CHAPTER
41 Paraesophageal and Other Complex
Diaphragmatic Hernias
Nicole A. Kissane 
l   David W. Rattner
P
araesophageal hernias merit consideration as a
separate entity from the more common sliding
hiatal hernia because they are associated with
life-threatening complications such as strangulation,
necrosis, or perforation of the stomach. Because of
the perceived high rate of complications, and the high
mortality of emergency surgery in this setting, the sur­
gical dogma has been to repair paraesophageal hernias
on diagnosis. Recent evidence, however, questions this
dogma. Evidence-based guidelines recommend watchful
waiting for the elderly patient who is asymptomatic or
minimally symptomatic. Only patients who are symptom-
atic require operative repair.
Principal components of surgery for paraesophageal
hernias include reduction of the herniated stomach and
other organs below the diaphragm, restoration of an
intraabdominal segment of esophagus, excision of the
hernia sac, and repair of the defect in the diaphragm.
Controversy exists as to the best approach (laparoscopic
vs. transabdominal vs. transthoracic), the need for
routine fundoplication, the role of prosthetic mesh, the
benefits of gastropexy, and the prevalence of “the short
esophagus.” These controversies will be examined in this
chapter.
Although this chapter will focus on paraesophageal
hernias, it will also discuss other complex hernias of the
diaphragm, including traumatic hernias, postoperative
diaphragmatic hernias, parahiatal hernias, and congeni-
tal diaphragmatic hernias in adults.
CLASSIFICATION AND PATHOPHYSIOLOGY
All hiatal hernias are characterized by a portion—if not
all—of the stomach protruding through an enlarged
esophageal hiatus into the mediastinum. Hiatal hernias
are thought to be caused by the combined forces of age,
stress (negative intrathoracic pressure, and positive
intraabdominal pressure), and degenerative processes
on the diaphragm. Hiatal hernias can be classified into
four types, depending on the anatomic location of the
gastroesophageal (GE) junction and on the extent of
herniated stomach or other organs (Figure 41-1).
A Type I hiatal hernia is known as a sliding hiatal
hernia and is characterized by the upward displacement
of the GE junction into the posterior mediastinum. The
stomach remains in its usual longitudinal alignment (see
Figure 41-1). The development of a hiatal hernia appears
to be related to age, and to the structural deterioration
of the phrenoesophageal membrane over time.1 This
deterioration is likely due to repetitive upward stretching
of the phrenoesophageal membrane during swallowing,
494
as well as the combined forces of negative intrathoracic
pressure and positive intraabdominal pressure. This pos-
tulate is supported by the fact that power lifters, who
develop high intraabdominal pressures during weight
training, have a higher incidence of sliding hiatal hernias
than nonweightlifting age-matched controls.2 A higher
incidence of hiatal hernia has also been found in people
with inguinal hernias.3 Although the majority of patients
with hiatal hernia are asymptomatic, the prevalence and
size of the sliding hiatal hernia correlate with increasing
severity of gastroesophageal reflux disease.4
Normally the position of the gastroesophageal junc-
tion is secured by the fibroelastic phrenoesophageal liga-
ment. This ligament consists of loose connective tissue,
collagen fibers, and elastic lamellae.5,6 It appears that the
elastic component is quantitatively depleted by as much
as 50% within both the phrenoesophageal ligament and
gastrohepatic ligaments of patients with large hiatal
hernias.7
Type II and Type III hernias are known as paraes­
ophageal hernias (see Figure 41-1). Type II—a “true”
paraesophageal hernia—is defined by a normally posi-
tioned intraabdominal GE junction, with the upward
herniation of the stomach alongside it. A type III hernia
is known as a “mixed” hernia, and is characterized by the
displacement of both the GE junction and a large portion
of the stomach cephalad into the posterior mediastinum.
The difference between a type I or sliding hiatal hernia,
and a type III or mixed paraesophageal hernia, is that
with a type III hiatal hernia, a portion of the stomach lies
cephalad to the GE junction.
A paraesophageal hernia develops when there is a
defect, possibly congenital, in the esophageal hiatus ante-
rior to the esophagus.8 The persistent posterior fixation
of the GE junction is the essential difference between a
paraesophageal hernia and a sliding hiatal hernia. A type
III or mixed hernia likely starts as a sliding hiatal hernia,
and over time as the hiatus enlarges, more and more of
the fundus and body of the stomach herniates into the
chest. Alternatively, a type III hernia could start as a type
II hernia, with eventual migration of the GE junction
cephalad.
In a type IV hernia, the esophageal hiatus has dilated
to such an extent that the hernia sac also contains other
organs such as the spleen, colon, or small bowel (see
Figure 41-1). Because of this altered anatomy, bowel
obstruction and other complications may develop. Para-
esophageal hernias initially develop on the left anterior
aspect of the esophageal hiatus. The anterior gastric wall,
or perhaps the epiphrenic fat pad itself, serves as a lead
point with the remainder of the stomach rolling up into
 Paraesophageal and Other Complex Diaphragmatic Hernias   CHAPTER 41
A Normal anatomy B Type I C Type II
D Type III E Type IV
FIGURE 41-1  Types of hiatus hernia. A, Normal anatomy. B, Type
I, or sliding, hiatal hernia. C, Type II or “true” paraesophageal
hernia. D, Type III or “mixed” paraesophageal hernia. E, Type IV
paraesophageal hernia, containing other intraabdominal organs.
(From Duranceau A, Jamieson GG: Hiatal hernia and
gastroesophageal reflux. In Sabiston DC Jr, editor: Textbook of
surgery and the biological basis of modern surgical practice, ed
15. Philadelphia, 1997, Saunders, p 775.)
the chest over time. The fundus must gain enough mobil-
ity from its intraabdominal attachments to travel cepha-
lad into the chest. This mobility is obtained by laxity in
the gastrocolic and gastrosplenic ligaments, which nor-
mally help to secure the stomach below the diaphragm.
It is this laxity that allows a volvulus to develop. A volvulus
occurs when the stomach twists on itself, and can lead to
obstruction of the stomach or esophagus, and possible
perforation.
Two types of volvulus can occur: organoaxial and mes-
entericoaxial (Figure 41-2). In organoaxial volvulus, the
greater curvature of the stomach moves anterior to the
lesser curve, along the axis of the organ. In mesenterico-
axial volvulus, which is less common, the stomach rotates
along its transverse axis. Gastric strangulation develops if
the blood supply is compromised by distention of the
herniated contents or a 360-degree twist of the stomach.
PREVALENCE
The actual prevalence of hiatal hernia in the overall
population is not known. Most patients are asymptom-
atic. Upper GI tract barium studies in patients with GI
complaints identify some type of hiatal hernia in 15% of
cases. The majority of cases identified are incidental
radiographic findings.
Greater than 95% of hiatal hernia are type I or sliding
hernias. Less than 5% are paraesophageal hernias. Of all
paraesophageal hernias, type III are the most common,
accounting for 90% of cases,9 type II are found in 3.5%
495
TABLE 41-1  Paraesophageal Hernias: Preoperative
Symptoms and Findings
Typical heartburn 47%
Dysphagia 35%
Epigastric pain 26%
Vomiting 23%
Anemia 21%
Barrett epithelium 13%
Aspiration 7%
From Pierre AF, Luketich JD, Fernando HC, et al: Results of laparoscopic
repair of giant paraesophageal hernias: 200 consecutive patients. Ann
Thorac Surg 74:1909, 2002.
Caveat: Many paraesophageal hernias are asymptomatic.
to 14%, and type IV are the least common, occurring in
only 2% to 5% of all paraesophageal hernias.4
Women are four times more likely to develop a
paraesophageal hernia than men. The incidence of para-
esophageal hernias increases with advancing age. Para­
esophageal hernia patients are on average significantly
older than sliding hiatal hernia patients: a mean of 61
years versus 48 years.10 Familial cases of hiatal hernia have
been well documented, with an autosomal dominant
mode of transmission.11
SYMPTOMS
More than 50% of patients with paraesophageal hernias
are considered to be asymptomatic though many of the
symptoms are minor and may be overlooked. When
patients are questioned carefully, 89% will actually have
symptoms related to their hernia.12 Symptoms include
chest pain, epigastric pain, dysphagia, postprandial full-
ness, heartburn, regurgitation, vomiting, weight loss,
anemia, and respiratory symptoms (Table 41-1).
Compared to a sliding hiatal hernia, symptoms of
dysphagia and postprandial fullness are more common
with a paraesophageal hernia. The symptoms of heart-
burn and regurgitation that commonly are associated
with a sliding hiatal hernia can also be present with a
paraesophageal hernia.
INCARCERATION AND STRANGULATION
The most serious complications from paraesophageal
hernias are incarceration with obstruction of the stomach
and gastric strangulation. Gastric dilation from incar-
ceration with obstruction can lead to ischemia, ulcer-
ation, perforation, and ultimately sepsis. Borchardt triad
consists of chest pain, retching with the inability to vomit,
and the inability to pass a nasogastric tube.13,14 This triad
indicates an incarcerated intrathoracic stomach and is
a true surgical emergency. The presentation is often
misdiagnosed as a myocardial infarction. Without timely
surgical intervention, a life-threatening situation soon
develops.
COMPRESSION OF THE ESOPHAGUS OR STOMACH
In large paraesophageal hernias, symptoms are usually
caused by the mechanical forces of the displaced stomach.
In patients with an organoaxial volvulus, that is, an
496 SECTION I  Esophagus and Hernia

FIGURE 41-2  Gastric volvulus associated with paraesophageal hernias. Top, Organoaxial volvulus. Volvulus occurs along the longitudinal
axis of the stomach leading to a true “upside down” stomach. The stomach becomes obstructed at both the cardia and the
pyloroduodenal area. This is the most common type of gastric volvulus. Bottom, Mesentericoaxial volvulus. The stomach folds on itself
along the transverse axis. This leads to a pyloroantral obstruction. (From Menguy R: Surgical management of large paraesophageal
hernia with complete intrathoracic stomach. World J Surg 12:415, 1988.)

“upside down stomach,” both the GE junction and pylorus
are relatively fixed (see Figure 41-2). Distention of a
gastric volvulus is akin to wringing out a towel. Fluid in
the stomach is trapped leading to nausea, pain, and vom-
iting. As the stomach distends, the esophagus may be
compressed, leading to dysphagia or chest pain. Some
patients complain of spitting up foamy fluid, that is,
oral secretions that could not transit the obstructed GE
junction. Interestingly, many patients with long-standing
heartburn relate that their heartburn resolved at or about
 Paraesophageal and Other Complex Diaphragmatic Hernias   CHAPTER 41 497

the same time as they began to complain of mechanically
related symptoms such as postprandial “dry heaves” or
chest pain. Vomiting is usually intermittent, but persistent
vomiting suggests obstruction of the stomach.
BLEEDING
Hematemesis or anemia is evident in about one-third of
patients with paraesophageal hernias. Bleeding can be
caused by ischemia of the gastric mucosa or by “riding
ulcers,” otherwise known as “Cameron ulcers.” These
linear ulcers are due to constant abrasive forces created
as the stomach rubs against, or is pinched by, the dia-
phragmatic hiatus.15,16 The continuous movement of the
stomach and esophagus as it travels up and down with
respiration and swallowing compounds the problem.
The most common location of these mucosal ulcerations
is on the lesser curve of the stomach at the diaphragmatic
hiatus. These lesions are seen during endoscopy in 5%
of patients with known hiatal hernias.16 The risk of having
Cameron lesions increases with hernia size.17 Cameron
lesions can be associated with intermittent bleeding.
Anemia secondary to bleeding from a paraesophageal
hernia resolves in 92% of the patients after surgical
repair.16
PULMONARY SYMPTOMS
Pulmonary symptoms associated with paraesophageal
hernias include dyspnea and chronic cough. Symptoms
are frequently progressive throughout the day, with
gradual increase in distention of the stomach. Recurrent
aspiration from regurgitation can lead to pneumonias
or chronic bronchitis, and even a restrictive pulmonary
defect.18 With operative repair of the hernia, significant
improvements in objective measurements of pulmonary
function are usually achieved in this subset of patients.19
DIAGNOSIS AND PREOPERATIVE
EVALUATION
Although some patients present with the symptoms
described above, many are asymptomatic or minimally
symptomatic. Physical examination can be remarkable
for decreased breath sounds or dullness to percussion in
the left chest. Bowel sounds can often be auscultated in
the chest in a type IV hiatal hernia. Paraesophageal
hernias in the asymptomatic or minimally symptomatic
are found during radiographic or endoscopic evalua-
tions performed for other reasons.
RADIOGRAPHIC STUDIES
Chest radiographs often show opacity in the left chest,
or an air-fluid level behind the cardiac silhouette. The
lateral view usually demonstrates this best (Figure 41-3).
A nasogastric tube that coils in the stomach can be used
to demonstrate that this opacity is indeed an intratho-
racic stomach. CT scans show these anatomic abnormali-
ties with much more precision and can display the
anatomy in multiple planes. CT scans can also determine
if other abdominal organs have migrated above the dia-
phragm into the hernia.20 Although perceived to be old-
fashioned, a barium esophagram can be quite useful to
assess anatomic detail. The barium esophagram provides
the diagnosis of a hiatal hernia in almost all cases (Figure
41-4). It remains the easiest way to determine the loca-
tion of the GE junction, which can help to differentiate
between a type II and type III hernia, although this can
also be identified with multislice coronal CT images.
ENDOSCOPY
Fiberoptic flexible endoscopy can readily diagnose a
paraesophageal hernia during the retroflexed evaluation

A B
FIGURE 41-3  Chest radiographs. Posteroanterior (A) and lateral (B) views, of a patient with a paraesophageal hernia. Notice the large
air-fluid level behind the cardiac silhouette because of the intrathoracic stomach.
498 SECTION I  Esophagus and Hernia
A B
FIGURE 41-4  Barium swallow of a patient with a paraesophageal hernia (same patient as in Figure 41-3). A, The majority of the stomach
is in an intrathoracic position. B, Esophageal narrowing is seen because of compression from the intrathoracic portion of the stomach.
of the GE junction. Diagnostic findings of a type II
paraesophageal hernia include a second orifice next
to the GE junction, with gastric rugal folds extending
up into the opening. A type III paraesophageal hernia
shows a gastric pouch extending above the diaphragm,
with the GE junction entering part way up the side
of this pouch. Having the patient sniff can help to
identify the crura. Endoscopy can also identify other
intraluminal abnormalities, including ulcerations, gastri-
tis, esophagitis, Barrett esophagus, or mucosal-based
neoplasms.
MANOMETRY AND 24-HOUR pH MONITORING
Manometry and 24-hour pH monitoring are not rou-
tinely useful because the anatomic distortion of a para-
esophageal hernia often makes interpretation of the
findings from these studies difficult. We rely on fluoro-
scopic evaluation for a crude measure of esophageal
motility. Because many patients are elderly, esophageal
peristalsis is often abnormal and symptomatology (pres-
ence or absence of dysphagia) is the best predictor of
whether a patient will tolerate a full fundoplication or
not. We recommend an antireflux procedure in most
circumstances (see Role of Fundoplication, later).
TREATMENT
Because paraesophageal hernia is an anatomic abnor-
mality, no medical treatment can correct it. Although
symptoms of gastroesophageal reflux disease (GERD)
may be alleviated by acid suppression, those symptoms
caused by mechanical forces such as ulceration, vomit-
ing, and postprandial chest pain respond only to surgical
restoration of normal anatomy. An endoscopic gastro-
pexy has been described for use in the highest-risk
patient, in which the stomach is partially reduced with a
gastroscope and fixed intraabdominally with a double
percutaneous endoscopic gastrostomy technique, with or
without laparoscopic assistance.19 In our experience, this
is rarely effective or durable.
INDICATIONS
Traditional surgical teaching recommended operative
reduction and repair of all paraesophageal hernias once
diagnosed, unless the patient was unfit for general anes-
thesia. The perceived need for prophylactic repair on
all patients with a paraesophageal hernia is based on
the theory that the mechanical complications leading
to catastrophic, life-threatening complications can occur
without warning. This belief was established in 1967
following the classic report by Skinner and Belsey who
followed 21 patients without surgery.21 Six of these 21
patients (29%) died of causes related to their parae-
sophageal hernia including strangulation, perforation,
bleeding, and acute dilation of the stomach. The authors
concluded that elective surgery, with a 1% mortality
rate, was preferable to the high mortality rate of emer-
gency surgery.21 The above study, even though based
on a small number of patients, was felt to characterize
the natural history of paraesophageal hernias as well as
the morbidity and mortality of elective and emergency
operations, and helped to determine surgical practice
for decades.
More recent evidence suggests that the risk of observ-
ing asymptomatic patients is much less, and therefore
elective surgery should be reserved only for symptomatic
patients. In a 1993 article by Allen et al,22 23 patients with
a paraesophageal hernia who were asymptomatic were
followed for 20 years, and only 4 of them eventually
developed symptoms.
 Paraesophageal and Other Complex Diaphragmatic Hernias   CHAPTER 41
Another recent study23 examined the outcomes of
watchful waiting versus elective laparoscopic paraesopha-
geal hernia repair in asymptomatic or minimally symp-
tomatic patients. This study used a Markov-chain Monte
Carlo decision analytic model based on pooled data from
all published studies and nationwide population-based
data from the Nationwide Inpatient Sample. The authors
found that published articles overestimated the mortality
of emergency surgery when compared to the population-
based data—17% versus 5.4%. The mortality of elective
surgery was 1.4% in the population-based study. The
annual probability of developing acute symptoms requir-
ing emergency surgery with the watchful waiting strategy
was 1.1%. Using data for laparoscopic paraesophageal
hernia repair as the benchmark for surgical treatment,
this study concluded that routine elective repair would
benefit only one out of five asymptomatic patients.
Furthermore, elective laparoscopic hernia repair in
asymptomatic patients might actually decrease the
quality-adjusted life expectancy for patients aged 65 and
older. Because progression of symptoms is slow and
seldom leads to emergency surgery, watchful waiting is
the preferred approach for patients with large but rela-
tively asymptomatic paraesophageal hernias. Supporting
this approach are multiple subsequent recent studies
that came to similar conclusions.14,22-26
A recent large-scale analysis of 1005 patients with para-
esophageal hernia focused on the morbidity and mortal-
ity in octogenarians after nonelective repair. A six- to
sevenfold increase in mortality was associated with non-
elective repair compared with elective repair.27 Likewise,
nonelective repairs were also associated with a 50%
longer length of stay (14.3 days) versus elective repair (7
days), and were found to be the sole predictor of inpa-
tient mortality in patients over age eighty.27 It is impor-
tant to differentiate asymptomatic patients from those
with paraesophageal hernia–related symptoms. Individu-
als who have obstructive symptoms, bleeding, or compli-
cations of GERD associated with a paraesophageal hernia
should undergo surgical repair. These patients are clearly
the subgroup at risk to develop life-threatening com­
plications requiring emergency surgery. The elderly,
high-risk patient who is symptomatic requires specific
consideration. Complex judgment is required in order
to balance the risk of surgery, the type of surgical
approach, and the extent of the procedure performed.
Recently a Finnish retrospective population-based
study attempted to describe the mortality associated with
the natural history of paraesophageal hernia.28 Over 5
years, 563 patients underwent surgical intervention for
their hernia, and 67 patients were treated conservatively.
There is nothing to suggest that the two groups were
comparable. In the group of patients treated conserva-
tively, 11 patients (16.4%) died during a hospitalization
within 42 months of diagnosis. Interestingly, of those
deaths, 4 were felt by the authors to be preventable with
surgical intervention (3%).28 The majority of the deaths
were in elderly patients with type III (50%) or type IV
(28.1%) hernias and multiple comorbidities.28
Predictive factors for postoperative morbidity and
mortality have also been examined. In a series of 354
patients who underwent paraesophageal hernia repair,
499
mortality was highest in patients over age 75.29 Morbidity
was greatest in patients with ASA class 3 or 4, and in
patients with type IV hernias. Body mass index was not a
predictive factor of morbidity or mortality.
SURGICAL APPROACH
Paraesophageal hernias can be reduced and repaired
using either a transthoracic or transabdominal approach.
It would be optimal if the surgeon caring for patients
with paraesophageal hernias were trained in all appr­
oaches and could truly individualize the approach to
each patient’s unique anatomy and risk profile. This,
however, is rarely true in real life practice. We do not
believe that one operation is appropriate for all para­
esophageal hernias and use the following guidelines to
select the approach. We preferentially repair paraesopha-
geal hernias with a laparoscopic approach, due to the
high success rate and lower morbidity compared with a
laparotomy or a thoracotomy. This approach requires
excellent advanced laparoscopic suturing and dissecting
skills. In experienced hands, mobilization of the esopha-
gus to the aortic arch can be routinely accomplished and
a Collis gastroplasty or wedge fundectomy added if neces-
sary. In inexperienced hands, however, this is the most
dangerous approach. Laparoscopic paraesophageal
hernia repair is much more difficult than a routine lapa-
roscopic antireflux operation and should probably not
be attempted by the occasional laparoscopic surgeon. It
is best for the patient if a surgeon performs an operation
that he or she is adequately trained to do, as this provides
the best chance for a safe and effective treatment.
Not all patients are good candidates for laparoscopic
paraesophageal hernia repair, and some should be con-
sidered for a transthoracic approach. Proponents for this
approach argue that it allows for complete esophageal
mobilization and the best exposure for the dissection of
the hernia sac. A thoracotomy also provides easy expo-
sure to perform a Collis gastroplasty. Disadvantages
include the morbidity of a thoracotomy with incisional
discomfort, pulmonary complications, and prolonged
length of stay, as well as difficulty assessing the intraab-
dominal organs. In our practice, open transabdominal
approaches are reserved for patients being converted
from a laparoscopic approach. We believe that laparo-
scopic visualization is superior to that obtained via
laparotomy—especially as one tries to work cephalad
through the hiatus. Therefore, there is little advantage
of laparotomy over laparoscopy in experienced hands if
one chooses a transabdominal approach.
LAPAROSCOPIC APPROACH
Laparoscopic paraesophageal hernia repair confers the
typical benefits of minimally invasive surgery—that is, less
blood loss and less third spacing of fluids, fewer pulmo-
nary complications, and a quicker recovery from surgery.
This benefit is magnified in patients with paraesophageal
hernias who tend to be elderly and debilitated, and may
not tolerate a thoracotomy or laparotomy well. The lapa-
roscopic approach has additional unique advantages in
that the view of the operative field is magnified facilitat-
ing precise identification of tissue planes and vessels.
Insufflation of CO2 frequently establishes the correct
500 SECTION I  Esophagus and Hernia
5 mm
10 mm
5 mm 5 mm
(Liver retractor)
10 mm
(Camera)
FIGURE 41-5  Trocar placement for laparoscopic paraesophageal
hernia repair. A five-trocar technique is usually used, with two
10-mm trocars and three 5-mm trocars. (Adapted from Hutter
MM, Mulvihill SJ: Laparoscopic management of pancreatic
pseudocysts. In Zucker KA, editor: Surgical laparoscopy, ed 2.
Philadelphia, 2001, Lippincott Williams & Wilkins, p 647.)
dissection plane as one separates the peritoneal and
pleural components of the hernia sac. The use of an
angled laparoscope also allows visualization of the medi-
astinum that cannot be obtained via laparotomy.
The disadvantages of a laparoscopic approach are the
long learning curve and need for advanced laparoscopic
experience to perform this difficult operation safely and
effectively. Some state that 30 to 50 laparoscopic fundo-
plications should be performed before attempting a lapa-
roscopic paraesophageal hernia repair.14 Such experience
makes it easier to identify the anatomy, safely dissect the
hernia sac from the mediastinum, and accurately place
the crural sutures deep in the crura close to the aorta.
LAPAROSCOPIC TECHNIQUE
The patient is placed supine, with the surgeon on the
patient’s right side. After a pneumoperitoneum is estab-
lished, a five-port technique is used, with the initial
10-mm port placed 2 cm to the left of the midline, and
a few centimeters above the umbilicus (Figure 41-5). The
taller and/or more obese the patient is the farther cepha-
lad this port should be placed. A 10-mm port is placed
in the left subcostal region, one or two fingerbreadths
below the costal margin, a 5-mm trocar is placed inferior
to this in the left anterior axillary line, a second 5-mm
port is placed in the midclavicular line beneath the right
costal margin and a third 5-mm port is placed in the right
in the anterior axillary line for the liver retractor. Using
atraumatic graspers, the stomach is grasped and traction
is placed on it to display the gastrohepatic ligament. The
gastrohepatic ligament is opened and then ultrasonic
coagulating shears are used to incise the peritoneum at
the anterolateral edge of the hiatus (Figure 41-6). It is
critical at this point in the procedure to develop the
natural tissue plane that exists between the peritoneal
and pleural layers of the hernia sac. This plane is often
areolar and bloodless. In patients who are highly symp-
tomatic, however, inflammation can develop, making it
more difficult to establish this plane. Once the plane is
established, it can be carried circumferentially around
the sac. Small vessels should be coagulated with the ultra-
sonic shears or cautery. At the cephalad margin, one
should identify the vagi and then roll the sac out of the
mediastinum and into the peritoneal cavity. Much of this
can be accomplished with gentle blunt dissection (Figure
41-7). A pneumothorax may develop during this dissec-
tion if the pleura itself is violated. Ordinarily, this is not
of consequence because the patient is on positive-
pressure ventilation. However, if the patient is hypovole-
mic or inadequately relaxed, a tension pneumothorax
can develop. Depressurizing the CO2 in the abdomen will
ameliorate this problem until volume status and depth
of anesthesia are corrected. Once complete dissection of
the sac is performed, the sac is excised close to its attach-
ment to the GE junction and removed, so as not to
interfere with the subsequent repair. The anterior and
posterior vagus nerves should be identified during the
dissection and preserved during the excision of the sac.
If there is concern about the location of the vagus nerves,
or the sac is very thick and vascular, it is better to leave
some excess sac than risk injury to the nerves or esopha-
gus. Occasionally freeing the sac from the lesser omentum
is difficult and bloody and we occasionally leave this
portion of the sac attached, so long as it does not inter-
fere with suture placement during the repair. It is,
however, essential that the sac is completely detached
from the crura and mediastinum. Residual attachments
of the sac to the crura will lead to recurrence. Dividing
the short gastric vessels helps with exposure of the caudal
portion of the left crus and should be done at some point
in the case. With a rubber drain or tape around the
esophagus, extensive mediastinal dissection with mobili-
zation of the esophagus to the level of the aortic arch can
be performed. The goal is to restore a suitable length
(2.5 cm) of tension-free esophagus into the abdomen.
This should be measured with the esophagus unstretched
after the crural closure has been completed. We like to
reapproximate the crura with 0 Ethibond sutures tied
over felt pledgets (Figure 41-8). The sutures are placed
starting caudally, moving cranially, and tied sequentially.
Additional pledgeted sutures are placed until there is
only a 1-cm gap surrounding the esophagus in the undis-
tended esophageal hiatus. Lowering the pressure of the
pneumoperitoneum to 8 to 10 mm Hg while closing the
crura is in our opinion an essential maneuver to take
pressure off the closure and also allow the esophageal
hiatus to relax closer to its natural dimensions. If there
is inadequate length of the esophagus on completion of
the crural closure, an esophageal lengthening procedure
should be performed. If there is adequate esophageal
length, one can proceed with a supplementary antireflux
 Paraesophageal and Other Complex Diaphragmatic Hernias   CHAPTER 41 501

FIGURE 41-6  Laparoscopic dissection of the hernia sac. The gastrohepatic ligament can be opened, and then ultrasonic coagulating
shears can be used to incise the peritoneum at the anterolateral edge of the hiatus (dotted line). It is critical at this point in the procedure
to develop the natural tissue plane that exists between the peritoneal and pleural layers of the hernia sac. This plane is often areolar and
bloodless. (From Lee R, Donahue PE: Paraesophageal hiatal hernia. In Cameron JL, editor: Current surgical therapy, ed 7. St. Louis,
2001, Mosby, p 44.)

procedure. Once the crura are reapproximated, a 360-
degree (Nissen) fundoplication or a posterior 240-degree
(Toupet) fundoplication is created (Figure 41-9). In
elderly patients or those with severe dysmotility seen on
videoeophagrams, we prefer a partial fundoplication.
The Toupet fundoplication also has the advantage of
providing four points of fixation of the wrap to the crura.
On completion of the repair, an upper GI tract endos-
copy can be useful if there is concern for an esophageal
injury or leak.
A barium swallow study may be obtained on the first
postoperative day to rule out a leak, and reherniation if
the dissection was difficult. Antiemetics should be given
as part of the anesthetic and past operative routine to
prevent vomiting or retching. Clear liquids are started on
the first postoperative day and the patient is discharged
home with instructions to start on a full liquid diet on
the second postoperative day and continue on it for 1
week, at which time the diet is slowly advanced.
OUTCOMES
Outcomes for paraesophageal hernia repairs are reported
in the literature from a few high-volume tertiary care
centers that specialize in these procedures. Data from
low-volume centers and population-based data are not
available. The following results therefore must be
interpreted with caution, as they may not reflect all set-
tings where these procedures are being performed.
Thoracic Approach.  Initially supradiaphragmatic repair
was described by Dr. Sweet30 in 1952. In a series of 111
consecutive patients, the thoracic approach involved
reduction of the hernia, plication or excision of the
hernia sac, and reapproximation of the hiatus with
pledgeted sutures from fascia lata if reinforcement was
necessary. Sweet also noted that although preoperative
imaging often suggested that patients had a foreshort-
ened esophagus, he intraoperatively encountered this
only 5% of the time.
The largest series of transthoracic paraesophageal
hernia repairs was reported by Patel et al31 from the Uni-
versity of Michigan in 2004. A Collis gastroplasty was
performed in 96% of their 240 cases. The mortality rate
was 1.7% and the complication rate was 8.5%, including
three leaks. At 42 months’ mean followup, 19 (8%) ana-
tomic recurrences were documented, of which 8 (3.3%)
required reoperation. Maziak et al32 from the University
of Toronto reported a series of 94 cases, 97% done trans-
thoracic, with 80% undergoing gastroplasty. In their
series the mortality rate was 2%, the major complication
rate was 19% (including four leaks), and 2% required
reoperation for recurrence.
Abdominal Approach.  In 2000, Geha et al33 from the
University of Illinois reported on 100 patients, 82 of
502 SECTION I  Esophagus and Hernia

FIGURE 41-7  Laparoscopic dissection of the hernia sac (continued). The hernia sac is dissected circumferentially and seems to “tumble”
down into the abdomen with gentle blunt dissection in the mediastinum using a laparoscopic peanut. (From Lee R, Donahue PE:
Paraesophageal hiatal hernia. In Cameron JL, editor: Current surgical therapy, ed 7. St. Louis, 2001, Mosby, p 45.)

which had an abdominal approach. Two percent also

FIGURE 41-8  Crural closure. The crura are closed with simple
interrupted pledgeted 0 braided polyester suture. Starting
posteriorly, additional sutures are placed until there is a 1-cm
space below the undistended esophagus. (From Lee R, Donahue
PE: Paraesophageal hiatal hernia. In Cameron JL, editor: Current
surgical therapy, ed 7. St. Louis, 2001, Mosby, p 46.)
required a Collis gastroplasty. There were two deaths in
patients undergoing emergent operations, and none in
the elective group. There were no recurrences; however,
long-term followup was not described. Williamson et al34
from the Lahey Clinic reported on 119 patients with
paraesophageal hernias who underwent a transabdomi-
nal repair. Followup from this study was for a median of
61.5 months; the mortality rate was 1.7%, and the com-
plication rate 11.8%. Eleven percent had symptomatic
recurrences.
Laparoscopic Approach.  Pierre et al35 from the Univer-
sity of Pittsburgh reported 200 patients undergoing lapa-
roscopic repair. Fifty-six percent underwent a Collis
gastroplasty, and 11% had prosthetic mesh–reinforced
cruraplasties. With an 18-month median followup, the
mortality rate was 0.5%, complication rate was 28%
including six (3%) leaks, and 2.5% required reoperation
for recurrences.
Outcomes of paraesophageal repair after one decade
at the University of Pittsburgh have recently been pub-
lished.36 In this group of 662 patients, postoperative
gastroesophageal reflux disease and health-related
quality-of-life scores were available for 489 patients.
Good to excellent results were noted in 90% of
 Paraesophageal and Other Complex Diaphragmatic Hernias   CHAPTER 41
FIGURE 41-9  Completed Toupet fundoplication. Eight sutures are
placed over a 54F bougie; the top two sutures (one on the right,
one on the left) include the esophagus, the fundus, and the edge
of the crus. Two other sutures are placed on each side of the
esophagus, containing just the esophagus and the fundus. One
must be careful to avoid the anterior vagus nerve. Three crural
sutures are seen toward the right on this diagram, and there are
two sutures placed posteriorly (not depicted), from the back of the
wrap to the crural closure. In total, there are four points of fixation
of the wrap to the crura. (From Champion JK, McKernan JB:
Laparoscopic Toupet fundoplication. In Zucker KA, editor: Surgical
laparoscopy, ed 2. Philadelphia, 2001, Lippincott, p 406.)
patients. Radiographic recurrence was noted in 15.7%.
Remarkably, all recurrences were asymptomatic. Over
a 10-year period, 3.2% of the patients required
reoperation.36
Several other large laparoscopic series show similar
mortality rates of 0% to 2.2%, and complication rates of
4% to 10%.37-39 Gastroplasty was used in less than 5% of
these cases. Although radiographic evidence of recur-
rence was seen in 22% to 33% of patients, reoperation
was required in only 2% to 3%. Many of the radiographi-
cally detected recurrences were small sliding hiatal
hernias and were not felt to be clinically significant.
Laparoscopic Versus Open Repairs.  Two single-institution
retrospective studies compared laparoscopic and open
repairs. Hashemi et al40 at the University of South
Carolina (USC) looked at 54 patients: half who
underwent a laparoscopic procedure, one quarter who
503
underwent laparotomy, and one quarter who underwent
thoracotomy. Though symptomatic outcomes were
similar in both groups, 42% of the laparoscopic group
had a recurrence on videoesophagram, compared with
15% in the open group. Schauer et al41 compared 95
consecutive cases, 70 performed laparoscopically and 25
performed with an open technique (19 transabdominal,
4 transthoracic). The laparoscopic group had a signifi-
cant reduction in blood loss, intensive care unit stay,
ileus, hospital stay, and overall morbidity compared to
the open group. Multiple studies also suggest that lapa-
roscopic repair of paraesophageal hernia is successful,
safe, and leads to a shorter hospital stay, with lower costs
and greater patient satisfaction compared with the open
results.42-60
The major concern this group had about laparoscopic
hernia repair was the recurrence rate. As mentioned
above, the USC group reported a 42% reherniation rate
in the laparoscopic group detected by videoesophagram,
compared with 15% in the open group.40 However, other
laparoscopic series show much lower rates and only 2%
to 3% require operative repair for these recurrences,
similar to the rate in the open studies. One plausible
explanation for high recurrence reported in some lapa-
roscopic series may reflect the difficulty of placing sutures
deeply into the crura or relaxed patient selection criteria
such that patients who were considered unfit for thora-
cotomy were triaged to laparoscopic surgeons.
Recently, a large literature review of open and laparo-
scopic paraesophageal hernia repairs discussed intra-
operative and postoperative findings. A total of 1525
laparoscopic and 766 open repairs were identified.61 The
median length of stay was shorter in the laparoscopic
group compared with the open group (3 vs. 10 days).
The median conversion rate was 2.4%. The range of
complication rates was 0% to 14% for the laparoscopic
group and 5.3% to 25% for the open group. In both
groups, respiratory-related issues were the most common
complication. The median mortality rate in the laparo-
scopic group was 0.3%, versus 1.7% in the open group.61
The median recurrence rate in the laparoscopic group
was 7% (range, 0% to 42%). The median recurrence rate
in the open group was 9.1% (range, 0% to 44%). In this
review, it was acknowledged that recurrence rates were
higher in studies that included routine radiographic
imaging in their followup.61
ROLE OF FUNDOPLICATION
Controversy persists over whether or not to add an anti-
reflux procedure to hiatal herniorrhaphy in patients with
paraesophageal hernias. There are many reasons to
perform an antireflux procedure during paraesophageal
hernia repair. First, an antireflux procedure can help
maintain the stomach in an intraabdominal position.
The bulky nature of the wrap and/or the suture fixation
to the crura makes it more difficult for the stomach to
reherniate into the chest. Second, it is very difficult to
preoperatively assess which patients will have reflux
symptoms once the hernia is reduced. Preoperative
symptoms may be due to distorted anatomy and poor
esophageal clearance rather than reflux. Preoperative
testing with pH probes and manometry in these patients
504 SECTION I  Esophagus and Hernia
does not provide much practical information because of
the effects of their abnormal anatomy. Third, the func-
tionality of the GE junction is likely to be compromised
by the operative dissection and reconstruction necessary
to reduce the hernia sac and repair the hiatus. Even if
the GE junction function were normal preoperatively,
the complete dissection of the hernia sac and mobiliza-
tion of the esophagus further destroys the posterior
esophageal attachments, predisposing to the develop-
ment of reflux. Failure to perform an antireflux proce-
dure can lead to symptomatic postoperative reflux in
20% to 40% of patients.53
The disadvantages of performing a fundoplication
include added time in the operating room and risk of
complications specific to the fundoplication such as dys-
phagia. However, because adequate dissection and crural
closure has already been performed, we find that the
addition of an antireflux procedure adds little time or
morbidity. The risk of creating dysphagia or relative
obstruction in a patient with inadequate esophageal
motility is lessened by liberal use of partial fundoplica-
tions rather than 360-degree wraps. Furthermore, not all
postoperative dysphagia is caused by the fundoplication
itself—intrinsically poor esophageal peristalsis, overly
tight closure of the hiatus, or severe postoperative fibro-
sis can also create dysphagia.
THE PREVALENCE OF THE SHORT ESOPHAGUS
Controversy persists over how often esophageal length-
ening procedures should be performed when repairing
paraesophageal hernias. This controversy arises from dif-
fering opinions about the prevalence of “the short esoph-
agus.” Most agree that a 2- to 3-cm segment of esophagus
must be restored to the abdomen in order to perform
an appropriate antireflux procedure and maintain reduc-
tion of the hiatal hernia.
The prevalence of the short esophagus seems mostly
to be related to the surgeon’s perspective, the surgical
approach, and how much effort the surgeon is willing to
put forth in fully mobilizing the esophagus. The fre-
quency of performing Collis gastroplasties during para-
esophageal hernia repairs ranges from 0% in some series
to as high as 96% in other series. Transthoracic series
have the highest rate, and laparoscopic series have the
lowest rate. Proponents of the liberal use of the Collis
gastroplasty point to the low recurrence rate of para­
esophageal hernias in their series and attribute their
success to decreased tension on the esophagus.
Patel et al,31 in their series of 240 cases undergoing
transthoracic repair, performed an esophageal-
lengthening Collis gastroplasty in 96% of the cases. In
another large series of patients with large paraesopha-
geal hernias approached through the chest, evidence of
a shortened esophagus required Collis gastroplasty in 75
of 94 patients (80%).32 One laparoscopic series has
shown the need for Collis gastroplasty in 27% of cases.32
Most series report that a shortened esophagus is present
in approximately 10% of cases, though not all of these
require gastroplasty.60 In most laparoscopic series, gastro-
plasty is performed in only 1% to 4% of cases.
There is no doubt that in certain circumstances, a
shortened esophagus does exist. Urbach et al found that
preoperative risk factors associated with finding a short-
ened esophagus requiring gastroplasty included the
presence of a stricture, paraesophageal hernia, Barrett
esophagus, and a redone antireflux surgery.62 Repeated
dilations or past perforations can also be risk factors.
Although an effective technique for getting the GE
junction below the diaphragm, there are concerns about
overly liberal use of the Collis gastroplasty. These include
the risk of placing gastric mucosa above the level of the
newly created esophageal sphincter. There is also poten-
tial for leaks and bleeding from the staple line. Further-
more, when the short gastric vessels are divided, as is
routine in laparoscopic approaches, the proximal end of
the gastroplasty can become ischemic, leading to stric-
ture or leak.
We have found that with adequate circumferential dis-
section of the hernia sac, and extensive mediastinal dis-
section of the esophagus, the prevalence of a truly “short”
esophagus is quite low. What appeared initially to be a
short esophagus can usually be brought easily into the
abdomen after adequate dissection and mobilization.
Others have also shown that with such mediastinal dis-
section selective rather than liberal use of Collis gastro-
plasty is appropriate.63,64
NEED FOR GASTROPEXY OR GASTROSTOMY
Gastrostomy and gastropexy have been suggested as
primary procedures for patients who are too ill to
undergo a major procedure. In 1919, Soresi described
suturing herniated viscera to the abdominal wall when
unable to close the diaphragm, in a procedure he
described as palliative.65 Similarly, Rudolph Nissen also
used anterior gastropexy as a primary treatment for para-
esophageal hernias. Ponsky et al reported a series of 28
patients with type III hiatal hernias undergoing laparo-
scopic paraesophageal hernia repair with an additional
anterior gastropexy. After 2 years, they reported no
hernia recurrences; however, longer-term followup data
are still pending.66
USE OF PROSTHETIC MESH
In the past decade, it was tempting to draw on the lessons
learned from inguinal and ventral hernia repair, and
conclude that prosthetic mesh should be utilized more
liberally in repairing paraesophageal hernias. However,
many senior surgeons were concerned that the repetitive
motions of swallowing and breathing would cause the
mesh to erode into the GI tract over time, as happened
with the Angelchik device years ago.67 These surgeons
also expressed frustration over the inadequacy of simple
suture closure of the hiatus, with reports showing recur-
rence rates as high as 42%.68
Consequently, the role of mesh augmentation of hiatal
cruraplasty has been hotly debated. In 2009, a survey of
275 members of the Society of American Gastrointestinal
and Endoscopic Surgeons (SAGES) was performed to
investigate the use of mesh in their practice.69 A total of
5486 hiatal hernia repairs were reported, and 77% of
those were repaired laparoscopically. The most common
indication for use of mesh was an increased hiatal
defect size, and the most commonly used types of mesh
were nonabsorbable polytetrafluoroethylene (PTFE)
 Paraesophageal and Other Complex Diaphragmatic Hernias   CHAPTER 41
and polypropylene.69 Suture anchorage was the most
common mesh fixation technique. The failure rate that
was reported was 3% and seemed to be more commonly
associated with biodegradable mesh. The stricture rate
was 0.2%. The erosion rate was 0.3%. Stricture and
erosion were most frequently seen with nonabsorbable
mesh.69
Ideally, the crura should be closed under as little
tension as possible, and prosthetic material should only
be used to reinforce closure—not bridge the gap. There
are multiple techniques described for the patch place-
ment, and both absorbable and nonabsorbable prosthe-
ses have been utilized.70-73 A circular prosthesis that
surrounds the esophagus with a keyhole cutout has been
developed using polypropylene,57,58 PTFE,74 and biologic
material.76,77 An A-shaped PTFE mesh patch that sur-
rounds the crura has also been described.75 Patches can
also be used to buttress the crural repair, without encircl-
ing the esophagus.
Several trials have compared mesh repair versus simple
hiatal cruraplasty, specifically with the use of PTFE and
biologic mesh. A randomized controlled trial of PTFE
patch repair versus simple cruraplasty was done in
patients undergoing a laparoscopic Nissen fundoplica-
tion with a hiatal defect greater or equal to 8 cm.76 A
keyhole was cut into a PTFE patch for the esophagus to
pass through, and the patch was secured to the dia-
phragm and crura with a straight hernia stapler. The
study showed a marked decrease in recurrence rate in
the prosthetic patch group—eight recurrences (22%) in
the simple cruraplasty group and no recurrences in the
PTFE patch group (P < .006).76 At a mean followup of
3.3 years, there have been no reported erosions, stric-
tures, or infections in the PTFE group.
In a recent multicenter randomized controlled pro-
spective study by Oelschlager et al,77 biologic-mesh hiatal
reinforcement was noted to be superior to primary crural
repair. This study examined 108 patients at four institu-
tions undergoing laparoscopic paraesophageal hernia
repair: 57 were randomized to primary repair, and 51
were buttressed with small intestinal submucosa (SIS)
biologic mesh. The SIS mesh that was used was 7 × 10 cm,
cut in a U configuration, and sutured to the diaphragm
with interrupted nonabsorbable sutures to ensure good
contact. Operative times, perioperative complications,
and postoperative symptoms were similar in both groups.
There were no mesh-related complications. The primary
outcome was postoperative recurrent hernia larger than
2 cm on barium swallow. At 6 months, 9% (n = 4) of
patients in the biodegradable mesh group developed
radiographic recurrence compared with 24% (n = 12) in
the primary repair group. Oelschlager et al77 concluded
that biologic prosthesis successfully reduces hernia recur-
rence without mesh-related complications.
Securing and handling biosynthetic mesh laparoscopi-
cally can be quite challenging. Specifically, tack and
staple placement into the diaphragm is potentially dan-
gerous. As a result, several simplified fixation techniques
have been introduced for placement of biologic mesh
such as the use of fibrin-based tissue glues. Biologic glue
is an absorbable solution of bovine serum albumin and
glutaraldehyde.78 DeMeester examined 35 patients who
505
underwent laparoscopic paraesophageal hernia repair
with the use of biologic or synthetic mesh secured
with biological.78 Results indicated that the use of glue
is a simple method for reinforcing the crural closure.
The recurrence rate at 1 year was 9.5%, and 91.3%
of patients 1 year after surgery reported satisfaction
with their repair. No mesh-related complications were
described.
Nonetheless, the use of mesh is not without potential
long-term complications. Stadlhuber et al79 examined
patients with known mesh complications who underwent
laparoscopic repair for large hiatal hernias. The types of
mesh used in this series were polypropylene (n = 8),
PTFE (n = 12), biologic (n = 7), and coated PTFE (n =
1). The complications attributed to mesh included intra-
luminal mesh erosion (n = 17), hiatal stenosis (n = 6),
and dense fibrosis (n = 5). Surgical repair for these com-
plications included esophagectomy, esophageal stenting,
partial gastrectomy, and total gastrectomy. Interestingly,
the authors did not identify a relationship between
mesh type and configuration with respect to the specific
complication.79
Complications secondary to mesh at the time of revi-
sional hernia surgery have also been studied. In a single-
institution retrospective study, Parker et al68 compared
surgical indications and perioperative outcomes between
patients with and without prior hiatal mesh placement.
The indications for surgery (i.e., anatomic failure or
recurrent symptoms) were similar for both groups of
patients. Reoperating on patients who had mesh in place
predictably resulted in longer operations and more
blood loss than in those who did not have in situ mesh.68
Patients with prior hiatal mesh were noted to have a
6.8-fold increased risk of major resection at the time of
revision. Of note, the presence of mesh, rather than the
number of prior upper abdominal operations, correlated
with the need for major resection.
In summary, the use of mesh in paraesophageal hernia
repair is increasingly common and appears to be helpful
in preventing recurrence. However, it is not without asso-
ciated complications. Mesh must only be used for rein-
forcement of the crural closure—not as simply a bridge
across the hiatus. Fixation is necessary, and best done
with interrupted precise sutures with or without addi-
tional biologic glue. According to the currently available
literature, it is difficult to make more definitive recom-
mendations about the routine use of mesh in paraesoph-
ageal hernia repairs.
OTHER COMPLEX DIAPHRAGMATIC HERNIAS
TRAUMATIC HERNIAS
Traumatic hernias can be caused by blunt force or pen-
etrating objects, and the management depends on
whether they are identified acutely or in a delayed
fashion. Seventy-five percent of published traumatic
hernias are due to blunt trauma, though the rate at a
specific trauma center will depend on the mix of pene-
trating versus blunt trauma.80 Approximately 1% of
patients admitted to the hospital after blunt trauma have
a diaphragmatic injury: 69% are left-sided injuries, 24%
506 SECTION I  Esophagus and Hernia
right-sided, and 1.5% bilateral. Fourteen percent are
diagnosed in a delayed fashion, and of the remaining
cases, half are identified preoperatively and half during
exploration. The mortality rate following an acute diag-
nosis is 3% to 17%, depending on the mechanism and
associated injuries.80,81 In blunt trauma, rupture is usually
due to increased intraabdominal pressure related to
falls or motor vehicle accidents. Diaphragmatic rupture
usually occurs at the apex of the diaphragm in this
situation.
Traumatic rupture of the diaphragm can be a diagnos-
tic challenge. Diagnosis depends on a high index of
suspicion, careful evaluation of the chest radiograph and
CT scans, and meticulous inspection of the diaphragm
when operating for concurrent injuries.80 Though there
have been advances in imaging the diaphragm,82 no spe-
cific radiographic study can rule out a diaphragmatic
injury, especially in penetrating trauma. The incidence
of occult diaphragmatic injury in penetrating trauma to
the left lower chest is high, approximately 24%.83 Delay
in diagnosis in penetrating trauma increases mortality
significantly—from 3% in the acute setting to 25% in the
delayed presentation group.81 Therefore, some trauma
surgeons recommend exploratory laparoscopy in patients
with left lower chest penetrating injuries, if they other-
wise do not have an indication for celiotomy.83
The surgical approach for repair of a diaphragmatic
injury can be either through the abdomen or the chest.
In the acute setting, most trauma surgeons use an abdom-
inal approach because greater than 89% will have an
associated abdominal injury.67 Patients who present in a
delayed fashion usually develop significant adhesions to
the intrathoracic organs, and so a transthoracic approach
should be considered. Surgical approach in the delayed
presentation is controversial, but one must be prepared
to operate on both sides of the diaphragm when under-
taking such a case. Laparoscopic explorations and repairs
have also been undertaken in both the acute and chronic
phases.83-85 Creating a pneumoperitoneum when there is
a diaphragmatic rupture can lead to a tension pneumo-
thorax, so one must be prepared to decompress the chest
urgently if necessary.
To fix the hernia defect, suture repair with inter-
rupted, large, nonabsorbable sutures is recommended.
Direct suture repair is usually possible in the acute
setting. In the chronic setting, a prosthetic patch is
usually needed. A chronic defect can be hard to close
without a patch, and because the defect is not usually
right at the GE junction, there is less concern about
erosion by the patch.
POSTOPERATIVE DIAPHRAGMATIC HERNIAS
Postoperative diaphragmatic hernias are due to altera-
tions in the normal anatomy from surgical dissection of
the hiatus. This may occur from previous hernia repairs
in this region, antireflux procedures, esophagomyotomy,
partial gastrectomy, misguided chest tubes, or thoracoab-
dominal incisions in which the diaphragm is taken down.
After laparoscopic Nissen fundoplication, up to 6.3%
of cases can develop an iatrogenic paraesophageal
hernia.86 Early dysphagia after a fundoplication can
be caused by wrap herniation, which can readily be
confirmed with a barium swallow. Symptomatic patients
should be repaired immediately. A laparoscopic repair is
usually possible, though one must be prepared to do an
open procedure.87
PARAHIATAL HERNIAS
Parahiatal hernias are fleetingly rare, and some question
their existence altogether in the absence of operative
manipulation or trauma. A parahiatal hernia by defini-
tion arises lateral to the crural musculature, not through
the esophageal hiatus itself. The clinical presentation can
be indistinguishable from that of a paraesophageal
hernia.88 Repair is similar to that of a paraesophageal
hernia, and can be performed laparoscopically or
through open approaches.88,89
CONGENITAL DIAPHRAGMATIC HERNIAS
Bochdalek hernias and Morgagni hernias occur due to
incomplete embryologic development of the diaphragm.
Most are repaired in children; however, 5% are found in
adults.90
Bochdalek hernias, otherwise known as posterolateral
hernias, make up 85% of congenital hernias. They occur
on the left side 80% of the time. They are diagnosed and
repaired in children a majority of the time. Primary
closure of small hernias can be performed with inter-
rupted mattress sutures of nonabsorbable suture, or
larger defects can be repaired with a prosthetic patch.
Both open and laparoscopic approaches have been
described.90
Foramen of Morgagni hernias (also referred to as
retrosternal hernias or Larrey hernias) occur in the tri-
angular space between the muscle fibers that make up
the diaphragm that extend from the xiphisternum and
the costal margin to the central tendon of the dia-
phragm.91 They are thought to be due to congenital
defects of lack of fusion of these muscle fibers in the
diaphragm, made worse by increased intraabdominal
pressure. Ninety percent are right sided, as the pericar-
dium itself prevents left-sided hernias.92 Foramen of Mor-
gagni hernias account for 3% to 4% of diaphragmatic
hernias requiring surgery in both adults and children.
Patients are usually asymptomatic, but have anterior
mediastinal masses incidentally found on chest
radiographs. Prompt surgical repair after diagnosis is
prudent, to avoid incarceration or strangulation of
abdominal organs. A transabdominal route is the pre-
ferred choice. Although these can be repaired laparo-
scopically, fixation of mesh and use of tacks requires skill
and discretion so as to gain adequate fixation anteriorly
and not to injure the pericardium and heart along the
left margin of the defect. Prosthetic mesh is usually
required to repair the defect.
REFERENCES
1. Eliska O: Phreno-oesophageal membrane and its role in the devel-
opment of hiatal hernia. Acta Anatomica 86:137, 1973.
2. Smith AB, Dickerman RD, McGuire CS, et al: Pressure-overload-
induced sliding hiatal hernia in power athletes. J Clin Gastroenterol
28:352, 1999.
3. Deluca L, DiGiorgio P, Signoriello G, et al: Relationship between
hiatal hernia and inguinal hernia. Dig Dis Sci 49:243, 2004.
 Paraesophageal and Other Complex Diaphragmatic Hernias   CHAPTER 41
4. Maish MS, DeMeester SR: Paraesophageal hernia. In Cameron JL,
editor: Current surgical therapy, ed 8. Philadelphia, 2004, Mosby,
p 38.
5. Kremer B, Meneck J, Lierse W: Phrenico-esophageal membrane:
Anchoring of the terminal esophagus and cardia at the diaphragm.
Langenbecks Arch Chir 371:59, 1987.
6. Kwok H, Marriz Y, Al-Ali S, et al: Phrenoesophageal ligament re-
visited. Clin Anat 12:164, 1999.
7. Curci JA, Melman LM, Thompson RW: Elastic fiber depletion in
the supporting ligaments of the gastroesophageal junction: A struc-
tural basis for the development of hiatal hernia. J Am Coll Surg
207:191, 2008.
8. Kleitsch WP: Embryology of congenital diaphragmatic hernia.
I. Esophageal hiatus hernia. Arch Surg 76:868, 1958.
9. Hashemi M, Sillin LF, Peters JH: Current concepts in the manage-
ment of paraesophageal hiatal hernia. J Clin Gastroenterol 29:8, 1999.
10. Peters JH, DeMeester TR: Gastroesophageal reflux and hiatal
hernia. In Zinner MJ, editor: Maingot’s abdominal operations, ed 10,
1997, Appleton and Lange, p 834.
11. Carre IJ, Johnston BT, Thomas PS, et al: Familial hiatal hernia in
a large five generation family confirming true autosomal dominant
inheritance. Gut 45:649, 1999.
12. Floch NR: Paraesophageal hernias: Current concepts (editorial).
J Clin Gastroenterol 29:6, 1999.
13. Carter R, Brewer LA, Hinshaw DB: Acute gastric volvulus. A study
of 25 cases. Am J Surg 140:99, 1980.
14. Johnson JA, Thompson AR: Gastric volvulus and the upside-down
stomach. J Miss State Med Assoc 35:1, 1994.
15. Cameron AJ, Higgins JA: Linear gastric erosion. A lesion associated
with large diaphragmatic hernia and chronic blood loss anemia.
Gastroenterology 91:338, 1986.
16. Maganty K, Smith RL: Cameron lesions: Unusual cause of gastro-
intestinal bleeding and anemia. Digestion 77:214, 2008.
17. Weston AP: Hiatal hernia with Cameron ulcers and erosions. Gas-
trointest Endosc Clin N Am 6:671, 1996.
18. Greub G, Liaudet L, Wiesel P, et al: Respiratory complications of
gastroesophageal reflux associated with paraesophageal hiatal
hernia. J Clin Gastroenterol 37:129, 2003.
19. Low DE, Simchuk EJ: Effect of paraesophageal hernia repair on
pulmonary function. Ann Thorac Surg 74:333, 2002.
20. Eren S, Ciris F: Diaphragmatic hernia: Diagnostic approaches with
review of the literature. Eur J Radiol 54:448, 2005.
21. Skinner DB, Belsey RH: Surgical management of esophageal reflux
and hiatus hernia. Long-term results with 1,030 patients. J Thorac
Cardiovasc Surg 53:33, 1967.
22. Allen MS, Trastek VF, Deschamps C, et al: Intrathoracic stomach.
Presentation and results of operation. J Thorac Cardiovasc Surg
105:253, 1993.
23. Stylopoulos N, Gazelle GS, Rattner DW: Paraesophageal hernias:
Operation or observation? Ann Surg 236:492, 2002.
24. Horgan S, Eubanks TR, Jacobsen G, et al: Repair of paraesophageal
hernias. Am J Surg 177:354, 1999.
25. Dahlberg PS, Deschamps C, Miller DL, et al: Laparoscopic repair
of large paraesophageal hiatal hernia. Ann Thorac Surg 72:1125,
2001.
26. Treacy PJ, Jamieson GG: An approach to the management of para-
oesophageal hiatus hernias. Aust N Z J Surg 57:813, 1987.
27. Poulose BK, Gosen C, Marks JM, et al: Inpatient mortality analysis
of paraesophageal hernia repair in octogenarians. J Gastrointest Surg
12:1888, 2008.
28. Sihvo EI, Salo JA, Rasanen JV, et al: Fatal complications of adult
paraesophageal hernia: A population-based study. J Thorac Cardio-
vasc Surg 116:267, 1988.
29. Larusson JH, Zingg U, Hahnloser D, et al: Predictive factors for
morbidity and mortality in patients undergoing laparoscopic para-
esophageal hernia repair: Age, ASA score and operation type influ-
ence morbidity. World J Surg 33:980, 2009.
30. Sweet RH: Esophageal hiatus hernia of the diaphragm. Ann Surg
135:1, 1952.
31. Patel HJ, Tan BB, Yee J, et al: A 25-year experience with open
primary transthoracic repair of paraesophageal hernia. J Thorac
Cardiovasc Surg 127:843, 2004.
32. Maziak DE, Todd TRJ, Pearson FG: Massive hiatus hernia: Evalua-
tion and surgical management. J Thorac Cardiovasc Surg 114:53,
1998.
507
33. Geha AS, Massad MG, Snow NJ, et al: A 32-year experience in 100
patients with giant paraesophageal hernia: The case for abdominal
approach and selective antireflux repair. Surgery 128:623, 2000.
34. Williamson WA, Ellis FH Jr, Streitz JM Jr, et al: Paraesophageal
hiatal hernia: Is an antireflux procedure necessary? Ann Thorac Surg
56:447, 1993.
35. Pierre AF, Luketich JD, Fernando HC, et al: Results of laparoscopic
repair of giant paraesophageal hernias: 200 consecutive patients.
Ann Thorac Surg 74:1909, 2002.
36. Luketich JD, Nason KS, Christie NA, et al: Outcomes after a decade
of laparoscopic giant paraesophageal hernia repair. J Thorac Cardio-
vasc Surg 139:395, 2010.
37. Diaz S, Brunt LM, Klingensmith ME, et al: Laparoscopic paraesoph-
ageal hernia repair, a challenging operation: Medium-term
outcome of 116 patients. J Gastrointest Surg 7:59, 2003.
38. Andujar JJ, Papasavas PK, Birdas T, et al: Laparoscopic repair of
large paraesophageal hernia is associated with a low incidence of
recurrence and reoperation. Surg Endosc 18:444, 2004.
39. Mattar SG, Bowers SP, Galloway KD, et al: Long-term outcome of
laparoscopic repair of paraesophageal hernia. Surg Endosc 16:745,
2002.
40. Hashemi M, Peters JH, DeMeester TR, et al. Laparoscopic repair
of large type III hiatal hernia: Objective follow-up reveals high
recurrence rate. J Am Coll Surg 190:553, 2000.
41. Schauer PR, Ikramuddin S, McLaughlin RH, et al: Comparison of
laparoscopic versus open repair of paraesophageal hernia. Am J
Surg 176:659, 1998.
42. Oddsdottir M, Franco AL, Laycock WS, et al: Laparoscopic repair
of paraesophageal hernia. New access, old technique. Surg Endosc
9:164, 1995.
43. Luketich JD, Raja S, Fernando HC, et al: Laparoscopic repair of
giant paraesophageal hernia: 100 consecutive cases. Ann Surg
232:608, 2000.
44. Wiechmann RJ, Ferguson MK, Naunheim KS, et al: Laparoscopic
management of giant paraesophageal herniation. Ann Thorac Surg
71:1080, 2001.
45. Wu JS, Dunnegan DL, Soper NJ: Clinical and radiologic assessment
of laparoscopic paraesophageal hernia repair. Surg Endosc 13:497,
1999.
46. Pitcher DE, Curet MJ, Martin DT, et al: Successful laparoscopic
repair of paraesophageal hernia. Arch Surg 130:590, 1995.
47. Hawasli A, Zonca S: Laparoscopic repair of paraesophageal hiatal
hernia. Am Surg 64:703, 1998.
48. Perdikis G, Hinder RA, Filipi CJ, et al: Laparoscopic paraesopha-
geal hernia repair. Arch Surg 132:586, 1997.
49. Willekes CL, Edoga JK, Frezza EE: Laparoscopic repair of para­
esophageal hernia. Ann Surg 225:31, 1997.
50. Gantert WA, Patti MG, Arcerito M, et al: Laparoscopic repair of
paraesophageal hiatal hernias. J Am Coll Surg 186:428, 1998.
51. Horgan S, Eubanks TR, Jacobsen G, et al: Repair of paraesophageal
hernias. Am J Surg 177:354, 1999.
52. van der Peet DL, Klinkenberg-Knol EC, Alonso Poza A, et al: Lapa-
roscopic treatment of large paraesophageal hernias: Both excision
of the sac and gastropexy are imperative for adequate surgical
treatment. Surg Endosc 14:1015, 2000.
53. Trus TL, Bax T, Richardson WS, et al: Complications of paraesopha-
geal hernia repair. J Gastrointest Surg 1:221, 1997.
54. Behrns KE, Schlinkert RT: Laparoscopic management of para­
esophageal hernia: Early results. J Laparoendosc Surg 6:311, 1996.
55. Huntington TR: Short-term outcome of laparoscopic paraesopha-
geal hernia repair. A case series of 58 consecutive patients. Surg
Endosc 11:894, 1997.
56. Krahenbuhl L, Schafer M, Farhadi J, et al: Laparoscopic treatment
of large paraesophageal hernia with totally intrathoracic stomach.
J Am Coll Surg 187:231, 1998.
57. Medina L, Peetz M, Ratzer E, et al: Laparoscopic paraesophageal
hernia repair. J Soc Laparoendosc Surg 2:269, 1998.
58. Edye MB, Canin-Endres J, Gattorno F, et al: Durability of
laparoscopic repair of paraesophageal hernia. Ann Surg 228:528,
1998.
59. Athanasakis H, Tzortzinis A, Tsiaoussis J, et al: Laparoscopic repair
of paraesophageal hernia. Endoscopy 33:590, 2001.
60. Horvath KD, Swanstrom LL, Jobe BA: The short esophagus: Patho-
physiology, incidence, presentation, and treatment in the era of
laparoscopic antireflux surgery. Ann Surg 232:630, 2000.
508 SECTION I  Esophagus and Hernia
61. Draaisma WA, Gooszen HG, Tournoij IA, et al: Controversies in
paraesophageal hernia repair. Surg Endosc 19:1300, 2005.
62. Urbach DR, Khajanchee YS, Glasgow RE, et al: Preoperative deter-
minants of an esophageal lengthening procedure in laparoscopic
antireflux surgery. Surg Endosc 15:1408, 2001.
63. O’Rourke RW, Khajanchee YS, Urbach DR, et al: Extended trans-
mediastinal dissection: An alternative to gastroplasty for short
esophagus. Arch Surg 138:735, 2003.
64. Madan AK, Frantzides CT, Patsavas KL: The myth of the short
esophagus. Surg Endosc 18:31, 2004.
65. Stylopoulus N, Rattner DW: The history of hiatal hernia surgery:
From Bowditch to laparoscopy. Ann Surg 241:185, 2005.
66. Ponsky J, Rosen M, Fanning A, et al. Anterior gastropexy may
reduce the recurrence rate after laparoscopic paraesophageal
hernia repair. Surg Endosc 17:1036, 2003.
67. Varshney S, Kelly JJ, Branaan G, et al: Angelchik prosthesis revis-
ited. World J Surg 26:129, 2002.
68. Parker M, Bowers SP, Bray JM, et al: Hiatal mesh is associated
with major resection at revisional operation. Surg Endosc 24:3095,
2010.
69. Frantzides CT, Carlson MA, Loizides S, et al: Hiatal hernia
repair with mesh: A survey of SAGES members. Surg Endosc 24:1017,
2010.
70. Granderath FA, Kamolz T, Schweiger UM, et al: Laparoscopic re-
fundoplication with prosthetic hiatal closure for recurrent hiatal
hernia after failed antireflux surgery. Arch Surg 138:902, 2003.
71. Carlson MA, Condon RE, Ludwig KA, et al: Management of intra-
thoracic stomach with polypropylene mesh prosthesis reinforced
transabdominal hiatus hernia repair. J Am Coll Surg 187:227, 1998.
72. Champion JK, Rock D: Laparoscopic mesh cruroplasty for large
paraesophageal hernias. Surg Endosc 17:551, 2003.
73. Edelman DS: Laparoscopic paraesophageal hernia repair with
mesh. Surg Laparosc Endosc 5:32, 1995.
74. Frantzides CT, Richards CG, Carlson MA: Laparoscopic repair of
large hiatal hernia with polytetrafluoroethylene. Surg Endosc 13:906,
1999.
75. Casaccia M, Torelli P, Panaro F, et al: Laparoscopic physiological
hiatoplasty for hiatal hernia: New composite “A”-shaped mesh.
Physical and geometrical analysis and preliminary clinical results.
Surg Endosc 16:1441, 2002.
76. Frantzides CT, Madan AK, Carlson MA, et al: A prospective, ran-
domized trial of laparoscopic polytetrafluoroethylene (PTFE)
patch repair vs simple cruroplasty for large hiatal hernia. Arch Surg
137:649, 2002.
77. Oelschlager BK, Pellegrini CA, Hunter J, et al: Biologic prosthesis
reduces recurrence after laparoscopic paraesophageal hernia
repair: A multicenter, prospective, randomized trial. Ann Surg
244:481, 2006.
78. Zehetner J, Lipham JC, Ayazi S, et al: A simplified technique for
intrathoracic stomach repair: Laparoscopic fundoplication with
Vicryl mesh and BioGlue crural reinforcement. Surg Endosc 24:675,
2010.
79. Stadlhuber RJ, Sherif AE, Mittal SK, et al: Mesh complications after
prosthetic reinforcement of hiatal closure: A 28-case series. Surg
Endosc 23:1219, 2009.
80. Shah R, Sabanathan S, Mearns AJ, et al: Traumatic rupture of dia-
phragm. Ann Thorac Surg 60:1444, 1995.
81. Degiannis E, Levy RD, Sofianos C, et al: Diaphragmatic herniation
after penetrating trauma. Br J Surg 83:88, 1996.
82. Iochum S, Ludig T, Walter F, et al: Imaging of diaphragmatic injury:
A diagnostic challenge? Radiographics 22(Spec No):S103, 2002.
83. Murray JA, Demetriades D, Asensio JA, et al: Occult injuries to the
diaphragm: Prospective evaluation of laparoscopy in penetrating
injuries to the left lower chest. J Am Coll Surg 187:626, 1998.
84. Meyer G, Huttl TP, Hatz RA, et al: Laparoscopic repair of traumatic
diaphragmatic hernias. Surg Endosc 14:1010, 2000.
85. Frantzides CT, Madan AK, O’Leary PJ, et al: Laparoscopic repair
of a recurrent chronic traumatic diaphragmatic hernia. Am Surg
69:160, 2003.
86. Watson DI, Jamieson GG, Devitt PG, et al: Paraoesophageal hiatus
hernia: An important complication of laparoscopic Nissen fundo-
plication. Br J Surg 82:521, 1995.
87. Seelig MH, Hinder RA, Klingler PJ, et al: Paraesophageal hernia-
tion as a complication following laparoscopic antireflux surgery.
J Gastrointest Surg 3:95, 1999.
88. Scheidler MG, Keenan RJ, Maley RH, et al: “True” parahiatal
hernia: A rare entity radiologic presentation and clinical manage-
ment. Ann Thorac Surg 73:416, 2002.
89. Rodefeld MD, Soper NJ: Parahiatal hernia with volvulus and incar-
ceration: Laparoscopic repair of a rare defect. J Gastrointest Surg
2:193, 1998.
90. Richardson WS, Bolton JS: Laparoscopic repair of congenital dia-
phragmatic hernias. J Laparoendosc Adv Surg Tech 12:277, 2002.
91. Minneci PC, Deans KJ, Kim P, et al: Foramen of Morgagni hernia:
Changes in diagnosis and treatment. Ann Thorac Surg 77:1956,
2004.
92. Comer TP, Clagett OT: Surgical treatment of hernia of the foramen
of Morgagni. J Thorac Cardiovasc Surg 52:461, 1966.