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HISTORY
In 1936, Dunphy reviewed the medical records of 12 patients dying
from intestinal ischemia and discovered that more than half (58%)
had evidence of chronic abdominal pain.20 This finding suggested
that timely surgical intervention may have prevented progression
to intestinal infarction and death. In 1957, Mikkelsen described
the arteriographic appearance of typical orificial atherosclerotic
lesions affecting the mesenteric arteries. That same year, the first
successful surgical procedure (SMA endarterectomy) for treatment of chronic intestinal ischemia was performed by Maynard
and Shaw.
21
Since then, numerous techniques have been developed to revascularize the mesenteric arteries. One debated issue is the optimal
number of vessels to revascularize. Proponents of multiple-vessel
or “complete” revascularization have worried that although singlevessel bypass is effective in relieving symptoms initially, there may
be a higher incidence of recurrent symptoms secondary to graft
failure. With a few exceptions, as noted subsequently, surgery of
some sort remains an integral part of the treatment of all etiologies
of mesenteric ischemia.
MULTIPLE-VESSEL REVASCULARIZATION
Multiple-vessel revascularization implies repair or bypass of all
diseased or occluded vessels, most often the CA and SMA. Most
agree that bypass to the IMA is unnecessary for successful revascularization except in unusual cases. Grafts can be oriented antegrade from the supraceliac aorta or retrograde from the infrarenal
aorta or an iliac artery.
An early report from the Mayo Clinic first suggested that “complete” revascularization resulted in decreased symptomatic recur-
22
rence.
A subsequent report including these patients and others
indicated that graft patency and survival in patients with threevessel revascularization were improved compared to single-vessel
revascularization.23 The authors speculated that this difference
in outcome was a result of complete revascularization, which
theoreti cally provides an additional measure of safety. These two
studies, however, were limited to patients with chronic intestinal
ischemia and did not use objective methods to determine postoperative graft patency. In the latter study, McAfee et al.23 noted
that symptoms of recurrent ischemia were an unreliable measure of graft patency because two of their three early occlusions
were asymptomatic. Lack of symptoms may have resulted from the
presence of additional patent grafts. Although these retrospective
studies suggest that complete revascularization resulted in fewer
recurrences and deaths, the results were not statistically significant.
Some believe that antegrade orientation provides better inflow
than retrograde orientation because prograde flow is less turbulent, there may be less graft kinking, and the supraceliac aorta is
usually less diseased than the infrarenal aorta or an iliac artery. In
the Mayo Clinic series published in 1981, the symptomatic recurrence rate was 26%; none of these grafts were antegrade.
current studies in which the majority of grafts are positioned antegrade, the recurrence rate is lower.
24
Clearly, the reduction in recur-
22
In more
rence is multifactorial and cannot be attributed solely to graft
orientation.
More recent data suggest the rate of symptomatic recurrence
is unaffected by the number of vessels revascularized or graft orientation. In a study of 91 patients treated for CMI with a bypass
procedure, there were patients with both single- and multiplevessel reconstructions and with grafts in either orientation. Survival
was unaffected by number of vessels revascularized. Patients with
retrograde grafts had decreased survival, but these patients were
older than those with antegrade grafts.
24
SINGLE-VESSEL REVASCULARIZATION
Proponents of single-vessel revascularization have reported longterm results similar to multiple-vessel revascularizations. Series
from France have shown SMA reconstruction alone to be a durable
form of treatment for intestinal ischemia. Kieny et al.25 performed
60 direct or indirect (using a short prosthetic segment) reimplantations of the SMA (10% of patients had additional vessels reconstructed) in patients with atherosclerotic lesions of the visceral
arteries. Mean follow-up was 8.5 years; five patients (8.3%) developed recurrences, and one patient died as a result. The 5-year actuarial survival was 69.6%.
Favorable results for single-vessel revascularization have also
been reported in the United States.
26,27
Stanton et al.26 performed
20 reconstructions in 17 patients, and at 60.9 months they found
no symptomatic recurrences. One method of mesenteric revascularization is transaortic endarterectomy (TAE), with antegrade
aortoceliac bypass reserved for older or poor-risk patients.
28
Transaortic endarterectomy usually involves revascularization of
both the celiac axis and the SMA. Similar recurrence rates have
been observed between the two techniques, with 86% of patients
in both groups being asymptomatic at 5 years. Durable relief of
symptoms did not appear to correlate with number of visceral
arteries repaired.
At Oregon Health & Science University, the surgical approach
to managing acute and CMI has changed in the last 2 decades.
In 1994, Gentile et al.27 reported 26 patients who had 29 isolated bypasses to the SMA for intestinal ischemia (23 chronic,
5 acute, 1 asymptomatic). Perioperative mortality was 10%.
Mean follow-up was 40 months, and the life table–determined
4-year primary graft patency rate and survival rate were 89%
and 82%, respectively. This compared favorably with contemporary reports in the literature. Based on this experience,
revascularization of the SMA alone is recommended for most
cases of intestinal ischemia.
Foley et al. recently reported a series of 50 SMA revascularizations, employing objective means to determine graft postoperative patency.
19
This series differed from others with respect to
the larger number of patients with previous attempts at revascularization (24%), higher percentage of patients presenting with
acute ischemia (42%), and higher percentage of patients requiring simultaneous bowel resection (28%). Overall perioperative
mortality (12%), however, was comparable to other recent series.
Perioperative mortality was 3% for patients operated on electively.
The incidence of perioperative graft occlusions (6%) was similar
to other recent series, only one of which contains a significant
number of patients presenting with acute intestinal ischemia.
Three graft occlusions occurred during long-term follow-up and
resulted in death in two patients, accounting for 22% of late deaths.
In this series, the number of symptomatic late graft occlusions,
number of deaths attributable to recurrent ischemia, and life
table–determined survival were comparable to other recent series
employing more complete visceral revascularizations (
Table 27-1).
Although acute mesenteric ischemia is accompanied by a
higher perioperative mortality rate, McMillan et al.29 found no differences in long-term patency of bypass grafts between patients
with acute or chronic ischemia. Two of the three late occlusions
in this series occurred in patients whose initial graft was placed
for CMI, but one of these occluded in the perioperative period and
was replaced. Revascularization of the SMA alone continues to
compare favorably with more complete mesenteric revascularizations. Several authors have noted that symptoms are an insensitive measure of graft failure.
scanning, several studies have objective data for long-term graft
patency.
29–31
23,29
With improvements in duplex
INDICATIONS FOR OPERATION
Revascularization is clearly indicated for symptomatic intestinal
ischemia. Revascularization for asymptomatic high-grade SMA
obstruction is recommended only in patients undergoing otherwise indicated aortic surgery for aneurysmal or occlusive disease.
In this group of patients, acute intestinal ischemia following aortic surgery has been well documented, and SMA reconstruction
seems prudent.
32
333
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TABLE 27-1 Recent Mesenteric Revascularization Outcomes
AUTHOR
Foley 2000 50 (42) 12
CH
Mateo 1999
27
Kihara 1999
Moawad 1997
McMillan 1995
*Symptomatic recurrences.
†
Life-table determined.
‡
Not available.
¶
Included multiple-vessel revascularizations.
From Foley MI, Moneta GL, Abou-Zamzam AM, et al: Revascularization of the superior mesenteric artery alone for treatment of intestinal ischemia. J Vasc Surg 32:37, 2000; Mateo RB, O'Hara PJ,
Hertzer NR, et al: Elective surgical treatment of symptomatic chronic mesenteric occlusive disease: early results and late outcomes. J Vasc Surg 29:821, 1999; Kihara TK, Blebea J, Anderson KM, et al:
Risk factors and outcomes following revascularization for chronic mesenteric ischemia. Ann Vasc Surg 13:37, 1999; Moawad J, McKinsey JF, Wyble CW, et al: Current results of surgical therapy for
chronic mesenteric ischemia. Arch Surg 132:613, 1997; and McMillan WD, McCarthy WJ, Bresticker M, et al: Mesenteric artery bypass: objective patency determination. J Vasc Surg 21:729, 1995.
¶
¶
¶
¶
TECHNIQUES OF SUPERIOR MESENTERIC
ARTERY BYPASS
Retrograde Bypass
The distal infrarenal aorta as an origin for an SMA bypass graft
has advantages and disadvantages. This exposure is familiar, and
risks of dissection and clamping are less than with more proximal
aortic exposures. In addition, the procedure can be readily combined with other intraabdominal vascular procedures. The primary
disadvantage is that the infrarenal aorta and iliac arteries are frequently calcified, increasing the technical difficulty of the proximal anastomosis.
Prosthetic grafts are used most often in cases of mesenteric
revascularization. Exceptions are cases complicated by bowel
necrosis. For these patients, vein grafts are preferred to minimize
the possibility of graft infection. Special attention to graft configuration must be paid to avoid graft kinking when the graft is placed in
a retrograde configuration. A preference for the origin of the graft
is from the area of the junction of the aorta and right common iliac
artery (CIA), although any suitable site on the infrarenal aorta
or either CIA is satisfactory. A single limb is cut from a bifurcation graft in the manner described by Wylie et al.; this provides a
“flange” for sewing and prevents anastomotic stricture (Fig. 27-13) .
The ligament of Treitz is dissected. The proximal (inflow) anastomosis is completed first. The graft is then arranged first cephalad,
then turning anteriorly and inferiorly a full 180 degrees to terminate in an antegrade anastomosis to the anterior wall of the SMA—
just beyond the inferior border of the pancreas (
graft is excluded from the peritoneal cavity by closing the mesenteric peritoneum, reapproximating the ligament of Treitz, and closing the posterior parietal peritoneum.
Antegrade Bypass
Antegrade bypasses originate from the anterior surface of the
aorta proximal to the CA. The proximal aorta is exposed through
the upper midline (
celiac aorta is calcified, using a low thoracoabdominal incision.
Antegrade bypass provides prograde flow to the mesenteric vessels and is clearly the preferred approach in patients with contraindications to use of the infrarenal aorta or an iliac artery as a
bypass origin. Visceral bypass grafts can be constructed to many
supraceliac aortas with partial-occlusion clamping of the aorta,
although in most cases the “partial” occlusion is near-total occlusion. Transient hepatic and renal ischemia is usually well tolerated but is a potential disadvantage to the antegrade approach.
To minimize the risk associated with supraceliac aortic surgery,
the procedure should be reserved for patients in whom this arterial segment is angiographically normal. Significantly diseased
supraceliac aortas are dangerous origins for a visceral artery
bypass.
PATIENTS
% ACUTE
85 (0) 8 3.5 16 21 64
42 (0) 10 0 4 33 70
24 (0) 4 4 2 25 71
25 (36) 12 4 0 0 N/A
PERIOPERATIVE
MORTALITY %
PERIOPERATIVE
OCCLUSIONS %
6 3 22 61
LATE
OCCLUSIONS*
% LATE DEATHS
FROM ISCHEMIA
Fig. 27-14). The
FIGURE 2713 Artist's depiction of technique of infrarenal aorta–to–
superior mesenteric artery (SMA) bypass. Graft is fashioned using one limb
of a bifurcated graft.
Antegrade grafts to the SMA are normally tunneled behind the
pancreas and anastomosed to the anterior wall of the SMA in end-
Fig. 27-15) or, when the intra abdominal supra-
to-side fashion (
Fig. 27-16). A disadvantage of antegrade bypass is
that the retropancreatic space is limited, and great care is necessary when tunneling the graft. Some surgeons advocate prepancreatic tunneling to avoid compression of the graft within the tunnel.
A prepancreatic tunnel, however, places the graft in opposition
to the posterior wall of the stomach and theoretically increases
the possibility of graft infection. Occasionally, in the setting of
very focal SMA origin disease and an easily mobilized pancreas,
the antegrade bypass can be constructed entirely superior to the
pancreas, obviating the need for a retropancreatic tunnel.
Postoperative Monitoring of Graft Patency
The authors use sterilized Doppler probes to confirm normal flow
signals in visceral artery bypass grafts and in the native mesenteric arteries distal to the anastomotic sites after graft completion.
SURVIVAL† %
5YEAR
‡
FIGURE 2714 Artist's depiction of a retrograde mesenteric bypass to
celiac and superior mesenteric arteries, with reimplantation of inferior
mesenteric artery (IMA).
335
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27
CliniCAl EvAluATion And TREATmEnT of mEsEnTERiC vAsCulAR disEAsE
FIGURE 2716 Artist's depiction of technique of antegrade bypass
from supraceliac aorta to celiac and superior mesenteric arteries.
FIGURE 2715 Artist's depiction of exposure of supraceliac aorta.
Arterial Doppler signals should be easily detected on the antimesenteric border of the revascularized bowel as well. It is important to
repeat Doppler insonation after all packs and retractors have been
removed and after the viscera have been returned to the peritoneum. This approach helps minimize technical failures from graft
kinking.
In contrast to the situation with other vascular repairs, continuous monitoring of the patency of visceral artery repairs is impossible in the postoperative period. Postoperative graft thrombosis
may be asymptomatic or confused with other causes of postoperative pain. When symptoms do occur with resumption of oral
intake, reoperation may be difficult or impossible because of
postoperative inflammatory scarring. Thus, routine imaging of
the reconstruction 5 to 7 days postoperatively to confirm visceral
revascularization patency is prudent (Figs. 27-17 and 27-18). If
the graft is occluded or otherwise unsatisfactory, reoperation is
mandatory.
Postoperative Care
Patients with chronic visceral ischemia often have significant ischemic bowel injury that requires time for recovery. “Food fear” due
to preoperative postprandial pain may persist at least temporarily.
FIGURE 2717 Postoperative arteriogram showing patent prosthetic
graft from iliac artery to superior mesenteric artery (SMA).
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27
FIGURE 2718 Postoperative computed tomographic angiogram (CTA)
of a patent prosthetic graft from iliac artery to superior mesenteric
artery (SMA).
Prolonged periods of inability to achieve adequate oral nutrition
are frequent following visceral revascularization. For this reason,
total parenteral nutrition is used liberally. Some patients with
severe preoperative ischemia develop postoperative revasculariza-
tion syndrome, which consists of abdominal pain, tachycardia, leukocytosis, and intestinal edema. It has been attributed to intestinal
vasospasm after revascularization.
33
Any departure from a normal
postoperative course should prompt arteriography, reexploration,
or both. Delayed diagnosis of graft occlusion or intestinal necrosis
is usually fatal.
ENDOVASCULAR THERAPY FOR MESENTERIC
OCCLUSIVE DISEASE
Catheter-based therapy has become an accepted method for the
treatment of mesenteric occlusive disease, especially in patients
who are frail and unable to tolerate an operation, and those who
have short-segment SMA disease. Whereas long-segment stenoses,
heavily calcified arteries, or irregular plaques are generally more
amenable to operative revascularization, short-segment SMA disease allows for angioplasty and stenting (
Figs. 27-19 and 27-20)
with good short-term and reasonable long-term results. Initial published series reported immediate technical success with endovascular therapy, but long-term success rates were disappointing early
on and inferior to open surgery. Mortality and complication rates
in these studies range from 0% to 6% and 0% to 32%, respectively.
In a study by Sharafuddin et al., 25 patients underwent angio-
plasty and stenting of the SMA or CA.
34
Primary patency determined by ultrasound was 92% at 6 months. Early series established
that endovascular treatment of mesenteric artery stenosis is technically feasible, but no data were available with respect to long-term
durability. More recently, Lee et al. showed a primary patency rate of
69% at 7 years, but freedom from recurrent symptoms was only 56%.
Although endoluminal therapy for CMI carries low morbidity and
mortality, long-term therapeutic benefit is not as reliably achieved;
catheter-based treatment should be reserved for patients without a
good surgical option.
35
SMA
stenosis
FIGURE 2719 Lateral aortogram demonstrating stenosis of superior
mesenteric artery (SMA) just prior to stent placement.
SMA with
stent
FIGURE 2720 Lateral aortogram demonstrating patency of superior
mesenteric artery (SMA) just after stent placement.
To date, there have been several studies, mostly retrospective,
comparing the durability of endovascular revascularization for
CMI with operative bypass. A comparison was made by Kasirajan
et al.36 where 28 patients were treated with percutaneous angioplasty (PTA) with and without stenting and compared to a previously reported series of 85 patients treated with a variety of
operative procedures for CMI. Early complication rates and mortality rates were similar, but the rate of recurrent symptoms was higher
in the PTA/stent group.
36
A second group, Sivamurthy et al.,37
evaluated 60 patients treated with either operative reconstruction
or angioplasty and stenting for CMI. Perioperative and 3-year mortality rates were similar between the groups, and overall patency
rates were not statistically different. The major difference between
these groups was the number of patients free from recurrent symptoms, which was worse in the angioplasty and stent group than in
the operative group (46% vs. 71%, respectively).
37
A recent paper by Davies et al.38 confirms prior conclusions.
Their group performed a retrospective review of 27 patients with
56 diseased vessels; 17 operative revascularizations were performed (38 vessels), and 15 endovascular reconstructions were
performed (28 vessels). Both groups were similar in comorbidities
and anatomy of disease. The primary patencies of the operative
revascularizations and endovascular reconstructions groups was
83% and 54%, respectively. More patients in the operative revascularization group were free from symptoms at 1 and 2 years than
in the endovascular repair group (100% vs. 73%, P = 0.014).38 In
another recent publication, Schermerhorn et al. looked at the
Nationwide Inpatient Sample to compare mortality and complication rates between patients treated with PTA and stenting and
patients treated with open surgery for mesenteric ischemia. This
study included over 6000 patients undergoing PTA/stent and over
16,000 patients undergoing open surgery. Overall mortality rates
were lower for those patients undergoing PTA/stent than after open
surgery for both acute mesenteric ischemia (16% vs. 28%) and CMI
(3.7% vs. 13%).
39
Given these data, endovascular reconstruction for mesenteric
ischemia is feasible and can be a good option, although longterm symptom recurrence is worse with angioplasty and stenting.
Endovascular options, however, could be considered in patients
requiring more time to improve nutritional status prior to undergoing elective bypass operations, or perhaps in those patients who
have an expected short-term lifespan.
Summary
Symptomatic CMI remains uncommon. Recognition and treatment
of CMI may avoid progression to acute ischemia, alleviate symptoms, and provide durable long-term relief. This may be accomplished by a number of techniques. Single-vessel bypass to the SMA
compares favorably in terms of graft patency, death from recurrent
ischemia, and survival to recent reports of intestinal revascularizations employing bypasses to multiple arteries.
With the small numbers of patients in previously published series,
as well as differences in patient selection, it has been difficult to
demonstrate a significant benefit of one technique over others. The
technical issues involved in mesenteric revascularization are basic
vascular surgical principles: choice of proximal anastomosis, distal
target, and conduit. It is largely accepted that prosthetic grafts are
effective for mesenteric revascularization. However, there has been
considerable debate surrounding the choice of inflow vessel, number of vessels revascularized, and orientation of the graft. Surgeons
should choose a revascularization procedure for CMI that fits the
patient. It is not necessary to rigidly adhere to a single approach.
If the operation is well planned and technically well performed,
excellent results can be expected.
Acute Nonocclusive Mesenteric Ischemia
SIGNS AND SYMPTOMS
Acute NOMI occurs as a result of severe and prolonged mesenteric arterial vasospasm without evidence of arterial or venous
obstruction and has been well documented. Twenty-five percent of
patients with acute mesenteric ischemia have NOMI, and mortality rates between 30% and 90% have been reported.
NOMI are often critically ill with decreased cardiac output and episodes of hypotension. They also tend to have significant comorbidities that can result in decreased intestinal perfusion. Although
a hypoperfusion state is present in most patients with NOMI, some
have NOMI due to visceral vasoconstriction alone, as is the case
with cocaine or ergot intoxication.
41,42
Early definitive diagnosis
and treatment are essential for patient survival.
40
Patients with
Recognition of factors associated with NOMI is critical to its
prompt diagnosis. These include acute myocardial infarction
(AMI), congestive heart failure (CHF), valvular heart disease,
aortic dissection, cardiopulmonary bypass (CPB), renal failure
requiring hemodialysis, sepsis, and the use of pharmacological
agents such as vasopressors and digitalis.
43–45
Findings on physical examination are varied and do not confirm
or exclude the diagnosis of NOMI. Abdominal pain may be present and can vary widely in character, location, and intensity but is
absent in 20% to 25% of patients with NOMI.
44
Abdominal distention with occult or frank gastrointestinal bleeding may be present.
As in occlusive acute mesenteric ischemia, laboratory values are
nonspecific.
RADIOLOGICAL DIAGNOSIS
Radiological evaluation of patients with NOMI is similar to that of
patients with occlusive acute mesenteric ischemia. Plain abdominal films are obtained to rule out a perforated viscus. If technically
feasible, duplex ultrasonography may detect persistent flow in the
mesenteric arteries and exclude occlusive disease.
Patients suspected to have NOMI should undergo urgent mesenteric angiography to confirm the diagnosis. Significant mortality
is associated with a delayed diagnosis. Images in the anteroposterior and lateral planes are obtained. Findings of NOMI include
patent mesenteric arterial trunks, with tapered or spastic narrowing of visceral artery branches and impaired filling of intramural
44
vessels.
TREATMENT
The primary treatment of NOMI is correction of the systemic condition leading to generalized hypoperfusion. The largest percentage of patients with NOMI have severe cardiac failure.
46–53
Etiology
of the cardiac failure is not as important as optimization of blood
pressure and cardiac output with as little dependence as possible
on agents that result in peripheral vasoconstriction.
In the past, digitalis was frequently used to treat congestive heart
failure. Although digitalis is used much less frequently in modern
practice, many patients remain on this drug or one of its derivatives. Patients treated with digitalis preparations are at risk for
NOMI in the setting of worsening congestive heart failure.
50
Animal
experiments indicate that baseline intestinal arterial resistance is
not altered by digitalis, but compared with controls, arterial resistance in animals treated with digitalis does increase in response
to intestinal venous hypertension.
54
Thus, patients who are treated
with digitalis and have increases in portal pressure, such as occur
with worsening heart failure, may be more susceptible to development of NOMI as a result of arterial mesenteric vasoconstriction.
In patients with possible NOMI, digitalis preparations must be withdrawn and alternative medications used to treat underlying cardiac abnormalities.
In patients with peritonitis, an operation is required to adequately evaluate bowel viability. For this reason, catheter-based
therapy alone is insufficient in patients with peritoneal findings. At
operation, the bowel is inspected for viability and necrotic intestine removed. A handheld Doppler instrument is used to assess the
mesenteric vessels proximally and distally.
55
Intravenous (IV) fluorescein is also used to evaluate areas of possible ischemia; absent,
perivascular, or patchy fluorescein patterns represent areas of isch-
56
emia.
A “second look” procedure within 24 to 48 hours allows for
reassessment of bowel viability, and additional bowel resection
can be performed if necessary.
Mesenteric Venous Thrombosis
SIGNS AND SYMPTOMS
Patients with MVT present with a wide range of symptoms ranging from asymptomatic state to an acute abdomen with peritoneal signs on physical exam. Acute mesenteric ischemia occurs
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in approximately 25% of patients as a result of MVT.
pain is the most common symptom and is present in approximately
80% of patients with documented MVT.
58
Typically, patients present
with prolonged abdominal discomfort associated with abdominal
distention related to increasing intestinal edema. With transmural
bowel infarction, peritoneal findings may be present in addition
CH
to other symptoms such as nausea, vomiting, and/or gastrointes-
27
tinal bleeding, which can be present in 20% to 30% of patients.
Leukocytosis and metabolic acidosis may accompany MVT that
has resulted in bowel infarction; these patients generally have
reduced intravascular volume as a result of fluid third-spacing. In
addition to urgent anticoagulation, they often need aggressive fluid
resuscitation. Ileus is also present in these patients, and bowel rest
and decompression with nasogastric suction is required.
Mesenteric venous thrombosis can be classified into primary or
secondary thrombosis. Primary MVT is associated with hereditary
or acquired hypercoagulation disorders including factor V Leiden
and deficiencies of protein C, protein S, and antithrombin III.
Secondary MVT can result from malignancy or inflammatory disorders, and is also associated with trauma, cirrhosis, portal hypertension, or oral contraceptives.
RADIOLOGICAL DIAGNOSIS
Plain abdominal radiographs are usually obtained in patients with
abdominal pain. Free air suggestive of a perforated viscus should
be ruled out. However, in most patients with MVT, plain abdominal radiographs show a nonspecific bowel gas pattern and are
generally nondiagnostic.
In patients who have minimal abdominal pain or are asymptomatic, duplex ultrasonography may be used to evaluate
patency of the mesenteric veins. The examination is performed
after a period of fasting, and blood flow velocities within the
aorta, inferior vena cava (IVC), hepatic veins, portal vein, hepatic
artery, splenic vein, and superior mesenteric vein are evaluated.
Additional information that can be obtained from duplex ultrasonography include the presence or absence of ascites, recanalized
umbilical vein, and/or liver mass. Hepatopetal (toward the liver)
or hepatofugal (away from the liver) flow within the portal vein
can also be determined.
Duplex ultrasonography is limited in the evaluation of the mesenteric veins when there is severe ascites, recent surgery or liver
biopsy, and obesity. Occasionally the liver is located high in the
right upper quadrant and is obscured by ribs. In patients with
peritoneal findings, duplex ultrasonography is difficult to perform
because of patient discomfort and significant amounts of bowel gas.
Currently, contrast-enhanced abdominal CT scanning is the
diagnostic study of choice in patients suspected of having MVT.
In addition to MVT, CT scanning can accurately detect portal and
ovarian vein thrombosis. Other suggestive findings include bowelwall thickening, pneumatosis intestinalis, or mesenteric edema. In
one series, contrast-enhanced abdominal CT scanning was diagnostic for MVT in 90% of patients.
58
Arterioportography is indicated when associated arterial ischemia is suspected or when findings on abdominal CT scanning
are equivocal. The mesenteric venous system cannot be directly
punctured, but is visualized indirectly through catheter-directed
contrast injections into the SMA and CA, followed by delayed filming (
Fig. 27-21). Mesenteric venous thrombosis is demonstrated by
a filling defect within the mesenteric veins.
TREATMENT
Urgent laparotomy is undertaken in patients with peritoneal findings. This is a minority of patients with MVT. Perioperative broadspectrum antibiotics are administered. Findings at laparotomy
consist of edema and cyanotic discoloration of the mesentery and
bowel wall with thrombus involving the distal mesenteric veins.
Complete thrombosis of the superior mesenteric vein is rare, occurring in only 12% of patients undergoing laparotomy for suspected
59
MVT.
The arterial supply to the involved bowel is usually intact.
57,58
Abdominal
Portal vein
Splenic vein
Superior mesenteric vein
FIGURE 2721 Aortoportography demonstrating patent portal vein,
superior mesenteric vein, and splenic vein.
Nonviable bowel is resected and primary anastomosis performed.
If viability of the remaining bowel is in question, a repeat “second
look” operation is performed in 24 to 48 hours. Thrombolytic therapy or surgical thrombectomy of mesenteric veins is not required;
these interventions are not usually technically successful.
In patients without peritoneal findings, anticoagulation with IV
unfractionated heparin (UFH) is promptly initiated, and the patient
is observed with serial abdominal examinations while maintaining
bowel rest. Ileus may be prolonged, so hyperalimentation should
be considered early. Once the patient's clinical status improves,
oral intake can be cautiously introduced. A search for a predisposing primary or secondary hypercoagulable condition is required.
In the interim, the patient is transitioned to oral anticoagulation
over 3 to 4 days, once intestinal function has returned. Lifelong anticoagulation is usually maintained, especially in cases of idiopathic
MVT or when an uncorrectable hypercoagulable state has been
identified.
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CliniCAl EvAluATion And TREATmEnT of mEsEnTERiC vAsCulAR disEAsE
PA RT VII
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VASCULOGENIC ERECTILE DYSFUNCTION
CHAPTER
28 Vasculogenic Erectile Dysfunction
Kirk A. Keegan, David F. Penson
Introduction
The first historical descriptions of erectile dysfunction (ED)
date back to Egyptian papyrus nearly 4000 years ago. Egyptian
scholars described two types of ED: a “natural” form in which the
man was incapable of performing the sex act, and a “supernatural” form rooted in evil charms and spells.
as Hippocrates and Aristotle also theorized on the etiology of ED.
However, the first accurate depiction of penile anatomy and rudimentary analysis of erection was not published until 1585, when
Ambroise Paré described it in his Ten Books on Surgery and the
Book of Reproduction.
tube with concentric coats of nerves, veins, arteries, two “ligaments”
composed of the corpora cavernosa, and the urinary tract.
Over the succeeding centuries, there has been considerable
investigation into the hemodynamic and anatomical mechanisms
of male erection. Modern understanding of erectile physiology has
been delineated only in the last 30 years. Central to our current theories of erectile physiology is the role of smooth muscle in control
of arterial and venous flow, the architecture of the tunica albuginea, the role of nitric oxide (NO) as the principal neurotransmitter regulating tumescence, and the function of phosphodiesterases
(PDEs) for detumescence. Recent research on the role of endothelial regulation of smooth muscle, the influence of ion channels, and
the integral function of endothelial gap junctions has furthered our
understanding. This chapter will review these findings, as well as
the prevalence, clinical evaluation, diagnostic testing, medical and
surgical management, clinical outcomes, and current guidelines
regarding vasculogenic ED in detail.
2
In these texts, Paré portrayed the penis as a
1
Ancient thinkers such
The 1992 National Health Social and Life Survey (NHSLS) was a
national survey of 1410 American men between the ages of 18
and 59. In the study group, the prevalence of ED in men aged 18
to 29 years was 7%, aged 30 to 39 was 9%, aged 40 to 49 was 11%,
and aged 50 to 59 was 18%.5 The Massachusetts Male Aging Study
(MMAS), a longitudinal population-based study, evaluated 1709
men between the ages of 40 and 70 who returned questionnaires
about a broad range of physiological measures, demographic
information, and self-reported sexual function. Participants were
surveyed between the years 1987 and 1989 and then reevaluated
between 1995 and 1997. In this series, the age-adjusted prevalence
of significant ED was 39% in men with coronary artery disease
(CAD), 25% in men with diabetes mellitus, and 15% in men with
hypertension. Incidence of ED on reevaluation was 25.9 cases per
1000 men per year (95% confidence interval [CI], 22.5-29.9).
these data, it was estimated that for Caucasian men, 617,715 new
cases of ED would present in the 40 to 69 age group each year.
Data from European and Brazilian researchers suggest a similar
incidence of ED in their respective countries.
8,9
6
Using
Functional Anatomy
The functional anatomy of the human penis is composed of
several key components. Principally, these are three cylindrical
structures—two corpora cavernosa surrounded by a tough tunica
albuginea, and the solitary corpus spongiosum which contains
the urethra. Vascular components include arteries and arterioles,
highly compliant sinusoids within the corpora cavernosa, and
compressible venules and veins.
7
Definition and Classifications
In 1992, the National Institutes of Health convened a Consensus
Development Conference on Impotence. The group renamed
impotence as male erectile dysfunction and defined it as “the
inability to achieve or maintain an erection sufficient for satisfactory sexual performance.”
dysfunction represents the most appropriate term, given that sexual
desire, orgasm, and ejaculation may be intact despite inability to
achieve or maintain erection.
Multiple schema have been proposed to classify the different types of ED. Broadly, ED can be described in terms of organic
and psychogenic dysfunction (
chapter will center on vasculogenic ED, which comprises impaired
endothelial function, arterial occlusive disease, veno-occlusive dysfunction, and structural changes to the corpora cavernosa.
3
Furthermore, they noted that erectile
Box 28-1). The main thrust of this
Prevalence and Incidence
Erectile dysfunction is quite common, affecting approximately 30 million men in the United States.
been performed to address male sexual function and specifically the
prevalence and incidence of ED in the American male population.
4
Several population-based studies have
Corporal Bodies, Sinusoids, and Glans
The corpora cavernosa are paired spongy cylinders that lie
on the superior aspect of the penis. They are enveloped by the
tunica albuginea. The proximal ends of the corpora are separate
structures anchored at the ischial ramus. The corpora then fuse
underneath the pubic ramus and share a common septum distally
towards the glans.
Within the corpora, interconnected sinusoids are enveloped
by trabeculae of smooth muscle, collagen, and elastin (
The sinusoidal smooth muscle is in intimate association with the
cavernous nerves and helicine arteries within the penis. The sinusoids are tonically constricted during the flaccid state. Arterial
blood flow diffuses through larger central sinusoids to smaller
peripheral sinusoids. In the flaccid state, this slow diffusion of
arterial blood results in blood gas values similar to venous blood.
During sexual stimulation, release of neurotransmitters causes
the smooth muscle around the sinusoids to relax. This results in
rapid influx of arterial blood, subsequent entrapment of blood
within these expanding sinusoids, and occlusion of veins traversing the tunica albuginea. Subsequent tumescence results in pressure increases of several hundred mmHg and blood gas values
approaching arterial levels.
10
Fig. 28-1).
341
342
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28
Box 28-1 International Society of Impotence
Research Classification of Erectile Dysfunction
Organic
I. Vasculogenic
II. Neurogenic
III. Anatomic
IV. Endocrine
Psychogenic
I. Generalized
A. Lack of Response
B. Inhibition
II. Situational
A. Partner related
B. Performance related
C. Distress related
semen. The glans is exquisitely sensitive, conical in shape, eases
intromission, and forms a cushion for the rigid corporal bodies.
These areas engorge in a similar fashion as the corpora cavernosa
but to a lesser degree, largely owing to an absence of the tunica
albuginea and diminished venous trapping.
Tunica Albuginea
The tunica albuginea is composed primarily of tough type I collagen with a minority component of more flexible type III collagen
and elastin. It is arranged in a bilayer, with inner circular layers and
outer longitudinal layers (see
the body of the corpora cavernosa and provide further support.
Fig. 28-1). Intervening struts traverse
11
The longitudinal layers of the tunica are present from the glans to
the proximal crura, where each corporal body inserts into its ischial
ramus to form a foundation for support of the erect penis. Emissary
veins (
Fig. 28-2) pierce the tunica albuginea. During engorgement,
these veins become compressed and allow entrapment of blood
within the penis.
Arterial System
The internal pudendal artery, a branch of the internal iliac artery
(IIA), is the principal source of blood flow to the penis. Up to 70%
of men may have accessory pudendal branches that originate from
the external iliac, obturator, or vesical arteries.
dal artery gives rise to the penile artery, which in turn branches
in to the dorsal, bulbourethral, and cavernous arteries (
The cavernous artery supplies the corpus cavernosum via helicine
arteries, which lie in close approximation to the sinusoidal tissue.
During erection, these vessels dilate, resulting in engorgement.
12
The internal puden-
Fig. 28-3).
FIGURE 281 Drawing of three-dimensional anatomy of human penis,
demonstrating inner circular layers and outer longitudinal layers of the
tunica albuginea, intervening supports, sinusoidal tissue in corpora
cavernosa, corpus spongiosum, and urethra.
The interior of the glans and corpus spongiosum share a similar sinusoidal architecture as the corpora cavernosa. However, the
tunica surrounding the spongiosum is thinner and is completely
absent around the glans. The corpus spongiosum is a highly compliant body that houses the urethra and facilitates expulsion of
Flaccid State
Emissary
vein
Venous System
Venous drainage originates from the three corporal bodies. Venules
interdigitate through the cavernosal sinusoids and coalesce below
the tunica albuginea into a subtunical plexus. The plexi then form
emissary veins that penetrate the tunica albuginea. From there,
numerous subcutaneous veins course along the shaft of the penis
to form the superficial dorsal vein and a deep dorsal venous system, which in turn drain into the saphenous vein and retropubic
venous plexus, respectively
13
(Fig. 28-4; also see Fig. 28-2).
Nervous System
Penile innervation occurs via both autonomic (parasympathetic and sympathetic) and somatic (motor and sensory)
pathways. Erection and detumescence are largely regulated
via the autonomic system. Sympathetic and parasympathetic
nerves coalesce to form the cavernous nerve, which penetrates
the corpora cavernosa to exert its effect on erection (
Sensation and contraction of penile musculature occurs via the
somatic nerves.
Erect State
Fig. 28-5) .
Tunica
albuginea
A
FIGURE 282 Penile erection. A, When flaccid, the corpora cavernosa, including arterioles, sinusoids, and arteries, are contracted. This allows free flow of blood
through intervening sinusoidal spaces. Blood exits the corpora cavernosa via emissary veins. B, During erection, arterioles, sinusoids, and arteries relax. This constricts
venules and veins and effectively compresses emissary veins under the tunica albuginea. Vascular inflow exceeds outflow, effectively creating an erection.
Subtunical
venous plexus
B
Expanded
sinuses
Compressed
subtunical
venous plexus
nosal a.
Circumflex a.
Internal iliac v.
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Cavernosal a.
Dorsal a.
FIGURE 283 Penile arterial supply.
Int. Pudendal a.
Bulbar a.
Circumflex caver
AUTONOMIC PATHWAYS
Between the T11 and L2 spinal segments, the sympathetic trunk
begins. These fibers then form the sympathetic chain ganglia, which
continue caudally to the inferior mesenteric and superior hypogastric plexi. Further sympathetic fibers exit to form the hypogastric
nerves, and ultimately the sympathetic portions of the pelvic plexus.
14
Between the S2-S4 spinal cord segments, the parasympathetic
pathway originates. These fibers also continue caudally to the
pelvic plexus (see
Fig. 28-5), where they join the aforementioned
sympathetic nerves. Together, these nerves then join to form a network of nervous tissue that passes along the lateral and posterior
aspect of the prostate to create the cavernous nerves.
15
Stimulation
of the sympathetic trunk via the cavernous nerves results in detumescence. Excitation of the parasympathetic aspects of the pelvic
plexus and cavernous nerves is responsible for erection. To avoid
iatrogenic ED, clear understanding of the location of these nerves
is critical during pelvic surgery such as radical prostatectomy or
abdominal perineal resection.
SOMATIC PATHWAYS
Sensory receptors in the penile skin and glans are unique in the
human body.
16
They are composed of free nerve endings comprising unmyelinated C fibers and thin myelinated A-delta fibers. These
coalesce into the dorsal nerve of the penis, which ultimately forms
the pudendal nerve. The pudendal nerve then enters the S2-S4
nerve roots at the spinal cord. Via spinothalamic and spinoreticular pathways, sensations such as touch, pain, and temperature are
Extenal
iliac v.
Internal
pudendal v.
Periprostatic
plexus
Saphenous v.
Superficial
dorsal v.
Deep
dorsal v.
Bulborethral v.
FIGURE 284 Penile venous drainage.
perceived.
17
Interestingly, research by Burnett et al.18 suggests that the
Circumflex v.
Subtunical plexus
Emissary v.
Crural v.
Cavernous v.
dorsal nerve of the penis carries both autonomic and somatic signals,
and therefore contributes to penile sensation, erection, and ejaculation.
Pathophysiology of Erectile Dysfunction
Vasculogenic Erectile Dysfunction
As noted in Box 28-1, ED often represents a multifactorial disease state. Although the focus of this chapter is on the vasculogenic determinants of ED, it is worth noting that within an
343
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28
VASCULOGENIC ERECTILE DYSFUNCTION
Dorsal nerve
Cavernous nerves
FIGURE 285 Penile nerves.
Pelvic plexus
Pudendal nerve
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