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50
Fig. 13.2 Mass of lymph node in preaortic area
13 Abdominal Aortic Aneurysm inaPatient withChronic Lymphocytic Leukemia
Fig. 13.4 Showing right external iliac artery occlusion
and 70% stenosis of left external iliac artery
Fig. 13.3 Showing AAA
165,000. Left ventricular ejection fraction was
65% with no valve abnormalities in the aortic or
mitral valve on 2D echocardiogram.
Procedure
Under general anesthesia, using a midline transabdominal incision, patient underwent open
aneurysm repair (OAR) in March 2014. Patient
was found to have large periaortic lymph nodes
which measured 5.7 × 3.6 × 3.5cm (Figs. 13.4
and 13.5). Proximal aortic clamp was applied
after mobilizing and dissecting the periaortic
lymph nodes with harmonic scalpel. Accessory
left renal artery was preserved and controlled
with a silastic loop. Aorto-bifemoral graft reconstruction with 18 × 9 mm knitted Dacron graft
was performed as patient had severe bilateral
Fig. 13.5 Operative picture of AAA and preaortic mass
iliac and femoral artery occlusive disease. Patient
was discharged on sixth postoperative day.
However, patient was readmitted 1 week after
discharge with left groin surgical site infection
with skin edge necrosis and serous drainage
(lymphocutaneous stula) which resolved with
local wound care, debridement, and antibiotics
Zyvox and Ceftin (Figs. 13.6 and 13.7).
Pathological report of the lymph nodes showed
ndings suggestive of chronic lymphocytic leukemia. Patient was seen in March 2019in satisfactory condition with stable CLL with normal
ankle brachial indices (Fig.13.8).
Discussion
In patients with chronic lymphocytic leukemia,
unusual manifestations occur in about 12%.
Median survival of patients with chronic lympho-
Discussion
Fig. 13.6 Specimen of preaortic lymph nodes
51
Fig. 13.7 Showing lymphocutaneous stula
cytic leukemia with enlarged lymph nodes is
8–10years. It is much reduced if there is associated anemia or thrombocytopenia. In this group of
patients, aortic wall infection is possible [1].
Induced thrombosis of inoperable abdominal aortic aneurysm with axillofemoral grafting was
described in 1978 by Berguer etal. [2]. If patient
does not have an associated iliac artery occlusive
disease, endovascular repair should be considered
in patients with periaortic mass with AAA.
Fig. 13.8 Subsequent healing of the groin
Groin lymphatic complications remain trou-
blesome in an aortofemoral bypass graft and less
commonly with infrainguinal bypass. The risk of
wound infection and subsequent graft infection
in a synthetic vascular conduit is of paramount
concern. The cause of lymphocutaneous stula
and lymphocele is often due to lymphatic disruption during groin dissection. Lymphocutaneous
stulas are diagnosed early, whereas lymphoceles are recognized later. Many surgeons advise
conservative treatment with limb elevation, local
wound care, pressure dressing, and prophylactic
antibiotics. Tyndall et al. and Kwaan et al.
described improved outcome with early reoperation in the form of closure of lymph leak subcutaneous tissues with absorbable sutures and
pressure dressing [3, 4].
Stadelman and Tobin treated 19 lymphoceles
by intraoperative exposure of the previous groin
incision and intradermal injection of the Isosulfan
blue dye (lymphazurin 1%, Ben Venue Labs Inc.
Bedford, Ohio) into distal extremity just above
the ankle [5]. The leg was massaged and elevated
to speed the migration of the dye. After about
15minutes, the blue dye can be seen emerging
52
13 Abdominal Aortic Aneurysm inaPatient withChronic Lymphocytic Leukemia
from the damaged lymphatic channel. These
lymphatic channels were directly ligated with
monolament absorbable suture with hemostatic
metal clips. Multiple layers of absorbable monolament sutures are used to obliterate lymphocele sac. In some instances, muscle ap or
adipofascial ap may be necessary if the dead
space cannot be completely obliterated.
Invited Commentary fromDipankar
Mukherjee, MD
Dr. Hans has reported and illustrated open repair
of a patient with an AAA with CLL.
This patient had extensive calcication and
occlusive disease in the access vessels making
endovascular repair options a difcult choice.
An aorto-bifemoral repair was done complicated by left groin wound infection and lymphocutaneous stula. Patient had a satisfactory
outcome with secondary healing of the groin
wound.
It is clear from the description of the open
repair that the operator is a skillful surgeon who
achieved a satisfactory result despite the many
challenges inherent in this case.
The problem of wound infection and possibly
late appearance of graft infection as a result of
potential immune compromise would be a serious concern with regard to the long-term outcome of this patient.
Could there have been an alternative less invasive treatment paradigm to manage this complex
problem? Aorto-uni-iliac endovascular repair
with left common femoral endarterectomy with
patch angioplasty followed by meticulous multilayered closure of the groin wound or even a
muscle ap may have averted the complication
that occurred.
Serial dilation of the left iliac access vessels or
even currently available shock wave technology
to overcome the calcium burden in these vessels
may have been an option. The chronically
occluded right iliac vessels may or may not need
to be addressed unless she was symptomatic from
the occlusion.
In the era of dwindling experience with open
repair of complex aneurysms of the abdominal
aorta, the young vascular surgeon would benet
from the details of open repair as described by
Dr. Hans.
References
1. Schwartz JA, Johnson G.Chronic lymphocytic leuke-
mia complicating abdominal aortic aneurysmectomy.
J Vasc Surg. 1986;3(1):159–61.
2. Berguer R, Schneider J, Wilner HL.Induced thrombo-
sis of inoperable abdominal aortic aneurysm. Surgery.
1978;84(3):425–9.
3. Tyndall SH, Shepard AD, Wilczewstai J, Reddy
DJ, Elliott JP, Ernst CB. Groin lymphocytic com-
plications after arterial reconstruction. J Vasc Surg.
1994;19:808–64.
4. Kwaan JHM, Berstein JM, Connothy JE.Management
of lymph stula in the groin after arterial reconstruc-
tion. Arch Surg. 1979;114:1416–8.
5. Stadelmann WK, Tobin GP.Successful treatment of
19 consecutive groin lymphoceles with the assistance
of intraoperative lymphatic mapping. Plast Reconstr
Surg. 2002;109:1274–88.
Inammatory Abdominal Aortic
Aneurysm Presenting
withTesticular Pain
Physical Examination
A 56-year-old male presented to his primary physician with testicular pain and underwent ultrasound evaluation of the abdomen which revealed
6.0 cm transverse diameter abdominal aortic
aneurysm. CTA abdomen and pelvis conrmed
6.0cm abdominal aortic aneurysm, 2.7cm right
common iliac aneurysm, and 2.9cm left common
iliac aneurysm (Figs.14.1 and 14.2). Patient had
undergone left carotid endarterectomy in March
2014. Medical comorbidities included hypertension, nicotine abuse, hyperlipidemia, and history
14
Fig. 14.2 3D reconstruction of AAA
of epiglottic mass. CT scan showed that the perianeurysmal tissue was thickened, and changes
Fig. 14.1 Shows AAA with thickened wall
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_14
were suggestive of inammatory type of AAA.
53
54
14 Inammatory Abdominal Aortic Aneurysm Presenting withTesticular Pain
After medical evaluation, patient was taken to the
operating room.
Procedure
In April 2004 endotracheal intubation was difcult due to the presence of epiglottic mass.
Aneurysm was found to be inammatory in type;
therefore, no attempt was made to separate the
third and fourth portion of the duodenum from
the aneurysmal wall. Bookwalter retractor was
applied, left renal vein was mobilized, and a
silastic vessel loop was passed around the left
renal vein. Bilateral external iliac arteries on
CTA and on evaluation in the operating room
were small (less than 6 mm) in diameter. After
ligating common iliac arteries, above their bifurcation, an aorto-bifemoral reconstruction was
performed. Inferior mesenteric artery was small
in caliber and was ligated. Patient had a follow up CT scan of the abdomen 6months later with
some residual inammatory changes in the wall
of the aneurysmal sac (Fig.14.3). An 18 × 9mm
Dacron graft reconstruction was performed.
Patient was seen in July 2019 in satisfactory
condition.
Discussion
Patients with inammatory abdominal aortic
aneurysm usually present with symptoms of
abdominal and back pain and weight loss and on
CT scan show inammatory changes in its wall.
In most patients the inammation subsides proximal to iliac bifurcation; therefore, a bilateral distal iliac anastomosis can be performed. However,
in this patient the iliac arteries were small in caliber; therefore, aorto-bifemoral reconstruction
was performed. Patient subsequently developed
recurrent left carotid stenosis and underwent
interposition grafting. Patient is doing well
15 years following abdominal aortic aneurysm
repair, and a recent CT scan of the abdomen
shows that the inammatory changes have completely resolved.
Fig. 14.3 Partial resolution of inammatory changes in the aortic wall following open repair
Abdominal Aortic Aneurysm
Repair inaPatient withFactor VII
Deciency
15
Physical Examination
A 72-year-old male was scheduled for open
repair of AAA in 1995. His abdominal aortic
aneurysm measured 6.0cm transverse diameter.
On pre-surgical screening, patient was found to
have a prolonged prothrombin time with a normal PTT and a hematology consultation revealed
factor VII deciency.
Procedure
Patient was treated with Proplex-T 1hour before
the operation and underwent open AAA repair
with aortoiliac graft placement via midline transperitoneal approach.
Discussion
Currently recombinant factor VII A is being
used increasingly to treat factor VII deciency,
hemophilia A and B, intracranial bleeding,
trauma and in patients undergoing cardiac surgery, prostatectomy, and liver transplantation.
The clot- promoting activity of RF VII A is primarily mediated through the tissue factor pathway, although direct activation of primary
hemostasis may also occur. Fresh frozen plasma
is usually not helpful in managing patients
undergoing surgery with factor VII deciency,
as was the case in this patient [1, 2]. Konyne
(factor IX complex) can also be used to treat
bleeding in patients with factor VII deciency.
The main aim of the treatment is to achieve an
increase of 15–25% from normal activity of factor VII.Factor IX concentrates also contain factor VII. NovoSeven RT (coagulation factor VII
A – recombinant) is highly effective (93%) in
stopping nonsurgical and surgical hemorrhage
in patients with factor VII deciency [3–7].
However, NovoSeven is an expensive recombinant protein with a price of $1540/mg.
Goodnough et al. recommended the following
treatment plan: (1) initial treatment with 2μg/kg
of recombinant factor VII A every 6hours for
24 hours, and (2) subsequent tapering of the
dose of recombinant factor VII A and its substitution with fresh frozen plasma. Normalization
of the PT or INR should not be the end point of
treatment [3–7]. The patient was lost to follow
up in 2006 after he had undergone repair of midline incisional hernia, 6 years following open
AAA repair.
Henriksen et al. hypothesized that occurrence of hernia is due to altered connective tissue mechanisms in patients with abdominal
aortic aneurysm [8]. Although radiographically
demonstrated incisional hernia is common following open AAA repair, clinically evident
hernias are much less frequently encountered.
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_15
55
56
15 Abdominal Aortic Aneurysm Repair inaPatient withFactor VII Deciency
Henriksen etal. from Danish Vascular Registry
reported 10.4% cumulative incidence of hernia
repair after 6years of follow-up. High body mass
index and abdominal aortic aneurysm repair were
two main risk factors for incisional hernia repair
in patients undergoing open aortic reconstruction
[8]. Incisional hernia is less common after aortobifemoral grafting for occlusive disease.
References
1. Greene WB, McMullan CW. Surgery for scoliosis
in congenital factor VII deciency. Am J Dis Child.
1982;136:411–3.
2. Yorke AJ, Matt MJ. Factor VII deciency and sur-
gery: Is preoperative replacement therapy necessary?
JAMA. 1977;238:424–5.
3. Arroyo A, Porto J, Gesto R.Congenital factor VII de-
ciency in a patient with abdominal aortic aneurysm. J
Vasc Surg. 1996;24:288–90.
4. Minno D, Napoletano M, Dolce A, Mariani G, STER
Study Group. Role of clinical and laboratory parameters for treatment choice in patients with inherited
factor VII deciency undergoing surgical procedures.
Evidence from the STER registry. Br J Haematol.
2018;180:563–70.
5. Rosental C, Volk T, Spies C, Zeimer S.Successful coronary artery bypass graft surgery in severe congenital
factor VII deciency. Perioperative treatment with factor VII concentrate. Thromb Haemost. 2007;98:900–2.
6. Gopalan PK, Clohisy JC, Casher AF, Eby CS. Use
of recombinant factor VIIA for surgery in a patient
with factor VII deciency. J Bone Joint Surg Am.
2007;89(2):389–91.
7. Goodnough LT, Lublin DM, Zhang L, Despotus G,
Eby CS. Transfusion medicine service policies for
recombinant factor VII administration. Transfusion.
2004 Sep;44(9):1325–31.
8. Henriksen NA, Helgstraud F, Vogt KC, Jorgensen LN,
Bigard T.Risk factors for incisional hernia repair after
aortic reconstructive surgery in a nationwide study. J
Vasc Surg. 2013;52:1526–30.
Part II
Open Repair of Ruptured Abdominal
Aortic Aneurysm
Open Repair ofRuptured
Abdominal Aortic Aneurysm
Complicated by Pancreatitis
andDuodenal Obstruction
History
A 56-year-old male was admitted to the hospital
on February 4, 1985, because of acute severe low
back and left ank pain. Prior medical history
included noninsulin-dependent diabetes mellitus
and cholecystectomy with history of pancreatitis
with calcication.
Procedure
16
He underwent emergent repair of a ruptured
abdominal aortic aneurysm with placement of a
20 × 10mm woven aorto-right common iliac and
left aortofemoral bypass graft. Six units of packed
red blood cells and ten liters of crystalloids were
administered during the open aneurysm repair. A
preoperative X-ray of the abdomen revealed retroperitoneal hematoma and calcication of the
pancreas.
Postoperatively, the patient had a large volume of bilious gastric output, averaging two liters
a day. A long tube (cantor) was inserted on March
9, 1985, and an upper gastrointestinal barium
series revealed duodenal obstruction at the junction of the second and third portions of the duodenum (Fig.16.1). The cantor tube could not be
advanced further into the small intestine. CT scan
of the abdomen showed enlarged head and body
of the pancreas, consistent with pancreatitis
(Fig.16.2). Serum amylase levels were elevated
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_16
Fig. 16.1 Upper GI study showing duodenal obstruction
at the junction of second and third portion of the duodenum
at 153 Somogyi units and serum lipase was 32
(normal 2-24 IU). Patient was re-explored
10 days after the initial operation as duodenal
obstruction did not improve with nasogastric suction and total parenteral nutrition. Patient was
found to have an enlarged body of the pancreas
59
60
Fig. 16.2 CT scan showing enlarged head of the
pancreas
16 Open Repair ofRuptured Abdominal Aortic Aneurysm Complicated by Pancreatitis andDuodenal…
with fat necrosis. Massive adhesions were found
between the loops of the small intestine.
Serosal tear of the duodenum developed during lysis of the adhesions; a jejunal patch was
applied, and a Baker tube was inserted through
the nose, beyond the duodenojejunal exure,
into the small intestine. Total parenteral nutrition
was continued. Patient developed pulmonary
emboli and was treated with anticoagulation. He
was discharged on April 23, 1985, in satisfactory
condition. Patient died in 1994 from intracerebral hemorrhage.
creatitis. A retrospective autopsy study demonstrated that in 95 patients after open abdominal
aortic aneurysm repair, the incidence of pancreatitis was higher in the ruptured group. Warshaw and
O’Hara reported a 12% incidence of acute pancreatitis following repair of intact abdominal aortic
aneurysm and 29% following repair of ruptured
abdominal aortic aneurysm [2]. Typical symptoms of acute pancreatitis like abdominal pain and
tenderness are either absent or masked by postoperative course. The incidence of pancreatitis following repair of ruptured aneurysm is difcult to
measure as many patients die from cardiac or
renal complications before manifestation of pancreatitis become apparent.
Duodenal obstruction occurs from mass effect
due to signicant enlargement of the pancreas [3,
4]. Hematoma in the paraduodenal area may also
be responsible for duodenal obstruction as well as
brinous adhesions between the jejunal loops and
duodenum. Any patient with prolonged ileus
should have serum lipase and amylase level evaluated following open AAA repair, and most patients
can be managed by nasogastric suction, management of electrolytes, and hydration. Total parenteral nutrition is necessary if patient is kept NPO
for more than a few days. Re-exploration should be
reserved for patients with persistent obstruction or
if peritoneal signs develop. Postoperative CT scan
should be obtained in a patient if persistent ileus
does not resolve following open AAA repair.
Discussion
Pancreatitis following repair of ruptured abdominal aortic aneurysm (AAA) was rst reported by
Castleman and McNeely in 1967. The same
authors reported a patient who died following
repair of ruptured aneurysm with autopsy revealing destruction of the pancreas [1]. They hypothesized embolization of the atheromatous debris
into the arteries of the pancreas, leading to pan-
References
1. Castleman B, McNeely BU. Case records of
Massachusetts General Hospital. N Engl J Med.
1972;286:442–28.
2. Warshaw A, O’Hara PJ. Susceptibility of pan-
creas to ischemic injury in shock. Ann Surg.
1978;188:197–201.
3. Aldridge MC, Eastcott HG.Prolonged gastroduodenal
ileus complicating aneurysm surgery. J R Coll Surg
Edinb. 1984;29:310–2.
4. Hans SS. Pancreatitis and duodenal obstruction fol-
lowing aortic surgery. Am Surg. 1989;55(3):177–9.