Theme: Frostbite and hypothermia. Pathogenesis, diagnostic and treatment

Theme: Frostbite and hypothermia. Pathogenesis, diagnostic and treatment


  1. What type of injuries can be caused by cold weather?

  2. factors that can lead to the cold injury

  3. Pathophysiology of Tissue Freezing

  4. The classification of cold injuries

  5. Treatment of frostbites

  6. Hypothermia

  7. Cold Stress Prevention: 7 Safety Tips to Prevent Hypothermia and Frostbite

  8. When the cold is good - cryotherapy



What type of injuries can be caused by cold weather?


 Cold weather-related injuries can be divided into two general categories. There are those injuries that occur without the freezing of body tissue, such as chilblains, trench foot, and frostnip, and those injuries that occur with the freezing of body tissue, such as frostbite. Hypothermia is a medical condition characterized by a core body temperature that is abnormally low.


Cold weather-related injuries without tissue freezing:




Chilblains (also known as pernio) are a common type of cold weather-related injury that can develop in predisposed individuals after exposure to nonfreezing temperatures and humid conditions. Chilblains typically develop because of an abnormal vascular response several hours after the area exposed to cold is re-warmed. Chilblains are itchy, painful, reddish, or purplish areas of swelling that usually affect the fingers, toes, nose, or ears. In some individuals, blisters or small open sores may also form, increasing the risk for developing an infection. Chilblains usually last for several days, and the affected area usually heals after several weeks. Though the affected area may remain sensitive to the cold in the future, there is usually no permanent damage. It is not uncommon for chilblains to recur in susceptible individuals.


Trench foot


 Trench foot was named after the condition suffered by many soldiers in the trenches during World War I, though it is a condition still encountered today, often found in homeless individuals. Trench foot develops after feet have a prolonged exposure to a wet, cold, environment and is typically a more serious condition than chilblains. Tight-fitting, constricting boots and footwear serve to exacerbate the condition. Trench foot does not require freezing temperatures, and can occur with temperatures of up to 60 F (15.5 C).


 The symptoms of trench foot may include pain, itching, numbness, and swelling. The affected foot may appear red, or blotchy (red and pale areas mixed together) or even bluish-black with advanced injury.


 As with chilblains, blisters and open sores can develop. With severe trench foot, the tissue dies and sloughs off, and the development of gangrene can occur, sometimes requiring amputation. The usual recovery period for uncomplicated trench foot can be several weeks.




Frostnip is a mild cold weather-related injury that typically affects the face, ears, toes, and fingers. After exposure to cold weather, the affected area may appear pale, and may be accompanied by burning, itching or pain. Tingling or numbness are frequently present. Simple re-warming restores normal color and sensation, and there is no subsequent permanent tissue damage.


Cold weather-related injuries with tissue freezing:





Frostbite occurs when there is freezing of body tissue, and it is the most serious of the cold weather-related injuries. Frostbite usually affects the hands, feet, nose, ears, and cheeks, though other areas of the body may also be affected. This type of injury results from decreased blood flow and heat delivery to body tissues resulting in damaging ice crystal formation, which ultimately leads to cell death. Upon re-warming of the affected tissue, vascular damage and complex cellular metabolic abnormalities lead to tissue death. Damage to tissue is most pronounced when there is prolonged cold weather exposure, the affected area slowly freezes, and the subsequent re-warming process is slow. Repeated thawing and refreezing of the affected tissue is particularly damaging, and should be avoided.


 Frostbite injuries can be classified as either superficial or deep, depending on the tissue depth of injury. Superficial frostbite injuries involve the skin and subcutaneous tissues, while deep frostbite injuries extend beyond the subcutaneous tissues and involve the tendons, muscles, nerves, and even bone. Superficial frostbite injuries have a better prognosis than deep frostbite injuries.




Cold can influence on the organism in such ways as :

1)    local - with appearing of frostbites of different areas and organs

2)    total -  hypothermia  of the organism.


Besides low temperature of the environment there are additional factors that can lead to the cold injury:

1.     Meteorological : high humidity , wind

2.     Mechanical that cause disorders of microcirculation: tight shoes or close, forced location

3.     Factors that are decreasing the local resistance of tissues to cold temperature - cold injuries and traumas in anamnesis, neurotrophic disorders, diseases of vessels (obliterating endarteritis, varicose veins of lower extremities).

4.     Factors that cause decreasing of total resistance of organism – blood loss, severe total diseases, total fatigue, alcohol intoxication, loss of consciousness, avitaminosis.


Pathogenesis: in case of cold injury functional and morphologic changes in vessel’ walls appear. Local blood circulation is changing: narrowing or closing of small vessels appear. Permanent paresis of vessels and lowering of blood circulation cause the loss of plasma, condensation of blood and erythrocytes sedimentation on vessel’s walls.


        Pathophysiology of Tissue Freezing - As tissue begins to freeze, ice crystals are formed within the cells. As intracellular fluids freeze, extracellular fluid enters the cell and there is an increase in the levels of extracellular salts due to the water transfer. Cells may rupture due to the increased water and/or from tearing by the ice crystals. Do not rub tissue; it causes cell tearing from the ice crystals. As the ice melts there is an influx of salts into the tissue further damaging the cell membranes. Cell destruction results in tissue death and loss of tissue. Tissue can't freeze if the temperature is above 32 degrees F. It has to be below 28 degrees F because of the salt content in body fluids. Distal areas of the body and areas with a high surface to volume ratio are the most susceptible (e.g ears, nose, fingers and toes - this little rhyme should help remind you what to watch out for in yourself and others).

Surface frostbite generally involves destruction of skin layers resulting in blistering and minor tissue loss. Blisters are formed from the cellular fluid released when cells rupture.

Deep frostbite can involve muscle and bone

Pathophysiology of accidental hypothermia


Accidental hypothermia is an uncommon problem that affects people of all ages, but particularly the elderly. This review briefly outlines the aetiological factors that may predispose to hypothermia, with particular reference to the effects of sepsis, although the specific situation of cold water immersion is not addressed. A more detailed analysis of the pathophysiology of hypothermia then examines the cardiovascular, haematological, neurological, respiratory, renal, metabolic, and gastrointestinal systems. Clinically relevant findings are highlighted and some associated management points are related to the physiological changes. Most of these changes are reversible on rewarming, and are resistant to pharmacological manipulation; some of the pathological effects are related more to the process of rewarming than to the hypothermia itself.


Accidental hypothermia is defined as an unintentional fall in core temperature to <35 °C, and is classified into mild, moderate, and severe in different ways, mild usually being 33–35 °C, 32–35 °C, or 32.2–35 °C, and severe usually being defined as <28 °C, <27 °C, or <26.7 °C. It is an uncommon cause of death: a study in Ireland found hypothermia to be responsible for 18.1 deaths per million 1 out of 53.6 cases per million population, and a smaller Glasgow study found a similar mortality equating to 22 per million, 2 out of 71 cases per million population. Official figures from death certificates give hypothermia as the cause of 300 deaths annually in the UK. Epidemiological studies, not surprisingly, have identified an at risk group which is isolated, socially deprived, and ill; accidental hypothermia is also primarily a problem of older people, with 85% of one series being over the age of 60.5




Normal thermoregulation involves a dynamic balance between heat production and control of heat loss, with the aim of providing a constant core temperature. This is achieved in part by adjustment of central thermogenesis, and in part by maintaining a differential temperature gradient between the body core and the peripheries directly exposed to the environment; the amount of heat gained from or lost to the environment is closely and rapidly regulated in response to changing circumstances. Two types of cutaneous receptors are involved: cold and warm. Exposure to cold increases activity in the afferent fibres from the cold receptors, which stimulate the preoptic nucleus of the anterior hypothalamus; direct reflex vasoconstriction reduces blood flow to the cooling skin, and colder blood also reaches temperature sensitive neurons in the hypothalamus. The hypothalamus then initiates various responses, immediate responses via the autonomic nervous system, more delayed responses through the endocrine system, adaptive behavioural responses, extra pyramidal skeletal muscle stimulation, and shivering. These responses aim either to increase heat production or to reduce heat loss.


Older people are particularly susceptible to accidental hypothermia because thermoregulatory ability is progressively impaired with age. They may have a reduced ability to generate heat because of reduced lean body mass, impaired mobility, inadequate diet, and reduced shivering in response to cold. Sympathetically activated thermogenesis in brown adipose tissue is attenuated from the end of infancy. In addition, older people are susceptible to increased heat loss through a reduced ability to vasoconstrict appropriately, are less able to discriminate changes in temperature, may have abnormal adaptive behavioural responses, and may be prone to exposure to cold through falls or illness. Predisposing socio economic factors may be particularly relevant to the elderly. Indeed, some elderly people suffer recurrent episodes of hypothermia, suggesting that they may have a particular predisposition to thermoregulatory failure that can be precipitated by a relatively minor insult.


In addition to this age related impairment of adaptability to a fall in temperature, various pathological conditions may be implicated in the development of hypothermia. For example, central thermoregulatory ability can be impaired in such situations as stroke, CNS trauma or infection, tumours, or haemorrhage, and in uraemia, Parkinson's disease, multiple sclerosis and Wernicke's syndrome. Impaired control of peripheral vasculature through autonomic dysfunction can also play a part in diabetes, infection and cardiac failure. Reduced heat production occurs in endocrinopathies such as hypothyroidism, hypoadrenalism, and hypopituitarism, and hypoglycaemia alone can predispose to hypothermia, particularly in the context of alcohol ingestion. Pancreatitis and diabetic ketoacidosis also need to be considered as precipitating causes of hypothermic episodes, even if they are not clinically apparent. Diabetes itself may also be a factor which increases the likelihood of accidental hypothermia, particularly in the context of malnutrition.


Perhaps the most frequent precipitating factor in older people is sepsis, which in several series has been found in about 80% of elderly patients with hypothermia. In the 9–10% of patients in whom an infection results in hypothermia rather than fever, there is a significantly worse prognosis: mortality is approximately doubled, perhaps in part because of the higher rate of shock in these patients. Sepsis may predispose to hypothermia either by causing a failure of vasoconstriction, or by inducing an abnormal hypothalamic response. The mechanism for this remains unclear, but there is evidence of an increased cytokine response, with raised levels of tumour necrosis factor alpha (TNFα) and interleukin 6, and elevated prostacyclin and thromboxane B2 metabolites in hypothermic septic patients. Animal work indicates that at lower ambient temperatures, injection of high doses of bacterial endotoxin in the form of lipopolysaccharide (LPS) induces a hypothermic response while lower doses result in pyrexia; it seems that LPS endotoxin can cause a lowering in the threshold temperature for activation of thermogenesis, and also has some behaviour modifying effects.


Some pharmacological agents can cause central thermoregulatory failure (for example barbiturates, opioids, tricyclic antidepressants, and benzodiazepines), and phenothiazines can both impair central thermoregulation and also inhibit peripheral vasoconstriction in response to cold by their alpha blocking activity. Other alpha blockers such as prazosin have been reported to cause hypothermia, and the elderly seem particularly susceptible to this effect of alpha blockade. Lithium toxicity has been reported to lead to a reduction in core temperature, and ethanol can lead to peripheral dilatation, impaired shivering, hypoglycaemia and environmental exposure to cold, as well as having a direct effect on the hypothalamus, by which it lowers the thermoregulatory set point, resulting in a fall in core temperature. Valproic acid has also been reported to cause hypothermia in a handful of cases, but the mechanism is unknown.


The end point of accidental hypothermia can, therefore, be considered as a failure of thermoregulatory control, which may have both underlying predisposing causes, including age, various pathologies both acute and chronic, and pharmacological agents, and also more immediate precipitating factors. These precipitating factors may vary between acute exposure to cold in an otherwise previously fit individual, through a more prolonged period in a less cold environment (so called chronic hypothermia), to a relatively brief exposure to mild cold in the context of illness, often sepsis, or enforced inactivity such as after a fall. For a previously fit, younger victim of cold exposure, the outlook is generally good in the absence of apnoea or circulatory arrest; rewarming alone generally leads to full recovery. The more commonly encountered situation in clinical practice, however, is when an elderly person becomes hypothermic because of another condition, and the outcome is then generally determined by the nature of this underlying illness. Attention therefore needs to be directed to finding and treating this precipitating condition—often sepsis—in parallel with measures to deal with the hypothermia.




Observational work since the early part of the last century, human and animal experiments, and monitoring of surgical patients undergoing induced hypothermia for cardiopulmonary bypass or neurosurgery, have provided much information about the physiological responses to cold. Whether the data from all these different situations can be extrapolated to that of accidental hypothermia, is not clear. The pathophysiological changes observed may be influenced by such things as underlying disease, hypovolaemia or drug ingestion, and will depend to some extent on the rate as well as depth of cooling, as there is some evidence that more severe problems with acid base, electrolyte and fluid balance can occur in chronic hypothermia. Apart from ischaemia induced tissue infarcts, the changes induced by hypothermia are generally reversible on rewarming, and in many instances attempts to normalize physiological variables in this context are not only futile but dangerous.


Cardiovascular changes


In mild hypothermia, there is an initial tachycardia and peripheral vasoconstriction, and a consequent increase in cardiac output. The blood pressure increases slightly. These sympathetically driven changes can mostly be suppressed by drugs, however, with a proportional decrease in heart rate, blood pressure and cardiac output. Ventricular ectopy is often suppressed by mild degrees of cold and reappears with rewarming. In vitro cooling of pig myocardium to 32 °C causes a prolongation of contraction, and an increase in contractile force by almost 40%. As the temperature falls to a moderate degree of hypothermia, a progressive bradycardia develops consequent on decreased spontaneous depolarization of the pacemaker cells, and this is refractory to atropine. The resultant reduction in cardiac output may also be balanced by an increased systemic vascular resistance consequent on autonomic reflex response and catecholamine release. This elevated systemic resistance may be perpetuated by haemoconcentration, increased viscosity and local vasomotor responses. Increased resistance in renal arteries has been found in animals while vasodilatation tends to occur in the splanchnic vasculature.


Repolarization abnormalities occur as evidenced by the appearance of a ‘J’ (Osborn) wave on the ECG, usually best seen in the lateral precordial leads; this tends to increase in amplitude with falling temperature, but is not otherwise affected by electrolyte disturbances. J waves are not pathognomonic of hypothermia, but can also be seen in subarachnoid haemorrhage and other cerebral injuries, as well as in myocardial ischaemia. Increasingly broad QRS complexes develop, indicating slowing of myocardial conduction, in combination with ST elevation or depression and T wave inversion; these ECG changes may be related to the increasing acidosis and ischaemia. At the cellular level, there is prolongation of the action potential duration, which is explained by delayed activation of the repolarizing potassium current, slowed inactivation of the sodium current, and delayed inactivation of the inward calcium current. The slowing of myocardial conduction is similarly attributable to reduced and delayed activation of the inward sodium current. There is a prolongation of systole, and conduction delay may be evidenced by an increased PR interval and second or thirddegree AV block. Delayed repolarization as reflected by QT prolongation may also be seen at lower temperatures. According to early observations, the QT prolongation may persist for hours or even days after rewarming, and atrioventricular block may develop days after normal temperature has been restored. Asystole 72 h after rewarming has also been reported.


The heart rate falls to 30–40 bpm at 28 °C; rates inconsistent with a patient's temperature should prompt a search for underlying pathology such as hypoglycaemia, hypovolaemia, or drug ingestion. At lower temperatures, the bradycardia may become extreme, with rates of about 10 bpm at 20 °C. Systemic vascular resistance falls as catecholamine release is blunted, and cardiac output decreases correspondingly. At temperatures less than about 24 °C, there is a high risk of asystole. Animal studies suggest that this threshold may be lowered in the presence of ethanol intoxication, which may explain some observations of improved outcomes in this situation. Transvenous pacing may be difficult, owing to higher thresholds being necessary, and indeed hazardous in terms of the risk of precipitating ventricular fibrillation, but animal work confirms that transcutaneous pacing in hypothermia is effective and safe, and is recommended by some.


It has been suggested that asystole is a primary manifestation of hypothermia, whereas ventricular fibrillation occurs secondary to rewarming, hypocapnia, alkalosis or physical manipulation. Ischaemia, increased adrenergic activity and electrolyte disturbances certainly predispose to myocardial irritability, and in moderate hypothermia this frequently results in arrhythmias, commonly atrial fibrillation or flutter or nodal rhythms, but also multifocal ventricular extrasystoles and tachyarrhythmias. Ventricular fibrillation is more common below about 27 °C, and is particularly likely to develop if there is a sudden change in parameters such as physical movement, pO2 or pCO2, myocardial temperature, or changes in biochemical or acid base status. It has been postulated that the development of a temperature gradient between the cooler endocardium and subendocardial conducting tissue and the relatively warmer myocardium facilitates conduction through the myocardium at the expense of normal neuromuscular transmission, which might explain why sudden changes in biochemistry or acid base status affect these tissues differently and predispose to the development of ventricular fibrillation. An alternative explanation is that the small temperature differentials between myocardium and endocardium may cause dispersion of the action potential duration, refractory period and conduction speed, which are significantly lengthened in hypothermia, resulting in an increased vulnerability to arrhythmias.


The risk of precipitating ventricular fibrillation by tracheal intubation may have been overstated and relates to a lack of preoxygenation. In severe hypothermia, ventricular fibrillation is usually extremely resistant to attempts at electrical cardioversion until rewarming has been achieved, although isolated case reports prove that there are exceptions to the rule. Unless extracorporeal circulation can be rapidly established, giving the best chance of recovery, prolonged cardiopulmonary resuscitation may be necessary until sufficient warming has occurred to allow defibrillation. In hypothermia, reduced chest wall elasticity and compliance of the heart and lungs makes chest compressions more difficult and probably less efficient, but survival of patients after up to 6½ h of cardiopulmonary resuscitation has been reported. Bretylium is the only antiarrhythmic agent of any use in this situation, and acts through increasing the refractory period and thus raising the ventricular arrhythmia threshold, without any apparent effect on conduction velocity or catecholamine levels.


Overall, there is no indication for prophylactic antiarrhythmic treatment in the absence of malignant arrhythmias. The administration of lidocaine is generally ineffective at temperatures less than about 30 °C, as indeed are procainamide, propranolol, diltiazem and verapamil. In general, pharmacological attempts to increase blood pressure or heart rate are similarly problematic, although inotropes such as low dose dopamine have been used in patients who are disproportionately hypotensive and who do not respond to volume replacement. This is not normally necessary, however, and indeed the utility of low dose dopamine in general has provoked much recent debate. In moderate hypothermia, peripheral vasculature is already maximally vasoconstricted and administration of vasoconstrictors only predisposes to arrhythmias; indeed, the administration of epinephrine may precipitate ventricular fibrillation. Animal studies suggest that at around 29 °C the initial activation of the sympathetic system switches off, and there may be a role for catecholamine support below that temperature. It should be emphasized that any medication should be administered intravenously: the intense peripheral vasoconstriction and consequent poor absorption means that intramuscular and subcutaneous injections should both be avoided.


Serum levels of HBD and creatine kinase are sometimes moderately elevated, but may not represent cold induced ischaemic myocardial damage; the rise in total CK is independent of temperature, and is not accompanied by ECG changes or histological evidence of myocardial infarction at post mortem, although small degenerative foci are seen on microscopic examination of the myocardium in two thirds of cases. Studies with more specific markers of cardiac damage, such as troponins, would be helpful.




The haematological changes that are associated with hypothermia are important, particularly the increase in blood viscosity, fibrinogen and haematocrit; these may underlie disorders in the function of many other organs. Changes in vascular permeability result in the loss of plasma to extravascular compartments, leading to haemoconcentration, and the accompanying hypovolaemia is compounded by a cold induced diuresis. The haematocrit increases by about 2% for every 1 °C decline in temperature, and a normal haematocrit in a moderately or severely hypothermic patient suggests preexisting anaemia or blood loss. Hypothermia has also been reported to cause marrow suppression and progressive marrow failure, and to induce erythroid hypoplasia and sideroblastic anaemia.


Cold directly inhibits the enzymic reactions of both intrinsic and extrinsic pathways of the clotting cascade, and hence a coagulopathy can develop. The prothrombin time and partial thromboplastin time can be deceptively normal if measured at 37 °C, but can be significantly increased if measured at lower temperatures, even when clotting factor levels are known to be normal. Rewarming, rather than administration of exogenous clotting factors, is the appropriate management. A disseminated intravascular coagulopathy has been reported on a number of occasions with no apparent cause other than the hypothermia; this might be related to release of tissue thromboplastin from ischaemic tissue, or the circulatory collapse itself may be the major factor. Hypothermia may also impair both the endothelial synthesis of prostacyclin (PGI2) and its inhibitory action on platelet aggregation, promoting platelet activation and thrombosis. Thrombocytopaenia can also occur; this usually results from sequestration in the liver and spleen, but can be related to a disseminated intravascular coagulation, or marrow depression. In addition, platelet production of thromboxane B2 is temperature dependent, promoting a decline in platelet activity with falling temperature.


Elevated cryofibrinogen levels may be found in hypothermia, which raise the blood viscosity, and they can do so in a dramatic way on exposure to further cold, impairing the microcirculation and, presumably, resulting in the widespread tissue micro infarcts which are sometimes observed. Excess cryofibrinogen occurs particularly with E. coli sepsis of the urinary tract, diabetes, folate deficiency and malignancy, all of which are more common in the elderly. Excessive purpura or bruising may suggest the presence of cryofibrinogenaemia, and is associated with an increased mortality. If antithrombotic prophylaxis is being considered for a hypothermic patient, it should be borne in mind that heparin (and dextran) can polymerize the cryofibrinogen in the presence of a cryofibrinogenaemia, and thus cause severe hyperviscosity; indeed, despite the increased susceptibility to thromboembolism, there is no evidence at present to support the routine use of prophylactic heparin in accidental hypothermia.


Leukocyte depletion can occur in response to hypothermia, and animal and in vitro studies suggest that neutrophil migration and bacterial phagocytosis are impaired, predisposing to infection, although this does not appear to have been demonstrated in man. In patients undergoing cardiopulmonary bypass, complement activation may be attenuated at lower temperatures. The common finding of sepsis in elderly patients who present with hypothermia may therefore be a consequence as well as a predisposing cause of the failure of thermoregulation, and this underlines the need for routine antibiotic cover in these patients.


Neuromuscular effects


The central neurological effects of cold are often apparent clinically, with initial confusion and sometimes amnesia in the mild stages. As the temperature falls further, apathy, impaired judgement and paradoxical undressing may occur. Dysarthria, progressive depression of consciousness and ultimately coma develop, and consciousness is commonly lost below about 30 °C. There is a loss of cerebrovascular autoregulation at about 25 °C as well as a reduction in cerebral blood flow by 6–7% per 1 °C drop in temperature. However, in severe hypothermia there is a markedly reduced metabolic rate, and hence a considerably increased cerebral ischaemic tolerance; at temperatures less than 20 °C, ischaemic tolerance is ten times the normothermic. The EEG becomes flat at below about 20 °C.


Shivering is initially increased in mild degrees of hypothermia, but then decreases as the temperature falls further; however the reported temperatures at which shivering is lost vary widely (24–35 °C), as in fact do the other neurological changes at a given depth of hypothermia. Synovial fluid becomes more viscous at lower temperatures, and so in moderate hypothermia, stiffness of muscles and joints appears. Ataxia and loss of fine motor control are seen in the initial stages, followed by hyporeflexia, an extensor plantar response and pupillary sluggishness in moderate degrees of hypothermia; rigidity, pupillary dilatation and areflexia appear as the temperature falls below about 28 °C. In severe hypothermia, muscle and joint stiffness may simulate rigor mortis, although the stiffness may paradoxically lessen as the temperature falls below 27 °C.


Animal studies have helped to explain these changes by showing that peripheral nerve conduction is impaired in the cold, with a progressive reduction in conduction velocity as the temperature falls; this seems to be related to a reduced flux of potassium and chloride ions across the axon membrane. The effect of this on autonomic circulatory control mechanisms may help to explain why marked postural hypotension is sometimes observed, and head up or sitting positions are to be avoided in transferring victims out of their cold environments. The synaptic delay time is also prolonged as the neuromuscular junction cools,81 and muscle contraction is partially temperature dependent, with a reduced rate of development of tension and maximal shortening velocity at lower temperatures, but little change in the maximum force obtained. With cutaneous temperatures as low as 12 °C, the precapillary sphincters cease to work, with a resultant vasodilatation, and the increased blood flow that follows may then cause sufficient warming to restore their function and reinstate local vasoconstriction. This oscillation between dilatation and constriction is known as the ‘Lewis Hunting Reaction’ and occurs primarily on the finger tips, toes, ears and face.


Respiratory problems


In mild hypothermia, there is an initial tachypnoea, followed by a reduction in minute volume and reduced oxygen consumption; bronchospasm and bronchorrhoea occur. As the temperature falls to moderate levels of hypothermia, protective airway reflexes are reduced because of impairment of ciliary function, and this predisposes to aspiration and pneumonia. Significant reductions in oxygen consumption and carbon dioxide production occur, both falling by about 50% at 30 °C. Core temperature control is very dependent on pCO2 level, which is detected by the carotid bodies and also more centrally, and these act on sources of thermogenesis and thermolysis. A direct cooling effect depresses ventilatory drive at the respiratory centres, and at temperatures below 34 °C sensitivity to pCO2 stimulation is attenuated, although the hypoxic drive is maintained to deeper levels of hypothermia. Physiological and anatomical respiratory dead space are increased through bronchial dilation, but alveolar dead space is unchanged. Local gas exchange is not affected by hypothermia, but there is an increase in pulmonary vascular resistance and a degree of ventilation perfusion mismatch in the lungs. In severe hypothermia, progressive hypoventilation and apnoea develop, and (more rarely) pulmonary oedema.


There is initially a left shift of the oxyhaemoglobin (HbO2) dissociation curve in response to falling temperature, which results in impaired oxygen delivery and tissue hypoxia, but this is balanced to some degree by the resultant lactic acidosis and by other factors contributing to an overall acidosis, both respiratory (reduced carbon dioxide excretion) and metabolic. Shivering may greatly increase lactate production, and its clearance by the liver is impaired; frequently the metabolic acidosis gets worse during rewarming as the products of anaerobic metabolism are returned to the circulation, and this can contribute to the increased risk of arrhythmias. In severe hypothermia, the acidosis is frequently profound, so that there is an overall right shift to the HbO2 dissociation curve. The significance of impaired oxygen delivery to the tissues is reduced because of the decline in oxygen demand at lower temperatures.


Management of acid base status during hypothermia has been controversial. Blood gases are normally warmed to 37 °C for analysis, which results in higher oxygen and carbon dioxide levels and lower pH values than the hypothermic patient's true state, while the presence of large temperature gradients in the body make accurate calculation of the corrected values difficult. In practice, some suggest that this calculation is unnecessary, and attempts should be made to maintain the temperature uncorrected pH around 7.40, as this helps to avoid over enthusiastic use of bicarbonate or hyperventilation. These may depress cardiac output further, and increase the predisposition to ventricular fibrillation; also transport of bicarbonate across hypothermic cell membranes is slow, and severe metabolic alkalosis may result during rewarming.


Renal and metabolic


In mild hypothermia, there is a cold induced diuresis, which occurs before any fall in body temperature. This is initially due to an increase in renal blood flow consequent on vasoconstriction, then with falling temperature, a loss of distal tubular ability to reabsorb water and a resistance to the action of vasopressin (ADH). The cold induced diuresis is accompanied by an increase in urinary electrolyte excretion, probably as a result of reduced tubular sodium reabsorption. In moderate hypothermia, the glomerular filtration rate falls as cardiac output and hence renal blood flow fall, the last of these being reduced by half at 27–30 °C. There is also a further reduction in tubular function, and renal clearance of glucose is reduced. At lower temperatures still, tubular capacity for H+ ion secretion is reduced, and hence there is a renal contribution to the acidosis. Clinically, acute renal failure is seen in over 40% of patients with accidental hypothermia who require admission to an intensive care unit. Biopsies have demonstrated ischaemic damage to the kidneys, which is thought to occur in the rewarming phase, following a period of relative protection at lower temperatures. This ‘prerenal’ failure, essentially consequent on the fall in renal blood flow, may therefore be preventable to some extent by careful volume replacement.


Total body metabolism reduces with increasing hypothermia, as measured by a fall in oxygen consumption, which is about 6% for every degree Celsius fall in temperature. The basal metabolic rate is therefore reduced by 50% at 28 °C. In animal studies, vasopressin and oxytocin secretion is reduced, but the associated reduction in ACTH secretion is not reflected by the plasma cortisol levels, which are usually raised; this is likely to be due to reduced hepatic clearance. Pituitary, adrenal and thyroid function is thought to be normal, although a depressed cortisol response to ACTH stimulation has been found by some. Plasma concentrations of TSH and thyroxine are normal, but should be measured to exclude hypothyroidism as an underlying cause. If a patient is resistant to attempts at rewarming, administration of hydrocortisone with or without liothyronine should be considered, in case occult hypothyroidism, hypopituitarism or previous chronic steroid use are contributory factors. Routine administration of steroids is not beneficial and is not recommended.


If the hypothermia has developed rapidly, many different processes may contribute to hyperglycaemia, which can contribute an osmotic component to the diuresis. Insulin release is inhibited by increased corticosteroid levels, as well as by a direct cooling effect on the islets of Langerhans; in addition, peripheral uptake of insulin at the tissues is impaired. Sympathetic activity is increased, with raised plasma norepinephrine and free fatty acid levels, and the catecholamine‐induced glycogenolysis and gluconeogenesis contribute to the hyperglycaemia. The glucagon level is increased, and plasma cortisol levels correlate with lactate and glycerol levels, implying active stimulation of glycogenolysis and lipolysis. In cases where hypothermia has developed more slowly or is long lasting, glycogen stores may be depleted, and then it is likely that hypoglycaemia will develop. Shivering may also deplete glycogen stores and in the longer term contribute to hypoglycaemia. With rewarming, the factors leading to a raised plasma glucose correct, and so moderate degrees of hyperglycaemia should be tolerated rather than be treated, in order to avoid profound hypoglycaemia on rewarming. Exogenous insulin has little effect in the hypothermic state, and high doses would be needed for any apparently beneficial effect. If hyperglycaemia persists during the process of rewarming, diabetic ketoacidosis and pancreatitis need to be considered, and insulin therapy instituted once the temperature has returned to >30 °C.


Hypokalaemia results from a shift of extracellular potassium into the cells, due to changes in both membrane permeability and the function of the sodium potassium pump. Hyperkalaemia, on the other hand, is a marker of acidosis and cell death and is therefore a sign of poor prognosis. The ECG is not helpful here, as the potassium induced changes in the ECG can be reduced in hypothermia, and lower temperatures enhance the cardiac toxicity of hyperkalaemia. Plasma sodium, calcium, magnesium and chloride concentrations do not change significantly above about 25 °C, but there are reports of severe hypophosphataemia on rewarming from profound hypothermia. This may be more common than is appreciated, because serial phosphate measurements are not routinely made, and moreover might be contributing significantly to the morbidity and mortality associated with rewarming. Further work in this area is needed.


Gastrointestinal effects


Intestinal motility decreases below about 34 °C, resulting in an ileus when the temperature falls below 28 °C, and therefore a nasogastric tube should be placed to reduce the chance of aspiration. Furthermore, the absorption of medication given orally or by nasogastric tube will be impaired in this situation, and this route should therefore be avoided. Punctate haemorrhages may occur throughout the gastrointestinal tract, and autopsy studies have found gastric erosions and submucosal haemorrhages to be common but not clinically significant. The shallow gastric ulcers are known as Wischnevsky's ulcers and are seen in the majority of cases at post mortem examination. A characteristic linear pattern is seen, said to be consistent with acute cold stress. Cystic dilatation of the capillaries is found on histological examination, presumed to be due to reperfusion after functional collapse of the microcirculation in the gastric mucosa. Animal work has shown that hypothermia increases gastric acid production and reduces duodenal bicarbonate secretion, predisposing to this mucosal damage in both the stomach and the duodenum.


Hepatic impairment can develop, probably consequent on the reduced cardiac output, and the decreased metabolic clearance of lactic acid contributes to the acidosis. It follows that if warmed intravenous fluids are given, these should not include Hartmann's solution, since the liver cannot handle the added lactate efficiently. The liver's functions of detoxification and conjugation are also depressed, affecting the half life of many drugs, and prolonging the effects of ethanol. This may be particularly relevant in the situation of an overdose, where the resultant hypothermia perpetuates the effects of the drug ingested.


Pancreatitis frequently occurs as a consequence of hypothermia, being found at autopsy in 20–30% of cases, and a mildly elevated serum amylase without clinical evidence of pancreatitis is even more common, being present in 50% of patients in one series. The reason for this is not well understood, but is thought to result from thrombosis in the microcirculation, and resulting ischaemia and perilobular necrosis in the pancreas; this may be a similar underlying process to that which causes micro infarcts in the gut, liver, brain, myocardium, and many other organs. Portal vein thrombosis has also been reported in conjunction with haemorrhagic pancreatitis. Animal studies have demonstrated impaired pancreatic exocrine function and increased serum amylase levels as a result of cooling the pancreas for a few hours. Other enzymes associated with cellular damage are often mildly elevated, such as AST, ALT and bilirubin.


Clinical presentation


The patient with mild hypothermia might present with vigorous shivering, a diuresis, cold white skin, and a tachycardia. With a moderate degree of hypothermia, one might see amnesia, apathy, and a loss of fine motor skills, paradoxical undressing, and reduced shivering. Speech might be slurred, and bradycardia and arrhythmias may be hard to detect peripherally. Joints become stiff and there is hyporeflexia. In the severe case it would be common to find loss of consciousness, extreme bradycardia and slow respiration or apnoea, hypotension and impalpable peripheral pulses, along with cold oedematous skin, areflexia, and fixed dilated pupils, which are not in this situation an indication of brain stem death. It must be emphasized, however, that the clinical picture does not in general correlate well with the degree of hypothermia, and there are many reports of situations at variance with this broad picture, and at least one instance of an elderly lady maintaining consciousness (albeit confused) at 24.3 °C core temperature.




Many factors predispose to accidental hypothermia, including socioeconomic, environmental, pharmacological, pathological, and the normal ageing process. Hypothermia has profound and widespread physiological effects which can result in diverse pathology; many of these changes are reversible on rewarming. Attempts to normalize physiological or biochemical variables may be misplaced as well as futile, and delayed metabolism and excretion of many drugs could result in overtreatment as the temperature is returned to normal. Full recovery is well documented from profound levels of hypothermia and the associated markedly abnormal physiological states, but arrhythmias and sepsis contribute to an appreciable mortality. In the elderly in particular, underlying predisposing or precipitating factors usually determine the outcome.


How We Lose Heat to the Environment

Radiation - loss of heat to the environment due to the temperature gradient (this occurs only as long as the ambient temperature is below 98.6). Factors important in radiant heat loss are the surface area and the temperature gradient.

Conduction - through direct contact between objects, molecular transference of heat energy

Water conducts heat away from the body 25 times faster than air because it has a greater density (therefore a greater heat capacity). Stay dry = stay alive!

Steel conducts heat away faster than water


Example: Generally conductive heat loss accounts for only about 2% of overall loss. However, with wet clothes the loss is increased 5x.

Convection - is a process of conduction where one of the objects is in motion. Molecules against the surface are heated, move away, and are replaced by new molecules which are also heated. The rate of convective heat loss depends on the density of the moving substance (water convection occurs more quickly than air convection) and the velocity of the moving substance.

Wind Chill - is an example of the effects of air convection, the wind chill table gives a reading of the amount of heat lost to the environment relative to a still air temperature.

Evaporation - heat loss from converting water from a liquid to a gas

Perspiration - evaporation of water to remove excess heat

Sweating - body response to remove excess heat

Respiration - air is heated as it enters the lungs and is exhaled with an extremely high moisture content

It is important to recognize the strong connection between fluid levels, fluid loss, and heat loss. As body moisture is lost through the various evaporative processes the overall circulating volume is reduced which can lead to dehydration. This decrease in fluid level makes the body more susceptible to hypothermia and other cold injuries.


According to the mechanism of the appearing of cold injury there are such groups :

1.     By the cold air

2.     In the environment with high humidity (trench foot). Appears because of medium but long lasting wet cold in case of special position of lower extremites. Such injury starts from desorders of tactile, temperature, pain sensation first on interior surface of first finger and than on all foot. Than edema appear that is not disappearing after warming.

3.     By cold water (immersion foot)

4.     By the contact with things ( metals) with low temperature

Trench and immersion foots appear more often during wars. First deals with long lasting standing on the snow, wet ground in wet shoes. Second – in cases of accidents in the sea in cold period of time.

In the peaceful time most of all frostbites by cold air appear. As a rule the distal parts (mostly arms and feet or nose, ears) of the body become involved.  

Periods of clinic in case of frostbites

1. before reactive (hidden)

2. reactive: early , late


Symptoms of before reactive period are :

                     - filling of cold

                      - itching

                     -  redness of skin that is changing on pailness and coldness;

-         decreasing or loss of sensitiveness of injured areas

-         in case of influence of not intensive but wet cold main symptoms are increasing pain in feet, edema and cyanotic color of skin.

Early reactive period starts from warming and restoring of body temperature and is caracterized by edema on area larger than injured, it increasing during first 6 days, and pain( the more superficial injury is – the more acute pain will be).

As for late reactive period it is carecterized by local symptoms of different degrees (1,2,3,4).


Determination of frostbite depth

1)    Bilrot method: determination of pain sansation by a needle from distal parts of extremity. We are trying to find border of full anaestesia and if after one day border will be the same it is the future demarcation line.

2)    Infrared thermography

3)    Creatincinasa test

4)    X-ray with radionuclids

5)    Electric neuromyography


The classification of cold injuries:

I and II are superficial and III, IV are deep.

Frostbite of the 1 degree

All symptoms are only functional and last 5-7 days. After warming  paleness is changing on hyperemia. Edema of tissues is progressing to 2 days and then it decreasing to 6-7 days when shelling (peeling) of epidermis appear. Tactile and pain sensitiveness (sensation) are preserved but sometimes with disorders. Moves of fingers of hands and feet too. Pain in injured areas could be severe, itching also could be.

Frostbite of  the 2 degree.

Edema of tissues spreads during first 2 days and bullas with limpid liquid, similar to plasma, like in case of burns, appear. Bullas appear on 2 day after injury.  Bottom of the opened bullas is papillar-epithelial layer of skin, covered by fibrin. It is of pink color and is sensitive for pain and temperature action. Regeneration as a rule appears without suppuration during 2 weeks. Cyanosis of skin, hard moves of between phalanges joints and decreasing of force of hands could last 2-3 month. Morphologically: necrosis of skin in case of injuries of 2 degree develops in keratic and granular layers. Growth layer of skin is not injured, that’s why restoration of the skin cover lasts 1-2 weeks. Nails are falling off but grow then again. Regeneration of lost skin areas is full, scars are not developed.

P. 1


Frostbite of  the 3 degree.

Necrosis of all skin layers or even fatty tissue appears. Inflammation develops: firstly aseptic and then on 5- 7 day purulent one. Bullas have blood contains. Decreasing of tactile and temperature sensation can develop. Edema of tissues spreads on the proximal areas. Firstly skin has cyanotic color then dark brown and black crust is formed. Sometimes if local treatment is not good wet necrosis is formed. After rejection or removing of crust wounds are healing during 2,5-3 months scars of connective tissue or chronic trophic ulcers are formed.  Different defects and deformations on the face are the results of frostbites of the 3 degree of nose, ears, lips.


Frostbite of 4 degree.

Necrosis of all skin, fat tissue and even bones and joints. Mummification or wet gangrene are formed. After warming, colour of skin is grey or dark-blue. Edema of tissues covers much bigger area than injured zone. Demarcative line appears at the end of the first week, but it could be determined exactly at the end of second week. The results of 4 degree of frostbites are loss of fingers, parts of organs, nose, ears.

P. 2



 X-ray changes on 25-30 days after trauma could be noticed. In case of cold injuries of 1, 2 degree osteoporosis on small areas of bones, mainly in the metaphysis could be noticed. In case of cold injuries of 3-4 degree – diffuse and cellular osteoporosis could develop. In phalanges of fingers and bones of wrist and tarsus there are clarifications of different forms and sizes.

In cases of superficial burns (1,2 degrees) total stage of patient is not changing a lot. Only in case of suppuration of bullas short lasting hyperthermia, leucocytosis appear. Such clinic also could be in cases of frostbites of 3, 4 degree of distal parts of fingers .

In cases of spread frostbites of 3, 4 degrees of limbs, ears as a rule inflammatory process appears, on 2-3 day intoxication caused by necrosis  and development of infection. During first 2 weeks after  trauma  chills, hectic temperature, loss of appetite, grey color of skin could appear. Tachicardia (  120-140/min), dull heart tones. Amount of leucocytes in blood 20-30 G/l. 

Electrolytic disorders, hypoproteinaemia, hyperbilirubinemia, proteinuria.

        Clinically frostbites on early terms are characterized by polyuria, acute catarrhal symptoms. Duration of intoxication and disorders of homeostasis depends on local treatment of cold injuries. After the separation of necrotic tissues the total stage of patient is becoming better. But during treatment different complications could appear.  


   TREATMENT of frostbites

Main aim of first aid is warming of the injured part, restoring of blood circulation and prophylaxis of infection.

So, first aid in case of cold injury includes (before reactive period).

1.     Taking off cold, wet shoes, socks, gloves very carefully

2.     Gradual warming using method of interior warming of limbs by means of 3, 4 layers special thermoregulative dressings during 24-36 hours.

3.     Wash the area with ethyl spiritus using it’s vessel widening and antibacterial function.

4.     Hot drinks, warm bed.

5.     Aseptic bandage with cotton wool after using antiseptics.

          6.   Inhalation of oxygen

Infusion therapy includes:

-         vasodilators ( 2% papaverin 2 ml every 6-8 hours, 0,1% novocain 150-200 ml every day  during first 3 days). We take in to account vessel spasm.

-         antigistamine drugs - 1% dimedrol 1 ml every 6-8 hours or pipolfen 2 ml every 8 hours

-           steroid hormones – dexametason 8 mg every 8-12 hours

-         inhibitors of kininscontrical 30-40 000 units every 12 hours. Because kinins make worser local microcirculation by means of increasing  of permeability of capillars.

-         anticoagulant – heparin 5 000 units every 4-6 hours during first 3 days under the coagulation control. It decreases coagulation and activates fibrinolitic functions of blood.

-         desagregantspentoxyfilin 5 ml every 12 hours during 10 days. It make better microcirculation by increasing of ability of erythrocytes to deformation  and it decrease producing of acute inflamatory mediators.

-         lowermolecular dextranreopolyglucin 200 ml one time a day 5-7 days. It prevents agregation of blood elements

-         trombolytic drugs ( fibrinolysin, streptokinasa) under the sceme. Theire function is to dissolve fibrin threads, provide lysis of microthrombs.

-         vitamins – B1 2 ml one time a day, B6 2 ml one time a day, B12 1 ml one time a day, C 6-8 ml 10% every 12 hours, nicotinic acid 2 ml 1% ones a day. They restore metabolism in tissues.

-         antiinflamatory  therapy: antibiotics of wide spectr of influence: cefatoxim 1 gr. every 8-12 hours, ceftriaxon 1 gr. every 12 hours, in severe cases accompaning with ftorhinolons: cefran, ciprinol.

-         in cases of disorders of  kidney function method of forced diuresis  is used by lasix, furosemid, manitol, with next correction of  electrolytic and  acidotic disorders by Na hidrocarbonate 5%.

-         in case of anemia  - washed erytrocytes,  erythrocyte mass

-         in case of hypoproteinemia – plasma, albumin, protein, lactoprotein

-         enteral and parenteral nutrition

-         immune therapy – antistafilococ globulin intramuscular 3-6 mg a day 1-2 weeks. Antisafilococ plasma intravenously 100-300 ml 3-5 times with brake in 2 days.

Volume of transfusions is 2- 4 l,or 30-60 ml/kg.

All these drugs is better to use i/a, i/bone, under apponevrotic spaces ( 0,25% novocain ). We can use blocks ( sympathic, paranefral) with their vasodilating and analgesic function.

Conservative therapy program:

-         in before reactive period and first days of early reactive period drugs that influence on microcirculation are most important

-         in early reactive period drugs with detoxication function should be added

-         in late reactive period when necrotic processes appear drugs with anti anemic and antiohypoproteinaemia  should be added.                   


Local treatment

1 degree of frostbites should be treated in such a way: primary cleaning of injured areas, dressing with water-soluble oinments, physiotherapeutic treatment. After the treatment at the hospital usage of medicine that improve reology of blood has to be recomended.

2 degree of frostbites should be treated in such a way:  primary cleaning of injured areas with cutting of all bullas, dressing with water-soluble oinments, position of extremites higer than body.

3-4 degree frostbites should be treated only at a burn department. After first sanation of wounds necrotomy, fasciotomy have to be used during first hours of reactive period. After that it is better to put the extremity into the special aerotheraputic sets for fastering of mumification of necrotic tissues and decreasing of intoxication. Everyday dressings should be provided. Separation of necrotic tissues by means of necrectomies and amputations after 4-6 days after the trauma are recomended.  After appearing of granulations (3-4 week) – free plastic or other methods of autotransplantation are used.

            New method of treatment of frostbites includes early necrectomy and xenografting.



         P. 3 Frostbite of II-III st.

P. 4 Early necrectomy

P. 5 Xenografting

P. 6 7th day after xenografting

P. 7  14th day after xenoplasty


        In case of III-IV st. xenografting is always combined with autoplasty.

P. 8  Frostbite of III-IV st.

P. 9 Early necrectomy

P. 10 Xenografting

P. 11 Granulating wound after xenografting

P. 12 Autografting

P.13 result of treatment


   Protezing is used after 3-4 month after healing and formation of scars. At the same time reconstructive operations for removing of defects (of nose, ears) should be provided.


                       Complications  of  frostbites

Early:      1) local:

a)     infection of bullas

b)    acute lymphangoitis, lymphadenitis

c)     abscesis, phlegmons

d)    acute pure artritis

                         2) total:

                      diseases of kidnees and lungs, anaerobic infection ( tetanus).

Late:                 a) osteomielitis

                          b) trophic ulcers

                          c) osteoporosis

                          d) obliterative diseases of  vessels

                 e) neuritises





It is the pathological hypothermia of the organism that in severe cases leads to death. In it’s development not only the temperature but also humidity, wind  play role.

In case of hypothermia main symptoms deal with depression of central nervous system, cardio-vascular and respiratory system. This symptoms are connected directly on temperature of the organism. 

How to Assess if someone is Hypothermic

If shivering can be stopped voluntarily = mild hypothermia

Ask the person a question that requires higher reasoning in the brain (count backwards from 100 by 9's). If the person is hypothermic, they won't be able to do it. [Note: there are also other conditions such as altitude sickness that can also cause the same condition.]

If shivering cannot be stopped voluntarily = moderate - severe hypothermia

If you can't get a radial pulse at the wrist it indicates a core temp below 90 - 86 degrees

The person may be curled up in a fetal position. Try to open their arm up from the fetal position, if it curls back up, the person is alive. Dead muscles won't contract only live muscles.


There are 4 stages :


1) Adynamic        35C  temperature of the body,  adynamia,  pail skin, acrocyanosis, pain in fingers,”goose” skin, chill, arterial pressure and breezing are normal as a rule, , total fatigue.

2) Stupor             320 C , adynamia, pail or even cyanotic skin,  bradycardia 50/min, hypotension, breezing 12/min, muscular weakness, sleepness, decreasing of reflexes.

3)  Cramp st.        – lower then 300 C, loss of conshesness , pulse lower 34/min,dull tones, hypotension, superficial, therminal breezing, cramps.

4) Terminal st.     -   lower 24C, when changes in the organizm will not be restored.



First aid : dry close, warming by some blankets, hot sweet tea,  transporting to the nearest hospital, reanimation.


CPR Procedures

Check radial pulse, between 91.4 and 86 degrees F this pulse disappears

Check for carotid pulse - wait at least a full minute to check for very slow heartbeat

If pulse but not breathing or slow breathing, give rescue breathing (also adds heat).

If no discernible heartbeat begin CPR and be prepared to continue - persons with hypothermia have been given CPR for up to 3.5 hours and have recovered with no neurological damage

Begin active rewarming


Things to avoid

Alcohol - a vasodilator - increases peripheral heat loss

Caffeine - a diuretic - causes water loss increasing dehydration

Tobacco/nicotine - a vasoconstrictor, increases risk of frostbite


At the hospital the aim of treatment is to restore the normal temperature, prophilaxis of complications after the warming.

Patients with easy injury could be warmed by infrared lamp. You have to change the wet close , give the warm tea , warm food, put the patient to the warm ward ( 28-30 C) . After some hours (8-10) they become active, and later could be transported to total regime and after 1-2 days  they can go home.

    In case of severe cooling (2,3 st.)  patient needs warm bath (37-40 C )with massage during 30 min – 1 hour . Cataterization of central vein. Intravenously warm infusions of 

   -   200-400 ml 10 % glucose with ascorbinic acid 10ml 5% ,

   -  200-300 ml 5% bicarbonate Na,

    -  1,0-1,5 0,025% strofantin

    -  100-150mg cocarboxilasy

    -   8-12 mg dexametazon

    -  5 ml pentoxyfilin

    -  1-2 ml 2% dimedrol

    -  10 ml 10% cloric Сa

    -  2 ml 1% nicotinic acid

    -  contrical 30-40 000 un. In  200 ml NaCl

    -   2-4 ml papaverin

     -  200-300 ml refortan

     - 2 ml 1% furosemid.

   When symptoms of edema of lungs appear – degidratative therapy.  Later this patients get infusive therapy  during  6-8 days 15-20 ml/kg a day.

    After the normalizing of patient’s stage – the prevention of disorders of function of central and peripheral nervous system , pneumonia, nephrities .

    After the patients’ recovery they need long lasting control (1-3 month) by  different specialists ( therapeutic, neurologic, nephrologic).


Particularities of hypothermia treatment in European countries and USA


Treating hypothermia at home


If you're treating someone with mild hypothermia at home, or waiting for medical treatment to arrive, the following advice will help to prevent further heat loss.

Move the person indoors or somewhere warm as soon as possible.

Once the person is in a warm environment, carefully remove any wet clothing and dry the person.

Wrap them in blankets, towels, coats (whatever you have available), protecting their head and torso first.

Your own body heat can help someone with hypothermia. Gently hugging them can help to warm them up.

Encourage the person to shiver if they're capable of doing so. 

If possible, give the person warm drinks (not alcohol) or high energy foods, such as chocolate, to help warm them up. However, it's important to only do this if they can swallow normally (ask them to give a cough to see if they can swallow).

Once the person’s body temperature has increased, keep them warm and dry.


Warm the center of the body. Focus on the chest, neck, head, and groin. If one is available, use an electric blanket. Otherwise, use skin-to-skin contact under loose, dry layers of blankets, clothing, towels, or sheets.[1] Whatever you apply should be warm rather than hot--no hot water, heating pad or heating lamp--and do not attempt to warm the arms and legs, as this will push cold blood back toward the heart, lungs and brain, making things worse


Treating Hypothermia

The basic principles of rewarming a hypothermic victim are to conserve the heat they have and replace the body fuel they are burning up to generate that heat. If a person is shivering, they have the ability to rewarm themselves at a rate of 2 degrees C per hour.


Mild - Moderate Hypothermia

1. Reduce Heat Loss

Additional layers of clothing

Dry clothing

Increased physical activity



2. Add Fuel & Fluids


It is essential to keep a hypothermic person adequately hydrated and fueled.


a. Food types

Carbohydrates - 5 calories/gram - quickly released into blood stream for sudden brief heat surge - these are the best to use for quick energy intake especially for mild cases of hypothermia

Proteins - 5 calories/gram - slowly released - heat given off over a longer period

Fats - 9 calories/gram - slowly released but are good because they release heat over a long period, however, it takes more energy to break fats down into glucose - also takes more water to break down fats leading to increased fluid loss


b. Food intake

Hot liquids - calories plus heat source

Sugars (kindling)

GORP - has both carbohydrates (sticks) and protiens/fats (logs)


3. Add Heat

Fire or other external heat source

Body to body contact. Get into a sleeping back, in dry clothing with a normothermic person in lightweight dry clothing


Severe Hypothermia


1. Reduce Heat Loss

Hypothermia Wrap: The idea is to provide a shell of total insulation for the patient. No matter how cold, patients can still internally rewarm themselves much more efficiently than any external rewarming. Make sure the patient is dry, and has a polypropylene layer to minimize sweating on the skin. The person must be protected from any moisture in the environment. Use multiple sleeping bags, wool blankets, wool clothing, Ensolite pads to create a minimum of 4" of insulation all the way around the patient, especially between the patient and the ground. Include an aluminum "space" blanket to help prevent radiant heat loss, and wrap the entire ensemble in plastic to protect from wind and water. If someone is truly hypothermic, don't put him/her naked in a sleeping bag with another person.


2. Add Fuel & Fluids

Warm Sugar Water - for people in severe hypothermia, the stomach has shut down and will not digest solid food but can absorb water and sugars. Give a dilute mixture of warm water with sugar every 15 minutes. Dilute Jello™ works best since it is part sugar and part protein. This will be absorbed directly into the blood stream providing the necessary calories to allow the person to rewarm themselves. One box of Jello = 500 Kilocalories of heat energy. Do not give full strength Jello even in liquid form, it is too concentrated and will not be absorbed.

Urination - people will have to urinate from cold diuresis. Vasoconstriction creates greater volume pressure in the blood stream. The kidneys pull off excess fluid to reduce the pressure so the person will urinate. In order to reduce the potential heat lost from wet clothing fashion a 'diaper" for the person inside the hypothermia wrap and wrap that with a garbage bag. That will serve to allow them to urinate and prevent the wetness from leading to evaporative heat loss. You will need to keep them hydrated with the dilute Jello solution described above.


3. Add Heat

Heat can be applied to transfer heat to major arteries - at the neck for the carotid, at the armpits for the brachial, at the groin for the femoral, at the palms of the hands for the arterial arch.

Chemical heat packs such as the Heat Wave™ provides 110 degrees F for 6-10 hours.

Hot water bottles, warm rocks, towels, compresses

For a severely hypothermic person, rescue breathing can increase oxygen and provide internal heat.



Is a situation in which the core temperature actually decreases during rewarming. This is caused by peripheral vessels in the arms and legs dilating if they are rewarmed. This dilation sends this very cold, stagnate blood from the periphery to the core further decreasing core temperature which can lead to death. In addition, this blood also is very acetic which may lead to cardiac arrythmias and death. Afterdrop can best be avoided by not rewarming the periphery. Rewarm the core only! Do not expose a severely hypothermic victim to extremes of heat.



Cold Stress Prevention: 7 Safety Tips to Prevent Hypothermia and Frostbite


Yesterday we discussed the importance of keeping work areas clear of snow and ice. By following proper procedures in getting rid of unwanted ice and snow, you avoid the heightened risk of slipping or falling on the job.

Unfortunately, the cold weather brings with it more risks that are invisible to the naked eye. Actually, they’re really invisible. With the dropping temperature across the nation, workers are under the threat of suffering from cold stress. Those who belong to the construction, agriculture, maritime and commercial fishing industries are the most exposed to the fatal hazards of cold weather.

Cold stress can be a fatal threat to every worker. Once exposed to cold or freezing temperature for long periods of time, they run the risk of losing a serious amount of body heat. If not treated immediately, this could lead to brain damage and even death.


Here are safety tips to prevent cold stress or cold-induced illnesses or injuries:


1. Train employees for the cold and changing weather.


Training sure is a timeless necessity in the workplace. In these colder days, workers must be trained not only about cold-induced illnesses and injuries, but also to determine environmental or work site conditions that may cause cold stress. They should be especially trained in recognizing the signs and symptoms of cold stress or cold-induced injuries like hypothermia and frostbite.


Here are signs and symptoms of hypothermia:

Cool skin

Slower, irregular breathing

Slower heartbeat

Weak pulse

Uncontrollable shivering

Severe shaking

Rigid muscles



Slurred speech

Memory lapses


The following are signs and symptoms of frostbite:

Paleness of the skin

Sensation of coldness or pain

Pain disappears after a while with the freezing of the tissues.

Tissues become increasingly whiter and harder.



2. Use a buddy system.

Sure, you may want to be left to yourself while working. But believe me, this is not the time to enjoy solitude while accomplishing your tasks outdoors. You don’t want to be working one minute and thawing your fingers the next.

So get a partner and work on monitoring each other for signs of cold stress. Don’t be stubborn because most of the time, it’s just difficult to determine danger signs when you only have yourself to rely on.


3. Adjust your work schedule to the cold or changing weather.

Don’t punish yourself too much. Just because you have to work outside and it feels like stepping into a walk-in freezer, it doesn’t mean you have to bask in the frigid winds all day.

Schedule work during the warmest part of the day. Break a task into shifts so you can take frequent, short breaks in warm dry shelters.


 4. Layer clothing.

At this time of the year, the saying “less is more” surely does not hold true. Well, maybe partly true since wearing less clothes means getting exposed to more cold-stress-related threats.

Remember that it’s better to go for several thin layers of clothing instead of wearing just a couple of thick layers. For clothes next to the skin, choose those with synthetic fabrics to avoid absorption of sweat. An ideal choice is polypropylene. For your outer layer, choose fabrics made of waterproof and wind-resistant material.


5. Wear complete PPE (personal protective equipment).

You know you need it. Wear warm gloves, hats and hoods. In extreme conditions, don a warm woolen hood that covers your neck, head and ears. If you get hot while working, just open your jacket. Don’t remove your hat and gloves. The key is in wearing clothing that can be adjusted to changing conditions.

Avoid wearing tight-fitting footwear as this restricts blood flow. Your shoes or boots should allow you to wear either one thick or two thin pairs of socks.


6. Eat and drink hot or warm foods and liquids.

You might have to say goodbye to hot coffee and choco for a while. Drinking caffeinated and alcoholic beverages is not recommended while working in cold weather. Instead, go for warm, sweet beverages like sports drinks and sugar water. Keep in mind that you are also at risk of dehydration under cold weather so make it a habit to drink up.

Good news, though. You can feast on hot pasta dishes, soups and other foods rich in calories. Remember, though, that if you’re sick or under medication, you are more at risk to get cold stress. This is especially true if you have hypertension, diabetes or a cardiovascular disease.


7. Wear eye protection.

Ice or snow + excessive ultraviolet rays = eye injury. Yes, this is one proven equation. Before working outside, check first if you may be exposed to glare or, worse, blowing ice crystals. If conditions point to the affirmative, then go wear the right kind of eye protection.


When the cold is good!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!



Cryotherapy is the use of cooling to treat injuries. The effects of cooling on damaged soft tissues has been researched and although the benefits are accepted, there are varying opinions on the duration of the cooling process in order to gain maximum benefit.



The body's reaction to an injury


An injury means tissues will have either been stretched or blood vessels damaged and the extent of bleeding will depend on the vascularity of the tissues involved. It is important to stop bleeding as it will increase inflammation which must be cleared before the healing can start.


Cells starved of nourishment due to injury will soon die. These dying cells stimulate the release of histamine causing the blood vessels to dilate which increases blood supply and extra nutrients to help repair the damaged tissues. With an increase in blood supply the capillary walls become much more permeable and Protein and inflammatory substances are pushed into the area causing swelling.


Muscle spasm may also occur causing the muscle to contract helping prevent further movement. This may restrict blood flow and place more pressure on nerve endings, leading to increased pain.




By applying ice immediately after a soft tissue injury the level of swelling and amount of blood allowed to leak out may be substantially limited. This can also be assisted by compression, elevation and rest, hence "ICER", (or more commonly "RICE)

Ice - Apply ice for up to 10 minutes as soon after the injury as possible - do not wait for the swelling to start. This may be repeated every 2 hours during the first two days after injury. It is important not to keep the ice on any longer than 10 minutes as the body then reacts by increasing blood flow to warm the area and therefore exacerbating the swelling. Do not apply ice directly to the skin. Use a wet flannel

Compression - After ice, apply a compression bandage to help minimise the swelling to the tissues

 Elevation - Elevate the injured part to help limit blood flow and prevent use of muscles to injured part

Rest - the injured part as much as possible to allow the healing of damaged tissues


Failure to follow the RICE protocol will increase the period of recovery from injury. If the injury is severe and not properly managed, it may create long term problems for the athlete.



Use of Ice


When applying ice never apply directly onto the skin as this may result in ice burns to the skin, instead wrap the ice in a damp cloth (a dry cloth will not transmit cold effectively).


There is on going debate over how long to apply ice. Current research suggests that during the first 24-48 hours after injury ice should be applied for 10 minutes and repeated every 2 hours.


If the ice pack is left on for more than 10 minutes, a reflex reaction occurs (Hunting effect) where the blood vessels dilate and blood is again pumped into the injured area, causing further bleeding and swelling.


Ice will have an analgesic effect on the injured part by limiting the pain and swelling, muscle spasm may also be reduced. Whilst this has obvious benefits, be cautious about reducing the pain, as this may mask the seriousness of the injury.


During the first 24 to 72 hours after an injury be sure to avoid any form of heat at the injury site (e.g. heat lamps, heat creams, spa's, Jacuzzi's and sauna's), avoid movement and do not massage the injured area as these will increase the bleeding, swelling and pain.


After the initial healing period of up to 72 hours (depending on the severity of the injury), ice massage may be incorporated into treatments. By applying stroking movements with an ice pack, the blood vessels will dilate and constrict alternately bringing an increased supply of blood and nutrients to the area, and so increasing the rate of healing. This may be done for more than 10 minutes to increase circulation.

Ice Baths


Ice baths have become popular in contact sports like rugby and American Football and with endurance athletes. For contact sports whole body ice baths can be considered and for sports that predominantly stress the legs, such as football, field hockey, running etc. immersion of the lower limbs only can be considered. Initially start with one minute sessions and progressing to a maximum of 10 minutes over a period of 10 weeks

Contra indications of using ice

 Check a person's general sensitivity to ice - some people find the application of cold immediately painful

Do not use ice on injuries in the chest region as in some instances this may cause a reaction in the muscles, bringing about angina pain, possibly from the constriction of coronary arteries

 Always check skin sensitivity before applying ice - if a person cannot feel touch before applying ice it may indicate other problems such as nerve impingement. In such instances ice would only serve to mask this and complicate the problem

Do not apply cold to someone with high blood pressure as vasoconstriction will increase the pressure within the vessels.


Can you really cure cellulite, acne and fatigue with just three minutes in a deep freezer?



Stepping into a cold chamber and being chilled to sub-zero temperatures for three minutes sounds less than enticing. Double your time in the chamber and you will almost certainly freeze to death. Now that sounds like pure madness.


Yet more and more people are lining up for the latest fad to hit Australia: Whole Body Cryotherapy.


The alternative health treatment that originated in Japan and is increasingly popular in Europe involves exposing yourself to cold, dry air for up to three minutes at a time.


Patients are blasted with nitrogen gas chilled to below minus 150 degrees, which shocks the body into action by revving up blood circulation and stimulating the immune system.


To give you an idea of just how bitterly cold that is, the lowest recorded temperature was minus 89 degrees in Antarctica.


So why would anyone voluntarily step into a Cryotherapy chamber?


The treatment has been embraced by elite athletes including F1 Racing Driver Mark Webber and England Rugby League captain James Graham who claim it speeds up their recovery process and enhances their performance.


But it is the long list of aesthetic benefits that has seen Whole Body Cryotherapy attract a growing number of fans.


The body-numbing sessions boost the complexion, improve skin tone, increase energy and banish the appearance of cellulite.


Acne, eczema, insomnia and psoriasis sufferers have also reported significant improvements in their condition following a treatment.


According to Karl Benn manager of the Cryolab in Sydney, after just one treatment a patient’s white-blood cells will have increased by four times and they will have burned around 1000 calories.


It is with these gilded promises in mind that I step into the Cryotherapy chamber.


Dressed in nothing more than underwear and fluffy slippers – any other material would be frozen – I have to shuffle around in the tiny chamber for the next two minutes to keep the circulation moving and prevent any nasty skin burns.


The first few blasts of nitrogen gas to enter the chamber are surprisingly bearable. Despite the temperature already having dropped to below minus 60 degrees, it feels no more uncomfortable than standing in a cool room.


However as the temperature plummets, the dry icy air takes my breath away.


Goosebumps cover my body and I shiver uncontrollably. The last twenty seconds of the treatment feels like an eternity and as the icy fog swirls around me I am desperate to get out of the chamber.


Finally after seven blasts of nitrogen gas chills the chamber to minus 170 degrees I am allowed to escape.


Surprisingly I don’t have the urge to wrap myself in a big fluffy blanket, however I do get the occasional urge to shiver.


Dressed back in my summer attire, my skin is blotchy, red and tingly all over kind like I’m badly sunburnt.


But I feel euphoric and energized as if I could run a marathon.


Later that feeling quickly turns to exhaustion and I am famished, namely due to burning excess calories (and perhaps the fact I skipped breakfast.)


In the days that follow the treatment, friends comment that my skin looks brighter and there is a noticeable improvement to the psoriasis that had plagued me since I was a child.


So how does it work?


The theory behind Whole Body Cryotherapy is that it tricks the body into believing it is in serious danger of freezing. The brain sends signals to the rest of the body to draw blood from the extremities and rush it to the core for protection. After the treatment the blood rushes back out again, increasing capillaries and white blood cells by up to 400 per cent.


The cold also triggers the nervous system to release feel-good endorphins and a natural anti-inflammatory, resulting in an energy boost, skin rejuvenation and pain relief.



What cryotherapy for cancer  is


Cryotherapy uses extreme cold to destroy cancer cells. It is also called cryosurgery or cryoablation. During cryotherapy treatment the doctor freezes the cancer cells to kill them. Cryotherapy is called a local treatment, which means that it only treats the area where you have treatment. It doesn’t treat any cancer cells in other parts of the body. After the treatment the body’s immune system gets rid of the dead tissue over a few weeks.

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Which cancers are treated with cryotherapy


Doctors use cryotherapy to treat a number of different types of cancer and precancerous conditions. Cryotherapy has been a treatment for abnormal cells on the cervix and for basal cell skin cancer for some time. It works well for these conditions.


Research has shown that cryotherapy is safe to use for some other types of cancer and kills the cancer cells in the treatment area. But we need more information about the long term outlook to find out if it is as good as other treatments at stopping the cancer coming back.


Even if cryotherapy isn’t a standard treatment for your type of cancer you may have it as part of a clinical trial.

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Where you go to have treatment


You have cryotherapy in hospital. For skin cancer or cervical changes you usually have the cryotherapy in the outpatient department. For internal cancers you may have treatment as an outpatient or in the operating theatre.

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Having cryotherapy for skin cancer


For skin cancer, a doctor sprays liquid nitrogen on to the area of cancer. Or they put it directly on to the area with a cotton swab. The liquid freezes the area. After treatment the liquid nitrogen dissolves and the area thaws. A scab forms in the area. Over the next month or so the scab falls off along with any dead cancer cells.

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Having cryotherapy for changes on the cervix


To treat precancerous changes on the cervix the doctor or nurse specialist puts a speculum into the vagina so they can see the cervix. They then put special instruments called cryo probes into the vagina so that they firmly cover the abnormal areas of cervical tissue. The liquid nitrogen in the cryoprobes then freezes the cells. The doctor or nurse may repeat this a couple of times. This treatment usually takes less than half an hour. You can find information about cryotherapy for cervical cancer and the possible side effects in the cervical changes section of CancerHelp UK.

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Having cryotherapy for cancer inside the body


For cancers inside the body the doctor puts a small probe next to or inside the tumour. This probe is called a cryoprobe. The cryoprobe is attached to a supply of liquid nitrogen controlled by the doctor. Your doctor or specialist nurse will talk to you beforehand about how you will have treatment and exactly what it involves for you.


Some cancers need to be frozen and thawed a number of times. Depending on the treatment area, it can take from a few minutes to a couple of hours.


To help the doctor position the cryoprobe you may have either an ultrasound scan or CT scan.


The position of the cancer in the body affects how the doctor puts the cryoprobe into the area. This may be

Through the skin (percutaneously)

Through a scope

Cryotherapy through the skin (percutaneously)


If you are having the cryoprobe put in through your skin you may have a general or a local anaesthetic. For example, men having cryotherapy for prostate cancer have the probes put into the skin of the perineum (the area of skin between your back passage and your testicles). For cryotherapy to the liver the doctor puts the probe in through the skin of the abdomen.


And for kidney cancer the doctor uses a thin, flexible tube called a laparoscope to help them position the cryoprobe. The laparoscope has a light and a tiny camera at the tip. The doctor makes a small cut in the skin on the side of the abdomen to put the laparoscope through. They can then position the cryoprobe.

Cryotherapy through a scope


The other way doctors can reach tumours inside the body is by using a scope without going through the skin. For example for lung cancer the doctor may use a bronchoscopy to position the probe. Or for cancers in the food pipe you may have an endoscopy.

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Side effects of internal cryotherapy


Before you agree to treatment your doctor will talk to you about the possible risks. The risks and possible side effects depend on the type of cancer you have and its position in the body. An advantage of cryotherapy is that it is not as invasive as having an operation. People usually recover within a few days after the treatment with very few side effects.


The side effects it can cause include the following.

Pain and discomfort in the treatment area – your doctor will prescribe painkillers to help to control this and it should settle within a few days

Bleeding from the treatment area – your nurse will check your blood pressure, pulse and wound on your skin (if you have one) regularly 

Damage by freezing normal tissue close to the treatment  area – your doctor will try to avoid this as much as they can


People having cryotherapy for a lung tumor may have a build up of fluid around the lung and damage to the lung tissue.


Men having cryotherapy for prostate cancer have a small risk of nerve damage, which can cause difficulty getting an erection (impotence).


IV.            References:

 Essential reading:

1. Rintamaki H; Predisposing factors and prevention of frostbite. Int J Circumpolar Health. 2000 Apr;59(2):114-21. [abstract]

2. Chilblains, Clinical Knowledge Summaries (November 2009)

3. Mechem CC; Frostbite. eMedicine, June 2007.

4. Murphy JV, Banwell PE, Roberts AH, et al; Frostbite: pathogenesis and treatment. J Trauma. 2000 Jan;48(1):171-8. [abstract]



Further reading:


  1. Francis TJR, Golden FStC. Non-freezing cold injury: The pathogenesis. J R Nav Med Serv. 1985;71:3–8.

  2. Francis TJR, Oakley EHN. Cold injury. In: Tooke JE, Lowe GDO, eds. A Textbook of Vascular Medicine. London,England: Arnold; 1996: 353–370.

  3. Francis TJR. Non–freezing cold injury: A historical review. J R Nav Med Serv. 1984;70:134–139.


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