The Role of Bypass Surgery in Diabetic Limb Ischemia
Prof Dr Hendro Sudjono Yuwono
Pajajaran University, Bandung, Indonesia
Presented :The 7thAsia-Pacific Congress of Diabetic Limb. Holliday Inn hotel,
Bandung, December 17, 2011
Diabetes mellitus is one of the frequent causes of chronic obstructed arterial disease. It
is characterized by several diseases in which chronic high blood glucose levels damage
all organs particularly the nerves, kidneys, eyes, and blood vessels.1,2,3Foot ulcerations
frequently develop in people with diabetes and may become complicated by sepsis and
seriously life-threatening.1,2 Diabetic foot problems accounts for more time spent by
diabetics in hospitals than for all other aspects of their disease combined. Diabetes
tends to affect all size arteries by causing progressive sclerosing (calcification) of the
vessel wall together with high blood lipid content known as atherosclerosis. 2The
circulatory insufficiency that occur decrease blood flow supply to the affected lower
extremity, causing damage of the distal limb tissues. Then the damage-tissue later leads
to skin ulceration, infection, necrosis, sepsis and gangrene.
Among people with diabetes, about 15% have type 1 (formerly known as
insulin-dependent diabetes), while about 85% have type 2 (formerly known as
non-insulin-dependent diabetes).
In type 1 diabetes, the major risk is microvascular complications, although
macrovascular complications are also increased. The primary risk factor is
hyperglycaemia, although other risk factors, such as hypertension and dyslipidaemia,
may occur secondary to uncontrolled hyperglycaemia or renal disease.1,2,3.
Complications are therefore usually acquired after diagnosis.
associated with other risk factors from early in the disease process, including abdominal
obesity, hypertension, dyslipidaemia, a prothrombotic state and insulin resistance.
Although macrovascular disease is the major cause of morbidity and mortality in type
2 diabetes, microvascular complications are often present when diabetes is diagnosed,
even in people with no symptoms.3 Prevalences at diagnosis are: retinopathy, about
20%; neuropathy, 9%; and overt diabetic nephropathy, up to 10%. Type 2 diabetes
increases the risk of coronary heart disease two- to fourfold and abolishes the
protectiveness of female sex observed in the non-diabetic population.4The presence of
diabetes also worsens the prognosis of coronary heart disease.4,5
The major mechanism of microvascular disease is the toxic effect of prolonged
hyperglycaemia, with hypertension a further exacerbating factor. Microvascular
complications seldom occur in isolation. Screening for microvascular disease enables
intervention at the earliest possible stage, maximising the effectiveness of treatment.
Data from trials over the past 10 years show that controlling hyperglycaemia and
hypertension reduces microvascular complications in both type 1 and type 2 diabetes.5-9
Large-vessel disease (macrovascular complications), including coronary heart disease
and stroke, is the greatest overall cause of morbidity and mortality in diabetes.
Preventing these complications in type 2 diabetes, which is often associated with other
cardiovascular risk factors, is a major challenge.3,4,5
Pathogenesis of hyperglycaemia promotes the reaction of glucose with components of
the arterial wall to form advanced glycation products. These products cross-link with
collagen, thereby increasing arterial stiffness. In dyslipidaemia, increased levels of
low-density lipoprotein (LDL) cholesterol, consisting mostly of small dense particles,
promote atherogenesis. Hypertension promotes the development and progression of
vascular disease.5,6
Finding strategies to reduce the development of macrovascular complications has been
challenging. The United Kingdom Prospective Diabetes Study (UKPDS), to date the
largest and longest prospective randomised trial in people with type 2 diabetes, showed
significantly, although it did reduce microvascular complications. However, the same
trial showed that treating hypertension did reduce macrovascular complications.
Since the UKPDS, the approach has broadened, with other trials confirming the benefit
of treating hypertension and showing significant benefits from treating dyslipidaemia.9
In major trials of lipid-lowering therapy, diabetic subgroups appeared to benefit more
than those without diabetes.9The recent publication of a trial of a multifactorial
approach to prevent cardiovascular disease in people with type 2 diabetes suggests that
the greatest benefits are seen when glucose, blood pressure and lipid levels are targeted
simultaneously.3
Control of hyperglycaemia:
The Diabetes Control and Complications Trial25 and the UKPDS5 established the
importance of intensive blood-glucose control in reducing the risk of microvascular
complications (target HbA1c level ≤ 7%). For both diabetic retinopathy and nephropathy, the benefit of good glycaemic control appears to be greatest in the early
stages. It has not been so clearly demonstrated that glycaemic control delays the
progression of overt nephropathy, and intensified glucose control may temporarily
exacerbate proliferative retinopathy.
The role of bypass surgery:
In advanced-diabetics, that is difficult to insert into the lumen of limb-arteries using
endovascular catheter or endovascular technique is not available, open bypass surgery
may be necessary.1,2,3A bypass graft is indicated in such serious critically ischemic limb.
This open surgical procedure uses either own vein/artery or PTFE-graft or the patients
own arteries or veins to improve blood flow to the affected distal limb tissue. In many
patients with critical limb ischemia, the ipsilateral greater saphenous vein is not
available for use as a conduit due to prior harvest or vein stripping.4 If the contralateral
greater saphenous vein is not available, then secondary sources of autogenous vein such
as the lesser saphenous vein or arm veins should be preoperatively mapped by duplex
scanning and utilized.1,2,3,4
In infragenicular bypass surgery, a pronounced difference is seen in the long-term
should be used, whether in situor reversed. Only a venous diameter less than 3–4mm
justifies a prosthetic reconstruction. The outcome of femorocrural bypasses is strongly
influenced by the number of calf vessels and their continuation to ankle and pedal level.
During the first year after infrainguinal revascularization, 50% of the reconstructions
will be at risk owing to stenosis. Intensive surveillance with noninvasive duplex
monitoring is required to detect these stenoses, most of which occur before they are
clinically obvious. The majority of short segment stenoses are localized and can be
treated successfully by means of minimally invasive endovascular techniques.3
Considering this, it is obvious that the treatment of chronic lower limb ischemia would
benefit from a multidisciplinary approach from both the vascular surgeon and the
interventional (endovascular) radiologist.1-5Both specialisms have to be involved in the
follow-up after infrainguinal revascularization.
Patients with diabetes presenting with limb ischemia should be treated as having very
high mortality risk and require intense treatment of cardiovascular risk factors at the
earliest possible stage applying any practicing-technique available.5
Incidence of major amputation or death was higher (57% increase; others resulted 55%
overall amputation-free survivalat 3 years, and 55% at 3 years) in patients with diabetes
after limb bypass surgery than in patients without, and diabetic patients had a shorter
amputation-free survival period after limb bypass surgery than individuals without.5,6,7
When PTAs (percutaneous transluminal angioplasty) are performed below the inguinal
ligament, the results are markedly worse. One-year patency rates of PTA in this group of
patients with threatened limbs are inferior to the patency rates of arterial bypass grafts,
even when these bypasses are performed with a prosthetic material. PTA should not be
considered as a primary treatment modality for patients with infrainguinal arterial
occlusive disease who also have limb-threatening ischemia, except in unusual
circumstances. 8-10 Pedal bypass can safely and effectively relieve critical ischemia in
diabetic patients.9 ,10
Conclusion, in diabetics open bypass surgery is the most important modality to prevent
limb loss.
1.Hughes K, Campbell D, Pomposelli Jr FB. Lower Extremity Arterial Reconstruction in
Patients with Diabetes Mellitus. Principles of Treatment. In:Veves A, Giurini JM, LoGerfo
FW. The Diabetic Foot.2nded. New Jersey:Humana Press2006.p.477
2.Sidawy AN. Diabetic foot. Lower extremity arterial disease and limb salvage.
Philadelphia :Lippincott Willliams&Wilkins.2006.p.473-88
3. de Vries JPPM, Moll FL, van den Berg JC. Surgical and endovascular treatment of
chronic ischemia of the lower limbs. In:White AW, Hollier LH. Vascular Surgery. Basic
science and clinical correlations. 2nd ed.Massachusetts: Blackwell Publishing.
2005.p.533-40
4.Sarkar R, Davies AH. Lower Limb Ischemia. In:Davies AH, Brophy CM. Vascular Surgery.
London:Springer-Verlag.2006.p.90-8
5.Malmstedt J, Leander K, Wahlberg E, Karlstrom L, Alfredsson L, Swedenborg J.
Outcome after leg bypass Surgery for Critical Limb Ischemia Is Poor in Patients With
Diabetes. A population-based cohort study. Diabetes Care.2008; 31:887-92
6.Adam DJ, Beard JD, Cleveland T, Bell J, Bradbury AW, Forbes JF, Fowkes FG, Gillepsie I,
Ruckley CV, Raab G, Storkey H: Bypass versus angioplasty in severe ischaemia of the leg
(BASIL): multicentre, randomised controlled trial. Lancet 2005; 366:1925–34
7.Feinglass J, Pearce WH, Martin GJ, Gibbs J, Cowper D, Sorensen M, Khuri S, Daley J,
Henderson WG: Postoperative and amputation-free survival outcomes after
femorodistal bypass grafting surgery: findings from the Department of Veterans Affairs
National Surgical Quality Improvement Program. J Vasc Surg 2001; 34:283–90
8. Parsons RE, Suggs WD, Lee JJ, Sanchez LA, Lyon RT, Veith FJ. J Vasc Surg
1998;28:1066-71
9. Panneton JM, Gloviczki P, Bower TC, Rhodes JM, Canton L, Toomey B. Ann Vasc Surg
2000;14(6):640-7
10. Bate KL, Jerums G. MJA 2003; 179 (9): 498-503
