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Therapeutic hypothermia- therapeutic effects on the patient’s body temperature in order to reduce the risk of ischemic tissue damage after a period of insufficient blood supply. Periods of insufficient blood supply can occur as a result of cardiac arrest or blockage of an artery due to embolism, as commonly occurs with a stroke. Therapeutic hypothermia can be administered by invasive methods, in which a special heat-exchange catheter is inserted into the patient's inferior vena cava through the femoral vein, or by non-invasive methods, which typically use a water-cooled blanket or vest on the torso and applicators on the legs, which are in direct contact with the body. patient's skin. Studies have shown that patients at risk of ischemic brain injury have better neurological outcomes when using therapeutic hypothermia.

Background

Hypothermia has been used as a therapeutic method since ancient times. The Greek physician Hippocrates (probably the only ancient doctor in the world whose views are supported in modern times) recommended covering wounded soldiers with snow and ice. Napoleon's surgeon, Baron Dominique Larrey, testified in writing that wounded officers who were kept closer to the fire were less likely to survive severe wounds than infantrymen who were not too pampered by such care. In modern times, the first medical article on hypothermia was published in 1945. This study focused on the effects of hypothermia on patients suffering from severe head injuries.

In the 1950s, hypothermia found its first medical use to create a bloodless surgical field during surgery for intracranial aneurysm. Most early studies focused on the use of deep hypothermia with body temperature in the range of 20–25 °C (68–77 F). This extreme reduction in body temperature generated a host of side effects, making the use of deep hypothermia impractical in most clinical situations. During the same period, isolated studies also appeared on milder forms of therapeutic hypothermia with a moderate decrease in body temperature to the range of 32–34 °C (90–93 °F). In the 1950s, Dr. Rosomoff demonstrated the beneficial effects of mild hypothermia following cerebral ischemia and traumatic brain injury in dogs. Additional animal studies in the 1980s demonstrated the ability of mild hypothermia to play a general neuroprotective role following blockade of blood flow to the brain. These animal findings were confirmed by two seminal human studies that were simultaneously published in 2002 in the New England Journal of Medicine. Both studies, one from Europe and the other from Australia, demonstrated the beneficial effects of moderate hypothermia after cardiac arrest. In response to these studies, in 2003 the American Heart Association (AHA) and the International Liaison Committee on Critical Care (ILCOR) mandated the use of therapeutic hypothermia after cardiac arrest. Today, an increasing number of clinics around the world are using AHA and ILCOR guidelines and have included hypothermic treatment as part of the standard care package for patients suffering from cardiac arrest. Some researchers have gone even further and argue that hypothermia provides better neuroprotection after blocking blood flow to the brain than medication.

RCHR (Republican Center for Health 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. At the moment, therapeutic hypothermia is considered as the main physical method of neuroprotective protection of the brain, since there is not a single method of pharmacological neuroprotection, from the standpoint of evidence-based medicine. 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 lesions of the brain or spinal cord without fever

Brain injury with neurogenic fever

I. INTRODUCTORY PART

Protocol name: Hypothermia (therapeutic) of a newborn

Protocol code:

ICD-10 code(s):

P81.0 Neonatal hypothermia due to environmental factors

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

CP - 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 the incidence of 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 (mandatory) diagnostic examinations performed 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 initiating hypothermia treatment, pharmacological agents should be administered to control shivering.

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 state that the patient's temperature should not fall below a threshold of 32°C.

The body temperature is then gradually raised to normal levels over 12 hours, under the control of the cooling/warming 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 the 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 cooling/warming systems with microprocessor control and patient feedback provide controlled therapeutic hypo/hyperthermia. The device monitors the patient’s body temperature using an internal temperature sensor and corrects it, depending on the specified target values, by 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 the side effects associated with hypothermia.

Therapeutic hypothermia of newborns cannot be performed without a tool for long-term dynamic analysis of brain activity, which effectively complements 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 amplitude-integrated EEG (aEEG) trends, a compressed spectrum and other quantitative indicators of the central nervous system, as well as the initial EEG signal in a small number EEG leads (from 3 to 5).

AEEG patterns have a characteristic appearance corresponding to various normal and pathological conditions of the 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 interventions.

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: no.

Diagnostic criteria

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

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

Laboratory tests: 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

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Treatment

Treatment goals:

Reducing the incidence of severe complications in the newborn from the central nervous system after 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).

Maintain 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.

Follow-up with a neurologist for 1 year.

Immunization with 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 of the brain.

More children treated with hypothermia have no changes on MRI;

General hypothermia at the time of resuscitation reduces the incidence of deaths and moderate and severe disturbances in 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 moderate to mild perinatal encephalopathy 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

Muscular hypotonia and hyporeflexia or

Severe hypertonicity and hyporeflexia or

Disorders of the pupillary reflex (narrowed and does not respond to darkening, dilated and does not respond to light, weak reaction of the pupil to changes in lighting).

Group “C” criteria based on CFM results

The upper edge of the curve teeth is more than 10 µV, the lower edge of the curve teeth is less than 5 µV. The curve may be interrupted by peaks or series of peaks greater than 25 µV or

The upper edge of the waves is less than 10 µV, the curve is interrupted and periodically appears as an isoline and/or is interrupted by a series of peaks less than 10 µV or

Continuous series of peaks with a voltage greater than 25 µV or

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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In 1960, a monograph by V.A. was published. Negovsky “Revitalization of the body and artificial hypothermia” summarizing the main world achievements in the field of experimental and clinical study of therapeutic hypothermia. The main reason for the classic resuscitator's turn to hypothermia was the search for means and methods of prolonging the period of clinical death for a period of more than 5-6 minutes, during which it is possible to achieve a complete and stable restoration of the vital functions of the body. In this approach, unlike hibernotherapy, the main role in prolonging the period of reversible changes in organs and tissues during total ischemia and hypoxia belonged to hypothermia, of course, with appropriate pharmacological accompaniment.

In cardiovascular surgery and neurosurgery, hypothermia has been used especially often to protect the brain from ischemic and reperfusion complications, combat shock and postoperative hyperthermia.

As a special method, artificial hypothermia has found its application primarily as a means of ensuring the safety of surgical interventions during cardiac manipulation, with the goal of protecting the brain in conditions of total circulatory depression. For the first time, such an intervention under conditions of hypothermia in a patient with blue-type heart disease was performed by McQuiston (1949). In the surgical correction of congenital heart defects, hypothermia was especially widely used by a group of Canadian scientists led by Bigelow (1950).

In the 50s of the last century, lowering body temperature during surgical interventions was used by Bakulev A.N., Shamov V.N., Vishnevsky A.A., Meshalkin E.N. and many other famous surgeons of the USSR. The success of the use of hypothermia was evidenced by the fact that mortality during cardiac surgery performed at low body temperature compared with operations performed under normothermia decreased from 13.7% to 5.5%. When correcting complex heart defects, the period of relatively safe shutdown of the general circulation without the use of a heart-lung machine was more than 15-20 minutes. Facts of this kind emphasized the convergence of research on the use of hypothermia in surgery and resuscitation with work on providing assistance in terminal conditions, with the problems of restoring fading or recently extinguished vital functions of the body.

In the surgical practice of those years, the most common methods of lowering the body temperature of patients was external cooling, for example, by immersing the patient in a bath of ice water (up to 2/3 of the body surface) and placing ice bubbles in the projections of the great vessels.

For a milder induction of hypothermia, special cooling blankets were used, in which there were tubes with circulating cold water, or “cold chambers”, where the naked surface of the body was blown with cold air. The use of this kind of techniques in the mid-twentieth century did not escape criticism, which was based on quite fair comments regarding the development of poorly controlled hypothermia, as well as in connection with the facts of cold damage to the integument of the body and damage to nerve trunks in the area of ​​heat removal. To prevent these disadvantages, various approaches have been developed. In particular, Laine P. proposed a technique for extracorporeal blood cooling to induce general hypothermia. In the experiments, blood from a large artery was passed through a silicone tube immersed in ice water and returned either to the same artery or to a vein. Methods of perfusion of organs, including the brain, with cold solutions were also used.

Since the main area of ​​application of hypothermia was surgery, it was extremely important to identify the necessary level of decrease in the temperature of the entire body, sufficient to protect various organs experiencing a long-term cessation of blood circulation. Experimental studies formed the basis for recommendations to lower the temperature during operations on the great vessels to +27-30ºС, and during heart operations to +26-28ºС. Deep hypothermia extended the permissible period of clamping of the vena cava and aorta for a period of 15-20 minutes or more without subsequent dysfunction of vital organs, whereas with normothermia it should not exceed 3-5 minutes. At a body temperature of +24-25ºС, even an hour and a half cessation of blood circulation did not lead to irreversible disorders associated with lesions of the spinal cord and brain in dogs.

Gradually, facts accumulated indicating a significant increase in the permissible time for turning off blood circulation, cardiac arrest and breathing, as hypothermia deepened, which was especially important when carrying out interventions without a heart-lung machine. However, here, too, limitations were discovered, associated, in particular, with the level of the average lethal temperature of a person during hypothermia, which was determined on the basis of numerous observations and turned out to be in the range of +24-26ºС. Reaching these extreme temperatures is necessarily accompanied by the appearance on the ECG of characteristic signs of cardiac dysfunction (prolongation of the P-Q interval, QRS complex, arrhythmias, electromechanical dissociation, etc.), including the appearance of a specific “damage potential” or Osborne waves.

An Osborn wave, also called a J wave or “hypothermic wave,” is a well-defined late upright wave following the QRS complex, or a notch on the downward limb of the R wave. The initial part of the ST segment is located high (there is an elevation of the J point), which reflects disturbances in early ventricular repolarization and manifests itself in hypercalcemia and other pathological conditions (Fig. 1).

Rice. 1. Osborn wave, recorded in a patient in a state of hypothermia.

The level of average lethal temperature is primarily due to increasing disturbances in the activity of the heart and a deep blockade of the functions of parts of the central nervous system. As the temperature of the brain decreased, the activity of the cerebral cortex (about +25ºС) first faded away, and at lower temperatures, the activity of the respiratory center.

The data on brain metabolism during hypothermia turned out to be very interesting. Back in 1950, it was found that oxygen consumption by the brain at a body temperature of +28ºС is reduced by 50% and by 80% at +25ºС. At the same time, the volumetric velocity of blood flow in brain tissue at this level of hypothermia decreases by more than three times. Under these conditions, despite a significant decrease in oxygen consumption, the arteriovenous difference increases by 20-30%, which is explained by a decrease in the volume of blood flow due to depression of the general circulation.

It was also found that as the temperature decreases, oxidative phosphorylation is progressively inhibited, reaching its minimum at a temperature of +25-26ºС, and a further decrease in body temperature does not make significant changes in the rate of metabolic processes in the brain.

The discovery of facts of metabolic depression even under conditions of mild hypothermia (up to +32°C) and a decrease in oxygen consumption by 5-9% when the brain temperature decreases by 1ºC (from +37 to +32°C) allowed us to consider therapeutic hypothermia as an effective way of preventing development of destructive processes in the central nervous system in terminal conditions, focal perfusion disorders.

Most experimental and clinical results demonstrating the protective effects of hypothermia were obtained with pre-cooling of the body. That is, surgical interventions, modeling of clinical death, reproduction of total ischemia and shock were carried out against the background of already formed (preventive) general hypothermia of varying depths.

In addition, it was noted that the rate of temperature increase upon recovery from hypothermia has a significant influence on the results of hypothermic protection. In particular, according to V.A. Negovsky, intensive heating after hypothermia worsened the results of resuscitation and contributed to an increase in the incidence of cardiovascular complications.

The positive effects of hypothermia were also manifested in the fact that after resuscitation of animals with a long period of clinical death (up to 30 minutes) against a background of low body temperature, cardiac activity was easily restored with transthoracic defibrillation. It turned out that in a state of hypothermia, successful defibrillation could be carried out by a discharge with a voltage half as much as that required in normothermic animals under similar conditions.

Under hypothermia conditions, experimental animals significantly increased survival after severe hemorrhagic, hemolytic and traumatic shock. However, cooling the body, undertaken in the later stages after the development of a shock state, turned out to be less effective. Let us recall that, according to A. Labori, hibernotherapy is very effective for shock in the first 6 hours after extreme exposure, primarily due to the use of a combined effect - “lytic cocktails” and hypothermia, which interrupt excessive excitation and inhibit metabolism.

In the mid-twentieth century, resuscitators successfully developed the principles of revival after clinical death, which developed from various causes in conditions of low body temperature. Much attention has been paid to preventive hypothermia in surgery. At the same time, experimental studies and clinical experience of using hypothermia in the treatment of terminal conditions formed under normothermia conditions were very limited.

It is important to note that the material discussed concerns primarily general cooling of the body, while almost no attention is paid to selective hypothermia of the brain. Believing that autonomic blockade in combination with general hypothermia provides systemic protection of the body, including neuroprotection, most authors believed that it was sufficient to provide a combination of these two factors. Moreover, during this period the prevailing opinion was that it was impossible to reduce brain temperature using only craniocerebral heat removal due to the fact that energetic central heat inflows neutralized local cooling effects. The same opinion dominates today, based on the imperative statement that the brain can be cooled only by lowering the temperature of the blood flowing to it, that is, by cooling the entire body.

Discussions on this issue will be given attention in subsequent sections of the work, however, it is appropriate to say that, presenting our own results of experimental and clinical studies of craniocerebral cooling at forums of anesthesiologists and resuscitators in 2010-2014, we have repeatedly encountered the following objections: “you cool the flat bones of the skull, not the brain”; or “craniocerebral cooling is local hypothermia of the cooled area, and not of the body, much less the brain.”

However, evidence that craniocerebral cooling, that is, cooling only the surface of the skin of the scalp, can induce a decrease in brain temperature, and with sufficient exposure and intensity cause a decrease in body temperature, was obtained in large studies carried out in the twentieth century and in a series of works our team.

Therapeutic hypothermia

Moderatetherapeutic hypothermia - controlled inducible decrease patient's core body temperature up 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. At the moment, therapeutic hypothermia is considered as the main physical method of neuroprotective protection of the brain, since there is not a single method of pharmacological neuroprotection, from the standpoint of evidence-based medicine.

Therapeutic hypothermia is included in the standards of treatment:

• International Committee for Interaction on Resuscitation (ILCOR)
• American Heart Association (AHA)
  

• Association of Neurosurgeons of Russia

Application of moderatetherapeutic hypothermia, for reducing the risk of irreversible changes in the brain, it is recommended at the following pathological conditions:

1. Encephalopathies of newborns

2. Heart failure

3. Strokes

4. Traumatic lesions of the brain or spinal cord without fever

5. Brain injury with neurogenic fever

Methodology of therapeutic hypothermia

Before initiating hypothermia treatment, pharmacological agents should be administered to control shivering.

The patient's body temperature drops to32-34°Cdegrees and is maintained at this level for 24 hours.Clinicians should avoid reducing the temperature below the target value. Accepted medical standards state that the patient's temperature should not fall below a threshold of 32 °C.

The body temperature is then gradually raised to normal levels over 12 hours, under the control of the cooling/warming 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 catheterinserted into the 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 the 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

For the non-invasive method of therapeutic hypothermia, specialized devices are used today, consisting of a blockwater-based cooling/warming systems and heat transfer 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 cooling systems /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 an internal temperature sensor and corrects it, depending on the specified target values, by 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.

Patient hypo-hyperthermia system BLANKETROL (CSZ, USA)

Protocol for controlled hypothermia in neonatology

Practice in the USA

Practice in the UK

Protocol for therapeutic hypothermia in neonatal hypoxicischemicencephalopathyAnd(HIE)

Indicators of morbidity and mortality of newborns are one of the most important criteria for the level of health care. Hypoxic-ischemic encephalopathy (HIE) is diagnosed as the most common pathological condition of the neonatal period. – 47% , or hypoxic damage to the central nervous system. According to various authors, it can be detected in 6-8% of newborns.

Hypoxic-ischemic encephalopathy (HIE) in full-term newborns, resulting from acute perinatal asphyxia, is an important cause of subsequent disorders of their neuropsychic development. The risk of death in infants with moderate HIEP is 10%, and in 30% of surviving children, neuropsychological development disorders are detected. With severe GIEP, 60% of infants die and almost all surviving children become disabled.

Clinical syndromes associated with perinatal hypoxia depend on the period of HIE: acute period syndromes include increased neuroreflex excitability, syndromes of general depression of the central nervous system, vegetovisceral dysfunction, hydrocephalic-hypertensive, convulsive, comatose state; The structure of the recovery period of HIE includes syndromes of delayed speech, mental, motor development, hypertensive-hydrocephalic, vegetovisceral dysfunction, hyperkinetic, epileptic, cerebroasthenic. Some authors identify syndromes of motor disorders and increased neuro-reflex excitability in the recovery period.

K. Nelson et al. noted in their studies that children with an Apgar score of less than 3 at 10, 15, 20 minutes and those who survived were more likely to have cerebral palsy, delayed psychomotor development, and seizures than children with a higher score. Prognostic signs depend on the severity of clinical manifestations. The mortality rate of newborns with perinatal damage to the central nervous system of a hypoxic nature is 11.5% (among children with moderate cerebral disorders - 2.5%, severe - 50%). In children with mild hypoxic-ischemic encephalopathy in the neonatal period, complications do not arise. According to M.I. Levene, in 80% of full-term newborns, severe CNS HIP leads to death or severe neurological impairment.

IN When a damaging factor (trauma, oxygen deprivation, etc.) affects the child’s brain, an acute period of encephalopathy begins, which lasts 3-4 weeks. It is in the acute period that active therapy is necessary, which can seriously affect the outcome of the disease.

It is known that general hypothermia (GH) at the time of resuscitation reduces the incidence of deaths and moderate and severe impairment of psychomotor development in newborns with hypoxic-ischemic encephalopathy (HIE) due to acute perinatal asphyxia. This has been confirmed in a number of multicenter studies in the USA and Europe. Moreover, selective head cooling soon after birth can be used to treat children with moderate to mild perinatal encephalopathy to prevent the development of severe neurological pathology. Selective head cooling is ineffective in severe encephalopathy.

Hypothermia in the treatment of HIE is associated with less damage to the gray and white matter of the brain. More children treated with hypothermia have no changes on MRI (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).

"Accumulating evidence supports the benefits of neuroprotective therapeutic hypothermia in term neonates with hypoxic ischemic encephalopathy" (Susan E. Jacobs) (Neonatal Services, Royal Women's Hospital, Victoria, Australia).

Whole body hypothermia consists of keeping the newborn at a target temperature of 33.5°C for 72 hours.

Therapeutic hypothermia was found to reduce the risk of death or major sensorineural disability at age 2 years

Only minimal negative effects of hypothermia are noted. Infants with hypothermia had a prolonged QT interval compared with control infants, but no arrhythmias requiring treatment or cessation of hypothermia were observed.

“The fifteen percent reduction in the composite primary outcome of death or major sensorineural disability is both statistically significant and clinically important.”

The result of the work of specialists was the creation of a number of clinical protocols in the USA and Great Britain. Currently, this method is also accepted by neonatologists in Australia.

In accordance with national multicenter studies in which leading US clinics participated (500 newborns, system Blanketrol ® II, СSZ), American Academy of Pediatrics ( AAP) passed a resolution in 2005 on the need for the use of hypothermia for HIE in the neonatal period to reduce neurological complications later in life.

In 2007, doctors at Children's Hospital in Boston developed a national protocol using blanket devices. Blanketrol ® II Hypo - Hyperthermia System , at which the newborn was cooled to 33.5° C (92.3° F)for 72 hours, followed by a gradual increase in temperature to normal. In development of the US National Protocol participated by Medical Director and Professor of Pediatrics at Harvard Medical School Anna Hansen ( Anne Hansen, MD, MPH).

The results of similar work in European clinics are reflected in a multicenter study TOBY (National Institute for Healthcare Standards, UK), which formed the basis of the UK Clinical Protocol. Clinics from Great Britain, Sweden, Israel, and Finland participated in the study. More information about this protocol can be found at http:/ /www.npeu.ox.ac.uk/toby

Therapeutic hypothermia is now the National standard of care for appropriate risk groups of newborns and is approved by the British Association of Perinatal Medicine.

The WHO Reproductive Health Library (RHL) of the Department of Reproductive Health and Research at WHO headquarters in Geneva, Switzerland, published the following review: “Cooling of neonates with hypoxic ischemic encephalopathy,” which noted that therapeutic hypothermia in term neonates with hypoxic ischemic encephalopathy ischemic encephalopathy appears to be effective. L.V. Usenko
Member of the European Resuscitation Council
A.V. Tsarev

”, consists of implementing complexamers aimed at reducing brain oxygen consumption, increasing its delivery, maintaining sufficient cerebral blood flow and preventing critical episodes of hypoxia and hypoxemia. To date, not many real tools have been proposed to combat ischemia. The basic principles of protecting the brain from ischemia are as follows.

Control of BP and CPP during brain protection. Hypotension is one of the most significant causes of secondary ischemic attacks. Currently, there are recommendations for the use of vasopressors and agents with a positive inotropic effect as a temporary measure to correct arterial hypotension. Obviously, vasopressors do not replace measures to restore circulating blood volume, but given the special sensitivity of the brain to hypotensive episodes, the temporary use of vasopressors is considered justified. According to some authors, the frequency of use of sympathomimetics during operations on intracranial aneurysms reaches 25%.

Glycemic control during brain protection. It is known that a decrease in blood glucose levels leads to damage to neurons due to disruption of energy balance, increased release of glutamate, aspartate, and Ca++ into the extracellular space, triggering mechanisms for the development of ischemia and cerebral edema. However, an increase in blood glucose levels during ischemia contributes to the development of neuronal damage. Hyperglycemia increases brain damage, both during general and focal ischemia.

During incomplete ischemia, the continued increase in the concentration of glucose in the cell, together with an insufficient supply of oxygen, shifts metabolism to an anaerobic level, which increases the lactate content in the brain and aggravates metabolic acidosis. At the same time, free radicals are formed, damaging cell membranes and causing cell death. Prevention of hypo- and hyperglycemia is necessary. It is advisable to maintain the level of glucose in the blood of patients within 5-9 mmol/l.

Hypothermia to protect the brain:
Neuroprotective effect hypothermia widely known and used in neurosurgery since 1955. The classical theory of brain protection is based on the concept that neuronal survival during times of inadequate blood supply can be ensured by reducing the metabolic demands of the brain. For a long time it was believed that hypothermic protection of the brain is based on a significant reduction in cerebral metabolism and neuronal oxygen demand.

So, with a drop in brain temperature for each degree Celsius, cerebral metabolism decreases by 5-7%, and with a decrease in metabolism to 50%, the “flash-suppression” phenomenon is observed on the electroencephalogram (EEG). That is, if the brain at 37°C is resistant to complete ischemia for 5 minutes, then at 27°C it is resistant to complete ischemia within 10 minutes. It is now obvious that the protective effect of hypothermia is provided not only by a decrease in cerebral metabolism.

It is assumed that when hypothermia the release of glutamate and aspartate is suppressed, and the production of nitric oxide, which is involved in the formation of free radicals and free fatty acids, is reduced.

Hypothermia prevents the penetration of Ca++ into the cell, which is fundamentally important for preventing the development of the ischemic cascade. Hypothermia helps stabilize cell membranes and restore BBB functions.
Without cardiopulmonary bypass It is possible to use only moderate hypothermia (31-32°C) due to the risk of serious cardiac disorders that occur with a significant decrease in body temperature.