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Blast Injury to the Lower Limb 123
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Since then a number of clinical and laboratory investigations have confirmed that
ligation of major veins in conjunction with repair of a traumatically injured arterial
system leads to significantly poorer clinical outcomes, such as decreased function or
even limb loss [17, 18]. Where possible vein repair should be attempted, particularly
in the presence of significant lower limb arterial injury, in an attempt to reduce
venous hypertension and associated morbidity. While there are few data regarding
the long-term outcome of venous repairs, it is the authors’ impression that maintaining venous patency, in the initial few days after injury, can significantly help
reduce acute post-injury swelling. If the superficial femoral vein requires ligation, it
is important to maintain patency of the ipsilateral long saphenous and profunda
femoris veins. Complex vein repair should never be attempted in unstable patients
who have sustained major blood loss and have significant problems with hypothermia and coagulopathy. In more stable patients, however, temporary intraluminal
venous shunting can facilitate the construction of larger calibre panel grafts
obtained from the contralateral long saphenous vein. [Q7: D, E]
Postoperative management of patients with complex limb injuries is critically
important. The majority of these patients have been transferred immediately to the
operating theatre and it is important that a thorough search for occult injuries is performed on admission to the intensive care unit. These patients are at risk of developing multiple organ dysfunction syndrome as a result of their large transfusion
requirements and likely reperfusion injury sustained [19, 20]. It is important that the
vascular surgeon communicates clearly with the staff in the intensive care unit
regarding the presence or absence of distal pulses, to ensure that vascular repair
remains patent. Young trauma patients with normal blood pressure and temperature
should have a palpable distal pulse. If there is any doubt regarding the integrity of the
vascular repair, the dressings should be removed and a careful assessment performed
by a vascular surgeon using handheld Doppler and/or portable ultrasound device.
Wounds should be reinspected 24–48 hours after initial surgery and at that stage
definitive plastic surgery may be required to obtain soft tissue and skin cover.
[Q8: D] Some centres advocate a selective policy with regard to fasciotomy based on
compartmental pressures, while many continue to advocate a more liberal policy
based on clinical grounds. Prolonged ischaemia time, combined arteriovenous
injuries, complex injuries including bone and soft tissue destruction and crush
injuries remain absolute indications for fasciotomy. The avoidance of compartment
syndrome and restoration of limb function far outweigh the low morbidity associated with liberal use of fasciotomy. These patients are at significant risk of wound
and other nosocomial infections and prolonged antibiotic use may be required.
The management of patients with complex injuries can be difficult; however, timely
surgery and the involvement of a multidisciplinary team can produce rewarding
results. One possible criticism of the above care could be failure to use the great toe,
from the amputated left lower limb, to replace the patient’s right thumb.
References
1. Itani KM, Burch JM, Spjut-Patrinely V, Richardson R, Martin RR, Mattox KL. Emergency center arteriography. J Trauma 1992;32(3):302–6; discussion 306–7.
2. Barros D’Sa AA. How do we manage acute limb ischaemia due to trauma? In: Greenhalgh RM,
Jamieson CW, Nicolaides AN, editors. Limb salvage and amputation for vascular disease. London:
WB Saunders, 1998.
124 Vascular Surgery
3. D’Sa AA. A decade of missile-induced vascular trauma. Ann R Coll Surg Engl 1982;64(1):37–44.
4. Elliot J, Templeton J, Barros D’Sa AA. Combined bony and vascular trauma: a new approach to treatment. J Bone Joint Surg Am 1984;66B:281.
5. Barros D’Sa AA. The rationale for arterial and venous shunting in the management of limb vascular
injuries. Eur J Vasc Surg 1989;3(6):471–4.
6. Barros D’Sa AA, Moorehead RJ. Combined arterial and venous intraluminal shunting in major
trauma of the lower limb. Eur J Vasc Surg 1989;3(6):577–81.
7. Harkin DW, D’Sa AA, Yassin MM, Young IS, McEneny J, McMaster D, et al. Reperfusion injury is
greater with delayed restoration of venous outflow in concurrent arterial and venous limb injury. Br
J Surg 2000;87(6):734–41.
8. Lovric Z, Lehner V, Kosic-Lovric L, Wertheimer B. Reconstruction of major arteries of lower extremities after war injuries. Long-term follow up. J Cardiovasc Surg (Torino) 1996;37(3):223–7.
9. Howe HR, Jr, Poole GV, Jr, Hansen KJ, Clark T, Plonk GW, Koman LA, et al. Salvage of lower
extremities following combined orthopedic and vascular trauma. A predictive salvage index. Am
Surg 1987;53(4):205–8.
10. Johansen K, Daines M, Howey T, Helfet D, Hansen ST, Jr. Objective criteria accurately predict amputation following lower extremity trauma. J Trauma 1990;30(5):568–72; discussion 572–3.
11. Helfet DL, Howey T, Sanders R, Johansen K. Limb salvage versus amputation. Preliminary results of
the Mangled Extremity Severity Score. Clin Orthop Relat Res 1990(256):80–6.
12. Russell WL, Sailors DM, Whittle TB, Fisher DF, Jr, Burns RP. Limb salvage versus traumatic amputation. A decision based on a seven-part predictive index. Ann Surg 1991;213(5):473–80; discussion
480–1.
13. McNamara MG, Heckman JD, Corley FG. Severe open fractures of the lower extremity: a retrospective evaluation of the Mangled Extremity Severity Score (MESS). J Orthop Trauma 1994;8(2):81–7.
14. Bonanni F, Rhodes M, Lucke JF. The futility of predictive scoring of mangled lower extremities. J
Trauma 1993;34(1):99–104.
15. Durham RM, Mistry BM, Mazuski JE, Shapiro M, Jacobs D. Outcome and utility of scoring systems
in the management of the mangled extremity. Am J Surg 1996;172(5):569–73; discussion 573–4.
16. Debakey ME, Simeone FA. Battle injuries of arteries in World War II: analysis of 2471 cases. Ann
Surg 1946;123:534–79.
17. Nanobashvili J, Kopadze T, Tvaladze M, Buachidze T, Nazvlishvili G. War injuries of major extremity arteries. World J Surg 2003;27(2):134–9.
18. Kuralay E, Demirkilic U, Ozal E, Oz BS, Cingoz F, Gunay C, et al. A quantitative approach to lower
extremity vein repair. J Vasc Surg 2002;36(6):1213–8.
19. Defraigne JO, Pincemail J. Local and systemic consequences of severe ischemia and reperfusion of
the skeletal muscle. Physiopathology and prevention. Acta Chir Belg 1998;98(4):176–86.
20. Foex BA. Systemic responses to trauma. Br Med Bull 1999;55(4):726–43.
13. Endoluminal Treatment of Traumatic
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Arteriovenous Fistula of the Axillary
Artery
Jonathan D. Woody and Rodney A. White
A 21-year-old male sustained a gunshot wound to the anterior right chest. The
entrance wound was at the midclavicular line. He was hemodynamically stable
upon arrival at the emergency department. He underwent initial resuscitation
with intravenous fluids. There was no evidence of hemothorax or pneumothorax
on chest X-ray. The right radial pulse was present but diminished when compared with the left. The patient had minor neurological symptoms in the right
upper extremity, which consisted mainly of weakness of the interosseous muscles
of the hand. An arteriogram was obtained, which revealed an arteriovenous
fistula (AVF) of the right axillary artery and vein (Fig. 13.1a). The patient
remained hemodynamically stable throughout the evaluation period.
Question 1
Acquired AVF is most commonly the result of:
A. Penetrating trauma.
B. Percutaneous puncture.
C. Erosion of arterial aneurysm.
D. Periarterial abscess.
E. Neoplasm.
Question 2
Which of the following are possible complications of AVF?
A. Bacterial endarteritis at the site of AVF.
B. Peripheral arterial insufficiency.
125
126 Vascular Surgery
a
(i)
(ii)
(iii)
Fig. 13.1. a Pre-treatment and b post-treatment images of an AVF of the right axillary artery after a gunshot
wound. i Arteriography, ii intravascular ultrasound, and iii duplex grey-scale ultrasound demonstrate the AVF
before treatment and the complete exclusion of the fistula after treatment. (Reprinted from J Vasc Surg, vol. 24,
White RA, Donayre CE, Walot I, et al., Preliminary clinical outcome and imaging criterion for endovascular prosthesis development in high-risk patients who have aortoiliac and traumatic arterial lesions, pages 569–571, ©
1996, with permission from The Society for Vascular Surgery.)
C. Venous congestion, venous valvular insufficiency, venous stasis, venous vari-
cosities and edema formation.
D. Tachycardia.
E. Cardiomegaly.
F. Congestive heart failure.
Endoluminal Treatment of Traumatic Arteriovenous Fistula of the Axillary Artery 127
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b
(i)
(ii)
(iii)
Fig. 13.1.
(continued)
Question 3
What is the gold standard for the diagnosis of AVF?
A. Magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA).
B. Computed tomography (CT).
C. Color-flow duplex ultrasound.
D. Arteriography.
128 Vascular Surgery
Treatment
The patient was transferred to the endovascular operating suite and placed under
general anesthesia. He was positioned on the interventional table with his right arm
on an arm board. A surface ultrasound was performed, which confirmed the location
of the AVF. The right arm and chest were prepared into a sterile field, and the
abdomen and upper legs were prepared into a separate sterile field. The right
brachial artery and vein were surgically exposed and isolated. A sheath was inserted
percutaneously into the right femoral artery. Under fluoroscopic guidance, a
guidewire was passed through the femoral sheath into the right axillary artery. It was
then passed across the injured segment of the right axillary artery and into the right
brachial artery to the surgical site. The wire was removed through a small transverse
arteriotomy, and a hemostatic sheath was inserted into the artery over the wire.
The length of the axillary artery was interrogated with intravascular ultrasound.
The diameter of the axillary artery was 7 mm. A 4-cm segment of deep brachial vein
was obtained and sutured to an appropriately sized Palmaz stent. This was crimped
onto an expandable balloon and, under fluoroscopic guidance, passed over the
guidewire to the site of injury. The balloon was expanded, and the endoluminal
device was deployed. The balloon was deflated and removed. The axillary artery was
again interrogated with intravascular ultrasound, which demonstrated excellent
apposition between the stent and the arterial wall. Complete exclusion of the fistula
was documented with both intravascular ultrasound and arteriography (Fig. 13.1b).
Flow was then restored to the arm. The arm wound was closed surgically, and pressure was applied to the femoral puncture site. Before awakening the patient, surface
ultrasound confirmed the closure of the fistula and normal flow through the axillary
artery.
Question 4
Which of the following is not considered to be one of the core principles of treatment of AVF?
A. Complete closure of the fistula.
B. Restoration of normal arterial flow.
C. Ligation of the arterial inflow
D. Restoration of normal venous flow.
Commentary
AVF is an abnormal communication between an artery and vein. By far the most
common cause of acquired AVF is trauma. This is usually the result of a penetrating
injury secondary to a knife or bullet, but it can also result from blunt trauma.
Iatrogenic injury from percutaneous puncture can also cause AVF. In addition, AVF
can be caused by erosion of an arterial aneurysm into an adjacent vein, by a periarterial abscess or by a neoplasm, although these are rare. [Q1: A]
Endoluminal Treatment of Traumatic Arteriovenous Fistula of the Axillary Artery 129
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Potential complications of AVF can be considered on both a peripheral and a systemic level. Peripheral effects may include peripheral arterial insufficiency, dilated
and thickened proximal arterial wall (predisposing to infection, i.e. bacterial endarteritis), venous congestion, venous valvular insufficiency, venous stasis, varicosities,
edema, and skin and soft tissue changes. Systemic effects may include increased
cardiac output, tachycardia, cardiomegaly, congestive heart failure, increased pulse
pressure, decreased diastolic pressure, increased blood volume, increased central
venous pressure, and increased stroke volume. [Q2: A, B, C, D, E, F]
The diagnosis of AVF is relatively straightforward. An audible bruit and palpable
thrill are often found, especially in peripheral lesions. The gold standard for diagnosis is arteriography. The most important point is to delineate clearly the anatomy of
the fistula so that treatment may be planned. Other diagnostic modalities include
color-flow duplex ultrasound, CT, and MRI and/or MRA. [Q3: D]
Treatment of AVF is best carried out early rather than late. The longer an AVF is
present, the more likely the patient will be to develop complications. Further, the
longer it exists, the more likely it is to develop significant collateral flow, which
increases the complexity of the repair. The principles of repair, whether conventional or endovascular, are the same: complete closure of the fistula and restoration
of normal arterial and venous flow. [Q4: C] Conventional repair can be undertaken in
a number of ways but will not be described here since conventional repair is not the
focus of this chapter.
The first report of successful endovascular repair of an arterial injury was by
Becker et al. [1]. Further reports by Parodi and Barone [2], Marin et al. [3] and May
et al. [4] have demonstrated a high rate of technical success with persistent fistula
closure, excellent long-term patency, and a low incidence of complications.
Endovascular treatment of AVF is ideal because most of these injuries are localized
to a small segment of artery with normal vessel wall on each end. Endovascular
treatment of these lesions also avoids the major morbidity of conventional open
repair, which can be significant. Endovascular access is achieved at a site remote
from the area of injury and can be performed percutaneously in many cases. There
is little damage to surrounding structures since only the affected vessel is manipulated. If endovascular treatment is successful, then the benefits for the patient
include a shorter hospitalization period and a quicker return to normal activity. The
only major concern is long-term patency and function of the endoluminal stent
graft, since these studies are not yet available. However, due to the relatively short
length of the stent graft, its placement in large-diameter vessels, and the high flow
rates in these vessels, it is reasonable to assume that the long-term patency would be
good [5]. It is of note that our patient was hemodynamically stable. Although
endovascular technology continues to evolve and improve, it must be emphasized
that a hemodynamically unstable patient who has sustained penetrating trauma
should undergo immediate open surgical exploration.
References
1. Becker GJ, Benenati JF, Zemel G, Sallee DS, Suarez CA, Roeren TK, Katzen BT. Percutaneous place-
ment of a balloon-expandable intraluminal graft for life-threatening subclavian arterial hemorrhage.
J Vasc Interv Radiol 1991;2:225–9.
2. Parodi JC, Barone HD. Transluminal treatment of abdominal aortic aneurysms and peripheral arteri-
ovenous fistulas. Paper presented at the 19th Annual Montefiore Medical Center/Albert Einstein
130 Vascular Surgery
College of Medicine Symposium on Current Critical Problems and New Technologies in Vascular
Surgery, New York, November 1992.
3. Marin ML, Veith FJ, Panetta TF, Cynamon J, Barone H, Schonholz C, Parodi JC. Percutaneous transfemoral insertion of a stented graft to repair a traumatic femoral arteriovenous fistula. J Vasc Surg
1993;18:299–302.
4. May J, White G, Waugh R, Yu W, Harris J. Transluminal placement of a prosthetic graft-stent device
for the treatment of a subclavian artery aneurysm. J Vasc Surg 1993;18:1056–9.
5. Donayre CE. Endovascular treatment of traumatic arteriovenous fistulas and pseudoaneurysms and of
arterial occlusive disease. In: White RA, Fogarty TJ, editors. Peripheral endovascular interventions,
2nd edn. New York: Springer, 1999;371–81.
14. Cardiovascular Risk Factors and
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Peripheral Arterial Disease
Stella S. Daskalopoulou and Dimitri P. Mikhailidis
A 62-year-old man with intermittent claudication was referred for vascular risk
factor modification. He had no history of myocardial infarction (MI) or stroke.
He was smoking 20 cigarettes/day. His family history was negative for premature
vascular events. He was not taking any medication. He was advised to start
aspirin 75 mg/day, but he stopped taking these tablets because of “stomach discomfort”. The patient’s total cholesterol was 228 mg/dl (5.9 mmol/l).
His blood pressure required treatment with amlodipine and a thiazide
diuretic. The patient eventually stopped smoking after referral to the smoking
cessation clinic in our hospital.
Question 1
Which of the following investigations would you order?
A. Fasting serum glucose.
B. Urine glucose to make a diagnosis of diabetes mellitus.
C. Fasting serum triglycerides.
D. Fasting serum high-density lipoprotein cholesterol (HDL-C).
E. Thyroid function tests.
A. Requesting a fasting serum glucose level is an essential test in all patients with
vascular disease. In this case the fasting glucose was 87 mg/dl (4.8 mmol/l); this is
satisfactory.
Interpretation of fasting glucose values:
There are three categories in which a patient can be placed relative to fasting serum
glucose levels:
• Normal: fasting glucose =110 mg/dl (=6.0 mmol/l).
133
134 Vascular Surgery
Table 14.1. Features of metabolic syndrome*. Updated
1.
Abdominal obesity (waist circumference):
Men >102 cm
Women >88 cm
2.
Triglycerides
=150 mg/dl (=1.7 mmol/l)
3.
High-density lipoprotein cholesterol (HDL-C):
Men <40 mg/dl (<1.0 mmol/l)
Women <50 mg/dl (<1.3 mmol/l)
4.
Blood pressure:
5.
Fasting glucose:
*According to the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III guidelines [1], any 3 or more
of these 5 features are diagnostic of the metabolic syndrome. Other factors that may coexist in these patients include a family
history of type 2 diabetes, South Asian ethnicity, decreased physical activity, smoking, elevated serum urate levels and
evidence of fatty liver (abnormal levels of aminotransferases, ALT/AST).
There is evidence (post-hoc analysis) from the Scandinavian Simvastatin Survival Study (4S) that IFG and diabetic patients
benefit from treatment with simvastatin [2]. More recently, a trial in type 2 diabetic patients without established vascular
disease showed a beneficial effect of atorvastatin 10 mg/day (vs. placebo) in reducing the risk of first cardiovascular events,
including stroke [3].
Both diabetes and metabolic syndrome are common in patients with peripheral arterial disease (PAD) [4]. Furthermore,
both diabetes and PAD are considered as coronary heart disease (CHD) equivalent and need to be treated aggressively [1].
<130/<85 mm Hg
=110 mg/dl (=6.0 mmol/l)
• Impaired fasting glucose (IFG): fasting glucose 110–125 mg/dl (6.0–6.9 mmol/l).
• Diabetes mellitus: fasting glucose =126 mg/dl (=7.0 mmol/l).
IFG is associated with an increased risk of vascular events and conversion to diabetes mellitus. Furthermore, a glucose level in the IFG range can be one of the features of the metabolic syndrome (also known as insulin resistance or Reaven’s
syndrome) [1] (Table 14.1).
B. This patient’s urine was tested when he was first seen in outpatients. The renal
threshold for glucose is a serum level of about 180–200 mg/dl (10–11 mmol/l).
Therefore, testing urine for glucose will not detect IFG or early/mild diabetes.
Clinicians must not rely on a urine glucose test to exclude IFG or early diabetes. In
view of the serum glucose value (see A, above), it is not surprising that the urine
glucose test was negative. However, testing the urine was an opportunity to exclude
proteinuria, another indicator of vascular risk.
C. The fasting triglyceride level in this patient was 141 mg/dl (1.6 mmol/l) – this is
satisfactory.
Interpretation of fasting triglyceride values:
There has been considerable confusion regarding the importance of triglycerides.
There are several reasons for this, including:
• Interactions with other lipid variables: serum triglyceride and HDL-C levels are
inversely related. HDL-C is a “protective” lipoprotein.
• Interactions with potential risk factors: elevated serum triglyceride levels are
associated with impaired fibrinolysis and possibly elevated plasma levels of
fibrinogen. Both type 2 diabetes and metabolic syndrome are associated with
raised serum triglyceride levels.
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