Leg Ulcer Treatment in Hyderabad

One of the most important messages Dr. Sharma gives every patient with a chronic leg wound is that 'leg ulcer' describes an appearance, not a cause — and treating the wound with dressings alone, without identifying why it will not heal, is why so many patients arrive at Renova Century Hospital after months or years of unsuccessful treatment elsewhere. A wound near the inner ankle behaves very differently, and needs a completely different approach, from a painful wound on the outer foot or a painless wound under a pressure point on a diabetic sole.

Roughly 70% of chronic leg ulcers in general practice are venous in origin, caused by long-standing venous hypertension from valve failure or previous DVT. Around 10–15% are primarily arterial, caused by insufficient blood supply reaching the skin. A significant proportion, especially in Hyderabad's high-diabetes population, are neuropathic or mixed, combining reduced sensation with impaired circulation. Correctly distinguishing between these categories at the very first visit — using ABI and duplex ultrasound rather than guesswork — is the single biggest determinant of whether an ulcer heals quickly or drags on for months.

This is also why compression bandaging, the mainstay of venous ulcer treatment, can be actively dangerous if applied to an ulcer that is actually arterial in origin — squeezing an already poorly perfused limb can worsen tissue damage. Every patient at Renova Century Hospital has an ABI checked before any compression is applied.

A venous ulcer typically appears just above the inner ankle bone, is shallow with irregular edges, and is often surrounded by brownish skin pigmentation, hardened tissue (lipodermatosclerosis) and mild-to-moderate swelling — the visible legacy of years of venous hypertension. Standard care combines multilayer compression bandaging, which mechanically reduces venous pressure and encourages healing, with correction of the underlying reflux, most often with endovenous laser or radiofrequency ablation of the faulty saphenous vein.

The evidence here is compelling: clinical trials have repeatedly shown that closing the reflux source early — rather than deferring vein treatment until after the ulcer heals — leads to significantly faster healing and dramatically lower recurrence. This is a shift from older teaching, which treated the vein only after the wound had closed; Dr. Sharma's practice now treats reflux concurrently with wound care wherever the ulcer bed allows it.

Without addressing the vein, even an ulcer that heals with compression alone carries a high chance of recurring within a year or two, since the underlying venous hypertension that caused it in the first place has never actually been corrected.

Arterial ulcers typically occur on the toes, heel or outer ankle, are often painful (sometimes dramatically so, worse at night or when the leg is elevated), and have a characteristic 'punched-out' appearance with a pale or grey base. These wounds will not heal with any dressing, however advanced, until blood flow is restored — angioplasty, stenting or, in more extensive disease, bypass surgery are the essential first step, with wound dressing playing a purely supportive role afterward.

Diabetic foot ulcers are often the most complex, frequently combining reduced sensation (so minor trauma goes unnoticed), impaired small and large vessel blood flow, and a higher susceptibility to infection due to elevated blood sugar. These ulcers commonly develop under pressure points on the sole where the patient has been unknowingly walking on an unhealed wound for weeks, and often need a combined approach of revascularisation, surgical debridement, offloading footwear and tight glucose control before meaningful healing begins.

In all three ulcer types, Dr. Sharma's approach follows the same underlying principle: identify and correct the vascular problem first, because no amount of advanced dressing technology substitutes for adequate blood flow reaching the healing tissue.

Once the underlying vascular problem has been addressed, the wound itself often still needs active management to close completely. Sharp surgical debridement — removing dead or non-viable tissue in the clinic or theatre — converts a chronic, stalled wound bed into an actively healing one by removing the biofilm and dead tissue that perpetuate a wound's inflammatory state.

Modern dressing choices are selected to match the wound's specific needs at each stage: hydrocolloid and foam dressings manage moderate exudate while maintaining a moist healing environment, while negative-pressure wound therapy (vacuum-assisted closure) is used for larger or deeper wounds to draw wound edges together and stimulate healthy granulation tissue.

For large, clean wounds that have stalled despite optimal circulation and dressing care, split-skin grafting can dramatically accelerate closure, taking a thin layer of the patient's own skin from a donor site (usually the thigh) to cover the ulcer. This is only undertaken once infection is controlled and the vascular supply has been confirmed adequate to support graft survival.