ABC of arterial and venous disease - Ulcerated lower limb

University of Nottingham, UK.
BMJ Clinical Research (Impact Factor: 14.09). 07/2000; 320(7249):1589-91. DOI: 10.1136/bmj.320.7249.1589
Source: PubMed

ABSTRACT Ulceration of the lower limb affects 1% of the adult population and 3.6% of people older than 65 years. Leg ulcers are debilitating and painful and greatly reduce patients' quality of life. Ulcer healing has been shown to restore quality of life. Lower limb ulceration tends to be recurrent, and the total annual cost of leg ulceration to the NHS has been estimated at £400m.

Causes of lower limb ulceration
Venous diseaseArterial diseaseMixed venous-arterial diseaseNeuropathyTraumaObesity or immobilityVasculitisMalignancyUnderlying osteomyelitisBlood dyscrasiasLymphoedemaNecrobiosis lipoidica diabetecorumPyoderma gangrenosumSelf inflicted

Venous disease, arterial disease, and neuropathy cause over 90% of lower limb ulcers. It is useful to divide leg ulcers into those occurring in the gaiter area and those occurring in the forefoot because the aetiologies in these two sites are different. At least two aetiological factors can be identified in one third of all lower limb ulcers.

Distribution of non-venous and venous ulcers of lower limb. The majority of venous ulcers are in the gaiter area and the majortiy of non-venous ulcers in foot

Venous ulcers most commonly occur above the medial or lateral malleoli. Arterial ulcers often affect the toes or shin or occur over pressure points. Neuropathic ulcers tend to occur on the sole of the foot or over pressure points. Apart from necrobiosis lipoidica, diabetes is not a primary cause of ulceration but often leads to ulceration through neuropathy or ischaemia, or both. The possibility of malignancy, particularly in ulcers that fail to start healing after adequate treatment, should always be borne in mind. The commonest malignancies are basal cell carcinoma, squamous cell carcinoma, and melanoma.

Common sites of venous, arterial, and neuropathic ulceration. Adapted from Tibbs et al

Patients with reduced mobility or obesity may develop ulceration in the gaiter area because of venous …

Download full-text


Available from: Professor Richard Donnelly, Jul 07, 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The ability to measure objectively wound healing is important for an effective wound management. Describing wound tissues in terms of percentages of each tissue colour is an approved clinical method of wound assessment. Wound healing is indicated by the growth of the red granulation tissue, which is rich in small blood capillaries that contain haemoglobin pigment reflecting the red colour of the tissue. A novel approach based on utilizing haemoglobin pigment content in chronic ulcers as an image marker to detect the growth of granulation tissue is investigated in this study. Independent Component Analysis is employed to convert colour images of chronic ulcers into images due to haemoglobin pigment only. K-means clustering is implemented to classify and segment regions of granulation tissue from the extracted haemoglobin images. Results obtained indicate an overall accuracy of 96.88% of the algorithm performance when compared to the manual segmentation.
    Visual Informatics: Sustaining Research and Innovations - Second International Visual Informatics Conference, IVIC 2011, Selangor, Malaysia, November 9-11, 2011, Proceedings, Part I; 01/2011
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Up to one million people suffer from chronic skin ulcers in the US. Little is known of the mechanisms leading to tissue breakdown, although inadequate circulation and ischemia are common elements in most dermal ulcers. Collagen is the principal source of mechanical strength in most tissues, and its molecular and fibrillar stability is dependent on adequate oxygen supply. In wound repair, localized ischemia leads to fibrogenic responses culminating in elevated collagen synthesis and remodeling. This study examines factors influencing collagen turnover and stabilization before ulceration in "at risk" patients. Severely ischemic but uninjured ischemic skin (IS) was compared with patient- and site-matched non-ischemic skin. Biochemical mechanisms of tissue repair were activated in IS, with increased lactate, transforming growth factor-beta, vascular endothelial growth factor, collagen synthesis and matrix metalloproteinases (MMPs)-1 and 2. The absence of MMP-9 and inflammatory cells confirmed that this upregulation was inappropriate and not in response to injury. Molecular stability of collagen was reduced in IS, and there was increased susceptibility to enzymic degradation. In conclusion, chronic ischemia and long-term hypoxia result in elevated collagen remodeling in an oxygen-poor environment. Unstable collagen molecules are synthesized together with upregulated MMPs, resulting in collagen denaturation, defective angiogenesis, weaker skin, and predisposition to ulceration.
    Journal of Investigative Dermatology 05/2007; 127(4):958-68. DOI:10.1038/sj.jid.5700651 · 6.37 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Extracellular matrix (ECM) metabolism and homeostasis is sensitive to changes in oxygen tension manifest in ischemia. We hypothesize that in chronically ischemic limbs, abnormalities in uninjured skin, secondary to hypoxia, predispose to dermal breakdown. Paired biopsies of uninjured distal ischemic and proximal non-ischemic skin were harvested at below knee amputation from 14 patients with peripheral vascular disease following quantification of ischemia. Age- and site-matched controls were taken at total knee replacement (TKR) and varicose vein (VV) operations. Matrix metalloproteinase (MMP)-2 and -9 expression was determined using gelatin zymography, MMP-1 by western blotting and ELISA and tissue inhibitor of MMP (TIMP) by reverse zymography. Collagen content was measured by determining hydroxyproline levels, and collagen type I synthesis by ELISA. Collagen type I synthesis was upregulated in ischemic tissue compared with non-ischemic matched pairs (p<0.001) and both TKR and VV controls, however, there was no increase in collagen deposition. Levels of MMP-2 (p<0.0005) and TIMP-2 (p<0.01), were elevated in ischemic samples. MMP-9 was unaltered, signifying no inflammatory changes. Tissue ischemia was linked to elevated ECM turnover, associated with matrix failure when compounded with problems of matrix stabilization, likely in ischemia. This represents a potential mechanism for ulcer formation.
    Journal of Investigative Dermatology 08/2005; 125(2):373-9. DOI:10.1111/j.0022-202X.2005.23789.x · 6.37 Impact Factor