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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.
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.
Treatment:
BEFORE THAWING
1. remove from environment
2. prevent partial thawing and refreezing
3. stabilize core temp. and treat hypothermia
4. protect frozen part ---- no friction or message
DURING THAWING
5. 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).
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.
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:
1. papular perniosis --- resemble EM. Lesions occur in crops. Prefers the side of the fingers. Last for many days
2. pustular chilblains
3. annular chilblains
4. perniotic lesions sometimes with necrosis on fingers, toes and ears may occur in elderly men in association with
monocytic leukemia.
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.
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.
CUTIS MARMORATA:
This is transient
A. Physiological
reticular cyanosis seen
Cutis marmorata
as a physiological
reaction to cold
B. Congenital
exposure which
Cutis marmorata telangiectatica congenital disappears on warming.
children and adults
C. Idiopathic especially obese women
Benign may develop these. The
Complicated characteristic bluish and
pink color is because of
D. Secondary venous blood alongwith
Arteriosclerosis incomplete oxygen
Vascular calcification dissociation.
Arteritis : Polyarteritis nodosa, allergic granulomatosis
Vascular occlution: emboli, thrombocythemia, cryoglobulins, cold IDIOPATHIC
agglutinins, LIVEDO
intraarterial injections RETICULARIS:
It is similar to
E. Miscelleneous cutis marmorata but is
Paralysis persistent. Etiology is
Cardiac failure unknown and occurs
Syphilis more between the ages
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.