25:558–61.
11. Mattioli S, Lugaresi M, Costantini M, etal. The short esophagus: intraoperative assessment of
esophageal length. J Thorac Cardiovasc Surg. 2008;136:834–41.
12. Bochkarev V, Lee YK, Vitamvas M, Oleinikov D.Short esophagus: how much length can we
get? Surg Endosc. 2008;22:2123–7.
13. Migaczewski M, Zub-Pokrowiecka A, Grzesiak-Kulk A, Pedziwiatr M, Major P, Rubinkiewicz
M, Winiarski M, Natkaniec M, Budzynski A.Incidence of true short esophagus among patients
submitted to laparoscopic Nisen fundoplication. Videosurgery Mininv. 2015;10:10–4.
14. Herbella FAM, Del Grande JC, Colleoni R.Short esophagus: literature incidence. Dis Esoph.
2002;15:125–31.
58
15. Swanstrom LL, Marcus DR, Galloway GQ.Laparoscopic Collis gastroplasty is the treatment
of choice for the shortened esophagus. Am J Surg. 1996;171:477–81.
16. Madan AK, Frantzides CT, Patsavas KL. The myth of short esophagus. Surg Endosc.
2004;18:31–4.
17. Hill LD, Gelfand M, Bauermeister D.Simplied management of reux esophagitis with stric-
ture. Ann Surg. 1970;172:638–51.
18. Larrain A, Csendes A, Strauszer T. The short esophagus: a surgical myth.
Actagastroenterologca Latinoam. 1971;3:125–33.
19. Demeester SR, Demeeser TR. The short esophagus: going, going, gone? Surgery.
2003;133:364–7.
20. Pearson FG, Cooper JD, Patterson GA, et al. Gastroplasty and fundoplication for complex
reux problems. Long-term results. Ann Surg. 1987;206:473–81.
21. Kauer WK, Peters JH, DeMeester TR, etal. A tailored approach to antireux surgery. J Thorac
Cardiovasc Surg. 1995;110:141–7.
22. Durand L, De Anton R, Caracoche M, Covian E, Gimenez M, Ferraina P, Swanstrom
L. Short esophagus: selection of patients for surgery and long term results. Surg Endosc.
2012;26:704–13.
23. Worrell SG, Greene CL, DeMeesterTR.The state of surgical treatment of gastroesophageal
reux disease after ve decades. J.Am Coll Surg. 2014;219:819.
I. Braghetto and O. Korn
Hiatal Hernia
KamilNurczyk, MarcoDi Corpo, andMarcoG.Patti
Hiatal hernia (HH) is a common nding in the general population, and given the
aging and the prevalence of obesity of the population in the United States, these
numbers will increase in the future [1]. It is a condition in which the stomach, in
some cases together with other structures, herniates through the esophageal hiatus
into the mediastinum. HH is a frequent nding in patients with gastroesophageal
reux disease (GERD) eliminating a key component of the antireux mechanism as
it interrupts the synergistic action between the lower esophageal sphincter (LES)
and the diaphragmatic crura [2]. HH has a distinct connection with obesity due to
increased intra-abdominal pressure [3, 4], which also increases the risk of recurrence [5].
7
Classification
The HH are divided into four groups [6]:
• Type I HH, so called sliding HH, is the most common, and it is responsible for
more than 95% of the cases. The gastroesophageal junction (GEJ) herniates
upward into the posterior mediastinum through the esophageal hiatus [7]
(Fig.7.1).
• Type II HH is the pure paraesophageal hernia (PEH). There is no displacement of
the GEJ, which is located below the diaphragm, but there is herniation of the
gastric fundus above the GEJ and lateral to the esophagus. Type II is the least
common among the PEH.
K. Nurczyk · M. G. Patti (*)
Departments of Surgery and Medicine, University of North Carolina, Chapel Hill, NC, USA
e-mail: marco_patti@med.unc.edu
M. Di Corpo
Department of Surgery, University of North Carolina, Chapel Hill, NC, USA
© Springer Nature Switzerland AG 2021
N. Zundel et al. (eds.), Benign Esophageal Disease,
https://doi.org/10.1007/978-3-030-51489-1_7
59
60
Fig. 7.1 Hiatal
hernia type I
K. Nurczyk et al.
• Type III PEH is the combination of types I and II as the GEJ and fundus are both
herniated into the mediastinum [6]. More than 90% of PEH are Type III (Fig.7.2).
• Type IV PEH is characterized by the presence of other structures, such as the
omentum, colon, small bowel, spleen, and/or pancreas within the hernia sac in
mediastinum (Fig.7.3).
Symptoms andComplications
Although many patients with HH are asymptomatic, each type of HH may present
with different symptoms. Complaints related to GERD, such as heartburn, regurgitation, chronic cough, laryngitis, and asthma, are the consequence of the antireux
mechanism disruption and are typical for type I HH.This may lead to GERD complications such as esophagitis, Barrett esophagus, and strictures. Respiratory complications vary from chronic cough to asthma, aspiration pneumonia, and even
pulmonary brosis. According to Schlottmann etal. patients with larger HH have
more frequent episodes of coughing and wheezing, decreased pressure of the lower
esophageal sphincter, weaker peristalsis, more acid reux (as documented by pH
7 Hiatal Hernia
Fig. 7.2 Hiatal hernia
type III
61
Fig. 7.3 Hiatal
hernia type IV
monitoring), and more severe esophagitis [8]. While in type I HH dysphagia is usually secondary to abnormal peristalsis, in PEH it may be caused by compression of
the distal esophagus by the hernia. Large PEH may lead to respiratory and cardiac
impairment caused by direct compression of the thoracic organs [9]. Another complication is anemia secondary to bleeding from venous stasis of the gastric wall or
62
Cameron lesions [10]. Acute symptoms are more common for PEH.Volvulus, strangulation, obstruction, ischemia, necrosis, and perforation are potentially lethal complications [11].
K. Nurczyk et al.
Evaluation
Most patients require an esophagogastroduodenoscopy, barium swallow examination, high resolution manometry, and pH monitoring. A chest and abdomen CT is
key for the diagnosis of a type IV hernia, which can be suspected in a chest X-ray.
Endoscopy
Endoscopy gives information about the presence of esophagitis or Barrett’s esophagus and rules out other gastric or duodenal pathology.
Barium Swallow
It determines the size and type of HH.While this test is important to delineate the
anatomy, it should not be considered diagnostic for GERD.
Esophageal Manometry
High-resolution manometry (HRM) determines the level of the crura, the respiratory inversion point, and the location of the lower esophageal sphincter (LES). It
may also give information regarding the size of sliding HH, the pressure of the LES,
and the quality of esophageal peristalsis. In addition, HRM enables a pH probe to
be properly positioned 5cm above the upper border of the LES.The manometry and
pH monitoring are often omitted in elderly patients with type III HH.
pH Monitoring
Ambulatory pH monitoring is used to determine the presence of abnormal reux,
and the correlation between symptoms experienced by the patient and episodes of
reux. This is key before planning surgical treatment of GERD with a
fundoplication.
Computed Tomography
CT scan is recommended when a type IV HH is suspected or in case of acute
complications.
7 Hiatal Hernia
63
Surgical Treatment
Asymptomatic HH do not need surgery. However, patients with large PEH should
have regular follow-up as the annual probability of developing acute symptoms is
around 1% [12]. The surgical approach and the indications for surgery differ depending on the type of HH.
Type I Most patients with GERD are treated with acid reducing medications. The
indications for surgery are intolerance to medical therapy or inadequate symptom
control despite optimal medical management, patient preference for surgery despite
successful medical management, complications of GERD, such as stricture while
taking PPI, and/or persistence of extra-esophageal symptoms despite medical therapy. The technique will be described in the chapter that treats GERD.
Types II, III, and IV Surgery is indicated when the patient is symptomatic. It is
usually elective surgery. When ischemia is present, urgent repair is needed [13].
Surgical techniques for HH evolved over time [14]. Previous studies have shown
that laparoscopic HH repair, as compared to open, was associated with signicantly
better postoperative outcomes in terms of morbidity, mortality, length of hospital
stay, and costs [15]. The following describes the technical steps of the repair of a
type III hiatal hernia. In most cases, the type IV hiatal hernia can also be treated
laparoscopically as it is possible to reduce all the organs. However, when severe
adhesions are present, a left thoracotomy might be necessary.
Patient Positioning
Laparoscopic HH repair is performed under general anesthesia. During the procedure, patient lies in supine position. The beanbag mattress is useful especially when
using the reverse Trendelenburg position. Patient’s legs are positioned on stirrups
with knees exed at 30 degrees. After inducing anesthesia, the anesthesiologist
inserts an oro-gastric tube to decompress the stomach. During the operation, the
surgeon’s position is between the patient’s legs with assistants on both sides of the
operating table (Fig.7.4).
Trocar Placement
The operation is performed using 5 trocars. After abdominal cavity insufation
using a Verres needle, trocar 1 is placed 14cm below the xiphoid process in the
midline or slightly to the left. Trocar 2 is placed in the left midclavicular line at the
level of trocar 1. Trocar 3 for the liver retractor is placed in the right midclavicular
line at the level of trocar 1. Trocars 4 and 5 are placed under the costal margins on
the left and right side, and are used for the dissecting and suturing instruments
(Fig.7.5).