Recent surveys converge on a picture of rapidly rising diabetes prevalence across Jammu and Kashmir. The ICMR-INDIAB study of 1520 participants reported diabetes prevalence of 18.9% overall in the Jammu region (26.5% urban, 14.5% rural), prediabetes of 10.8%, and high rates of coexisting hypertension (27.1%), generalized obesity (41.7%), and abdominal obesity (62.7%) [6]. NFHS-6 data show elevated blood glucose in 13% of women and 11.3% of men aged 15 and above, up from 8.7% and 8% respectively in NFHS-5 (2019-21), with a pronounced urban-rural gradient (17% urban versus 11.9% rural women; 14.6% urban versus 10.3% rural men) [7]. These two figures are not directly comparable: the ICMR-INDIAB estimate is a clinically ascertained diabetes prevalence confined to the Jammu region, while the NFHS-6 figure is a screening-level elevated-blood-glucose prevalence reported for the Union Territory as a whole; they are presented together here only to indicate overall direction and magnitude, not as a single combined statistic. Both surveys highlight a large undiagnosed pool, roughly 40% of cases in the ICMR-INDIAB sample, which has direct implications for foot-complication prevention, since undiagnosed patients receive no structured foot screening, glycaemic counselling, or footwear advice until a complication, sometimes a foot ulcer itself, brings them to medical attention.

Foot problems were reported to affect more than half of patients with diabetes duration exceeding ten years [3], broadly consistent with the national pattern in which 15% - 25% of Indian diabetics develop a foot ulcer in their lifetime, half of these become infected and require hospitalisation, and a fifth require amputation [2]. Applied to Jammu and Kashmir, these remain national extrapolations rather than locally measured figures. Applied to a region with rising prevalence, a high proportion of undiagnosed disease, and a severe winter climate, these national figures imply a substantial and likely growing local burden of preventable foot complications, one that is not yet quantified by dedicated regional registries.

The cost implications of allowing diabetic foot disease to progress rather than intervening early are considerable even in absolute terms. Indian cost analyses [2] have estimated ambulatory treatment of an uncomplicated neuropathic ulcer at roughly $56 per episode, rising to approximately $165 for an infected neuropathic foot, $1080 for advanced limb-salvage care, $960 for amputation alone, and as high as $2650 when salvage is followed by amputation (Table 1). As with the burden estimates above, these cost figures originate from a conference-abstract-level evidence synthesis [2]; they are presented as approximate, indicative figures pending confirmation from a full peer-reviewed cost-of-illness study. Given that around half of patients who undergo one amputation experience a second within two years, the lifetime cost trajectory for a single preventable ulcer can escalate substantially, an argument that applies with particular force in a resource-constrained hill-state health system where such expenditure competes directly with other essential services.

Table 1. Approximate per-episode treatment costs for diabetic foot disease in India (USD).

The 2023 IWGDF Prevention Guideline identifies loss of protective sensation (from peripheral neuropathy), peripheral arterial disease, foot deformity, and prior ulcer/amputation history as the principal determinants of foot ulcer risk, and recommends risk-stratified screening and integrated preventive foot care accordingly [1] [8]. Winter conditions interact with each element of this triad rather than introducing an independent, unrelated hazard.

Cold exposure triggers reflex peripheral vasoconstriction to conserve core temperature; in a foot with pre-existing peripheral arterial disease, itself markedly more prevalent in diabetic than non-diabetic populations, this can convert marginal perfusion into frank ischaemia [1] [8] [9]. Preliminary evidence from wearable in-shoe sensor technology is consistent with a seasonal effect on foot temperature, though this evidence is indirect and requires cautious interpretation. A 2026 feasibility study using wearable temperature and pressure sensors recorded a statistically detectable drop in foot temperature in December, which its authors described only as “potentially indicating reduced circulation or vasoconstriction due to colder weather”—a hypothesis-generating observation, not a confirmed physiological finding [13]. Critically, that study was conducted in healthy adult volunteers with no diabetes, neuropathy, or foot pathology, as a methodological baseline for future clinical work rather than a study of diabetic patients; its authors explicitly caution that the detected anomalies “should not be interpreted as clinically confirmed DFU-related pathology” [13]. It is cited here only as a possible risk indicator worth testing in diabetic cohorts, and should not be read as direct evidence that winter vasoconstriction reduces perfusion or raises ulceration risk in people with diabetes—that remains a plausible, biologically grounded hypothesis extrapolated from general cold-physiology principles [1] [8] [9], not a demonstrated finding in this population. In practical terms, a foot that could tolerate a given degree of pressure or minor trauma in summer may be unable to do so once winter vasoconstriction has reduced its perfusion reserve, even without any change in the patient’s underlying vascular disease; confirming this mechanism in diabetic patients specifically remains an important direction for regional research (Section 10).

Sensorimotor neuropathy is the pathway through which cold climates most directly threaten the diabetic foot, because it removes the protective withdrawal response to both extremes of temperature. Frostbite scoping reviews identify diabetes and neuropathy as recognized predisposing factors, since impaired cold-induced pain perception delays recognition of freezing injury [14] [15]; frostbite pathophysiology itself progresses through extracellular ice nucleation, microvascular thrombosis, and reperfusion injury on rewarming, producing long-term sequelae—chronic pain, cold hypersensitivity, vasomotor disturbance, and reduced sensation—in 63.3% of patients in one scoping review that pooled outcome data across included studies [16], alongside frostbite arthritis resembling osteoarthritis and, in children, growth-plate damage [14] [16]. Systematic review evidence further identifies personal and psychosocial predisposing factors for frostbite and frostbite-related amputation, including impaired judgement of cold exposure duration and delayed protective behaviour, factors plausibly compounded by neuropathic sensory loss [15]. Conversely, the same sensory loss removes the pain response that would normally prevent prolonged contact with a heat source, the mechanism underlying kangri- and bukhari-related thermal burns discussed below. Cold weather has also been separately reported to intensify neuropathic pain itself, through cold-allodynia mechanisms involving transient receptor potential (TRP) channels, independent of any injury [17], meaning patients may simultaneously experience heightened pain from intact nerves at rest while retaining dangerously reduced protective sensation to acute injury.

The kangri, an earthenware pot of hot embers woven into a wicker casing and carried beneath the pheran, is a centrally important traditional Kashmiri warming device, particularly in rural households and during the frequent winter power outages that sustain its continued use; the bukhari (wood/coal stove) and hot-water bottles serve related purposes.

Chronic kangri ulcer and malignant transformation.Kashmiri dermatological literature describes a distinct chronic cutaneous entity, the “kangri ulcer” (also termed “Kangri cancer” when malignant change has occurred), arising from years of repeated, low-grade ember contact against the abdomen and thighs rather than from a single exposure. Hospital-based histopathological series from Srinagar have documented a spectrum of Kangri-associated skin change—erythema ab igne, Bowen’s disease, and squamous cell carcinoma—in patients with long-standing Kangri use [18], and larger retrospective series describe Kangri-cancer squamous cell carcinoma with a substantial risk of loco-regional metastasis [19]. This chronic, cumulative pathway to malignancy is a regional variant of the broader phenomenon of heat-contact-associated Marjolin’s ulcer, also described as “kairo burn cancer” in Japan and “kang ulcer” in China [20] [21]. It is mechanistically and clinically distinct from the acute thermal burns discussed next: the chronic kangri ulcer develops over years in the general Kashmiri population independent of diabetes status, carries a cancer risk rather than an immediate limb-threat, and is managed primarily by dermatological surveillance and biopsy of suspicious lesions, whereas acute diabetic foot burns, described below, present within hours to days, carry an immediate risk of infection and amputation, and are managed as acute wounds.

Acute thermal burns in the diabetic foot.In diabetic patients, neuropathy compounds the hazard of direct-contact heat sources acutely: case literature has documented diabetic individuals sustaining severe thermal burns after using direct heat therapy to relieve neuropathic discomfort, resulting in secondary infection and extensive debridement despite the absence of pain during the causative exposure [22]. Burn-registry evidence corroborates the disproportionate impact of thermal injury on diabetic feet specifically: diabetic patients with foot burns present later (delayed recognition due to reduced sensation), and single-institution and comparative retrospective studies report significantly higher rates of amputation, longer hospitalisation, more frequent regrafting, and reduced functional status at discharge among diabetic versus non-diabetic foot-burn patients, with one comparative study reporting 33% amputation in the diabetic group versus 0% in controls, and significantly fewer diabetic patients prescribed pressure garments despite comparable need [23] [24]. Regarding treatment, a single regional burn centre’s retrospective comparison reported that its patients managed with local wound care had less morbidity, shorter wound-closure times, and better functional outcomes than those managed operatively, and that centre has accordingly adopted a non-operative-first institutional protocol [23]. This is a single-institution, abstract-level retrospective comparison in which treatment was not randomly allocated—patients selected for surgery may have had more severe injuries at baseline—so it should not be read as establishing a general preference for non-operative care. The more defensible clinical message is that every diabetic foot burn warrants prompt specialist (burns or diabetic-foot multidisciplinary) assessment, with the choice between operative and non-operative management individualised according to burn depth, presence of infection, and limb perfusion, rather than defaulting to either approach [23] [24].

Low ambient humidity outdoors and drying indoor heating reduce skin moisture; diabetic skin, already prone to autonomic-mediated reduced sweating, becomes more prone to fissuring, particularly over the heel, in winter. Fissures constitute a portal of entry for pathogens in a population already documented to have high rates of polymicrobial and multidrug-resistant diabetic foot infection in Indian case series [9] [25], raising the stakes of any skin breach; one Indian cohort found multidrug-resistant organisms in 69% of bacterial isolates from diabetic foot infections, with methicillin-resistant Staphylococcus aureus accounting for over 80% of resistant Gram-positive isolates [25], underscoring how quickly a minor winter fissure could seed a difficult-to-treat infection.

IWGDF guidance identifies appropriate footwear and structured self-care education as core pillars of ulcer prevention for at-risk patients [8]. Winter footwear—heavy socks, insulated boots, layered wrappings—can increase in-shoe pressure and friction while simultaneously making daily visual foot inspection more cumbersome. Snow and ice add mechanical and frostbite risk to exposed or thinly covered toes, and reduced daylight, difficult terrain, and seasonal isolation in high-altitude areas of the Union Territory plausibly delay care-seeking for early lesions, compounding the known association between diagnostic delay and adverse diabetic foot outcomes documented across Indian tertiary-care cohorts [4] [5].

Screen all persons with diabetes at least annually for loss of protective sensation (10g monofilament and/or vibration perception) and pedal pulses, per IWGDF risk categories [1] [8], with more frequent review (every 1 - 3 months) for those at high risk and every 3 - 6 months for moderate risk, and continue this schedule through winter months when attendance often falls.Give special attention to patients with a prior ulcer or amputation, who IWGDF and Indian cohort data identify as being at the highest recurrence risk and among whom lifelong preventive foot care is warranted [5] [8].Record any new lesion using a consistent classification system (SINBAD or Wagner) to standardize communication between primary care, specialist, and referral centres [10] [26] [28].

Inspect both feet daily, including soles and inter-digital spaces, using a mirror or the assistance of a family member when visual acuity or flexibility is limited.Wash feet daily in lukewarm water, verifying temperature with the elbow or a thermometer rather than the foot itself if sensation is impaired; dry thoroughly, especially between the toes.Apply moisturiser to soles and heels (avoiding web spaces) to counter winter-related dryness and fissuring.Refer corns, calluses, thickened or ingrown nails for professional podiatric management rather than self-treatment with blades, acids, or heat.

There is no cloth barrier or contact-time limit that makes direct contact between a kangri, hot-water bottle, heating pad, or bukhari and an insensate foot safe. Because impaired protective sensation prevents the patient from feeling developing tissue damage regardless of barrier or duration, direct or prolonged contact between any such heat source and the foot should be avoided altogether in patients with confirmed or suspected neuropathy, not merely minimised [22]-[24].Where feasible, prefer thermostatically controlled electric heaters with automatic shut-off over open-ember devices for individuals with confirmed neuropathy, while recognizing the cultural significance and continued necessity of the kangri during frequent winter power outages.Warm the room, not the foot directly: insulated footwear and warmed (not hot) bedding reduce reliance on direct-contact heat sources.Educate family members and caregivers of elderly or neuropathic patients to actively check for evolving burns, since the patient may not perceive the injury developing.Where a thermal injury does occur, seek prompt assessment by a burns or diabetic-foot specialist rather than assuming conservative management is preferred by default; the choice between operative and non-operative treatment should be individualised according to burn depth, presence of infection, and limb perfusion, recognising that operative management is necessary for deep, infected, or poorly perfused wounds [23] [24].

Wear well-fitting, insulated, waterproof footwear with adequate toe room; avoid constrictive boots or excessive sock layering that compresses the foot and impairs circulation.Inspect the interior of footwear for foreign objects, seams, or moisture before each use.Change damp socks promptly; avoid prolonged bare or thinly covered exposure to snow, ice, or cold flooring, which can cause unrecognized frostnip in an insensate foot.Never walk barefoot on cold stone or concrete floors indoors.

Maintain glycaemic control (targeting HbA1c ≤ 7% where individually appropriate), given the documented association between poor control and both DFU incidence and amputation in Indian cohorts [4] [5].Manage coexisting hypertension, dyslipidaemia, and tobacco use, all of which are prevalent regionally and compound peripheral arterial disease risk [6].Maintain diabetes clinic attendance through winter months despite travel and weather difficulty, recognizing the risk of care discontinuity in remote and high-altitude areas.

Treat any new redness, blister, discoloration, numbness, or wound as urgent regardless of pain, since neuropathic feet may not signal injury through pain.Avoid home remedies, hot compresses, or unsupervised topical treatment of any foot lesion, a documented precipitant of severe thermal injury in neuropathic patients [22].Ensure prompt referral pathways from primary care to specialist diabetic foot or wound services, given the strong association between delayed presentation and amputation demonstrated across Indian and international burn and DFU cohorts [4] [23] [24].