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282 Part II Abdominal Wall
32 mm; (2) aortic neck length of 10 mm or greater; (3)
proximal aortic neck angulation 60 degrees or less; (4) iliac
artery xation diameter of 8–22 mm; (5) distal iliac artery
xation length of 10 mm or greater (preferably >15 mm);
(6) access vessel diameter of 7.5 mm or greater. Other considerations include the degree of iliac tortuosity, circumferential thrombus or calcication, and the aortic length.
Successful application of EVAR technology in treatment
of ruptured AAAs requires an experienced surgical team;
adequate endovascular imaging capabilities; and an adequate
supply of grafts, sheaths, guidewires, and balloons.
single most important consideration is the ability to expeditiously proceed with endovascular aortic control and suitable repair in the patient with a ruptured AAA before irreversible shock occurs. Multiple centers have described their
techniques and operative strategy, and some variation exists;
however, the fundamental principles are identical to our center’s technique. e preoperative management and anesthetic
considerations are the same as for open repair. Either local
or general anesthesia is utilized; the advantage of the former being that the fall in blood pressure with induction is
avoided. is is most advantageous while balloon control is
being obtained. In most cases the repair is completed under
general anesthesia to facilitate control of the patient’s airway
and minimize motion.
Access is obtained through both femoral arteries simultaneously. One artery may be accessed percutaneously with
placement of a closure device. Once access is obtained by
a Seldinger technique, bilateral 6F sheaths are placed over
oppy wires and subsequently exchanged for a sti wire over
a guiding catheter to the level of the proximal descending
aorta. Contralateral to the side proposed for deploying the
80
e
RA
FIGURE 13-20 Intraoperative angiogram showing suprarenal
occlusion balloon in place (arrow) and sheathed stent graft in position
for deployment (dotted arrow).
sheath and a compliant 45-mm aortic balloon is introduced
to the level of T12. Although a 12F sheath is the minimum
size for the compliant aortic balloon, we prefer larger sheaths
to allow for simultaneous pigtail catheter placement. If the
patient is hemodynamically stable, the procedure can proceed
with the balloon in place but not inated. A marking pigtail
catheter is introduced over a second oppy wire, aortogram
is performed, and the position of the renal arteries marked.
e main body graft is then introduced through the opposite femoral artery over the sti wire and placed in appropriate position (Fig. 13-20). e deated aortic balloon and its
sheath are pulled back and the graft is deployed as is normally
done for an elective EVAR. e contralateral gate of the graft
is then cannulated, and the contralateral limb is introduced
and deployed. If the patient becomes unstable, the aortic
occlusion balloon may be reintroduced through the sheath
of the contralateral limb and inated in the suprarenal aorta.
e ipsilateral limb deployment is then completed and
any ipsilateral limb extensions (if needed) are introduced
and deployed. Once the endografting has been performed,
all xation sites are molded with the compliant balloon and
a completion aortogram performed to document absence of
endoleak (Fig. 13-21). A type I (attachment or perigraft leak)
or type III endoleak (modular disconnection) warrants further repair before leaving the operating room, whereas a type
FIGURE 13-21 Completed endograft for ruptured abdominal aortic
aneurysm (AAA) showing complete exclusion of the aneurysm.
Chapter 13 Abdominal Vascular Emergencies 283
II (branch endoleak) or type IV (graft porosity) endoleak may
be followed conservatively.
e femoral arteries are then closed primarily. If heparin
had not been administered, in ow and back bleeding should
be assessed prior to closure, and, if judged to be poor, a thrombectomy catheter may be passed gently to retrieve thrombus.
Although the above describes one approach for ruptured
EVAR, multiple options exist, and the surgeon should be
well acquainted with the options based on anatomic criteria
should an endovascular approach be undertaken. ese may
include conversion to an aortouniiliac device with a femoralfemoral crossover graft or a proximal aortic extension in the
case of a type I endoleak. It is anticipated that the future generation of endografts, along with greater surgeon experience,
will lead to greater use of EVAR for ruptured AAA.
Results
Although some variation exists among individual series,
pooled data suggest an overall perioperative mortality of
approximately 50% after open repair for ruptured AAA.
Attempts have been made to correlate both pre- and postoperative variables with the probability of survival. Poor
prognostic preoperative predictors include hypotension on
induction (systolic blood pressure <90); age over 80 years,
preoperative cardiac arrest, and low hematocrit.
82
logistic regression analysis has identi ed postoperative myocardial infarction, respiratory failure, coagulopathy, and renal
dysfunction as strong predictors of postoperative mortality;
the probability of survival decreases dramatically with two or
83
more complications or with the need for dialysis.
Studies suggest that 40–60% of patients with ruptured
AAA may be treated by endovascular means. Encouraging
81
Similar
survival results have been reported following EVAR for ruptured AAA, with perioperative mortality of less than 20%
and decreased renal, cardiac, and respiratory complications
when compared to historical (open repair) controls.
ses of institutional algorithms and larger databases suggest
that endovascular repair of AAA is increasing and mortality
80,
84,
is signi cantly lower than with open repair.
ruptured AAA can be complicated by the development of
compartment syndrome requiring decompressive laparotomy
in a signi cant number of patients, and this must remain
a consideration when this approach is undertaken.
these admirable results cannot be applied universally, given
the small number of specialized centers routinely performing
ruptured EVAR, there is hope that increased dissemination of
EVAR technology and its application in ruptured AAA will
lead to a global decrease in the mortality of ruptured AAA.
Visceral Artery Aneurysms
Aneurysms of the visceral arteries are uncommon, seen in
0.01–0.02% of autopsy studies.
utilization of routine body imaging has resulted in greater
recognition and discovery of asymptomatic visceral artery
aneurysms, and thus their true prevalence is likely higher. e
elective treatment of visceral aneurysms is outside the scope
of this chapter. e major complications of these aneurysms
are rupture or distal embolization and prevention of these
complications is the rationale for elective treatment. Table
13-1 summarizes the relative frequency of these aneurysms,
their estimated risk of rupture, and recommended treatment.
Approximately 25–30% of splanchnic artery aneurysms are
ruptured at the time of presentation
are associated with aneurysms elsewhere in the arterial tree.
87
However, the increased
88
and about one-third
79
Analy-
85 EVAR for
86
While
89
TBLE 13-1: VISCERAL ARTERY ANEURYSMS
Location
Splenic 60 Low Symptomatic; pregnant or
Hepatic 20 High Symptomatic; asymptomatic
SMA 6 High All Ligation (with
Celiac 4 High All Ligation; resection
Gastric/Gastroepiploic 4 Very high All Ligation
Peripancreatic Rare High All Transcatheter embolization
Frequency
(%)
Risk of
Rupture Indications for Surgery Type of Repair
Ligation; splenectomy;
childbearing age
>2 cm (or all)
transcatheter embolization
Ligation (common hepatic);
endoaneurysmorrhaphy
with arterial reconstruction;
endovascular stent graft or
transcatheter embolization
revascularization if
compromised bowel)
with revascularization;
aneurysmorrhaphy
284 Part II Abdominal Wall
is chapter does not concern itself withthe elective management of visceral aneurysms, but rather the proper surgical
approach once rupture has occurred.
Splenic Artery Aneurysms
Splenic artery aneurysms are the most frequent visceral
aneurysms (60%), are the only aneurysms with a female predominance (3:1), and have the lowest risk of rupture. Splenic
artery aneurysms have the lowest risk of rupture, perhaps no
more than 10% overall and less than 2% in low-risk patients.
However, the risk of rupture rises dramatically among pregnant patients, with maternal and fetal mortality rates of over
70%, and after liver transplantation,
for recommending repair of asymptomatic aneurysms in
91
these groups.
Both arterial medial dysplasia (more common
in females) and the underlying vascular eects of multiple
pregnancies (both hormonal and hemodynamic) have been
proposed as contributing factors.
include portal hypertension and splenomegaly, pancreatitis or
pseudocyst-associated local inammation, and trauma. Ruptured splenic artery aneurysm initially presents with abdominal
pain referable to hemorrhage in the lesser sac without abdominal distention or shock. ese signs may become apparent
later after continued hemorrhage spills into the peritoneal cavity through the foramen of Winslow (“double rupture”).
In most cases, ruptured splenic artery aneurysms are
treated by laparotomy and ligation. Restoration of arterial
continuity is rarely necessary because of the collateral supply
to the spleen, and therefore either open or endovascular obliteration of the aneurysmal segment is appropriate. Operative
repair of proximal and midsplenic artery aneurysms entails
exposure through the lesser sac, proximal and distal control,
and simple ligation of the aneurysm without arterial reconstruction. It is important to ligate all feeding vessels; this may
require opening the aneurysm and ligation from within the
sac. Aneurysms of the splenic hilum require mobilization of
the spleen and may be treated by ligation of all branches or
splenectomy, if necessary. As in trauma, early control of the
proximal splenic artery is important for the treatment of hilar
aneurysms. While laparoscopic techniques have been reported
for the elective resection of splenic aneurysms,
place in the acute setting. Endovascular approaches are generally reserved for patients at high operative risk such as those
whose aneurysms are associated with pancreatitis, advanced
portal hypertension, or liver transplantation. In these cases,
if the patient is stable, vascular access to the splenic artery
is obtained through the celiac artery from a femoral or brachial approach. Using guiding sheaths and microcatheters,
the splenic artery is engaged and coils are placed distal to
the aneurysm, in the aneurysm sac and then proximal to
the aneurysm. ere is a 10–15% risk of rebleeding
endovascular techniques, as well as a risk of splenic infarction
when hilar aneurysms are treated. However, the diculties
of open surgery in patients with pancreatitis or advanced
liver disease justify attempts at endovascular treatment as a
90
which is the rationale
92
Other possible etiologies
93
they have no
94
using
rst eort. Endovascular stent graft placement has also been
95
described
and may be particularly useful in certain subsets,
such as patients in whom preservation of splenic blood ow
need be maintained (as for portal-systemic shunts) or in
high-risk patients with pancreatitis-associated aneurysms and
severe inammation.
Hepatic Artery Aneurysms
Hepatic artery aneurysms, unlike splenic artery aneurysms,
occur more frequently in men. ere is some evidence
that posttraumatic hepatic artery aneurysms are increasing
in frequency. Etiologies include medial degeneration,
atherosclerosis, trauma (up to 20% of cases), infection (usually
secondary to illicit drug use), vasculitis, and as a consequence
of orthotopic liver transplantation.
have a rupture risk of no less than 14%
About half the ruptured hepatic artery aneurysms present with
signs and symptoms of intraperitoneal hemorrhage, while the
other half will rupture into the biliary tract, manifesting as
either hemobilia or gastrointestinal hemorrhage.
A variety of treatment options exist for hepatic artery
aneurysms, including ligation, excision, repair with arterial
grafting and reconstruction, hepatic resection, and endovas-
87,96–98
cular approaches.
Treatment of ruptured hepatic artery
aneurysms generally depends on their location and the status
of hepatic blood ow. When feasible, preoperative arteriography is helpful in planning the operative approach. Arteriography can provide information on the collateral ow to the
liver, demonstrate anomalies such as a replaced right or left
hepatic artery, and identify multiple aneurysms, especially in
the case of intrahepatic lesions.
Ruptured common hepatic artery aneurysms are treated
by simple ligation and exclusion, unless the liver appears
ischemic after clamping. Collaterals from the right gastric
and gastroduodenal arteries will maintain hepatic artery ow
in most cases. Arterial reconstruction is indicated for most
aneurysms of the proper hepatic artery and its extra hepatic
branches unless the patient is too unstable to tolerate attempts
at bypass. In most instances, this requires interposition grafting (preferably with autologous saphenous vein) aneurysmectomy, or endoaneurysmorrhaphy. Because of their proximity
to the bile duct and portal vein, dissection of the more distal
hepatic or extrahepatic branch arterial aneurysmal segments
may be tedious, and proximal and distal control may be easier
from within the aneurysm itself. Ruptured aneurysms may
require concomitant control at the supraceliac aorta level. If
an interposition graft is not possible (as with distal common
or proximal proper hepatic artery aneurysms), an aortohepatic
bypass can be performed by exposing the right anterolateral
border of the aorta through an extended Kocher maneuver
and medial visceral rotation. e aortic anastomosis is performed rst; the graft is tunneled retroduodenal to the porta
hepatis and anastomosed to the hepatic artery after opening
the aneurysm. If the patient is unstable, ligation of the hepatic
artery, at any level, is acceptable as long as the portal vein is
96
Hepatic artery aneurysms
96
and possibly higher.97
Chapter 13 Abdominal Vascular Emergencies 285
patent; the risk of hepatic infarction is low and is less than that
of an extended procedure in a compromised patient.
Intrahepatic aneurysms are best treated by catheter-based
embolization unless they are large. Options for endovascular treatment of hepatic artery aneurysms include both coil
embolization and stent graft placement. Embolization has
been most useful for small, saccular intrahepatic pseudoaneurysms, as may be seen following trauma or percutaneous
biliary procedures with iatrogenic arterial injury. Large intrahepatic aneurysms may require liver resection. Endovascular
approaches have also been described for extrahepatic aneurysms, including both coil embolization and the placement
of endovascular covered stents.
94
Superior Mesenteric Artery Aneurysms
Superior mesenteric artery (SMA) aneurysms have been associated with an infectious etiology, dating back to DeBakey
and Cooley’s 1953 report of successful resection of a mycotic
aneurysm,
endocarditis) continues to be a signicant factor in their
development. Other less common causes of SMA aneurysms
include atherosclerosis, connective tissue disorders, vasculitis,
and trauma. e risk of rupture of SMA aneurysms is in the
range of 40–50%. e majority of SMA aneurysms occur in
the proximal 5 cm of the vessel. SMA aneurysms are usually
symptomatic, presenting with abdominal pain and sometimes signs of intestinal angina. Treatment of ruptured SMA
aneurysms is complicated by their frequent infectious etiology
and diculty with arterial reconstruction. Unlike the situation with trauma to the SMA, resection and reconstruction of
aneurysms is often more dicult because the lesion is more
extensive. While early teaching mandated proximal SMA
reconstruction, larger, contemporary series suggest that ligation
without revascularization can be considered in most patients.
In these cases, test occlusion of the vessel to assess the extent of
intestinal ischemia is critical prior to a decision on the need for
reconstruction. When collateral circulation from the celiac and
inferior mesenteric arteries, through the pancreaticoduodenal
and middle colic vessels, respectively, is sucient to maintain
intestinal viability after test occlusion of the SMA, ligation can
be performed. If extensive intestinal ischemia is present after
test occlusion, bypass grafting is required. is is usually performed as an interposition graft or a bypass from the infrarenal aorta, using autogenous vein. More distal aneurysms of
the SMA can often be treated by ligation with resection of the
compromised small bowel as needed. Access to the origin of
the SMA is obtained by left medial visceral rotation. e more
distal segments of the SMA are exposed by elevating the mesocolon and dissecting through the small bowel mesentery, using
the middle colic artery as a guide.
small bleeding aneurysms in a hemodynamically stable patient.
Assessment of bowel viability by angiographic determination
of collateral ow and celiotomy is mandatory after the procedure is completed.
99
and systemic infection (usually associated with
100
Transcatheter embolization is usually reserved for multiple
Celiac Artery Aneurysms
Medial degeneration is the most common etiology of
celiac artery aneurysms. is is particularly true in those
cases associated with anatomic anomalies such as a com-
101
mon celiomesenteric trunk.
On occasion, aneurysmal
dilation occurs distal to compression by the median arcuate
ligament, although the incidence of rupture in these cases
is unknown. Atherosclerosis is also associated with celiac
aneurysms. Ruptured celiac artery aneurysms are usually
treated by ligation, which is generally well tolerated. In saccular or very focal aneurysms, aneurysmectomy, and arte-
102
rial reconstruction may be considered.
In the patient with
preexisting liver disease or evidence of portal hypertension,
reconstruction is indicated to maximally preserve hepatic
nutrient ow. When necessary, arterial continuity may be
established using either an aortoceliac bypass, originating
from the supraceliac aorta or, less commonly, with an interposition graft. In some cases, the aneurysm may be conned
to a portion of arterial wall; aneurysmorrhaphy may be
accomplished with excision of that portion of aneurysmal
wall provided the remaining wall is healthy. Exposure and
control of the celiac artery is best obtained through a transabdominal incision and medial visceral rotation, allowing
for visualization and subsequent division of the crura and
median arcuate ligament. Alternatively, a direct approach
through the lesser sac may be used.
Gastric, Gastroepiploic, Gastroduodenal,
Pancreatic, and Pancreaticoduodenal
Aneurysms
Gastric and gastroepiploic aneurysms represent 4% of
splanchnic aneurysms, the majority of which are solitary
and involve the gastric artery. e etiology is undened
but likely results from either medial degeneration or an
associated inammatory process. ese aneurysms have a
very high incidence of rupture, either into the peritoneum
or the gastrointestinal tract and 70% present with gastrointestinal bleeding. ese aneurysms are best treated by
ligation, including resection of involved organs as necessary. e excellent collateral supply of the stomach and
the urgent nature of the operation make reconstruction
inadvisable.
Aneurysms of the gastroduodenal, pancreatic, and pancreaticoduodenal arteries are usually associated with either acute
or chronic pancreatitis.
seen after liver transplantation or pancreaticoduodenectomy,
particularly when complicated by postoperative pancreatic
stula. Most are symptomatic; rupture and gastrointestinal hemorrhage are common occurrences. Because of their
association with pancreatic inammation, gastroduodenal
and pancreaticoduodenal aneurysms are best managed with
transcatheter embolization and obliteration, especially in the
setting of active hemorrhage.
103
Occasionally these aneurysms are
286 Part II Abdominal Wall
Aneurysms of Mesenteric Branches and
the Inferior Mesenteric Artery
Jejunal, ileal, and colic branch aneurysms are usually small and
often solitary.
angiography to investigate gastrointestinal bleeding or on CT
scans for evaluation of abdominal pain. e presence of multiple mesenteric aneurysms suggests a systemic pathology such as
polyarteritis nodosa, septic emboli from bacterial endocarditis,
or a connective tissue disorder. Rupture is most commonly
seen in aneurysms involving colonic branches. Rupture most
often occurs into the mesentery, although free intraperitoneal
rupture can occur. Management is operative ligation, with
resection of involved bowel as necessary. Transcatheter embolization has a very limited role, because laparotomy is required
in any case to assess intestinal viability.
Aneurysms of the inferior mesenteric artery are exceedingly rare and little is known about their etiology or natural
history. ese aneurysms can usually be managed by ligation,
with revascularization using autogenous vein if collateral
circulation is inadequate.
103
ese aneurysms are often identied during
COMPLICATIONS AFTER RUPTURED
ABDOMINAL ANEURYSMS
Local and systemic complications are frequent after rupture
of an abdominal aortic or visceral aneurysm. A high index
of suspicion, prompt recognition, with early treatment of
complications is mandatory for survival. Mortality rates
range from 10–60% for ruptured visceral artery aneurysm
and 40–75% ruptured aortoiliac aneurysms. Postoperative
bleeding may occur as the result of ongoing coagulopathy
(“medical bleeding”) or from a technical defect (“surgical
bleeding”). Correction of hypothermia and coagulopathy
(using blood component therapy) should be prompt, and
abdominal reexploration, if bleeding continues, is mandatory.
In the face of extensive blood loss and resuscitation, abdominal
compartment syndrome may occur and should be promptly
recognized. Abdominal compartment syndrome results in
increased peak airway pressures, progressive hypoxemia, renal
dysfunction and visceral ischemia from direct compression of
mesenteric and hepatic capillary ow and venous compression,
reduced cardiac output, and increased intracranial pressure.
e diagnosis is suspected on clinical grounds and conrmed
by bladder manometry. Bladder pressures that exceed 20 mm
Hg should be treated with decompressive celiotomy. Once the
edema has resolved (usually within 7 days), the abdomen is
closed, either primarily or with mesh.
Residual visceral ischemia may occur after resection of aortic or visceral aneurysms. Patients who have persistent fever,
leukocytosis, or ileus after surgery should be evaluated for
residual visceral ischemia, pancreatitis, or intra-abdominal
abscess. is is particularly true when resection of abdominal
organs has been performed. Colon ischemia occurs in up to
30% of patients after ruptured AAA repair, with an associated
104
105
mortality of more than 50%.
It occurs unpredictably, and
can present with a range of signs and symptoms. Diarrhea,
which may or may not be bloody, that occurs within 24 hours
of AAA resection should raise suspicion of colonic ischemia;
exible sigmoidoscopy should be promptly performed in
questionable cases. If the diagnosis of colonic ischemia is
conrmed, dierentiation between transmural and mucosal
ischemia may be dicult, and the decision between nonoperative treatment (with broad spectrum antibiotics, uids,
and bowel rest and repeat colonoscopy) or celiotomy and
resection should be based on the patient’s clinical course. In
questionable cases, it is better to err on the side of operative
intervention and colon resection.
Rupture of the aorta or a major visceral vessel often results
in shock and multisystem organ failure. Cardiac (myocardial infarction, heart failure, arrhythmias) and respiratory
(respiratory failure, adult respiratory distress syndrome)
problems predominate. Renal dysfunction occurs in about
one-third of patients undergoing ruptured AAA repair; the
need for dialysis portends a poor prognosis, with mortality
106
rates of greater than 75%.
Gastrointestinal and infectious
complications may also occur, usually in the later stages of
protracted convalescence. Finally, the culmination of these
manifests as multisystem organ failure, which is the most
common cause of death beyond 48 hours in patients with
ruptured AAA.
Limb ischemia may be seen in patients after resection of ruptured AAA and is caused by distal embolization of aortic debris.
If femoral or popliteal pulses are absent at the conclusion of
surgery, prompt vascular exploration, usually by a groin incision, is indicated. In most cases the oending thrombus can be
removed with an embolectomy catheter. If femoral and popliteal
pulses are present, but pedal Doppler signals are diminished or
absent, more distal embolization has occurred. is sometimes
manifests as “blue toes” and may be associated with microembolization of atherosclerotic debris to the buttocks, spinal cord,
and sometimes abdominal and pelvic viscera. Treatment of this
condition is generally supportive, because retrieval of microemboli is not feasible. Outcome depends on the severity and
location of embolization and attendant ischemia and may range
from full recovery to amputation and death.
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ESOPHAGUS
III
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BENIGN ESOPHAGEAL DISORDERS
Saurabh Khandelwal • Brant K. Oelschlager
14
e esophagus is a muscular tube whose function is to
transport ingested material from the pharynx to the stomach.
Its function is the result of a complex symphony of neuromuscular coordination. e esophagus is subject to a variety
of disorders, both congenital and acquired. is chapter deals
with the most common benign disorders encountered by
the surgeon. ese include paraesophageal hernias (PEHs),
esophageal diverticula, and motility disorders. Our goal is
to provide a logical and e cient approach to the evaluation
and management of these disorders. Esophageal malignancy
and gastroesophageal re ux disease (GERD) are addressed
elsewhere in this book.
PARAESOPHAGEAL HERNIA
Paraesophageal hernias (PEHs) result from a defect at the
diaphragmatic hiatus. Upward displacement of abdominal
contents into the mediastinum occurs due to widening of the
hiatal aperture between the right and left crura. e negative
pressure of the chest creates a downward pressure gradient
from the abdomen further facilitating this shift. Herniation
may result from congenital anatomic causes, or it may be a
result of trauma or iatrogenic causes. Prior surgery involving
the gastroesophageal junction (GEJ), including esophageal
mobilization, crural repair, or fundoplication, can result in
PEH formation. e stomach is the organ most frequently
involved; other organs including the colon, omentum, spleen,
liver, and pancreas may also be associated.
Etiology And Anatomic Classi cation
Hiatal hernias are classi ed according to the location of the
GEJ in relation to the diaphragmatic hiatus and also by the
contents of the hernia sac. Type I hiatal hernias are by far most
common and are characterized by cephalad displacement of
the GEJ above the hiatus into the mediastinum ( Fig. 14-1 ).
Type I hiatal hernias are often referred to as sliding hiatal
hernias and are typically reducible. Patients with type I hiatal
hernias often su er from gastroesophageal re ux (GER) as a
consequence of the altered anatomy and mechanical function
of the lower esophageal sphincter (LES) and hiatal complex.
Loss of intra-abdominal esophageal length and alteration
of the angle of His contribute to this. If type I hiatal hernias enlarge signi cantly, they may become xed above the
hiatus.
Type II hiatal hernias are considered true paraesophageal
hernias and result from cephalad displacement of the fundus
of the stomach into the mediastinum. e GEJ itself remains
in its normal intra-abdominal location ( Fig. 14-2 ). Dysphagia
is a common symptom associated with a type II hiatal hernia,
usually due to compression of the esophagus by the stomach.
ese types of hernia are also referred to as “rolling” hernias.
Herniated portions of the stomach are typically found in the
posterior mediastinum. ese are the least common type of
hiatal hernia.
Type III hiatal hernias are also true paraesophageal hernias and are best thought of as a combination of types I and
II whereby both the GEJ and a portion of the stomach have
herniated above the diaphragmatic hiatus ( Fig. 14-3 ). ese
can become quite large and may involve complete herniation
of the stomach into the thorax. e anchoring attachments of
the stomach such as the gastrosplenic ligament and phrenogastric ligaments can become quite attenuated and stretched. is
type of hernia can result in partial or complete outlet obstruction as well as in volvulus. Both organoaxial volvulus, where
the stomach twists along its longitudinal axis, and mesoaxial
volvulus, where the stomach ips anteriorly along its transverse
axis, can occur. Organoaxial volvulus is more common. Patients
will typically complain of re ux, dysphagia, regurgitation, and
respiratory symptoms, all resulting from the displacement and
altered mechanics of both the GEJ and the stomach.
Type IV hiatal hernias are distinguished by herniation of
other abdominal viscera or omentum above the diaphragm.
is can occur in association with either a type II or III PEH.
e transverse colon and omentum are frequently involved,
but other organs such as the spleen, liver, and pancreas may
also be involved. Presenting symptoms can vary with particular
organ involvement.
291