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Cold-Injuries by Dr. Basumatary

Cold-Injuries by Dr. Basumatary

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Published by airfix1999
What happens to the human body if exposed to cold? What happened to the french soldiers during the retreat from Moscow in 1812.
What happens to the human body if exposed to cold? What happened to the french soldiers during the retreat from Moscow in 1812.

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Categories:Types, Research, History
Published by: airfix1999 on Jun 08, 2010
Copyright:Attribution Non-commercial

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01/25/2013

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COLD INJURIES
HEAT LOSS OCCURS BY 5 MECHANISMS:
RADIATION (55-65% of heat loss)
CONDUCTION (10-15% of heat loss)
CONVECTION
EVAPORATION
RESPIRATIONRISK FACTORS OF HYPOTHERMIA:I.AGE EXTREMES
Elderly
neonatesII.OUTDOOR ACTIVITIES
occupational
sports related
inadequate clothingIII.DRUGS AND INTOXICATIONS
Ethanol
Phenothiazines
Barbiturates
Anaesthetics
Neuromuscular blockade
othersIV.ENDOCRINE RELATED
Hypoglycemia
Hypothyroidism
Adrenal insufficiency
HypopituitarismV.NEUROLOGIC RELATED
stroke
hypothalamic disorders
parkinson’s disease
spinal cord injuryVI.MULTISYSTEM
malnutrition
sepsis
shock
hepatic and renal failureVII.BURNS AND EXFOLIATIVE DERMATOLOGIC CONDITIONSVIII.IMMOBILITY OR DEBILITATIONBIOMETROLOGY 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 areavailable. The most popular methods are based on thermal conductance and infrared or microwave thermography. They suffer fromrelatively poor sensitivity.The most widely used method to assess skin blood flow relies on LASER – DOPPLER FLOWMETRY. They create a color coded imageof 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 continuousrecording of light intensity scattered by the skin. The signal is generated by the amount of light in the given skin area. The higher thehemoglobin content, the higher is the amount of light that is absorbed. HENCE THE METHOD IS BLOOD VOLUME SENSITIVE. Thevelocity of erythrocytes also may influence the readings through changes in the optical transmittance due to changes in theorientation 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 theendocrine system.Autonomic nervous system responses include the release of nor epinephrine, increased muscle tone and shivering leading tothermogenesis and increase of BMR.Prolonged cold exposure also stimulates the hypothalamic release of thyrotropin releasing hormone; this leads to increasedlevels 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 tomaintain the core temperature but at the expense of the skin. Conversely cold induced vasodilatation represents a protectivemechanism against skin necrosis. This physiologic response known as HUNTING REACTION OF LEWIS involves transient cyclicvasodilatation caused by the opening of AV anastomosis. E.g. when a finger is immersed in water at 0 degree C, an initial drop in skintemperature to 2-4 degrees is followed by a rise of 7-13 degrees. With continued cold exposure, the temperature drops again and thecycle is repeated over and over again especially in acclimatized people. WHEN CORE TEMPERATURE IS THREATENED, THIS HUNTINGREACTION 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)
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 tohemoglobin.DISEASES CAUSED OR AGGRAVATED BY COLD:1.FROSTBITE2.TRENCH FOOT3.PERNIOSIS4.ACROCYANOSIS5.ERYTHROCYANOSIS6.LIVEDO RETICULARIS7.RAYNAUD’S PHENOMENON8.CRYOGLOBULINEMIA9.COLD HEMOLYSINS
10.
COLD AGGLUTININS11.COLD URTICARIA12.COLD ERYTHEMA13.DELAYED COLD SENSITIVITY14.COLD REFLEX URTICARIA.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 LIPIDSsuch 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 cellmembranes.
 Thawing may be as damaging as freezing itself and repeated freeze and thaw cycles compound the injury making availablemore water. The rewarming rate is also important. In slow rewarming, ice crystals become larger and more destructive. Cellsalso 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 venouspressure decreased capillary perfusion and sludging. Also, cooling creates a left shift in the oxygen dissociation curve andhemoglobin 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 themicrovasculature. 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 -7degree C. This explains the hypopigmentation after cryotherapy and that frostbite occurs more in blacks. Nerve axons arealso easily damaged but nerve sheaths are resistant. Autonomic fibres are also affected and this may account for theabnormal 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 lighttouch, pain and temperature perception.
 The clinical presentation falls into 3 catagories corresponding to mild frostbite or frostnip, superficial frostbite and deepfrostbite with tissue loss.
Frostnip involves only the skin and cause no irreversible damage. There is a sensation of severe cold progressing tonumbness followed by pain. Erythema over the affected area without edema or blebs. This is the only form of frostbite thatcan 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 progressionof pain subsiding to feelings of warmth. This is a sign of severe involvement. THE SKIN HAS A WAXY APPEARANCE BUT THEDEEPER TISSUES REMAIN SOFT AND RESILIENT. WITHIN 24-36 HOURS OF THAWING, clear blebs form accompanied by edemaand 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 afterrewarming. Frostbite blisters contain high amount of prostaglandins F2a and thromboxane A2. these mediators maycontribute to increased vasoconstriction, platelet aggregation, leucocyte adhesiveness and ultimately progressive tissueinjury. 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
 
Constitutional signs of tissue necrosis such as fever and tachycardia
Cyanotic or dark red skin persisting after pressure.
Freeze-thaw- refreeze injury.
 Treatment:BEFORE THAWING1.remove from environment2.prevent partial thawing and refreezing3.stabilize core temp. and treat hypothermia4.protect frozen part ---- no friction or messageDURING THAWING5.rapid rewarming is the keystone of treatment ---- with water bath no warmer than 40-42 degrees until themost distal part is flushed (10-45 min).6.administer ibuprofen 400mg PO 8-12 hourly.7.large amount of narcotic analgesics are needed.
8.
encourage patient to gently move the part.9.several adjunctive treatments like vasodilators, throbolysis and hyperbaric oxygen are sometimes useful.AFTER THAWING
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 AREHELPFUL.
SCC
EPIPHYSEAL PLATE DAMAGE or premature fusion may occur in children. Premature fusion can result in shorteneddigits, joint deviation and dystrophic nails.
Frostbite arthritis resembling osteoarthritis may occur weeks or years later. TRENCH FOOT OR IMMERSION FOOT:
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:
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 factoras it increases the conductivity of air). It is seen less often in very cold climates where the people take adequate precautionsagainst cold and are acclimatized.
Both acrocyanosis and chilblains are more common in women, children and persons with low body mass. Anorexia nervosa isalso 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 inadults 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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