17 FEB 2025 CUTANEOUS REACTIONS TO COLD.pptx

Cutenous manifestation on exposure to cold

1. CUTANEOUS REACTIONS TO COLD PRESENTER – DR AKSHIK A SHETTY MODERATOR – DR VINMA SHETTY

2. INTRODUCTION Cutaneous reactions to cold occur when the skin is exposed to low temperatures, leading to various dermatological conditions. These reactions can range from mild, such as temporary redness and irritation, to severe, like frostbite or cold urticaria. Certain individuals are more susceptible due to genetic predisposition, underlying medical conditions (e.g., autoimmune diseases), or prolonged exposure to cold environments. Understanding these reactions is essential for proper prevention and management, especially in colder climates or among individuals at higher risk

3. PHYSIOLOGICAL REACTIONS TO COLD Factors Influencing Cold-Induced Skin Effects : Environmental Factors: Temperature, humidity, wind chill, altitude Clothing Factors: Light, tight, wet, permeable, inadequate clothing Individual Factors: Age, fitness, injuries, fatigue, dehydration, smoking, alcohol, psychotropic drugs.

4. PHYSIOLOGICAL REACTIONS TO COLD Onset of Vasoconstriction : Starts when skin temperature falls below 35°C Maximal vasoconstriction at 31°C Three mechanisms: •Reflex cooling (other areas vasoconstrict in response) •Local cooling (direct effect on exposed skin) •Deep body cooling (core temperature drops)

5. PHYSIOLOGICAL REACTIONS TO COLD Physiological Mechanisms of Vasoconstriction •Early phase: Norepinephrine & α2- adrenergic receptors •Later phase: Reactive oxygen species & Rho kinase reduce blood flow •Core temperature regulation: TRPM8 receptor ( transient receptor potential melastatin 8)

6. PHYSIOLOGICAL REACTIONS TO COLD Heat Conservation via Blood Redistribution: •Vasoconstriction of arterioles & venules → Blood moves from superficial to deep veins •Arteriovenous (AV) anastomoses close → Reduces heat loss •Sympathetic activation via hypothalamus. Prolonged Cold Exposure: Hunting Reaction of Lewis •Cycles of vasoconstriction → vasodilation •Prevents skin necrosis •If core temperature drops too much, hunting reaction stops, and vasoconstriction persists

7. PHYSIOLOGICAL REACTIONS TO COLD Cold-Induced Skin Injury & Hysteresis Effect : • Nonlinear response: Mild cooling can still significantly reduce blood flow • Prolonged ischemia + high metabolic rate → Tissue necrosis, neuropathy • Hysteresis effect: Mismatch between cooling & rewarming responses

8. DISEASES CAUSED OR AGGRAVATED BY COLD Diseases of Cold Exposure Frostbite Trench foot Diseases of Abnormal Susceptibility to Cold •Raynaud phenomenon •Livedo reticularis • Cryoglobulinaemia •Cold agglutinins •Cold haemolysis •Cold urticaria • Perniosis •Acrocyanosis • Erythrocyanosis •Cold erythema •Cold panniculitis •Neonatal cold injury

9. FROSTBITE Frostbite is the term used to describe tissue damage caused by freezing. Skin and subcutaneous tissues are at risk of frostbite when exposed to cold air, liquids or metals. Frostnip – this is a milder form of cutaneous cold damage than frostbite and is characterised by reversible redness of the skin. The risk of frostbite increases with alcohol use and smoking. The parts of the body that can be least protected from cold are affected – the toes, feet, fingers, ears, nose and cheeks. Frostnip involves the skin only and is characterised by painful red patches, which normalise with rewarming.

10. FROSTBITE In superficial frostbite there is involvement of the skin and subcutis with redness accompanied initially by pain and then a sense of warmth. Investigations Technetium-99 bone scintigraphy may be helpful in evaluating outcome in frostbite injury and indicating the level of amputation needed in severe cases. Magnetic resonance angiography Bone scintigraphy

11. FROSTBITE Management: First line : Rapid rewarming by immersion in water at 37–39∘C is recommended. Use a thermometer to measure water temperature, or a caregiver’s hand, to ensure that an additional thermal burn injury is not imparted. The area should be air dried or patted dry to avoid shearing forces damaging tissue. Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen have been recommended although the evidence for their use is weak. Topical aloe vera gel has been suggested on the basis that it may also reduce inflammatory prostaglandins

12. FROSTBITE Second line: intra-arterial infusion of tissue plasminogen activator (tPA) is given within 48 h of the injury . Following tPA, patients are treated with low- moelcular -weight heparin for a week and then aspirin 325 mg daily for 1–3 months. Third line Surgical removal of gangrenous tissue should be delayed until there is a distinct demarcation between viable and non-viable tissue

13. TRENCH FOOT Aka - Immersion foot It is described as combination of stasis, non-freezing cold injury and wet conditions leading to numbness and skin changes on the distal legs and feet. Predisposing factors- Smoking and peripheral vascular disease. Affected individuals develop numbness of the feet and distal legs accompanied by skin changes caused by non-freezing cold injury. This is compounded by wet conditions and aggravated by leg dependency, immobility and constrictive footwear. R edness, oedema, tenderness and, in severe cases, areas of superficial gangrene.

14. TRENCH FOOT Affected individuals develop numbness of the feet and distal legs accompanied by skin changes caused by non-freezing cold injury. This is compounded by wet conditions and aggravated by leg dependency, immobility and constrictive footwear. Management The best approach is prevention bed rest, elevation and analgesics Conservative excision of necrotic tissue may be necessary Antibiotics should be given if there is evidence of infection.

15. A 91-year-old patient who had been trapped in the bath for 4 days. The foot is grey, with maceration and wrinkling of the skin

16. PERNIOSIS Aka – Chilblains It is described as localised inflammatory lesions on the acral skin, which occur as an abnormal reaction to cold in susceptible individuals. Presentation is typically in the late thirties, with a large female preponderance . Aetiological factors include poor nutrition, anorexia nervosa and systemic diseases, most typically lupus erythematosus (LE) and haematological malignancy. The lesions are red-purple and usually macular, papular or nodular .

17. PERNIOSIS Plaque-like perniosis also occurs. It develops symmetrically on the acral skin, in particular the fingers and toes, but other body extremities may also be involved including the heels, lower legs, nose and ears. a/w - Pruritus and burning pain. In severe cases blistering and ulceration may occur. Chilblain LE (also known as Hutchinson lupus) is a form of cutaneousLE that presents in a similar way to idiopathic perniosis . Chilblain LE may be accompanied by discoid LE or other forms of cutaneous LE.

18. Perniosis over the distal right middle toe

19. PERNIOSIS Management: Warm clothing and central heating generally prevent perniosis . Susceptible individuals must avoid cold, damp conditions and should not smoke.

20. ACROCYANOSIS It is a persistent cyanotic or erythrocyanotic mottled discoloration of the hands and, less commonly, feet and face. Decreased acral blood flowmay be further compromised by plasma hyperviscosity . Idiopathic acrocyanosis usually starts in adolescence and persists into adult life. There is a painless mottled duskiness of both hands in the presence of normal peripheral pulses. Trophic changes, such as ulceration,are absent. Acrocyanosis must be distinguished from the Raynaud phenomenon, which occurs episodically with triphasic colour changes and often involves just a few digits.

21. Aetiology of acrocyanosis

22. ACROCYANOSIS Capilleroscopy has been used to demonstrate dilated and congested capillary loops at the base of the fingernail. Management There is no effective medical treatment for acrocyanosis. Vasodilator therapies, such as the calcium-channel antagonists, do not appear to be beneficial. Drug-induced acrocyanosis will be improved by cessation of the culprit drug. Treatment of an underlying systemic disorder may improve the appearance in secondary acrocyanosis.

23. ERYTHROCYANOSIS Erythrocyanosis is a persistent, dusky redness of the skin occurring at sites with a thick layer of underlying subcutaneous fat, such as the thighs and lower legs. It has been hypothesised that the subcutaneous fat in these sites acts to insulate the superficial vessels from thewarmth of the underlying blood supply, thus rendering them susceptible to cold exposure. It is exacerbated by cold and therefore usually more prominent during the winter.

24. ERYTHROCYANOSIS It is characterised by dusky discoloration of the skin and may be accompanied by keratosis pilaris, angiokeratomas and telangiectases . The area is cold to touch. Nodular perniotic lesions occurring after cold exposure may complicate erythrocyanosis . Oedema and fibrosis may be seen as chronic manifestations of erythrocyanosis . Management Warm clothing, exercise, weight reduction and elastic support may be helpful. Vasodilators, such as calcium-channel antagonists.

25. LIVEDO RETICULARIS Livedo reticularis is a mottled, cyanotic discoloration of the skin, which has a characteristic network pattern. It is accentuated by cold. Livedo reticularis may be physiological, idiopathic or secondary to intravascular obstruction or vessel wall disease. Physiological livedo reticularis also known as cutis marmorata, this is a transient cyanotic mottling of the skin that occurs as a physiological response to cold exposure and disappears with warming.

26. LIVEDO RETICULARIS It is usually encountered in healthy infants and resolves during the first year of life. Involvement of the trunk as well as the limbs is common. Physiological livedo reticularis rarely occurs in adults, but in this situation is often associated with a disorder that causes stasis within blood vessels, for example paralysis

27. LIVEDO RETICULARIS It is usually encountered in healthy infants and resolves during the first year of life. Involvement of the trunk as well as the limbs is common. Physiological livedo reticularis rarely occurs in adults, but in this situation is often associated with a disorder that causes stasis within blood vessels, for example paralysis.

28. A reticular red patch and subtle cutaneous atrophy over the right thigh extending to the midsection of the shin, consistent with cutis marmorata telangiectatica congenita, in a 3-month-old girl.

29. RAYNAUD PHENOMENON It is defined as episodic digital ischaemia occurring in response to cold or emotional stimuli. It is characterised by sequential colour changes: white (pallor), blue (cyanosis) and red (rubor). Raynaud phenomenon (also called Raynaud disease) is idiopathic and occurs as an isolated innocuous disorder. Secondary Raynaud phenomenon occurs in association with underlying diseases, or is caused by physical factors or drugs.

30. Criteria for the diagnosis of primary Raynaud phenomenon

31. RAYNAUD PHENOMENON It affects the hands and, less often, the feet , changes elsewhere are exceptional, although the tongue can be involved. A typical attack consists of sudden pallor of one or more digits, followed after a few minutes by cyanosis or sometimes by redness. In primary Raynaud phenomenon the condition is usually symmetrical and involves several digits. Attacks are usually precipitated by cold, either local or of the whole body, or by psychological stimuli.

32. RAYNAUD PHENOMENON MANAGEMENT Conservative management includes taking measures to keep the hands and feet warm and reducing cold exposure and also emotional stress. Calcium-channel antagonists can be useful in decreasing the frequency, duration and severity of attacks. Recommended doses of nifedipine range from 30 to 180 mg daily and for amlodipine between 5 and 20 mg daily. Sildenafil 50 mg twice daily demonstrated significant improvement in mean attack rates and duration.

33. CRYOGLOBULINAEMIA It refers to the presence of immunoglobulin complexes that precipitate in vitro when cooled below body temperature. The most usual skin manifestation is purpura on the lower legs, which may develop after cooling of the extremities. In cryoglobulinaemia of all types, other skin signs are livedo reticularis, Raynaud phenomenon, atypical ulceration of the legs, digital skin necrosis and cold urticaria. Treatment of mixed cryoglobulinaemia is aimed at reducing immune complex activity by immunosuppression (with prednisolone and cyclophosphamide) and plasmapheresis

34. COLD AGGLUTININS It is a disorder of autoimmune haemolysis in which cold-sensitive immunoglobulins react against erythrocyte surface antigens. Cutaneous features occur mainly on acral sites and include Raynaud phenomenon, acrocyanosis and skin necrosis. MANGEMENT Non-pharmacological treatments involve avoiding or mitigating against cold exposures. This may include wearing gloves for example when accessing fridges or freezers, making sure patients have a warm environment on hospital wards and warming intravenous infusions.

35. REFERENCES Rook's_Textbook_of_Dermatology,_10th_Ed_4 IADVL TEXTBOOK OF DERMATOLOGY FIFTH EDITION