STUDY - Technical - New Dacian's Medicine
Hypothermia
Translation Draft
Hypothermia is arbitrarily defined as a central body temperature of 35 degrees Celsius or less and is classified as mild (from 35 to 32 degrees Celsius), moderate (from 32 to 28 degrees Celsius) or severe (less than 28 degrees Celsius).
It can have a few causes and usually has multifactorial origin. Precise estimates of incidence are difficult to obtain, because nonfatal hypothermia is often undetected or unreported and fatal hypothermia is likely underreported. Most cases occur in the winter months, in areas with cold climates, but hypothermia can occur in areas with mild climates in any season.
Risk factors include extreme ages (especially the elderly), homeless people, alcohol users, malnutrition, poverty, mental illness, neuroleptic use and hypothyroidism. A common context is chronic exposure to the cold in the house in a poor elderly person with a pre-existing disease and immobility.
Heat is generated in most tissues of the body and is lost by radiation (55%), evaporation (5% through the airways, 25% through the skin), conduction (15%) convection (5%). Immersion in water causes hypothermia faster as the thermal conductivity of water is 20 to 30 times that of air.
The balance between production and heat loss in the body is regulated by the hypothalamus (preoptic and posterior regions). Exposure to cold activates the cold-cut receptors that transmit the signal through the lateral spinotalamy tracts to the preoptic cords in the hypothalamus.
The posterior hypothalamus activates the sympathetic nervous system to increase muscle tone and causes trembling, which in turn increases the metabolic rate from a normal level of 40 to 60 kcal/hour to a value of 300 kcal/hour. Even at maximum metabolic rates, heat loss in the body can exceed heat production. As body temperature drops below 30 degrees Celsius, metabolic processes slow down and trembling stops, thus accelerating the process of hypothermia development.
Extreme environmental conditions can cause hypothermia in healthy individuals, but it rarely requires medical attention. The most severe hypothermia occurs in people with pre-existing medical problems, which lead to excessive heat loss (usually involving exposure to the environment - keep in mind that body temperature never drops, under normal conditions, below the average temperature, most of the environmental exposures being accidental) or inadequate heat production.
Iatrogen hypothermia can occur when obnubilpatients are left unwrapped in reserves or during surgical procedures, when large body areas are exposed for long periods of time in the operating room. This is especially possible due to the fact that the response consisting of trembling is inhibited by anesthesia, increasing the risk of hypothermia.
The only manifestation in this situation may be the difficulty of obtaining hemostasis due to the inactivation of coagulation factors at low temperatures. Increased blood flow to the skin (burns, psoriasis) can also cause hypothermia in the presence of minimal change in the environment, as the preservation of heat through peripheral vasoconstriction is inadequate.
Low heat production can contribute to hypothermia especially against the background of malnutrition and/ or inaniation, by decreasing the glycogen and fat deposits needed for actual heat production. Hypothermia occurs in more than 10% of patients with sepsis (usually bacterial) and is often associated with a severe prognosis.
Approximately 40% of resting oxygen consumption is regulated by thyroid hormones and hypothermia is common in severe hypothyroidism, when metabolic rate can be reduced to 40% below normal. Hypothermia from liver failure is commonly due to a combination of hypoglycaemia from inadequate hepatic gluconeogenesis and altered hypothalamic function (decrease in trembling).
Hypoglycaemia of any cause (glucocorticoid deficiency, alcohol consumption, hyperinsulinism), uremia and diabetic ketoacidosis, also predispose to hypothermia. Hypothalamic lesions (tumors, inflammation) can cause thermoregulatory instability and hypothermia. Spinal cord injuries to or above the first root of the thoracic nerve can lead to hypothermia by blocking trembling and interrupting cold-induced compensatory reflexes mediated by the lateral spinotalamy tracts.
Spontaneous episodic hypothermia with hyperhidrosis is a rare condition associated with excessive sweating in the absence of tremor (almost half of these patients have calos body agenesis - Shapiro syndrome), suggesting a central nervous system (CNS) etiology.
Some drugs may contribute to hypothermia, such as phenothiazines, barbiturates, opiates, benzodiazepines and ethanol, inhibiting tremor through their effects on CNS.
Acute exposure to cold causes tachycardia, increased cardiac activity, peripheral vasoconstriction and increased peripheral vascular resistance secondary to sympathetic stimulation. As body temperature drops below 32 degrees Celsius, cardiac conduction is impaired and heart rate and heart rate decreases.
Low ventricular response atrial fibrillation is common below 32 degrees Celsius and ventricular fibrillation may occur below 28 degrees Celsius. Peripheral vasoconstriction sprints the blood to the central circulation and increases the central blood volume, defending diuresis (cold diuresis), tending to decrease intravascular volume in a compensatory manner.
Through prolonged exposure to cold, the combination of diuresis to cold, additional volume losses due to altered resorption of sodium and water by the kidneys (due to inadequate function of epithelial transport mechanisms) and exchanges of intravascular fluid to intracellular fluid and peripheral edema can cause severe volume and hypotension.
In turn, volume deletation leads to increased hemoconcentration and blood viscosity that predisposes to thrombosis. On the contrary, bleeding due to ineffective clotting at low temperatures, thrombocytopenia and disseminated intravascular coagulation can even cause minor trauma, resulting in significant blood loss.
Acid-base and electrolyte imbalances depend on the duration of exposure to cold. Lactic acidosis, due to decreased peripheral tissue infusion, can lead to compensatory respiratory alkalose. In case of severe hypothermia, breathing depression can cause respiratory acidosis. Electrolyte levels in the serum are usually normal, but the entry of potassium into the cells can cause hypokalemia in the absence of trauma or rhabdomyolysis.
Exposure to cold can induce bronchorea and bronchospasm. Early tachypnea is followed by hypoventilation as hypothermia becomes more severe. Decreased mental status predisposes to aspiration due to loss of cough and eructation reflex and pulmonary edema may occur.
The displacement of the hemoglobin oxygen dissociation curve at low temperatures affects oxygen intake to hypothermic tissues, which decreases by decreasing tissue oxygen needs due to low metabolism.
The manifestations of the nervous system are varied. Brain blood flow decreases and nervous conduction speed is slowed as neuronal metabolism decreases. Manifestations include dysartria, ataxia, amnesia, hallucinations, confusion, slowed pupillary reflexes and delayed deep tendinous reflexes, the last phenomenon that can make hypothyroidism difficult to recognize in the presence of hypothermia.
Chronic hypothermia may be primary or a cause that contributes to changes in mental status in older people. Hypothermic individuals can take their clothes off because they feel warm ("paradoxical undressing"). Coma from severe hypothermia may be associated with death but the EG does not indicate this and may be reversible.
Increased secretion of hypothalamic hormones releasing through exposure to cold causes an increased secretion of ACTH and thyroid stimulating hormone (TSH). Serum cortisol and catecholamine levels increase along with other acute changes.
Acute release of vasopressin by increasing central blood volume contributes to diuresis to the cold. Serum thyroid hormone levels only increase slowly and free thyroxine levels remain normal in euthyroid individuals. Moderate to severe hypothermia inhibits the action of insulin and leads to low glucose use and hyperglycaemia, unless hypoglycaemia is a cause of hypothermia. Severe hypothermia eventually inhibits the release and action of ACTH and steroid hormones.
Intestinal hypomotility is common in moderate hypothermia. Low liver metabolism can prolong the serum half-life of components normally purified by the liver. Pancreatitis and hyperamylazema occur in half of patients after reheating. It is unclear whether hypothermia itself causes pancreatitis due to alcohol abuse, a common factor in hyperthermia, or is of an independent cause.
Reheating techniques can be active or passive, internal or external. External passive reheating includes covering the patient with blankets and clothes in a warm environment to allow endogenous heat production to correct hypothermia (it is important to keep the head covered because up to 30% of body heat is lost at this level).
This method is the easiest and safest and should be used first in most patients with mild hypothermia (an increase in body temperature of 0.5 to 2 degrees Celsius/hour may be expected).
External active reheating involves the direct application of heat sources (heating blankets, radiators, immersion in hot water) on external body surfaces. This procedure, if not applied correctly, may make the situation worse in two ways if it is not applied correctly.
First, direct application of heat to the skin can cause shock by improving cold-induced vasoconstriction, thus removing an important factor in supporting blood pressure in the volume-depling patient.
Secondly, the improvement of peripheral vasoconstriction allows colder peripheral blood to enter the central circulation and can cause the central temperature to fall even more (the reference to this phenomenon being "subsequent fall"). There is, of course, also a risk of burn damage when heat sources are applied directly to the skin. Direct heat should only be applied to the thorax if external active reheating is to be used.
Internal active reheating can be achieved by several techniques. The simplest method is the reheating of the airways, in which the patient breathes humidified oxygen heated to 42 degrees Celsius, through a facial mask or endotraheal tube. Reheating rates of 1 to 2 degrees Celsius/hour can be obtained by reheating the airways.
Intravenous fluids should be heated to 40 degrees Celsius, but their use has minimal effects on central reheating. Peritoneal and pleural lavage induces heating rates of 2 to 4 degrees Celsius/ hour, but should only be used in moderate to severe hypothermia, when there is cardiovascular instability or when external reheating is ineffective.
The most effective reheating technique is extracorporeal blood heating by hemodialysis or cardiopulmonary bypass, which can increase the central temperature by 1.2 degrees Celsius every 3.5 minutes. These procedures are reserved for the most severe cases of hypothermia (e.g. when cardiac arrest occurs due to it) and when peritoneal and/ or pleural lavage are ineffective.
Hypothermia is arbitrarily defined as a central body temperature of 35 degrees Celsius or less and is classified as mild (from 35 to 32 degrees Celsius), moderate (from 32 to 28 degrees Celsius) or severe (less than 28 degrees Celsius).
It can have a few causes and usually has multifactorial origin. Precise estimates of incidence are difficult to obtain, because nonfatal hypothermia is often undetected or unreported and fatal hypothermia is likely underreported. Most cases occur in the winter months, in areas with cold climates, but hypothermia can occur in areas with mild climates in any season.
Risk factors include extreme ages (especially the elderly), homeless people, alcohol users, malnutrition, poverty, mental illness, neuroleptic use and hypothyroidism. A common context is chronic exposure to the cold in the house in a poor elderly person with a pre-existing disease and immobility.
Heat is generated in most tissues of the body and is lost by radiation (55%), evaporation (5% through the airways, 25% through the skin), conduction (15%) convection (5%). Immersion in water causes hypothermia faster as the thermal conductivity of water is 20 to 30 times that of air.
The balance between production and heat loss in the body is regulated by the hypothalamus (preoptic and posterior regions). Exposure to cold activates the cold-cut receptors that transmit the signal through the lateral spinotalamy tracts to the preoptic cords in the hypothalamus.
The posterior hypothalamus activates the sympathetic nervous system to increase muscle tone and causes trembling, which in turn increases the metabolic rate from a normal level of 40 to 60 kcal/hour to a value of 300 kcal/hour. Even at maximum metabolic rates, heat loss in the body can exceed heat production. As body temperature drops below 30 degrees Celsius, metabolic processes slow down and trembling stops, thus accelerating the process of hypothermia development.
Extreme environmental conditions can cause hypothermia in healthy individuals, but it rarely requires medical attention. The most severe hypothermia occurs in people with pre-existing medical problems, which lead to excessive heat loss (usually involving exposure to the environment - keep in mind that body temperature never drops, under normal conditions, below the average temperature, most of the environmental exposures being accidental) or inadequate heat production.
Iatrogen hypothermia can occur when obnubilpatients are left unwrapped in reserves or during surgical procedures, when large body areas are exposed for long periods of time in the operating room. This is especially possible due to the fact that the response consisting of trembling is inhibited by anesthesia, increasing the risk of hypothermia.
The only manifestation in this situation may be the difficulty of obtaining hemostasis due to the inactivation of coagulation factors at low temperatures. Increased blood flow to the skin (burns, psoriasis) can also cause hypothermia in the presence of minimal change in the environment, as the preservation of heat through peripheral vasoconstriction is inadequate.
Low heat production can contribute to hypothermia especially against the background of malnutrition and/ or inaniation, by decreasing the glycogen and fat deposits needed for actual heat production. Hypothermia occurs in more than 10% of patients with sepsis (usually bacterial) and is often associated with a severe prognosis.
Approximately 40% of resting oxygen consumption is regulated by thyroid hormones and hypothermia is common in severe hypothyroidism, when metabolic rate can be reduced to 40% below normal. Hypothermia from liver failure is commonly due to a combination of hypoglycaemia from inadequate hepatic gluconeogenesis and altered hypothalamic function (decrease in trembling).
Hypoglycaemia of any cause (glucocorticoid deficiency, alcohol consumption, hyperinsulinism), uremia and diabetic ketoacidosis, also predispose to hypothermia. Hypothalamic lesions (tumors, inflammation) can cause thermoregulatory instability and hypothermia. Spinal cord injuries to or above the first root of the thoracic nerve can lead to hypothermia by blocking trembling and interrupting cold-induced compensatory reflexes mediated by the lateral spinotalamy tracts.
Spontaneous episodic hypothermia with hyperhidrosis is a rare condition associated with excessive sweating in the absence of tremor (almost half of these patients have calos body agenesis - Shapiro syndrome), suggesting a central nervous system (CNS) etiology.
Some drugs may contribute to hypothermia, such as phenothiazines, barbiturates, opiates, benzodiazepines and ethanol, inhibiting tremor through their effects on CNS.
Acute exposure to cold causes tachycardia, increased cardiac activity, peripheral vasoconstriction and increased peripheral vascular resistance secondary to sympathetic stimulation. As body temperature drops below 32 degrees Celsius, cardiac conduction is impaired and heart rate and heart rate decreases.
Low ventricular response atrial fibrillation is common below 32 degrees Celsius and ventricular fibrillation may occur below 28 degrees Celsius. Peripheral vasoconstriction sprints the blood to the central circulation and increases the central blood volume, defending diuresis (cold diuresis), tending to decrease intravascular volume in a compensatory manner.
Through prolonged exposure to cold, the combination of diuresis to cold, additional volume losses due to altered resorption of sodium and water by the kidneys (due to inadequate function of epithelial transport mechanisms) and exchanges of intravascular fluid to intracellular fluid and peripheral edema can cause severe volume and hypotension.
In turn, volume deletation leads to increased hemoconcentration and blood viscosity that predisposes to thrombosis. On the contrary, bleeding due to ineffective clotting at low temperatures, thrombocytopenia and disseminated intravascular coagulation can even cause minor trauma, resulting in significant blood loss.
Acid-base and electrolyte imbalances depend on the duration of exposure to cold. Lactic acidosis, due to decreased peripheral tissue infusion, can lead to compensatory respiratory alkalose. In case of severe hypothermia, breathing depression can cause respiratory acidosis. Electrolyte levels in the serum are usually normal, but the entry of potassium into the cells can cause hypokalemia in the absence of trauma or rhabdomyolysis.
Exposure to cold can induce bronchorea and bronchospasm. Early tachypnea is followed by hypoventilation as hypothermia becomes more severe. Decreased mental status predisposes to aspiration due to loss of cough and eructation reflex and pulmonary edema may occur.
The displacement of the hemoglobin oxygen dissociation curve at low temperatures affects oxygen intake to hypothermic tissues, which decreases by decreasing tissue oxygen needs due to low metabolism.
The manifestations of the nervous system are varied. Brain blood flow decreases and nervous conduction speed is slowed as neuronal metabolism decreases. Manifestations include dysartria, ataxia, amnesia, hallucinations, confusion, slowed pupillary reflexes and delayed deep tendinous reflexes, the last phenomenon that can make hypothyroidism difficult to recognize in the presence of hypothermia.
Chronic hypothermia may be primary or a cause that contributes to changes in mental status in older people. Hypothermic individuals can take their clothes off because they feel warm ("paradoxical undressing"). Coma from severe hypothermia may be associated with death but the EG does not indicate this and may be reversible.
Increased secretion of hypothalamic hormones releasing through exposure to cold causes an increased secretion of ACTH and thyroid stimulating hormone (TSH). Serum cortisol and catecholamine levels increase along with other acute changes.
Acute release of vasopressin by increasing central blood volume contributes to diuresis to the cold. Serum thyroid hormone levels only increase slowly and free thyroxine levels remain normal in euthyroid individuals. Moderate to severe hypothermia inhibits the action of insulin and leads to low glucose use and hyperglycaemia, unless hypoglycaemia is a cause of hypothermia. Severe hypothermia eventually inhibits the release and action of ACTH and steroid hormones.
Intestinal hypomotility is common in moderate hypothermia. Low liver metabolism can prolong the serum half-life of components normally purified by the liver. Pancreatitis and hyperamylazema occur in half of patients after reheating. It is unclear whether hypothermia itself causes pancreatitis due to alcohol abuse, a common factor in hyperthermia, or is of an independent cause.
Reheating techniques can be active or passive, internal or external. External passive reheating includes covering the patient with blankets and clothes in a warm environment to allow endogenous heat production to correct hypothermia (it is important to keep the head covered because up to 30% of body heat is lost at this level).
This method is the easiest and safest and should be used first in most patients with mild hypothermia (an increase in body temperature of 0.5 to 2 degrees Celsius/hour may be expected).
External active reheating involves the direct application of heat sources (heating blankets, radiators, immersion in hot water) on external body surfaces. This procedure, if not applied correctly, may make the situation worse in two ways if it is not applied correctly.
First, direct application of heat to the skin can cause shock by improving cold-induced vasoconstriction, thus removing an important factor in supporting blood pressure in the volume-depling patient.
Secondly, the improvement of peripheral vasoconstriction allows colder peripheral blood to enter the central circulation and can cause the central temperature to fall even more (the reference to this phenomenon being "subsequent fall"). There is, of course, also a risk of burn damage when heat sources are applied directly to the skin. Direct heat should only be applied to the thorax if external active reheating is to be used.
Internal active reheating can be achieved by several techniques. The simplest method is the reheating of the airways, in which the patient breathes humidified oxygen heated to 42 degrees Celsius, through a facial mask or endotraheal tube. Reheating rates of 1 to 2 degrees Celsius/hour can be obtained by reheating the airways.
Intravenous fluids should be heated to 40 degrees Celsius, but their use has minimal effects on central reheating. Peritoneal and pleural lavage induces heating rates of 2 to 4 degrees Celsius/ hour, but should only be used in moderate to severe hypothermia, when there is cardiovascular instability or when external reheating is ineffective.
The most effective reheating technique is extracorporeal blood heating by hemodialysis or cardiopulmonary bypass, which can increase the central temperature by 1.2 degrees Celsius every 3.5 minutes. These procedures are reserved for the most severe cases of hypothermia (e.g. when cardiac arrest occurs due to it) and when peritoneal and/ or pleural lavage are ineffective.
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