Theme:
Frostbite and hypothermia. Pathogenesis, diagnostic and treatment
Plan
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
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
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
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
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
Aetiology
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.
Pathophysiology
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
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.
Haematology
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
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
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.
Conclusion
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 kinins – contrical
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.
-
desagregants – pentoxyfilin 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 dextran – reopolyglucin 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-
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
Hypothermia
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 –
2) Stupor –
3) Cramp st. – lower then
4) Terminal st. -
lower
Treatment
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-
In case of
severe cooling (
- 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 Ña
- 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
Shelter
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.
Afterdrop
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
Drowsiness
Exhaustion
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
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.
RICE
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
The alternative health
treatment that originated in
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
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.
Back to top
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.
Back to top
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.
Back to top
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
Back to top
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.
Back to top
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,
Further
reading: