Medical hibernation is a method of controlled reduction in the temperature of the body or its organs in order to reduce the intensity of metabolism, the level of function of tissues, organs and their physiological systems, and increase their resistance to hypoxia.

When the body is deeply cooled, it slows down metabolic processes, and tissue oxygen demand decreases. This feature of oxygen metabolism, in particular of the brain, is taken into account by surgeons during operations on different organs under artificial hypothermia in conditions of a significant decrease or even temporary cessation of blood circulation, which is called operations on dry organs (heart, blood vessels, brain, other organs). Typically, anesthesiologists focus on the temperature in the rectum in the range of 28-30 ° C, but if necessary, deeper hypothermia can be created (thermolysis, according to Labori, a specialist in medical hibernation) using hardware cardiopulmonary bypass, muscle relaxants, metabolic inhibitors and other manipulations. For general cooling of the body, liquids with a temperature of +2 to -12 ° C are used, circulating in special “cold” suits worn on the patient, or “cold” blankets with which they are covered. In a number of cases, local hypothermia is used, for example, of the head, using a special helmet placed on the patient’s head, pierced with thermode tubes through which coolant circulates.

In order to eliminate or reduce pronounced adaptive reactions of the body in response to hypothermia and limit the stress reaction, before cooling begins, the patient is given anesthesia and administered muscle relaxants and neuroplegic substances (lytic cocktail). Taken together, these manipulations ensure a gradual decrease in general and cellular metabolism, oxygen consumption by cells, release of carbon dioxide and other metabolites, and prevent disturbances in acid-base balance, imbalance of ions and water in tissues.

The benefits of medical hibernation are that

· not observed vitally dangerous violations cortical functions cerebral hemispheres and reflex activity nervous system,

· excitability and conductivity are reduced and the automation of conductive pacemaker cells is limited heart systems,

· is being formed sinus bradycardia,

cardiac minute and stroke volumes fall,

· arterial blood decreases blood pressure,

· functional activity and level of metabolism in organs and tissues of the body are inhibited.

Locally controlled hypothermia individual organs and tissues (brain, kidneys, stomach, liver, prostate gland and others) is used if necessary surgical interventions or other therapeutic manipulations on them: correction of blood flow, plastic processes, metabolism and other purposes.

A very important and not yet fully resolved problem is the removal of the patient from a state of artificial hypothermia. If this condition is deep enough and continues relatively long time, significant changes occur in almost all types of metabolism in the body. Their normalization in the process of removing the body from hypothermia is important aspect application of this method in medicine.

Hypothermia is a condition of the body that occurs as a result of a decrease in core body temperature to a level below 35 ° C.

Normally, a person has a temperature in the cranial cavity, lumen large vessels, abdominal organs and chest cavity maintained at a constant level – 36.7–38.2 °C. This internal temperature is called core temperature (or core temperature), and the hypothalamus is responsible for maintaining it at the proper level.

Temperature of the “shell” of the body ( skeletal muscles, subcutaneous tissue, skin) is always lower than the central one by several tenths of a degree, and sometimes by several degrees.

Degrees of hypothermia

Causes

The constancy of body temperature is maintained by the balance of heat production, that is, the ratio of heat production and heat transfer. If heat transfer begins to prevail over heat production, a state of hypothermia develops.

The main causes of hypothermia:

• long-term regional or general anesthesia;
• prolonged exposure to the cold, immersion in cold water;
• volumetric infusion of cold solutions, whole blood or its drugs.

People at risk for developing hypothermia include:

• children;
• aged people;
• persons under the influence of alcohol;
• patients are unconscious or immobilized (due to acute disorder cerebral circulation, hypoglycemia, extensive injuries, poisoning, etc.).

In addition to pathological hypothermia, which occurs as a result of hypothermia, there is therapeutic hypothermia. It is used to reduce the risk of irreversible ischemic tissue damage due to insufficient blood circulation. Indications for therapeutic hypothermia are:

• severe hypoxia of newborns;
• ischemic stroke;
• heavy traumatic injuries central nervous system;
• neurogenic fever resulting from brain injury;
• heart failure.

Kinds

Depending on the level of decrease in core temperature, hypothermia is divided into several types:

• light (35.0–32.2 °C);
• medium (32.1–27 °C);
• severe (less than 27 °C).

The constancy of body temperature is maintained by the balance of heat production, that is, the ratio of heat production and heat transfer. If heat transfer begins to prevail over heat production, a state of hypothermia develops.

IN clinical practice Hypothermia is divided into moderate and severe. With moderate hypothermia, the patient retains the ability to independently or passively warm. In severe cases of thermoregulation disorder, this ability is lost.

Signs

Signs of moderate hypothermia (body temperature - from 35.0 to 32.0 ° C):

• drowsiness;
• disturbance of orientation in time and space;
• apathy;
• muscle tremors;
• rapid breathing;
• tachycardia.

Spasms are observed blood vessels(vasoconstriction) and increased plasma glucose concentrations.

A further decrease in core temperature leads to depression of respiratory and cardiovascular systems, impaired neuromuscular conduction, decreased mental activity and slowing down metabolic processes.

When the central body temperature decreases to 27 °C or less, it develops coma, clinically manifested by the following symptoms:

• lack of tendon reflexes;
• lack of pupillary reaction to light;
• an increase in the amount of urine excreted (polyuria, cold diuresis) due to a decrease in the secretion of antidiuretic hormone, which increases hypovolemia;
• cessation of muscle tremors;
• a fall blood pressure;
• frequency reduction breathing movements up to 8–10 per minute;
• severe bradycardia;
• atrial fibrillation.

Diagnostics

The main method for diagnosing hypothermia is determining the core body temperature. In this case, you cannot rely on temperature readings in the axillary (axillary) region, since even in normal conditions the difference between the central and axillary temperatures is 1–2 degrees. In hypothermia it is even greater.

Normally, in humans, the temperature in the cranial cavity, the lumen of large vessels, and the abdominal and thoracic organs is maintained at a constant level of 36.7–38.2 °C.

Core temperature is measured in the external auditory canal, esophagus, nasopharyngeal region, bladder or rectum using special electronic thermometers.

For rate general condition laboratory examination of existing metabolic disorders and functions of vital organs is carried out:

• general blood analysis;
• biochemical blood test with determination of urea, creatinine, glucose, lactate;
• coagulogram;
• blood test for acid-base balance and the level of electrolytes (chlorides, magnesium, potassium, sodium);
• general urine analysis.

Monitoring of the patient's condition is necessary (ECG monitoring, pulse oximetry, measurement of blood pressure, body temperature, hourly measurement of diuresis).

If damage to internal organs or bone fractures is suspected, radiography or computed tomography corresponding part of the body.

Treatment

For moderate hypothermia, the patient (if he is conscious) is placed in a dry warm room and warmed up by covering the head with a warm blanket and giving a hot drink. This may be enough.

In case of severe hypothermia, it is also necessary to actively warm the patient, taking into account a number of points. You should not try to warm the entire victim by placing him, for example, in a bath with hot water, which will lead to expansion of peripheral blood vessels and massive flow of cold blood into the main vessels and to internal organs. As a result there will be sharp drop blood pressure and decreased heart rate, which can have critical consequences.

In addition to pathological hypothermia, which occurs as a result of hypothermia, there is therapeutic hypothermia. It is used to reduce the risk of irreversible ischemic tissue damage due to insufficient blood circulation.

The most effective and safe way to internally warm a patient is by using one of the following methods:

• inhalation of oxygen humidified and heated to 45 °C through an endotracheal tube or mask;
• intravenous infusion of warm (40–42 °C) crystalloid solution;
• lavage (washing) of the stomach, intestines or Bladder warm solutions;
• lavage chest using two thoracostomy tubes (most effective method warming even in the most severe cases of hypothermia);
• lavage abdominal cavity warm dialysate (indicated in patients with severe hypothermia accompanied by severe electrolyte imbalance, intoxication or acute necrosis skeletal muscles).

Active internal rewarming should cease as soon as the core temperature reaches 34°C. This will prevent the development of a subsequent hyperthermic state. When carrying out active warming, ECG monitoring is necessary, since there is a high risk of heart rhythm disturbances ( ventricular tachycardia, atrial fibrillation).

Prevention

Prevention of hypothermia includes measures aimed at preventing hypothermia:

• organization correct mode work and rest in winter time years for people working outdoors;
• use suitable for weather conditions warm clothes and dry shoes;
• medical control over the condition of participants in winter sports competitions, exercises, and military operations;
• organization of public heating points during frosts;
• avoiding drinking alcohol before being in the cold;
• hardening procedures that improve adaptability to changing climatic conditions.

Consequences and complications

Hypothermia is a life-threatening condition, the consequences of which can be:

• Heart arythmy;
• cerebral edema;
• pulmonary edema;
• hypovolemic shock;
• acute renal and liver failure;
• pneumonia;
• phlegmon;
• pyelonephritis;
• otitis;
• tonsillitis;
• arthritis;
• osteomyelitis;
• sepsis.

RCHR ( Republican Center healthcare development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2014

Other thermoregulatory disorders in the newborn (P81)

Neonatology

general information

Short description

Approved by the Expert Commission

On health development issues

Ministry of Health of the Republic of Kazakhstan

Moderate therapeutic hypothermia- controlled induced decrease in the patient’s central body temperature to 32-34°C, in order to reduce the risk of ischemic damage to brain tissue after a period of circulatory disorders

Hypothermia has been proven to have a pronounced neuroprotective effect. Currently, therapeutic hypothermia is considered as the main physical method neuroprotective protection of the brain, since there is none, from the standpoint evidence-based medicine, a method of pharmacological neuroprotection. Therapeutic hypothermia is included in the treatment standards of: the International Liaison Committee on Resuscitation (ILCOR), the American Heart Association (AHA), as well as the clinical recommendation protocols of the Association of Neurosurgeons of Russia.

The use of moderate therapeutic hypothermia, to reduce the risk of irreversible changes in the brain, is recommended for the following pathological conditions:

Encephalopathies of newborns

Heart failure

Strokes

Traumatic injuries to the brain or spinal cord no fever

Brain injury with neurogenic fever

I. INTRODUCTORY PART

Protocol name: Hypothermia (therapeutic) of a newborn

Protocol code:

ICD-10 code(s):

P81.0 Hypothermia of the newborn due to factors external environment

P81.8 Other specified disorders of thermoregulation in the newborn

P81.9 Disturbance of thermoregulation in the newborn, unspecified

Abbreviations used in the protocol:

HIE - hypoxic-ischemic encephalopathy

KP - clinical protocol

CFM - monitoring of cerebral functions by αEEG

EEG - electroencephalography

αEEG - amplitude-integrated EEG

NMR - nuclear magnetic resonance

Date of development of the protocol: year 2014

Protocol users: neonatologists, anesthesiologists-resuscitators (children), pediatricians, general practitioners

Classification

Clinical classification:

Therapeutic hypothermia of newborns is a method of controlled cooling of the child's body. There are:

Systemic hypothermia;

Craniocerebral hypothermia;

Therapeutic hypothermia is given to children with a gestational age of more than 35 weeks and a body weight of more than 1800 g.

Therapeutic hypothermia reduces mortality and incidence neurological disorders in children with hypoxic-ischemic brain damage

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

Basic (required) diagnostic examinations carried out on an outpatient basis: no.

Additional diagnostic examinations performed on an outpatient basis: no.

Minimum list of examinations that must be carried out when referring for planned hospitalization: none.

Basic (mandatory) diagnostic examinations carried out at the hospital level:

Methodology of therapeutic hypothermia

Before starting hypothermia treatment, administer pharmacological agents to control tremors.

The patient's body temperature drops to 32-34°C and is maintained at this level for 24 hours. Clinicians should avoid reducing the temperature below the target value. Accepted medical standards stipulate that the patient's temperature should not fall below a threshold of 32°C.

Then the body temperature is gradually raised to normal level for 12 hours, under the control of the cooling/heating system control unit computer. Warming of the patient should occur at a rate of at least 0.2-0.3 ° C per hour to avoid complications, namely: arrhythmia, lowering the coagulation threshold, increasing the risk of infection and increasing the risk of electrolyte imbalance.

Methods for implementing therapeutic hypothermia:

Invasive method

Cooling is carried out through a catheter inserted into femoral vein. The fluid circulating in the catheter removes heat outside without entering the patient. The method allows you to control the cooling rate and set body temperature within 1°C of the target value.

The procedure should only be performed by a well-trained doctor who knows the technique.

The main disadvantage of the technique is serious complications- bleeding, deep vein thrombosis, infections, coagulopathy.

Non-invasive method

The non-invasive method of therapeutic hypothermia today uses specialized devices consisting of a water-based cooling/warming system unit and a heat exchange blanket. Water circulates through a special heat transfer blanket or a tight-fitting vest on the torso with applicators on the legs. To reduce temperature at an optimal rate, it is necessary to cover at least 70% of the patient's body surface area with heat transfer blankets. A special helmet is used to locally reduce brain temperature.

Modern systems cooling/warming with microprocessor control and feedback from the patient, ensure the creation of controlled therapeutic hypo/hyperthermia. The device monitors the patient's body temperature using a sensor internal temperature and corrects it, depending on the specified target values, changing the temperature of the water in the system.

The principle of patient feedback ensures high precision in achieving and controlling the temperature of the patient's body first, both during cooling and during subsequent rewarming. This is important to minimize side effects associated with hypothermia.

Therapeutic hypothermia of newborns should not be performed without an instrument for prolonged dynamic analysis brain activity, effectively complementing the vital signs monitoring system.

The dynamics of changes in the brain activity of a newborn, which cannot be tracked during a short-term EEG study, is clearly presented during long-term EEG monitoring with the display of trends in amplitude-integrated EEG (aEEG), compressed spectrum, and others. quantitative indicators CNS, as well as the original EEG signal from a small number of EEG leads (from 3 to 5).

aEEG patterns have characteristic appearance, corresponding to various normal and pathological conditions brain.

aEEG trends display the dynamics of changes in EEG amplitude during multi-hour studies in a compressed form (1 - 100 cm/hour) and allow you to assess the severity of hypoxic-ischemic disorders, sleep patterns, identify convulsive activity and predict the neurological outcome, as well as monitor aEEG changes in conditions leading to brain hypoxia in newborns and observe the dynamics of the patient’s condition during therapeutic effects.

Additional diagnostic examinations carried out at the hospital level:

AEEG is carried out after 3 hours and 12 hours during the therapeutic hypothermia procedure.

Table 1. Typical options for EEG lead circuits for monitoring cerebral functions

table 2. Examples of aEEG patterns

Diagnostic measures carried out at the emergency stage emergency care: No.

Diagnostic criteria

Complaints and anamnesis: see CP “Asphyxia of a newborn.”

Physical examination: see CP “Asphyxia of the newborn”.

Laboratory research: see CP “Asphyxia of a newborn”.

Instrumental studies: see CP “Asphyxia of a newborn”.

Indications for consultation with specialists:

Consultation with a pediatric neurologist to assess the dynamics of the newborn’s condition before and after therapeutic hypothermia.

Differential diagnosis

Differential diagnosis: No.

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Treatment abroad

Get advice on medical tourism

Treatment

Treatment goals:

Frequency reduction severe complications in a newborn from the central nervous system, after suffering asphyxia and hypoxia during childbirth.

Treatment tactics

Non-drug treatment:

The level of cooling during craniocerebral hypothermia is 34.5°C±0.5°C.

The cooling level during systemic hypothermia was 33.5°C (Fig. 3).

Maintenance rectal temperature 34.5±0.5°C for 72 hours.

The duration of the procedure is 72 hours.

The warming rate should not exceed 0.5°C/hour

Drug treatment: No.

Other treatments: no.

Surgical intervention: No.

Further management:

Monitoring the condition of a child in the ICU/NICU.

Dispensary observation with a neurologist for 1 year.

Immunization preventive vaccinations according to indications.

Indicators of treatment effectiveness and safety of diagnostic and treatment methods described in the protocol:

Hypothermia in the treatment of HIE is associated with less damage to the gray and white matter brain.

U more children undergoing hypothermia have no changes in NMR;

General hypothermia during resuscitation reduces the frequency deaths, and moderate and severe disturbances of psychomotor development in newborns with hypoxic-ischemic encephalopathy due to acute perinatal asphyxia. This has been confirmed in a number of multicenter studies in the USA and Europe;

Selective head cooling soon after birth can be used to treat children with perinatal encephalopathy middle and light degrees severity to prevent the development of severe neurological pathology. Selective head cooling is ineffective in severe encephalopathy.

Hospitalization

Indications for hospitalization indicating the type of hospitalization*** (planned, emergency):

Group A criteria:

Apgar score ≤ 5 at 10 minutes or

Continued need for mechanical ventilation at 10 minutes of life or

In the first blood test taken during the first 60 minutes of life, (umbilical cord, capillary or venous) pH<7.0 или

The first blood test taken within 60 minutes of life (umbilical cord, capillary or venous) shows a base deficit (BE) of ≥16 mol/L.

Group “B” criteria:

Clinically significant seizures (tonic, clonic, mixed) or

Information

Sources and literature

1. Minutes of meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2014
   1. 1) Jacobs S, Hunt R, Tarnow-Mordi W, Inder T, Davis P. Cooling for newborns with hypoxic ischemic encephalopathy. Cochrane Database Syst Rev 2007;(4):CD003311. 2) Hypothermia for newborns with hypoxic ischemic encephalopathy A Peliowski-Davidovich; Canadian Paediatric Society Fetus and Newborn Committee Paediatr Child Health 2012;17(1):41-3). 3) Rutherford M., et al. Assessment of brain tissue after injury moderate hypothermia in neonates with hypoxic–ischaemic encephalopathy: a nested substudy of a randomized controlled trial. Lancet Neurology, November 6, 2009. 4) Horn A, Thompson C, Woods D, et al. Induced hypothermia for infants with hypoxic ischemic encephalopathy using a servo controlled fan: an exploratory pilot study. Pediatrics 2009;123:e1090-e1098. 5) Sarkar S, Barks JD, Donn SM. Should amplitude integrated electroencephalography be used to identify infants suitable for hypothermic neuroprotection? Journal of Perinatology 2008; 28: 117-122. 6) Kendall G. S. et al. Passive cooling for initiation of therapeutic hypothermia in neonatal encephalopathy Arch. Dis. Child. Fetal. Neonatal. Ed. doi:10.1136/adc. 2010. 187211 7) Jacobs S. E. et al. Cochrane Review: Cooling for newborns with hypoxic ischemic encephalopathy The Cochrane Library. 2008, Issue 4. 8) Edwards A. et al. Neurological outcomes at 18 months of age after moderate hypothermia for perinatal hypoxic ischemic encephalopathy: synthesis and meta-analysis of trial data. BMJ 2010; 340:c363

   
   Indication of the conditions for reviewing the protocol: Review of the protocol after 3 years and/or when new diagnostic/treatment methods with a higher level of evidence become available.

   
   

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Cold sickness (hypothermia)

Introduction
Body temperature is an important physiological constant, and maintaining it within a certain range is a necessary condition for the proper functioning of all organs and systems. Even small deviations in body temperature from normal can lead to serious changes in metabolism with the development of heat or cold illness. Severe forms of heat and cold illness pose a threat to life, which determines the importance of their timely recognition and treatment in emergency care practice. This work covers the main issues of etiology, pathophysiology, clinical picture and emergency care for hypothermia, the most severe form of cold illness.
Hypothermia: definition, classification
Hypothermia is a pathological condition caused by a decrease in core body temperature to 35°C or less. Depending on the temperature level, hypothermia is classified as mild (32-35°C), moderate (28-32°C), severe (28-20°C) and deep (< 20°С).
There are primary and secondary hypothermia. Primary (“accidental” or unintentional) hypothermia develops in healthy individuals under the influence of unfavorable external conditions (meteorological or immersion in cold water) of sufficient intensity to reduce core body temperature. Secondary hypothermia occurs as a complication of another, primary pathological process or disease, such as alcohol intoxication, trauma or acute myocardial infarction.
Epidemiology
Each year, hypothermia causes about 100 deaths in Canada, 300 in the UK, and 700 in the USA. It is assumed that the true incidence of hypothermia as a cause of death must be higher since it is not always recognized.
Cases of hypothermia occur in urban and rural areas, but are more common in cities. The typical victim of hypothermia in sparsely populated areas is an ill-prepared or lost traveler, or a person who has lost the ability to move due to injury, injury, or illness. In cities, hypothermia usually occurs in individuals without adequate shelter due to illness or other circumstances. Hypothermia can occur at any time of the year (not only in winter).
Primary hypothermia usually affects young men and children. The risk of secondary hypothermia is higher in the elderly, homeless, suffering from mental disorders, often alone, and living in insufficiently heated rooms. In general, the problem of hypothermia is more pressing for the elderly: in one study, 85% of patients with hypothermia were over 60 years of age.
Etiology
Normal thermoregulation involves a dynamic balance between heat production and loss to ensure a constant core body temperature. This is achieved both by tuning central thermogenesis and by maintaining a certain temperature gradient between the inside of the body and the periphery facing directly to the external environment. The amount of heat received from the outside or released into the environment is precisely and quickly regulated in response to changing conditions with the participation of two types of skin receptors - heat and cold. When cooling, the activity of afferent fibers from cold receptors increases, which stimulates the supraoptic nucleus of the anterior hypothalamus; reflex vasoconstriction reduces blood flow to cooled skin. In addition, a decrease in blood temperature is perceived by thermosensitive neurons of the hypothalamus. A series of adaptive reactions are triggered through the hypothalamus: immediate, through the autonomic nervous system; delayed, with the participation of the endocrine system; adaptive behavioral response; extrapyramidal stimulation of skeletal muscles and muscle tremors. These reactions are aimed at either increasing heat production or reducing heat loss.

Risk factors for hypothermia include all states and conditions that increase heat loss, decrease heat production, or thermogenesis, or impair thermoregulation or the behavioral ability to seek shelter.
Risk factors for hypothermia:

1. increased heat transfer:

• environmental factors (intensive cooling, immersion in cold water);
• pharmacological;
• toxicological;
• burns;
• psoriasis;
• exfoliative dermatitis;
• ichthyosis;

decreased heat production/thermogenesis:

• extreme degree of physical overstrain;
• extreme age limits;
• hypoglycemia;
• hypofunction of the thyroid gland;
• adrenal hypofunction;
• hypopituitarism;
• kwashiorkor;
• marasmus;
• reduced nutrition;
• inactivity;
• absence of muscle tremors;

violation of thermoregulation:

• acute spinal injury;
• anorexia nervosa;
• stroke;
• subarachnoid hemorrhage;
• CNS injury;
• diabetes;
• hypothalamic dysfunction;
• multiple sclerosis;
• neoplastic process;
• neuropathy;
• Parkinson's disease;
• pharmacological factors;
• toxicological factors;

other:

• episodic hypothermia;
• giant cell arteritis;
• pancreatitis;
• sarcoidosis;
• sepsis;
• uremia.

Accidental hypothermia in a young, initially healthy person usually proceeds favorably (except for cases with respiratory and circulatory arrest); Simple warming is usually enough for recovery. However, more often in clinical practice there are situations when hypothermia occurs in elderly people against the background of other diseases, the nature and severity of which in such cases determine the success of treatment and the outcome of hypothermia.
Clinic and pathophysiology
A patient with hypothermia can be encountered under a wide variety of circumstances. When it is known that a person has been exposed to prolonged hypothermia, it is not difficult to conclude that hypothermia is present. The task may be more difficult, and the diagnosis incorrect or untimely, when hypothermia occurs without obvious hypothermia, for example, in a patient with mental disorders, poisoning or trauma. With secondary hypothermia, signs of the underlying disease may come to the fore, determining the clinical picture. In addition, many manifestations of hypothermia themselves are nonspecific and can be noticed and correctly interpreted only with a sufficient degree of alertness and familiarity with the clinic and pathophysiology of this condition. For example, a patient with mild or moderate hypothermia may complain of nausea, dizziness, weakness, and hunger. Confusion, slurred speech, and impaired consciousness may occur. In severe hypothermia, depression of the central nervous system is observed, up to the development of coma, disorders of the cardiovascular system, breathing, and renal function.
There is a certain correlation between the level of core body temperature and the pathophysiological manifestations of hypothermia (Table 1). Although not absolute, this dependence provides the key to the initial clinical assessment of the patient’s condition and the selection of the correct treatment tactics. It is only necessary to immediately note that the changes caused by hypothermia are for the most part reversible and disappear after warming, so attempts to normalize physiological parameters in many cases turn out to be not only useless, but also dangerous.
It is obvious that with hypothermia, the activity of all organs and systems, including the cardiovascular, respiratory, and nervous systems, is impaired to one degree or another; significant changes are observed in the energy supply of tissues, the state of fluid balance, acid-base balance, and the blood coagulation system. Initially, an adaptive reaction to cold develops in the form of tachycardia, tachypnea, and increased diuresis. If cooling of the body continues, this response is replaced by bradycardia, depression of consciousness and breathing, and shutdown of kidney function. Thus, hypothermia is a progressive pathological condition that, in the absence of intervention, leads to the death of the victim.
The cardiovascular system
In mild hypothermia, the initial response to cold stress is tachycardia, peripheral vasoconstriction, increased cardiac output, and a slight increase in blood pressure. Characteristic is inhibition of ventricular ectopic activity (for example, extrasystole) with its resumption after warming.
Moderate hypothermia is accompanied by progressive bradycardia. The latter is caused by a decrease in the rate of spontaneous diastolic repolarization in pacemaker cells and is resistant to the action of atropine. The decrease in cardiac output under these conditions is partially compensated by a further increase in peripheral vasoconstriction. An additional contribution to the increase in peripheral vascular resistance is made by hemoconcentration and increased blood viscosity.
On the ECG, in the early phase of ventricular repolarization, the J wave, or Osborne wave, characteristic of hypothermia, is recorded, initially more noticeable in leads II and V6. The Osborne wave increases as it cools and disappears completely after warming up. Other ECG changes include variable degrees of atrioventricular conduction slowing, widening of the QRS complex due to slowing of ventricular myocardial conduction, prolonged electrical systole (QT interval), ST segment depression, and T wave inversion. Atrial fibrillation and junctional rhythm are common.
In severe hypothermia, systemic vascular resistance decreases due to a decrease in catecholamine levels, which is accompanied by a decrease in cardiac output. At temperatures around 27°C, the risk of ventricular fibrillation increases sharply. Its development is facilitated by any sudden changes in the patient’s body - from a sharp change in body position to fluctuations in myocardial temperature, shifts in biochemical parameters or acid-base balance. The high readiness for ventricular fibrillation during deep hypothermia is explained by the fact that even a small temperature gradient between endocardial and myocardial cells is accompanied by dispersion in the duration of the action potential, refractory periods and conduction velocity. This, together with a significant slowdown in conduction, determines an increased tendency to develop arrhythmias during hypothermia. At a temperature of 24°C and below, there is a high risk of asystole.
Hematological changes
Hypothermia is accompanied by an increase in blood viscosity, an increase in fibrinogen and hematocrit levels, which significantly impairs the function of other organs. Some of the fluid leaves the vessels due to an increase in their permeability, some is excreted by the kidneys due to cold diuresis; as a result, the volume of intravascular fluid decreases, hypovolemia and hemoconcentration occur. For every 1°C decrease in body temperature, the hematocrit increases by 2%. A normal or decreased hematocrit level in a patient with moderate or severe hypothermia indicates preexisting anemia or blood loss.
Moderate and severe hypothermia may be accompanied by coagulopathy due to inhibition, under the influence of cold, of the activity of enzyme proteins of the coagulation cascade. The release of tissue thromboplastin from ischemic tissue initiates disseminated intravascular coagulation; thrombocytopenia develops.
The white blood cell count is normal or low, even in the setting of infection.
Neuromuscular changes
The nervous system is especially sensitive to hypothermia. Mild hypothermia is accompanied by confusion and memory impairment. As the degree of cooling increases, slurred speech, apathy, ataxia, decreased level of consciousness, and paradoxical undressing are observed. Finally, with severe hypothermia, progressive depression of the nervous system leads to the development of coma and death of the patient. Consciousness is usually lost at temperatures around 30°C. Autoregulation of cerebral blood flow stops at a temperature of about 25°C; a decrease in body temperature by 1°C is accompanied by a decrease in cerebral blood flow by 6-7%. Cerebral ischemia during hypothermia is well tolerated due to a significant slowdown in metabolic processes during cooling. When the temperature reaches 20°C, the electrical activity of the brain stops - an isoline is recorded on the EEG.


With mild hypothermia, muscle tremors are pronounced, but as body temperature decreases, this protective phenomenon fades. Cooling leads to an increase in the viscosity of the synovial fluid, so moderate hypothermia is accompanied by stiffness, stiffness of joints and muscles. In the early stages, ataxia and impaired fine motor skills are observed, and when cooled to 28°C and below, muscle rigidity, dilated pupils and areflexia occur. In severe hypothermia, joint stiffness and muscle rigidity may mimic rigor mortis, although these effects may paradoxically be reduced at temperatures below 27°C.
With hypothermia, severe postural hypotension is possible, which is explained by impaired autonomic control of blood circulation due to the effects of cold on peripheral nerves; therefore, victims of hypothermia must be transported in a horizontal position.
Respiratory system
The initial response to hypothermia is to increase the respiratory rate with the development of respiratory alkalosis. As the degree of hypothermia increases, the minute volume of ventilation and oxygen consumption decrease, bronchospasm and bronchorrhea occur. Moderate hypothermia is accompanied by impaired protective reflexes of the respiratory tract, which predisposes to aspiration and pneumonia. Oxygen consumption and carbon dioxide formation are significantly reduced (up to 50% at t = 30°C). As the body cools and breathing rate decreases, carbon dioxide is retained and respiratory acidosis develops. Acidosis during hypothermia is complemented by a metabolic component due to tissue ischemia, lactate production during muscle tremors and impaired lactate metabolism in the liver. During warming, metabolic acidosis may be aggravated due to the return of anaerobic metabolic products into circulation, which increases the risk of developing arrhythmias. With deep hypothermia, breathing stops.
Kidney function
The first reaction to cold exposure from the kidneys is increased function and increased diuresis. This is due to an increase in renal blood flow under conditions of peripheral vasoconstriction and relative central hypervolemia. Increased diuresis under bad weather conditions (cold, damp) is familiar to many and may precede a decrease in core body temperature.
With moderate hypothermia, cardiac output, renal blood flow and glomerular filtration rate are reduced, the latter at a body temperature of 27-30°C decreases by 50%. Severe hypothermia leads to the development of renal failure and loss of renal function. About 40% of hypothermic patients requiring intensive care have acute renal failure.
Hyperkalemia is a marker of acidosis, cell death and is considered a poor prognostic sign.
Diagnostics
The diagnosis of hypothermia is confirmed by simply measuring body temperature. In order not to miss hypothermia, you must remember to measure the temperature when assessing the patient’s physical data, use an accurate thermometer, take measurements in the oral cavity or external auditory canal, and correctly take into account the thermometer readings. In the emergency department, if hypothermia is suspected, rectal temperature should be taken.
The assumption of hypothermia is confirmed by the registration of the Osborne wave on the ECG (Fig. 1). This positive deflection of the ECG waveform at the junction of the QRS complex and the ST segment appears at a temperature of about 32°C, initially in leads II and V6. With a further decrease in body temperature, the Osborne wave begins to be recorded in all leads.
Pre-hospital assistance
In the prehospital setting, the initial assessment of a patient with hypothermia is carried out in the same way as for other potentially life-threatening illnesses and injuries. If hypothermia is suspected, the patient should be removed from wet clothing and, if possible, placed in a warm, dry, insulating material such as a sleeping bag. To reduce heat loss, it is more important to place something under the patient than to cover him on top.
Although physical activity is accompanied by increased heat production, it creates the danger of dilation of peripheral vessels and a secondary decrease in core body temperature due to the flow of cooled blood from the periphery (the “afterdrop” phenomenon). In this regard, the patient should remain at rest for as long as possible. Massage of cold extremities is also contraindicated due to the possibility of increased peripheral vasodilation.
If conditions permit, venous access should be provided for intravenous administration of heated solutions. For breathing, whenever possible, warm and humidified air or oxygen is supplied.
Patients with severe hypothermia must be moved extremely carefully due to the high readiness of the myocardium for ventricular fibrillation. Defibrillation can be used to treat ventricular fibrillation in the prehospital setting, but if three attempts are unsuccessful, aggressive rewarming of the patient should be undertaken before repeat defibrillation.
Treatment in the emergency department
There is no single algorithm for the treatment of hypothermia. In each specific case, therapeutic intervention is determined by the severity of hypothermia and the patient's condition. The increase in pathophysiological changes with an increase in the degree of hypothermia requires a more active therapeutic approach. Warming the patient plays a decisive role in the treatment of hypothermia. For example, many arrhythmias associated with hypothermia resolve after body temperature normalizes: bradycardia during hypothermia is resistant to the action of atropine, but disappears with warming. Correction of coagulopathy is also achieved by warming, rather than by prescribing factors that affect the blood coagulation system.
To assess the effectiveness of rewarming, monitoring of core body temperature is necessary, which is achieved by continuous or repeated measurement of rectal or esophageal temperature. Monitoring allows timely detection of a secondary decrease in body temperature after the onset of warming (“afterdrop”). The mechanism of this phenomenon is that when the peripheral parts of the body are warmed, vascular spasm is relieved, and a large volume of cooled blood enters the circulation from the periphery. As a result, the patient's core temperature may paradoxically decrease after rewarming begins. The “afterdrop” phenomenon increases physiological disturbances and increases the risk of developing arrhythmias and cardiac arrest. Temperature monitoring is indicated for all patients with a decrease in temperature to 32°C or less.
All drugs should be administered intravenously, since cooling of the body is accompanied by peripheral vasospasm, which impairs absorption during intramuscular and subcutaneous injections.
Since hypothermia is accompanied by hypovolemia and dehydration, patients are advised to administer intravenous saline, preferably with 5% glucose, under conditions of careful monitoring (risk of volume overload). The administration of infusion solutions containing lactate should be avoided, since under conditions of hypothermia its metabolism in the liver is disrupted.
Attempts to increase heart rate and blood pressure with inotropic drugs are usually unsuccessful. Low doses of dobutamine may sometimes be helpful, especially if hypotension persists after fluid resuscitation or the degree of temperature reduction is inadequate.
Arrhythmias associated with hypothermia are little sensitive to the action of antiarrhythmic drugs and usually disappear after the patient is warmed up. At temperatures below 30°C, lidocaine, procainamide, propranolol, verapamil and diltiazem are usually ineffective.
Warming methods for hypothermia are divided into active and passive, as well as invasive and non-invasive.
Passive warming is used for mild hypothermia, when the patient has not yet lost the ability to generate heat due to muscle tremors. In this case, insulation from the cold is sufficient for the patient to gradually warm up due to his own thermogenesis.
With active external warming, heat is supplied to the patient from external sources. It is the method of choice for patients with mild to moderate hypothermia whose ability to thermize is impaired by low temperature (especially below 32°C), illness, intoxication, or medication. There are many methods of active external warming: using heat lamps, heated blankets, immersion in warm water, active heated air systems. The main disadvantage of active external warming is the risk of developing the “afterdrop” phenomenon.
Active internal rewarming is used to treat moderate to severe hypothermia. The simplest and most accessible method of internal warming is the administration of warm solutions intravenously and inhalation of warm humidified air/oxygen. This is the optimal treatment option for stable patients with moderate hypothermia. The liquid is heated to a temperature of 44°C and injected through a needle (catheter) with a large lumen diameter, using a system of minimal length. Humidified air or oxygen should also be warmed to 42-44°C. There are special systems for heating air in the treatment of hypothermia; they allow you to increase the patient’s body temperature by 1-2.5°C/h.
For active internal warming, a number of invasive methods have been proposed: washing cavities with warm solutions (stomach, bladder, peritoneal and pleural cavity); extracorporeal blood warming; mediastinal lavage. These methods can quickly increase body temperature, but due to the invasiveness and risk of complications, they are used only in the most severe cases - with hypothermic cardiac arrest, lack of response to other methods of warming, complete frostbite of the extremities, rhabdomyolysis and electrolyte disturbances.
Extracorporeal blood warming is used in patients with severe hypothermia resistant to other treatments. There are several methods of extracorporeal blood warming: hemodialysis; arteriovenous, venovenous and cardiopulmonary bypass surgery. The main advantage of these methods is the high rate of warming of the blood, and therefore the patient. Additional advantages are associated with the ability to supply oxygenated blood into the circulation in the absence of mechanical activity of the heart. Extracorporeal rewarming is used in patients with severe hypothermia who do not have contraindications for resuscitation, and in cases of complete frostbite of the extremities.
Cardiac arrest due to hypothermia is difficult to treat. For a number of reasons (suppression of the mechanical activity of the heart, absence of a peripheral pulse), the very fact of circulatory arrest in a patient with hypothermia may not be obvious. At the prehospital stage, it is difficult to establish the mechanism of cardiac arrest - asystole or ventricular fibrillation. In severe hypothermia, ventricular fibrillation is usually extremely resistant to defibrillation, the latter becoming effective only after active warming of the patient. Drug treatment of ventricular fibrillation in patients with hypothermia is usually ineffective; there are only reports of the preventive effectiveness of bretylium.
Cardiac arrest due to hypothermia requires cardiopulmonary resuscitation (CPR). Cooling is accompanied by chest rigidity and deterioration of cardiac compressibility, which makes CPR difficult; In addition, patients with hypothermia usually require prolonged resuscitation. However, CPR improves survival in patients with cardiac arrest due to hypothermia. Cases of successful resuscitation and complete recovery have been recorded in patients who had no signs of life at the time CPR began. There is a report of a surviving hypothermic patient in whom CPR was administered for 6.5 hours.
Conclusion
Many factors predispose to the development of hypothermia, including socioeconomic, pharmacological, environmental influences, the presence of underlying diseases, and aging. Under the influence of hypothermia, a wide range of pathophysiological disorders develop, many of which are potentially reversible with warming. Attempts to actively normalize various biochemical parameters during hypothermia may be inappropriate and unsafe. Although supportive care is useful in treating hypothermia, keeping the patient warm is critical. For mild hypothermia, passive external warming is effective, for the treatment of moderate and severe hypothermia, active external warming methods are used, and for severe and profound hypothermia, the use of active internal warming methods is indicated. A fairly high mortality rate in patients with severe hypothermia is due to the development of arrhythmias or sepsis. However, even with severe hypothermia, complete recovery is possible. The prognosis of hypothermia in the elderly often depends on the diseases that caused it.

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Therapeutic hypothermia can be carried out using invasive and non-invasive methods and is divided into general and local.

Invasive methods involve infusion of cooled saline into a central vein. The advantage of this technique is the controllability of hypothermia, which allows you to achieve a temperature value within ~ 1°C of the target, regulate the cooling rate and the warming rate. The main negative side of this method is the systematic nature of hypothermia, which provides a high probability of developing the above side effects. There is also a possibility of bleeding, thrombosis, and infectious complications, which are especially dangerous in conditions of hypothermia.

Non-invasive techniques involve cooling the patient's body through the outer covering. One option is a heat exchange blanket, which has several cooling and warming speeds, which allows you to achieve controlled general hypothermia of the entire body. A separate group is represented by methods of local surface cooling, one of which is craniocerebral hypothermia.

Craniocerebral hypothermia.

Craniocerebral hypothermia (CCH) is cooling of the brain through the outer covering of the head in order to increase its resistance to oxygen starvation.

For this, various means were used: rubber or plastic bubbles filled with ice, cooling mixtures (snow with salt, ice with salt), rubber helmets with double walls, between which cooled liquid circulates, and fairing bands, air hypotherms with low circulation of cooled air . However, all these devices are imperfect and do not lead to the desired result. In 1964, in our country, the “Holod-2F” device was created (by O.A. Smirnov) and is currently being mass-produced by industry, which is based on the original jet method of cooling the head, and then the air-cooled “Fluido-Craniotherm” . CCG with the help of these devices has a number of advantages over general cooling, since first of all the temperature of the brain, especially the cortex, i.e. the structure most sensitive to oxygen starvation, decreases.

When the temperature of the upper layers of the brain adjacent to the cranial vault is 26 - 22 ° C, the temperature in the esophagus or rectum remains at 32 - 30 ° C, i.e. within limits that do not significantly affect cardiac activity. The “Holod-2F” and “Fluido-Craniotherm” devices allow you to urgently begin cooling during an operation without interrupting it or interfering with the surgeon’s work; use hypothermia in the postoperative period for resuscitation purposes; automatically maintain the temperature of the coolant and the patient’s body during the cooling process; warm the patient; control the patient’s body temperature at four points simultaneously and the temperature of the coolant.

Obviously, it is possible to achieve a guaranteed uniform decrease in the temperature of brain tissue only with general hypothermia. The removal of heat from the surface of the head leads to cooling of the surface tissues and bones of the skull, and only after that to a decrease in the temperature of the surface areas of the brain. At the same time, the central influxes of heat remain quite powerful, which forms a pronounced temperature heterogeneity of the brain, the role of which in pathology has not been studied. However, due to the listed side effects, the temperature and time limits of general hypothermia are strictly limited, which reduces the neuroprotective effect of this technique.

CCG is used:

• · during operations accompanied by a short shutdown of the heart from the blood circulation, such as suturing a secondary atrial septal defect, valvuloplasty for pulmonary stenosis, valvuloplasty for aortic stenosis and, in some cases, for Fallot’s triad;
• · in case of danger of severe hypoxia due to the nature of the surgical intervention itself, for example, the application of interarterial anastomoses in “blue” patients, when eliminating coarctation of the aorta or reconstructive operations on the brachiocephalic branches of the aortic arch;
• · in emergency neurosurgery. CCG is especially effective in patients with severe traumatic brain injury, accompanied by severe cerebral edema and disturbances of cardiac activity and breathing. When the temperature in the external auditory canal decreases to 31 - 30 ° C and the rectal temperature remains in the range from 34 to 35 ° C, there is a significant improvement in cardiac activity and respiration, which is explained by a decrease in cerebral edema, hypoxia and secondary changes;
• · during resuscitation of patients (therapeutic hypothermia). CCG in clinical death can be decisive in the outcome of revival, as it prevents or reduces cerebral edema.

General anesthesia for CCG does not differ from that for general hypothermia. Cooling begins after induction of anesthesia and intubation. The patient's head is placed in a helmet equipped with numerous holes for streams of cold water or air. The optimal temperature of the coolant (water, air) should be considered 2°C. Lower temperatures are dangerous due to frostbite of the skin. The patient's body temperature is measured at several points (inside the ear canal at the level of the eardrum, in the nasopharynx, esophagus and rectum). The temperature inside the ear canal at the level of the eardrum corresponds to the temperature of the cerebral cortex at a depth of 25 mm from the internal vault of the skull; body temperature is judged by the temperature in the rectum. The rate of cooling of the brain using devices ranges from 7 to 8.3 °C/min, and of the body - 4.3-4.5 °C/min. Cooling is continued until the temperature in the rectum is not lower than 33 - 32 ° C, in the esophagus 32-31 ° C.

CCG causes a gradual decrease in blood pressure and a decrease in heart rate. ECG changes depend on the nature of the surgical intervention and the duration of exclusion of the heart from the circulation. Studies of the bioelectrical activity of the brain do not reveal any significant changes when cooled in this manner to a temperature of 25 ° C in the external auditory canal. During cooling, a decrease in blood buffer bases and pCO2 is observed, a decrease in the amount of protein and its fraction, a decrease in fibrinogen and an increase in fibrinolytic activity. However, these changes are reversible and return to normal when the patient is warmed to the initial temperature.

The patient is warmed using electric heating pads, which are placed on the operating table under the patient's back. After the operation is completed, warming is continued using a polyethylene cape, under which warm air is pumped by a thermostat.