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RISK FACTORS OF HYPOTHERMIA: I. AGE EXTREMES  Elderly  neonates II. OUTDOOR ACTIVITIES  occupational  sports related  inadequate clothing III. DRUGS AND INTOXICATIONS  Ethanol  Phenothiazines  Barbiturates  Anaesthetics  Neuromuscular blockade  others IV. ENDOCRINE RELATED  Hypoglycemia  Hypothyroidism  Adrenal insufficiency  Hypopituitarism V. NEUROLOGIC RELATED  stroke  hypothalamic disorders  parkinson’s disease  spinal cord injury VI. MULTISYSTEM  malnutrition  sepsis  shock  hepatic and renal failure VII. BURNS AND EXFOLIATIVE DERMATOLOGIC CONDITIONS VIII. IMMOBILITY OR DEBILITATION BIOMETROLOGY APPLIED TO COLD EXPOSURE: Assessment of skin following cold exposure is possible using a series of BIOMETROLOGIC METHODS. Thermography is the measurement and recording of temperature at the skin surface. Contact and non contact devices are available. The most popular methods are based on thermal conductance and infrared or microwave thermography. They suffer from relatively poor sensitivity. The most widely used method to assess skin blood flow relies on LASER – DOPPLER FLOWMETRY They create a color coded image . of tissue perfusion. It records changes in the blood volume and velocity. The data are collected without touching the skin. Photoplethysmography using red or infrared emitting diodes is well correlated with laser Doppler velocimetry. It consists of continuous recording of light intensity scattered by the skin. The signal is generated by the amount of light in the given skin area. The higher the hemoglobin content, the higher is the amount of light that is absorbed. HENCE THE METHOD IS BLOOD VOLUME SENSITIVE. The velocity of erythrocytes also may influence the readings through changes in the optical transmittance due to changes in the orientation relative to their speed. THERMOREGULATION AND HUNTING REACTION: Local and systemic thermoregulation is complex. The preoptic anterior hypothalamus normally orchestrates thermoregulation. The immediate defense of thermoneutrality is via the autonomic nervous system whereas delayed control is mediated by the endocrine system. Autonomic nervous system responses include the release of nor epinephrine, increased muscle tone and shivering leading to thermogenesis and increase of BMR. Prolonged cold exposure also stimulates the hypothalamic release of thyrotropin releasing hormone; this leads to increased levels of TSH which simulates the thyroid gland to produce thyroxine ------ a hormone that increases the BMR. Cold exposure produces an initial massive cutaneous vasoconstriction resulting in fall of skin temperature. This change serves to maintain the core temperature but at the expense of the skin. Conversely cold induced vasodilatation represents a protective mechanism against skin necrosis. This physiologic response known as HUNTING REACTION OF LEWIS involves transient cyclic vasodilatation caused by the opening of AV anastomosis. E.g. when a finger is immersed in water at 0 degree C, an initial drop in skin temperature to 2-4 degrees is followed by a rise of 7-13 degrees. With continued cold exposure, the temperature drops again and the cycle is repeated over and over again especially in acclimatized people. WHEN CORE TEMPERATURE IS THREATENED, THIS HUNTING REACTION CEASES AND VASOCONSTRICTION PERSISTS. PHYSIOLOGIC REACTIONS TO COLD:  ALL ENZYMES AND VITAL PROCESSES ARE DEPRESSED  CONSTRICION OF ARTERIOLES AND VEINS BY DIRECT MECHANISM (veins> arterioles)

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Reflex increase in sympathetic tone arising from (a) cold receptors of the skin (b) heat regulating centre of the hypothalamus. Increase in viscosity of blood

Changes in platelet adhesiveness, diminished conduction in sympathetic nerves, slow dissociation of Oxyhemoglobin to hemoglobin.


11. 12. 13. 14.


FROSTBITE:  It occurs when the tissue temperature drops below 0 degree C after exposure to extreme cold air, liquids and metals.  The components of tissue that may lead to damage when frozen are WATER with the formation of ice crystals AND LIPIDS such as fat globules or cell membrane constituents.  The rate of freezing determines the focus of freezing injury.  Slow freezing produces extra cellular ice whereas rapid freezing produces intracellular ice.  Intracellular ice destroys the cellular architecture.  Extracellular ice disturbs the osmotic properties of the tissues and disturbs the flow of water and electrolytes across the cell membranes.

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Thawing may be as damaging as freezing itself and repeated freeze and thaw cycles compound the injury making available more water. The rewarming rate is also important. In slow rewarming, ice crystals become larger and more destructive. Cells also are exposed to a high concentration of electrolytes for a longer period than with rapid rewarming. As the body cools, there is reflex constriction of the arteries and veins in the extremities. This result in increased venous pressure decreased capillary perfusion and sludging. Also, cooling creates a left shift in the oxygen dissociation curve and hemoglobin gives up its oxygen less readily. This results in hypoxia and damage to both capillaries (endothelial damage ----leading to thrombosis) and surrounding tissues. Oxygen tension is further decreased by thrombus formation in the microvasculature. In addition, segmental vascular necrosis occurs in areas of erythrostasis. Cell types vary in their susceptibility to cold injury. Melanocytes are very sensitive to cold and damage may occur at -4 to -7 degree C. This explains the hypopigmentation after cryotherapy and that frostbite occurs more in blacks. Nerve axons are also easily damaged but nerve sheaths are resistant. Autonomic fibres are also affected and this may account for the abnormal sweating and cold sensitivity that stay long after the non freezing type of cold injuries. 3 stages of cooling are recognized:  Massive vasoconstriction which causes rapid fall in skin temperature  Hunting reaction follows with a cyclic rise and fall in skin temperature.  Ultimately the skin temp falls to approach the ambient temperature. Sites: FINGER, TOES, EAR, NOSE OR CHEEK. The initial presentation of frostbite is relatively benign. The symptoms always include a sensory deficiency affecting the light touch, pain and temperature perception. The clinical presentation falls into 3 catagories corresponding to mild frostbite or frostnip, superficial frostbite and deep frostbite with tissue loss. Frostnip involves only the skin and cause no irreversible damage. There is a sensation of severe cold progressing to numbness followed by pain. Erythema over the affected area without edema or blebs. This is the only form of frostbite that can be safely treated in the field with first aid. Superficial frostbite involves the skin and immediate SC tissue. It includes the previously described signs but with progression of pain subsiding to feelings of warmth. This is a sign of severe involvement. THE SKIN HAS A WAXY APPEARANCE BUT THE DEEPER TISSUES REMAIN SOFT AND RESILIENT. WITHIN 24-36 HOURS OF THAWING, clear blebs form accompanied by edema and erythema. Lesions may become eroded. Deep frostbite extends to deep SC tissue. The injured skin becomes white or bluish white with a variable degree of anesthesia. The tissue is totally numb, indurated with immobility of the joints and extremities. Muscle may be paralysed. Nerves, large blood vessels and even bone may be damaged. Large blisters, some hemorrhagic, form 1-2 days after rewarming. Frostbite blisters contain high amount of prostaglandins F2a and thromboxane A2. these mediators may contribute to increased vasoconstriction, platelet aggregation, leucocyte adhesiveness and ultimately progressive tissue injury. The blister is resorbed in 5-10 days leading to the formation of HARD BLACK GANGRENE. Weeks later, a line of demarcation occurs and the tissues distal to the line undergo autoamputation. Prognostic signs of frostbite: 1. good prognostic signs:  large clear blebs extending to the tips of the digits  rapid return of sensation  rapid return of normal temperature to the injured area  rapid capillary filling time after pressure blanching.  Pink skin after rewarming. 2. poor prognostic signs:  Hard, white, cold, insensitive skin  Cold and cyanotic skin without blebs after rewarming  Dark hemorrhagic blister  Early evidence of mummifaction

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Constitutional signs of tissue necrosis such as fever and tachycardia Cyanotic or dark red skin persisting after pressure. Freeze-thaw- refreeze injury. BEFORE THAWING remove from environment prevent partial thawing and refreezing stabilize core temp. and treat hypothermia protect frozen part ---- no friction or message DURING THAWING 5. 6. 7. rapid rewarming is the keystone of treatment ---- with water bath no warmer than 40-42 degrees until the most distal part is flushed (10-45 min). administer ibuprofen 400mg PO 8-12 hourly. large amount of narcotic analgesics are needed. encourage patient to gently move the part. several adjunctive treatments like vasodilators, throbolysis and hyperbaric oxygen are sometimes useful. AFTER THAWING

Treatment: 1. 2. 3. 4.


10. the damaged part is elevated and blisters left as it is, pledgets are put between the fingers if macerated.
11. consider TT and streptococcal prophylaxis. 12. hydrotherapy at 37 degrees to continue. 13. surgical debridement is often delayed by 1-3 months after demarcation.  Sequelae of frostbite include:  Hypersensitivity to cold  paresthesias  Hyperhidrosis

These occur because of neuronal injury and persistently abnormal sympathetic tone. SYMPATHECTOMY AND VASODILATORS ARE HELPFUL.  SCC EPIPHYSEAL PLATE DAMAGE or premature fusion may occur in children. Premature fusion can result in shortened digits, joint deviation and dystrophic nails. Frostbite arthritis resembling osteoarthritis may occur weeks or years later.


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It results from repetitive exposure to wet cold above the freezing point. Limb dependency due to immobility and constrictive footwear were important pathogenic factors. 3 stages:

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Stage I: Foot folds cold, cyanotic and anaesthetic Stage II: It followed within 24 hours with paresthesia, marked edema, numbness and sometimes blisters. Stage III: Progression to superficial gangrene.

Smoking and Peripheral vascular disorders predispose. Nonfreezing cold injury may be followed by cold sensitivity and hyperhidrosis which may persist for years. Treatment consists of --------- rest, analgesics and antibiotics. Surgery should be delayed.

CHILBLAINS:  SYNONYM: Pernio or perniosis  These are localized lesions caused by continued exposure to cold above the freezing point.  Absolute temperature is less important than cooling of nonadapted tissue.  Dampness and wind increase the chances  It shows a genetic predisposition  It is described mostly in temperate regions where the winters are occasionally cold and damp (humidity is an important factor as it increases the conductivity of air). It is seen less often in very cold climates where the people take adequate precautions against cold and are acclimatized.  Both acrocyanosis and chilblains are more common in women, children and persons with low body mass. Anorexia nervosa is also a predisposing factor.  It also shows a genetic predisposition.  It is also seen in hypothyroidism and myeloproliferative disorders.  Chilblains tend to start in early part of winter in children and women with obvious erythrocyanosis and in spring months in adults who work outdoors and are exposed to a combination of greater cold and light.  They develop acultely as single or multiple, erythematous or purplish swellings.  Patients may complain of burning, itching or pain  In severe cases, blisters pustules and ulceration may occur.  The characteristic locations include the proximal phalanges of the fingers and toes (dorsal aspect) and the planter aspect of toes, heels, nose and ears.  Lesions usually resolve in 1-3 weeks.  In presence of arterial disease, systemic disease or prolonged exposure to cold or friction, irreversible changes of fibrosis, hyperkeratosis and lymphoedema may occur and lesions may persist for many weeks or months. E.g. senile perniosis.  Less common forms of chilblains:

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papular perniosis --- resemble EM. Lesions occur in crops. Prefers the side of the fingers. Last for many days pustular chilblains annular chilblains perniotic lesions sometimes with necrosis on fingers, toes and ears may occur in elderly men in association with monocytic leukemia.

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D/D includes ---- chilblains LE and lupus pernio. Natural history: acute lesions are self limiting. In children, some recurrences occur. Later there is complete recovery. Senile chilblains get worser each year unless the precipitating factors are avoided. Treatment consist of : 1. adequate, loose, insulating clothing 2. warm housing and workplace 3. regular exercise 4. a short course of UVR at the beginning of winter. 5. once chilblains has occurred treatment is symptomatic with rest, warmth, topical antipruritic, CCBs. 6. in crippling severity: sympathectomy.

COLD URTICARIA AND POLYMORPHOUS COLD ERUPTION: Cold urticaria occurs at the sites of localized cooling usually when the area is rewarmed. It may be idiopathic or associated with serologic abnormality like cryoglobulinemia. Most cases fall into the group of essential cold urticaria. They are divided into familial and an acquired form. IgE is implicated in the pathogenesis The antigen is a normal metabolite produced on cold exposure. Histamine is a important mediator but leukotreines, PAF and others have been incriminated. Exposure to cold causes prolonged edematous swellings often with headache, fever, arthralgia and leucocytosis. Swelling of the oral mucosa and esophagus occurs on ingestion of cold food. Death may occur on swimming in cold water. Alarming signs resembling histamine shock are responsible for loss of consiousness. Familial cold urticaria is a rare AD condition with onset at an early age. Urticaria develops when the patient is exposed to generalized cooling particularly chilling wind rather than local cold application. The delayed type of familial cold urticaria is characterized by localised angioedema developing 9-18 hours after the cold exposure. Diagnosis of cold urticaria is confirmed by placing an ice cube wrapped in a plastic bag on the skin of the forearm for periods varying from 30s to 10 min. Weals form on rewarming. Cold erythema seems to be a related disorder with erythema and pain without urticaria. Treatment includes avoiding cold wind exposure and swimming in cold water. Antihistaminics lower the clinical signs. Desensitization is done by immersing one arm on a daily basis into water at 15 degrees for 5 min. COLD PANNICULITIS: IT IS COMMON IN CHILDREN. Affects the cheeks and legs mostly. 1-3 days after the cold exposure there develops tender SC nodules. They subside spontaneously within 2-3 weeks. Ice cube challenge to the child’s skin for 10 minutes results in the development of an erythematous plaque 12-18 hours later. ACROCYANOSIS:  IT IS A BILATERAL DUSKY MOTTLED DISCOLORATION OF THE ENTIRE HANDS, FEET AND SOMETIMES THE FACE.  It is persistent and accentuated by cold exposure.  Pulses are present  Trophic changes and pain are absent.  It is GENETICALLY DETERMINED AND USUALLY STARTS IN ADOLESCENCE.  It is distinguished from Raynaud’s phenomenon which is clearly episodic and often segmental.  Chronic vasospasm of small cutaneous arterioles or venules with a secondary dilation of the capillaries and subpapillary venous plexuses has been postulated.

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These patients are liable to develop chilblains, livedo reticularis and erythrocyanosis. No treatment is curative. In cases that develop in adults, suspect myeloproliferative diseases.

ERTHROCYANOSIS:  It is a dusky cyanotic hue of the skin brought about by cold temperature.  It occurs mostly over the thigh, calfs, buttocks and forearms that have abundant SC fat.  The fat acts as insulator, lowering the skin surface temperature making the vessels more susceptible to cold induced vasoconstriction.  Seen commonly in adolescents and middle aged people.  It may be associated with nodular lesions, KP and scaling.  Treatment consists of avoidance of cold. Exercise to reduce weight. UV radiation has been tried in few cases. LIVEDO RETICULARIS:   It is reddish blue mottled and blotchy discoloration of the skin which forms a net like pattern. It is postulated that the darkened areas correspond to the sites of anastomosis between the blood vessels where the blood supply is relatively less. There is dilatation of small capillaries and venules at these sites resulting in stagnation of blood and hence the cyanotic discoloration. Initially the vessel changes are reversible in the early stages but later on they become permanently dilated. It is usually asymptomatic but sometimes there may be tingling and numbness. There are a number of causes of livedo reticularis.

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A. B. C.

Physiological  Cutis marmorata Congenital  Cutis marmorata telangiectatica congenital Idiopathic  Benign  Complicated Secondary  Arteriosclerosis  Vascular calcification  Arteritis : Polyarteritis nodosa, allergic granulomatosis  Vascular occlution: emboli, thrombocythemia, cryoglobulins, intraarterial injections


This is transient reticular cyanosis seen as a physiological reaction to cold exposure which disappears on warming. children and adults especially obese women may develop these. The characteristic bluish and pink color is because of venous blood alongwith incomplete oxygen dissociation. cold agglutinins,

IDIOPATHIC LIVEDO RETICULARIS: It is similar to cutis marmorata but is E. Miscelleneous persistent. Etiology is  Paralysis unknown and occurs  Cardiac failure more between the ages  Syphilis of 25-45 years, women  Lymphomas more affected than  Mycosis fungoides men. Changes are symmetrical and diffuse. Complicated forms have systemic involvement in the form of hypertension and arterial disease in the peripheral, coronary, renal and cerebral blood vessels. They have poor prognosis. CRYOGLOBULINEMIA:  Cryoglobulins are immunoglobulins that undergo reversible precipitation at low temperatures.  They are found in a variety of neoplastic, inflammatory and infectious disorders.  Cyroglobulinemia may be single component or mixed cryoglobulinemia.  Single component cryoglobulinemia is found in multiple myeloma, lymphoma, macroglobulinemia. It may lead to acral cyanosis, tingling, numbness, RP, pigmentation of skin, purpura, blisters, ulcerations and gangrene. Livedo reticularis, cutis marmorata and cold urticaria may also be seen. Systemic features like chills, fever, dyspnoea and diarrhea are common.

Mixed cryoglobulinemia is a systemic disorder characterized by a triad of purpura, weakness and arthralgias and visceral complications like liver (Hepatosplenomegaly) and renal involvement (glomerulonephritis). They are seen in association with kala azar, SABE, leprosy, syphilis, malignancy, HBV and HCV infections, collagen vascular disorders. Diagnosis is made by drawing venous blood at 37 degree and allowing it to clot. Then the serum is allowed to cool at 4-5 degree and any precipitate is noted. It redissolves on warming. Levels less than 25mg/100ml are usually asymptomatic. Therapy is directed to underlying diseases. avoid cold. Cyclophosphamide, splenectomy, urethane and stilbamidine have been advocated. Plasmapheresis may occasionally be helpful. Recombinant interferon alpha 2 a (3mIU thrice weekly) has been used with good results.

CRYOFIBRINOGENEMIA:  May be idiopathic or associated with underlying diseases like ----- metastatic prostatic carcinoma, pulmonary, gastric or ovarian carcinoma, CLL and rheumatic fever.  Primary type is rare and usually asymptomatic. Secondary type is associated with number of symptoms like ----- cold intolerance, numbness, cyanosis, RP, livedo, petechia, ecchymoses, acral necrosis and gangrene.  The crofibrinogen is detected by cooling the plasma at 0-4 degree C for 24 hours. It forms a precipitate or gel if cyrofibrinogens are present. COLD AGGLUTININ DISEASE:  The condition is caused by macroglobulins which agglutinate erythrocytes of all groups at 0-5 degree C.  The agglutination occurs in cooler parts of the body and result in acrocyanosis, RP, ulceration and gangrene.  It may be associated with conditions like infectious mononucleosis, atypical pneumonia, trypanosomiasis, CT diseases, malignant tumors, lymphomas and cirrhosis of liver. COLD HEMOLYSIS SYNDROME:  This syndrome is caused by hemolysins which combine with RBCs below 20 degree C and produce hemolysis when rewarmed to 25 degree C or above.  Symptoms include hemoglobinuria, chills, fever, backache, weakness, abdominal cramps, N/V, asthma and tachycardia. Icterus and Hepatosplenomegaly may occur in sever hemolytic anemia.  In the skin, RP and cold urticaria may occur.

The chronic form occurs with late and congenital syphilis and resolves with treatment with penicillin whereas the acute form occurs after viral infections and is not helped satisfactorily by any treatment.

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