Here - EWMA 2013

◄ Transcutaneous oxygen pressure (tcpO2) below 30 mmHg has been considered to predict
that the infection will not resolve and the ulcer not heal. The accuracy of these
measurements in patients with critical leg ischemia has been questioned, especially in the
presence of tissue edema. Notwithstanding, tcpO2 may be a useful method to identify tissue
lesions that may heal with conservative treatment. Ulceration of the foot in diabetes will
generally heal if the tctcpO2 >50 mmHg.
Low levels of ABI, ankle pressure, toe pressure and tcPO2 suggest that diabetic ulcer may
not heal, but always in the consideration of limitations of each technique. Furthermore,
measurements of mere macrocirculation are not adequate for the assessment of perfusion
impairment in a diabetic foot. As a consequence, there is a need for investigational
techniques that not only look at the macrocirculation of the foot and the presence of an
occlusive disease but also evaluate the perfusion in an ischaemic foot. Unfortunately,
techniques such as laser doppler, skin perfusion pressure, spectral imaging, capillary microscopy
and indocyanine green imaging are not available for common clinical use. Importantly,
clinicians must recognise that a diagnosis of neuroischaemia is not only based on
the presence of obstructive arterial disease. Therefore, decreased perfusion or impaired
circulation needs to be introduced and recognised as an indicator for intervention in the
diabetic foot in order to achieve and maintain healing and to avoid or delay a future
amputation. Therefore, vascular imaging and subsequent revascularization should be
considered if no healing has occurred within six weeks of appropriate conservative treatment
irrespective of non-invasive vascular test results .
Patient characteristics, co-morbidities and life expectancy as well as extremity-related factors
such as limb survival, wound-related factors such as tissue loss, and emerging technologies
are to be considered whether to revascularize or not. Systemic risk factors as well as poor
functional capacity may be contraindications for revascularisation.
Rest pain, claudication and oedema increase the probability of delayed healing and
amputation in the case of a neuroischaemic foot ulcer. The size and site of the ulcer have
been related to the outcome especially in neuropathic ulcers. Ulcers located in the heel are
frequently regarded as refractory: proper perfusion through the posterior tibial artery seems
essential for the healing. Multiple ulcers in the same foot are also associated with severe
PAD, multi-organ disease as well as poor outcome. The extent of tissue loss at the time of
intervention influences the outcome of diabetic neuroischaemic ulcers.
Summary: There is a clear need for a paradigm shift from neuropathic to neuroischaemic
ulcers. The presence of ischaemia should always be suspected and evaluated. Early
vascular review and revascularisation with lower threshold is likely to improve outcomes of
ulcerated diabetic foot as “time is tissue”.
Key references:
Schaper NC et al. Specific guidelines for the diagnosis and treatment of peripheral arterial dis-ease in a patient
with diabetes and ulceration of the foot 2011. Diab Metab Res Rev 2012; 28 (suppl 1). 236-237
Hinchliffe RJ et al. A systematic review of the effectiveness of ravascularization of the ulcerated foot in patients wit
diabetes and peripheral arterial disease. Diab Metab Res Rev 2012; 28 (suppl 1): 179-217
Apelqvist J & Lepäntalo M. The ulcerated leg: when to revascularize. Diab Metab Res Rev 2012; 28 (suppl 1):
30-35
Lepäntalo M et al. Chapter V: Diabetic Foot. Eur J Vasc Endovasc Surg 2011; 42 (suppl 2): S60-74.
Key Session: Recent Evidence – Vascularisation and Amputation
107
When to revascularize?
Mauri Lepäntalo 1
1 University of Helsinki (Helsinki, Finland).
The role of peripheral arterial disease (PAD) in ulcerated diabetic feet has long been
underes-timated due to the paucity of warning signs, claudication and rest pain, as well as
the presumed neuropathic nature of the ulcer. Consequently, 30%–50% of individuals with
diabetes and foot ulcers already have gangrene at admission and are therefore often
considered unsuitable for revascularization. Furthermore, the healing of a neuroischaemic
ulcer is worsened by microvascular dysfunction, causing AV-shunting, capillary ischaemia,
leakage and venous pooling. Therefore, the threshold of revascularizing neuroischaemic
ulcers should be lower than that of purely ischaemic ulcers. Co-morbidity, ulcer
characteristics and infection affect the decision as to when to intervene, as do the severity
and extent of occlusive arterial lesions.
The window of opportunity for vascular intervention in the neuroischaemic diabetic foot
should not be missed, and the need for early vascular intervention as an integrated part of a
strategy to achieve healing should be emphasised. Non-invasive vascular testing should be
performed on all individuals with an ulcerated diabetic foot. The arterial tree should be
imaged if non-invasive tests indicate ischaemia or when mild or questionable ischaemia is
diagnosed and conservative treatment does not promote ulcer healing in six weeks.
Revascularization should be performed whenever feasible to repair distal perfusion in order
to achieve ulcer healing.
Ischaemia should not be excluded as a cause of any diabetic foot ulcer unless proven
absent. In neuroischaemic legs, healing is primarily affected by the severity of ischaemia.
Therefore, from the practical point of view, neuroischaemic and ischaemic lesions should be
considered together as both may require revascularisation. Pulse palpation is the cornerstone
of vascular examination although it is not necessarily a method of good reproducibility.
In case of any uncertainty as to foot perfusion the measurement of ankle pressure, ankle/
brachial systolic pressure index (ABI) and toe pressures should be included. The normal
values of ABI range between 0.9 and 1.3, as high values suggest non-com pressible arteries
(pseudohypertension) characteristic of advanced mediasclerosis, typical for diabetes. Less
severe calcification may result in a normal ABI despite clinically significant PAD. Ankle
pressures were immeasurable in 35% among 554 diabetics with vascular impairment. Trust
ABI when low but not when high. An ABI 0.6 has little predictive value (IWGDF). Toe
pressure may give more reliable information of the level of distal flow capacity but were
immeasurable in 16% due to previous amputation or gangrene of the big toe. Vascular
intervention has been suggested feasible for diabetics with ulcer and ankle pressures below
80 mmHg, and toe pressure below 55 mmHg. Probability of ulcer healing is clearly related to
available perfusion pressures and regardless of assessment method follows a sigmoid curve.
ABI < 0.4-0.45, absolute systolic ankle pressure