Traumatic Brain Injury in Children: Clinical Guidelines

List of Abbreviations

ICD-10 – International Classification of Diseases, 10th Revision

TBI – traumatic brain injury

ATP – adenosine triphosphate

BBB – blood-brain barrier

Con – concussion

SCT – spiral computed tomography

GCS – Glasgow Coma Scale

DAI – diffuse axonal injury

ICP – intracranial pressure

DC – decompressive craniectomy

ICH – intracranial hypertension

US – ultrasound examination

Dura – dura mater

STBI – severe traumatic brain injury

AEH – acute epidural hematoma

CT – computed tomography

MRI – magnetic resonance imaging

ECG – electrocardiography

EEG – electroencephalography

Terms and Definitions

Evidence-based medicine is an approach to medical practice where decisions regarding the use of preventive, diagnostic, and therapeutic measures are made based on available evidence of their efficacy and safety, and such evidence is sought, compared, synthesized, and widely disseminated for use in the best interest of patients.

Working group — two or more individuals of the same or different professions working together and in coordination to develop clinical guidelines and bearing joint responsibility for the results of this work. Condition — changes in the body arising from the impact of pathogenic and/or physiological factors and requiring medical care;

Level of certainty of evidence – reflects the degree of confidence that the found effect of a medical intervention is true.

Level of recommendation — reflects not only the degree of certainty regarding the reliability of the intervention's effect, but also the degree of certainty that following the recommendations will yield more benefit than harm in a given situation. Surgical intervention — an invasive procedure that may be used for diagnostic purposes and/or as a treatment method for diseases.

Standard — universally accepted principles of diagnosis and treatment that may be considered as mandatory therapeutic tactics (efficacy confirmed by multiple randomized trials, meta-analyses, or cohort clinical studies). Recommendation. Therapeutic and diagnostic measures recommended for use by the majority of experts on these issues. May be considered as treatment choices in specific clinical situations (efficacy confirmed by individual randomized trials or cohort clinical studies).

Option — therapeutic or diagnostic measures that may be useful (efficacy confirmed by expert opinion in specific clinical cases). Not recommended — therapeutic and diagnostic measures that have no positive effect or may cause harm (any level of evidence).

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Traumatic brain injury (TBI) is damage to the skull and intracranial contents, including brain tissue, cerebral vessels, cranial nerves, and meninges, caused by mechanical energy. The diagnosis is established when there is a clear history of head trauma (history of trauma).

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

The modern concept of brain injury in TBI is based on the concept of primary and secondary injury factors. The traumatic factor causes primary (irreversible) damage within milliseconds, which triggers a cascade of secondary destructive biochemical and immunological reactions. Secondary brain injury factors are subdivided into intracranial (brain edema, intracranial hematomas and hemorrhages, intracranial infection, etc.) and extracranial (hypoxia, arterial hypotension, hypo-, hypercapnia, hypo-, hyperglycemia, hyperthermia, arterial hypertension, infection, etc.)

Secondary injuries combined with primary structural damage to the brain tissue significantly aggravate the severity of the patients' condition and can cause an unfavorable outcome. Secondary brain injury is viewed as a potentially reversible process with timely intervention.

The main pathogenetic links of TBI develop independently of the patient's age. At the same time, the younger the child, the more pronounced are the anatomical and physiological differences that determine the specific features of the brain's reaction to trauma — these include high metabolic rate; low tolerance to blood loss; low tolerance to hypoxia and hypotension; predisposition to brain edema and swelling; low tolerance to hyperthermia; predominance of generalized, diffuse cerebral reactions over focal local manifestations; high compensatory capabilities with sudden and rapid functional decompensation.

1.3 Epidemiology of the Disease or Condition

Traumatic brain injury (TBI) in children occurs more frequently than in adults. Mortality among children with severe TBI ranges across different regions from 12 to 30% or more [2,9]. The results of a survey conducted at the Research Institute of Emergency Pediatric Surgery and Traumatology in 2008 across various federal districts showed that the incidence of TBI among the pediatric population is highly variable, which may largely be due to the lack of a unified reporting and registration system. At the same time, statistical analysis showed that among hospitalized children with neurotrauma, the proportion of severe traumatic brain injury is 6%, which amounts to about 4,000 disabled individuals annually [2].

1.4 Features of Coding the Disease or Condition

S06.0 Concussion

S06.1 Traumatic cerebral edema

S06.2 Diffuse brain injury

S06.3 Focal brain injury

S06.4 Epidural hemorrhage

S06.5 Traumatic subdural hemorrhage

S06.6 Traumatic subarachnoid hemorrhage

S06.7 Intracranial injury with prolonged coma

S06.8 Other intracranial injuries

S06.9 Intracranial injury, unspecified.

1.5 Classification of the disease or condition

The classification of TBI is based on its biomechanics, type, nature, form, severity of injuries, clinical phase, period of course, as well as the outcome of the trauma [Potapov A.A. et al., 2003; Konovalov A.N. et al., 1998 – 2002].

Mild TBI (mTBI) is an acutely developed impairment of brain function resulting from traumatic impact, which may be accompanied by transient loss of consciousness (up to 30 minutes) and/or amnesia (up to 24 hours). It includes a single nosology — cerebral concussion.

Cerebral concussion (concussion) is the mildest clinical form of diffuse transient brain injury based on metabolic, ionic, neurotransmitter disturbances and neuroinflammation, characterized by the absence of visible changes on computed tomography (CT), and clinically presenting as a single functionally reversible form [3].

Moderate TBI includes mild and moderate brain contusions, epidural-subperiosteal hematomas without brain compression.

Severe traumatic brain injury includes

• severe brain contusion,

• intracranial hematomas with compression (acute epidural, subdural, intracerebral hematoma),

• diffuse axonal injury [1,3,7].

To assess the severity of traumatic brain injury globally, the Glasgow Coma Scale (GCS) (Appendix G1), developed in 1974 by G. Teasdale and B. Jennett, is widely used. The significance of the GCS lies in its ability to provide an objective assessment of brain injury severity using a quantitative scale. For pediatric patients, taking into account age-related features, a pediatric scale has been developed (Appendix G2).

Mild TBI: 13–15 GCS points (corresponds to concussion and mild brain contusion).

Moderate TBI: 9–12 GCS points (corresponds to moderate brain contusion).

Severe traumatic brain injury: 3–8 GCS points (corresponds to severe brain contusion).

Both classifications are well compatible [3].

According to biomechanics, TBI is classified into: 1) impact-counterimpact, 2) acceleration-deceleration, 3) combined.

By type of injury: 1) focal, 2) diffuse, 3) combined.

By the genesis of brain injury in TBI, a distinction is made between: 1) primary injuries, which result from the direct impact of traumatic factors — focal contusions and lacerations of the brain, diffuse axonal injuries, primary intracranial hematomas, and combinations thereof;

a) secondary intracranial injuries resulting from factors such as impaired blood-brain barrier permeability, increased brain volume or swelling due to edema, hyperemia or venous engorgement, elevated intracranial pressure, brain displacement and deformation, delayed hematomas (epi-subdural, intracerebral), impaired hemato- and CSF circulation due to subarachnoid or intraventricular hemorrhage, intracranial infection, etc. b) secondary extracranial factors: arterial hypotension, hypoxemia, hypercapnia, anemia, etc. [Reilly P., Bullock R., 2005]. Secondary factors can be prevented or treated, which depends on timely and correct diagnosis, organization, and quality of neurosurgical care.

The following clinical forms of TBI are distinguished: 1) concussion, 2) mild brain contusion, 3) moderate brain contusion, 4) severe brain contusion, 5) diffuse axonal injury, 6) brain compression, 7) head compression.

In TBI, three basic periods of traumatic brain disease are distinguished [Likhterman L.B. et al., 2012]: 1) acute, 2) intermediate, 3) remote.

Acute period is the time interval from the moment of mechanical energy impact on the brain with a sudden disorder of its integrative-regulatory and local functions until the stabilization of impaired general cerebral and systemic functions at a certain level, or the death of the victim. The duration of the acute period ranges from 2 to 10 weeks depending on the clinical form of TBI. Approximate durations of the acute TBI period are: for concussion — up to 2 weeks, mild brain contusion — up to 3 weeks, moderate brain contusion — up to 4–5 weeks, severe brain contusion — up to 6–8 weeks, diffuse axonal injury — up to 8–10 weeks, brain compression — from 3 to 10 weeks (depending on the baseline condition).

Intermediate period is the time interval from the stabilization of systemic, general cerebral, and focal functions impaired by the trauma until their complete or partial recovery or stable compensation. Duration of the intermediate period: in mild TBI — up to 2 months, in moderate TBI — up to 4 months, in severe TBI — up to 6 months.

Remote period is the period of clinical recovery, or maximally achievable rehabilitation of impaired functions, or the emergence and/or progression of new pathological conditions caused by the sustained TBI. Duration of the remote period: in clinical recovery — up to 2 years, in progressive course — unlimited [Likhterman L.B. et al., 2012].

Based on dura mater (DM) damage, penetrating (DM damaged) and non-penetrating (DM intact) severe TBI are distinguished.

Types of TBI include: isolated (if there are no extracranial injuries), combined (if mechanical energy simultaneously causes extracranial injuries), and complex/combined (if different types of energy — mechanical and thermal, or radiation, or chemical — act simultaneously) injuries [1, 3].

1.6 Clinical presentation of the disease or condition

Head examination may reveal signs indicating a past injury (bruises, abrasions, wounds) and skull base fractures (bruising in the mastoid process area [Battle's sign], periorbital hematomas ["raccoon eyes"], leakage of fluid from the external auditory canals, nose, mouth), facial emphysema, mobility of the facial skeleton bones, exophthalmos, and soft tissue hematomas.

Following the general examination, the patient's neurological status is assessed, including: 1) assessment of the level of consciousness using the Glasgow Coma Scale (Appendices G1, G2), 2) pupil state (diameter, symmetry, light reflexes), 3) motor response to painful stimulation (pain localization, flexion response, extension response, lack of motor response), 4) cranial nerve functions, 5) reflex status, 6) meningeal syndrome, 7) oculomotor disorders. All patients with TBI require repeated dynamic neurological examinations.

During the neurological examination, it must be taken into account that acute epidural hematoma in 10% of cases, and acute subdural hematoma in 5% of cases, may feature a triphasic course — initial loss of consciousness, followed by a lucid interval and secondary deterioration with a drop in the level of consciousness to stupor or coma (Konovalov A.N., 2001; Krylov V.V. et al., 2019). It should be kept in mind that in addition to the classic "lucid" interval after initial loss of consciousness, there may be a reduced "lucid" interval or its absence.

Acute subdural hematoma can be either isolated or combined with brain contusion foci. Severe brain contusion is characterized by loss of consciousness lasting from several hours to several days, a decrease in wakefulness to stupor or coma, and may be accompanied by psychomotor agitation, brainstem signs, hormotonia, meningeal signs, epileptic seizures, and vital function disorders. The onset of bradycardia in TBI is due to reflex irritation of the vagus nerve nuclei caused by intracranial hypertension and dislocation. Anisocoria most commonly develops on the side of the hematoma during the initial phase of tentorial herniation, more frequently in acute subdural hematomas, though not in all cases (up to 30% according to the Sklifosovsky Research Institute of Emergency Medicine, 2019). When anisocoria was present, in 82% of cases it was noted on the side of the hematoma, and in 18% on the contralateral side (Krylov V.V. et al., 2019).

The clinical picture of acute epidural hematoma depends on its rate of development and localization; with rapid development of the herniation syndrome, patients may be admitted to the hospital in a severe condition, with the frequency of stupor and coma reaching up to 60% (Konovalov A.N. et al., 2001; Krylov V.V. et al., 2019). Frequently, with this type of hematoma, there is an absence of a lucid interval in up to 40% of cases.

As the herniation syndrome progresses, general cerebral, hypertensive, and meningeal symptoms, drowsiness, psychomotor agitation, bradycardia, and subsequent decrease in the level of wakefulness develop. In 7% of patients, seizures may occur (Krylov V.V. et al., 2019). A feature of the clinical course of epidural hematomas is the possibility of their delayed progression over time; therefore, all victims with severe TBI who experience clinical deterioration or who are found to have a small-volume acute epidural hematoma require a repeat brain spiral computed tomography (SCT). Up to 90% of patients with acute epidural hematoma have a skull fracture. Unlike epidural hematomas, subdural hematomas are not limited in their spread and can be located over 2 or more lobes of the brain; meanwhile, skull fractures in acute subdural hematomas are less common than in acute epidural hematomas — up to 45% (Krylov V.V. et al., 2019).

Unlike acute epidural hematomas, herniation syndrome develops more slowly in acute subdural hematomas, with general cerebral symptoms and mental disorders prevailing in the clinical picture, and epileptic seizures occurring somewhat more frequently (up to 12%). A triphasic course in acute subdural hematomas is rare, whereas anisocoria (up to 56%) and bradycardia (50%) are more pronounced, and up to 28% of patients have contralateral pyramidal deficit. The severity of the patient's condition with acute subdural hematoma is determined by its volume; thus, with a hematoma volume of up to 50 cm³, patients do not exhibit severe impairment in the level of wakefulness.

Diffuse axonal injury of the brain is characterized by a prolonged (up to 2–3 weeks) comatose state, pronounced brainstem symptoms (upward gaze paresis, vertical ocular divergence, bilateral depression or loss of pupillary light reflex, impaired or absent oculocephalic reflex, etc.). Disturbances in respiratory rate and rhythm and hemodynamic instability are frequently observed. A characteristic feature of the clinical course of diffuse axonal injury is the transition from prolonged coma into a persistent or transient vegetative state, indicated by the onset of previously absent eye opening, either spontaneously or in response to various stimuli. At the same time, there are no signs of tracking, gaze fixation, or execution of even elementary instructions (this condition is referred to as apallic syndrome).

The vegetative state in such patients lasts from several days to several months and is characterized by functional and/or anatomical dissociation of the cerebral hemispheres and the brainstem. As the patient emerges from the vegetative state, neurological symptoms of dissociation are predominantly replaced by deficit symptoms. These are dominated by extrapyramidal syndrome with pronounced muscle rigidity, dyscoordination, bradykinesia, oligophasia, hypomimia, minor hyperkinesia, and ataxia. Simultaneously, aspontaneity (indifference to the surroundings, untidiness in bed, lack of any drives for activity), amnestic confusion, and dementia manifest. At the same time, gross affective disorders in the form of irritability and aggressiveness are observed.

2. Diagnostics, medical indications and contraindications for diagnostic methods

Criteria for establishing the disease or condition:

• anamnestic data: presence of a history of trauma according to the victim's description or eyewitness accounts.

• physical examination: clinical presentation of traumatic brain injury (impaired consciousness, focal, meningeal symptoms, herniation syndrome), presence of wounds and abrasions, signs of cranial bone fractures, presence of bleeding, cerebrospinal fluid leakage, and brain tissue discharge through the wound.

• instrumental examination: brain CT, skull radiography

Comments:

Assessment of the patient's general condition includes assessment of the level of arousal (GCS), airway status and breathing pattern (free, labored, superficial, pathological, rhythmic, presence or absence of pneumo-hemothorax), assessment of the cardiovascular system (character of the pulse on the carotid and radial arteries [if the pulse is absent on the radial and present on the carotid, systolic pressure is within 50–70 mmHg], heart sounds, HR, BP), and assessment of the level of arousal.

At the prehospital stage, especially in patients in a comatose state, it is important to assess the state of brainstem functions, within the structure of which the state of the pupils is of fundamental importance (pathology: pupil asymmetry [anisocoria], fixed bilateral pupil dilation [mydriasis], absence of reaction to bright light).

Depression of the level of arousal below 9 points on the GCS, symmetric or asymmetric increase in pupil diameter (anisocoria) with impaired light reaction, symmetric or asymmetric increase in muscle tone up to decerebrate rigidity, blood pressure instability, and bradycardia indicate a severe and extremely severe condition of the patient and the development of herniation syndrome.

Monitoring of vital functions is continued in the ambulance. Along with the assessment of the cardiovascular and respiratory systems, special attention is paid to the dynamics of consciousness disorders, the state of the pupils, and the presence and progression of motor disorders (paresis and paralysis) and muscle tone to detect a potential increase in herniation syndrome

2.1 Complaints and Anamnesis

• When taking the anamnesis, it is recommended to determine the mechanism, location, and time of the injury to clarify the nature and severity of the damage. When taking the history, it is important to take into account the features of the child's psychomotor development. Due to the fact that a patient with severe TBI is in a comatose state, it is necessary to ascertain the anamnesis and circumstances of the injury from relatives or accompanying persons whenever possible [36].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

2.2 Physical Examination

• A thorough general examination of a patient with severe TBI is strongly recommended, including external inspection, palpation of the spine, chest and ribs, abdomen, and facial skeleton to rule out associated injuries. It is mandatory to search for extracranial injuries, as any TBI may be associated [37–39].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

Comments:

During the initial assessment of a patient with severe TBI, it is necessary to establish its nature (closed/open; penetrating/non-penetrating; isolated/associated/combined) and the substrate of injury (DAI/contusion foci/meningeal hematomas; bone structure damage; presence or absence of subarachnoid hemorrhage; and to describe in detail the damage to soft tissues and extracranial structures [thoracic/abdominal cavity; cervical spine; skeletal trauma, pelvis]).

Comments:

When assessing neurological status, the effect of pharmacological sedation is taken into account. Special attention is paid to patients (children, adolescents) in a state of alcohol intoxication, who may exhibit focal neurological symptoms in mild TBI. A separate assessment of focal, general cerebral, meningeal, and brainstem lesion symptoms is performed.

When assessing brainstem reflexes in unconscious patients, the following algorithm is applied:

1) assessment of response to pain stimulus (opens/does not open eyes, localizes/does not localize pain/flexion/extension response/no response);

2) assessment of light reaction, presence of anisocoria, pupil sizes,

3) assessment of corneal reflexes,

4) assessment of oculocephalic and oculovestibular reflexes (contraindicated in cervical spine trauma),

5) assessment of the cough reflex (during tracheal suction)

2.3 Laboratory Diagnostics

• All patients with severe TBI upon admission are recommended to undergo:

  1) general (clinical) blood count with platelet count to identify the condition [40]:

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

• 2) general biochemical blood test, coagulogram (exploratory assessment of the hemostatic system), general (clinical) urinalysis to assess the state of internal organs (liver, kidneys, pancreas, gallbladder, etc.), identify/exclude an active inflammatory process, as well as water-electrolyte balance disorders [141, 142];

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

• 3) coagulogram (exploratory assessment of the hemostatic system) to identify the condition [41, 42];

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

• 4) study of acid-base balance and blood gases to identify the condition [43].

GPP BLOE 3Level of Evidence B (Level of Likeness/Evidence — 3)

2.4 Instrumental Diagnostics

Comments:

High risk factors for intracranial injuries

1. GCS score less than 15

2. decrease in GCS by 2 points during clinical monitoring

3. amnesia lasting more than 30 minutes

4. focal neurological symptoms

5. diagnosed or suspected skull fracture

6. presence of a large scalp hematoma (in children under 2 years of age)

7. suspected open traumatic brain injury (profuse hemorrhage/suspected cerebrospinal fluid leak from the nasopharynx or ears, "raccoon eyes" sign, ecchymosis over the mastoid process)

8. post-traumatic seizures

9. loss of consciousness following trauma

10. repeated vomiting in the absence of other causes

11. intense post-traumatic headache, general agitation, behavioral changes

12. head trauma in patients with coagulopathy

13. history of neurosurgical pathology

14. intoxication with alcohol or other CNS depressants

15. fall from a height

16. age under 2 years

17. high-energy mechanism of injury

CT data allow for the quantification of the extent of injuries and can be considered as outcome predictors.

Adverse outcomes correlate with the progression of diffuse brain injury from grade I to IV according to the Marshall CT classification (Appendix G4), the presence of blood in the basal cisterns, and the presence of intracranial hematomas and brain contusions causing a mass effect. Compression or effacement of the basal cisterns on CT is a high risk factor for intracranial hypertension [3,7,10,11,18].

In cases of suspected craniovertebral trauma or cervical spine fracture (according to the Canadian C-spine high-risk criteria), spiral computed tomography of the cervical spine with intravenous bolus contrast enhancement is recommended for pediatric patients;

Comments:

Canadian C-spine high-risk criteria:

1) Fall from a height of more than 1 m

2) Axial load to the head (diving)

3) Motor vehicle collision at high speed, rollover motor vehicle crash, or bicycle/motorized vehicle (scooter) accident

4) Presence of extremity paresthesias

5) Additional: unconscious patients with an unknown history.

• Computed tomography brain monitoring (repeat scan) is recommended for pediatric patients with worsening neurological deficits, escalating intracranial hypertension/refractory intracranial hypertension, or when neurological status cannot be assessed due to prolonged sedation or neuromuscular blockade [47, 108, 109].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

• All patients with severe TBI (GCS 3–8) upon admission are recommended to undergo an electrocardiogram to assess cardiac function [48].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

• All patients with severe TBI upon admission are recommended to undergo spiral computed tomography or radiography of the chest to rule out polytrauma [144].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

• All patients with severe TBI upon admission are recommended to undergo abdominal CT or comprehensive abdominal ultrasound to rule out polytrauma [49, 51, 115].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

Comments:

If necessary, BICS (infrared brain scanning) is performed dynamically every 20 minutes.

Mild TBI accounts for 90% of all head injuries. Only 25% of patients undergo a CT scan, while 75% of pediatric patients receive no instrumental examination. Visual diagnosis of cerebral hemorrhage in mild TBI (GCS 14–15) in children is difficult and sometimes impossible due to the atypical clinical presentation and absence of symptoms typical for children. Delayed diagnosis of cerebral hemorrhage generally leads to complications, prolonged treatment, extended rehabilitation, and mortality.

• If CT/MRI is unavailable, neurosonography is recommended for infants (first year of life) to rule out life-threatening intracranial injuries and for clinical and sonographic monitoring [1, 52].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

Comments:

An indication for MRI in children may be the very fact of TBI accompanied by the onset of focal neurological symptoms.

MRI findings can be used to predict TBI outcomes in children.

The scope of the examination is determined by the severity of the child's condition. The MRI technique represents a compromise between achieving the highest possible image quality, completeness, and reliability of information regarding the region of interest, on the one hand, and minimizing total scan time, on the other. This is due to the low tolerance of patients experiencing pain or traumatic shock, the need for multiplanar imaging necessitated by the complex configuration of the pathological process, and the requirement for multiparametric characterization of traumatic lesions. The duration of the scanning protocol can be reduced to 5–10 minutes by increasing acceleration factor values, altering relaxation times, voxel or matrix dimensions, or decreasing signal-to-noise ratio values.

Basic brain MRI protocol for TBI (Appendices G5, G6):

rapid scout sequences to obtain brain slices in the sagittal, axial, and coronal planes;

axial T2-weighted TSE, slice thickness 3–4 mm, up to 31 slices;

axial T2-weighted FLAIR, slice thickness 3–4 mm, up to 31 slices;

T2*-weighted GE = SWI (typically 3D in the primary axial plane);

sagittal T2-weighted FLAIR, slice thickness 3–4 mm, 27 slices;

coronal T1-weighted FLAIR or T1-weighted GE, slice thickness 3 mm;

3D DWI in the primary axial plane.

When analyzing MRI data in TBI patients, alongside visual assessment of the brain tissue via signal intensity changes, a series of measurements is performed to quantify mass effect. The following parameters are measured: midline shift, volumes of contusions and hematomas, ventricular volumes, degree of cisternal compression, and linear dimensions.

Midline shift is measured at the level of the septum pellucidum. Areas are calculated by tracing the contours of the region of interest. Volume is determined using the ellipsoid volume formula:

V=1/6∙π∙A∙B∙C

where V is the volume of the contusion or hematoma, and A, B, C are its principal diameters.

When analyzing cerebrospinal fluid spaces, special attention must be paid to visualizing the cisterns: ambient, basal, lateral, transverse, quadrigeminal, pontine, vein of Galen cistern, and cerebellar vermis cistern.

To assess the degree of ambient cistern deformation, its configuration, relationship to adjacent brain structures, width, and the angle formed by the intersection of its lateral angle planes (normally varying from 90° to 105°) are evaluated.

2.5 Other Procedures

• General (clinical) cerebrospinal fluid analysis is recommended for children (0–18 years) when developing intracranial purulent-inflammatory complications are suspected. Lumbar puncture is recommended in the absence of clinical and CT signs of herniation syndrome and preserved patency of CSF pathways to prevent the development or worsening of brain herniation and dislocation processes [145, 146].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

Delayed care, secondary brain injury, incomplete examination, unskilled surgical intervention, and inadequate intensive care are the primary causes of patient mortality and disability.

3.1. Conservative management

3.1.1. Prehospital stage

The prehospital stage, or the stage of first medical aid for patients with severe traumatic brain injury (TBI), is one of the most critical and vulnerable phases. The effectiveness of the provided care depends on the time factor and the optimal scope of care, which is why we considered it necessary to include this section in these guidelines.

The main tasks of the prehospital stage in children with TBI include assessing the severity of the injury and general condition, determining and providing the priority needs of the injured child, and ensuring the fastest possible transport to a specialized hospital with appropriate diagnostic and therapeutic capabilities [5, 9, 18, 19].

For pediatric patients with severe TBI (GCS 3–8 points), restoring and maintaining vital functions and preventing secondary brain injury are of paramount importance. When necessary, resuscitation measures should be initiated as close to the injury site as possible [1–3, 5, 10, 17, 18].

Emergency medical service specialists should have a clear understanding of the main pathogenetic links in the development of «traumatic disease» of the brain.

Documentation completed at the prehospital stage should reflect the provisional diagnosis, hemodynamic status, dynamics during observation, and the scope of emergency care provided at the scene and during transport [5, 10].

3.1.1.1. Initial patient examination

Comments:

Foreign bodies and bone fragments from the cranial cavity in penetrating wounds must not be removed.

• To transport the patient, it is recommended to use a vacuum mattress that allows immobilization of the entire musculoskeletal system. If a vacuum mattress is unavailable, a cervical collar and splints to immobilize injured limbs (in case of polytrauma) should be applied [56, 57].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

3.1.1.2. Restoration of oxygenation at the prehospital stage

Patency of the airway is secured. If necessary, the oro/nasopharynx is suctioned and an airway is inserted. In the presence of signs of respiratory failure during spontaneous breathing, oxygen mask ventilation is provided. Adequacy is assessed based on clinical data and monitoring parameters.

Comments:

Avoid episodes of hypoxia.

• If intubation is impossible in pediatric patients (0–18 years) with impaired consciousness down to coma grade I (GCS score less than 9), conicotomy (A16.08.022) is recommended [60].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

3.1.1.3. Correction of arterial hypotension at the prehospital stage

In children, hypotension is defined as systolic blood pressure below the 5th percentile of the age norm (Appendix 3). The lower limit of systolic blood pressure (5th percentile) of the age norm can be calculated by the formula: 70 mmHg + (2 × age in years) (2).

• Bradyarrhythmia and cardiac arrest are indications for initiating cardiopulmonary resuscitation. It is recommended for the pediatric category of patients (0–18 years) to use closed-chest cardiac massage for artificial circulation support. The primary drug used in cardiac resuscitation is epinephrine** (ATX code C01CA24). If vascular access is unavailable, endotracheal administration of drugs or a single administration into the root of the tongue is possible [11].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

3.1.1.4. Drug therapy

3.1.1.5. Transport conditions

Comments:

Infusion therapy aimed at maintaining systolic blood pressure at the upper limits of the age norm.

3.1.2. Specialized inpatient facility

Optimal timing implies admission of the patient within the first hour after trauma with notification of the receiving medical facility.

Treatment of children with severe isolated and polytrauma TBI is carried out in a specialized hospital. A specialized hospital is a multidisciplinary pediatric hospital with round-the-clock CT, laboratory-diagnostic, intensive care, surgical, traumatological, and neurosurgical services [1, 9, 10].

Transportation/transfer to a specialized hospital is carried out in the following cases [9-11, 14, 18]:

1. GCS <14 points,

2. Open TBI

3. Fall from a height of more than 2 meters

4. High-energy trauma mechanism

5. Prolonged extrication of the victim (more than 20 minutes) from rubble, vehicles, etc.

6. Age under 5 years

Comments:

The main purpose of hospitalization is the fastest possible diagnosis of injuries and elimination of the main life-threatening pathophysiological mechanism.

The overall severity of the patient's condition and brain injury is assessed with the involvement of all necessary specialists (anesthesiologist-resuscitologist, traumatologist, surgeon, etc.) united by a unified treatment and diagnostic program that implies the continuity and consistency of the therapeutic process.

Neurological status is monitored to control brainstem functions—the level of consciousness (Glasgow Coma Scale) is reassessed, and pupil status is evaluated (pathology: pupillary asymmetry of one millimeter or more (anisocoria), fixed bilateral pupillary dilation (mydriasis), absence of reaction to bright light).

3.1.2.1. Monitoring of vital functions

3.1.2.1 Respiratory monitoring

• Tracheal intubation with possible subsequent mechanical ventilation is recommended for victims with impaired consciousness down to coma grade I (less than 8 points on the GCS) [3, 7, 9, 11, 18, 20].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

Comments:

In children with TBI ≤8 (on the GCS), airway status must be controlled to prevent hypoxemia, hypercapnia, and aspiration. Oxygenation and ventilation must be assessed continuously using pulse oximetry and CO2 monitoring (capnography with determination of end-tidal CO2 concentration), and/or by dynamic blood gas analysis and blood acid-base status testing [14, 15, 17-19].

Upon loss of consciousness to the level of coma (less than 8 points on the GCS), the patient must be intubated, and if spontaneous breathing is ineffective through the endotracheal tube, mechanical ventilation (MV) should be performed. To prevent episodes of patient-ventilator dyssynchrony during MV that cause a sharp increase in ICP, the selection of ventilation modes or the administration of non-depolarizing neuromuscular blockers and sedatives is necessary. End-tidal CO2 or PaCO2 concentration must be maintained within 36-40 mmHg. To prevent cerebral hypoxia, all manipulations associated with the depressurization of the ventilator circuit must be accompanied by pre- and post-oxygenation with 100% oxygen.

Short-term hyperventilation can be used in case of a sharp deterioration in neurological status (threat of herniation syndrome development) and increasing intracranial hypertension when sedation, muscle relaxation, cerebrospinal fluid drainage from the cerebral ventricles, and osmotic diuretics are ineffective.

3.1.2.3. Hemodynamic monitoring

Comments:

Arterial hypotension is corrected by restoring circulating blood volume. In children, hypotension is defined as systolic blood pressure below the fifth percentile of the age norm or in the presence of clinical signs of shock. The lower limit of systolic blood pressure (fifth percentile) of the age norm can be calculated using the formula: 70 mmHg + (2 × age in years). Vasopressor and inotropic support are used if necessary.

Comments:

Cerebral perfusion pressure (CPP) is the difference between mean arterial pressure and ICP—the pressure gradient that determines cerebral blood flow.

Cerebral perfusion pressure within 40-65 mmHg (depending on age) is optimal [11, 17, 19].

3.1.2.4. ICP monitoring

• ICP monitoring is recommended for children with sTBI (GCS ≤8). The use of intracranial pressure monitoring may also be considered in infants in the first year of life with sTBI [3, 7, 9, 11, 18, 20, 86, 87]

GPP BLOE 3Level of Evidence B (Level of Likeness/Evidence — 3)

Comments:

Children with severe TBI (GCS ≤8) have a high risk of intracranial hypertension. Intracranial hypertension can accompany diffuse brain injury and post-traumatic sinus thrombosis. At higher GCS scores, ICP monitoring may be indicated for patients with severe polytrauma who require prolonged mechanical ventilation, sedation, and relaxation, i.e., those in conditions that limit the possibility of clinical monitoring.

Intracranial hypertension is a key pathophysiological variable in the development of secondary injuries (1–3). Since the late 1970s, a breakthrough in the treatment of severe TBI has been associated with the introduction of guidelines focused on intracranial pressure control (4). A meta-analysis of 15 studies including 857 children with sTBI showed the dependence of unfavorable outcomes on elevated ICP (>20 mm Hg) [15]. The appropriateness of using ICP monitoring is confirmed by data on the high incidence of ICP development in children with sTBI, the correlation of adverse outcomes with high intracranial pressure values, and improved treatment outcomes in patients with controlled ICP values. Although these studies correspond only to Class III evidence, their results demonstrate a relationship between the control of intracranial hypertension and neurological outcome. Several studies have shown the dependence of unfavorable outcomes after severe TBI on intracranial hypertension and/or systemic hypotension [17–19, 23].

ICP monitoring makes it possible to determine the optimal volume of treatment based on objective indicators, facilitating the adequate choice of methods such as hyperosmolar therapy, sedation, muscle relaxation, the use of barbiturates and their derivatives, and decompressive craniotomy.

3.1.2.5. Treatment of intracranial hypertension

Comments:

The treatment of severe TBI in children, just like in adults, is largely focused on controlling ICP and preserving CPP. A short-term increase in ICP with a return to normal values within <5 minutes is permissible, but a prolonged increase in ICP ≥20 mm Hg for ≥5 minutes requires treatment (1). Optimal threshold and target ICP values in pediatric TBI are still being refined and depend on age [17–19]. Publications on this issue are practically non-existent; only in one study did the ICP thresholds for initiating therapy vary depending on age and were 15, 18, and 20 mm Hg in children aged 0–24 months, 25–96 months, and 97–156 months, respectively [23].

Basic (prophylactic) and emergency therapy for intracranial hypertension are distinguished [10].

Basic (prophylactic) therapy is aimed at preventing and eliminating factors that can worsen or accelerate the development of intracranial hypertension. Specific factors that can lead to an increase in intracranial pressure include impaired venous outflow from the cranial cavity (incorrect head position of the patient, psychomotor agitation), respiratory disorders (airway obstruction, hypoxia, hypercapnia), hyperthermia, arterial hypo- and hypertension, and seizure syndrome.

3.1.2.6. Emergency therapy

3.1.2.6. Basic therapy for intracranial hypertension

Ventricular drainage

Comments:

Ventricular drainage is installed in patients with sTBI with a GCS level of consciousness <8 points if the manipulation can be performed (after neuroimaging). After opening the ventricular drain, release no more than 2 ml of CSF. ICP monitoring should be performed with a closed drain after 15–20 seconds. If there is no effect, perform repeated drainage. The drainage rate should not exceed 20 ml per hour.

Hyperosmolar solutions

(Solutions affecting water-electrolyte balance) (ATX code B05BB)

Comments:

#Mannitol** is used as a bolus at a dose of 0.25–1.0 g/kg of body weight. The daily dose of administered #mannitol** should not exceed 140–180 g [11, 18, 149].

Mannitol** is widely used for elevated ICP in children with TBI and, despite the lack of an evidence base, has established itself as an effective and safe drug in the treatment of intracranial hypertension. It is advisable to use #mannitol** before starting ICP monitoring if there are signs of transtentorial herniation or neurological deterioration not related to the effects of extracranial factors [17, 18].

Use of barbiturates

Comments:

When performing therapeutic barbiturate anesthesia, it is advisable to monitor the arteriovenous oxygen difference, since there is a risk of developing oligemic cerebral hypoxia [6].

Clarify the form and dose according to the instructions for Sodium thiopental** (N01AF barbiturates): loading dose 8 mg/kg; maintenance dose: 3–5 mg/kg/hour [88, 122]

Initially, the drug is administered at a dose of 8 mg/kg per hour, followed by an infusion of 3 doses of 5 mcg/kg per hour and maintenance of the achieved plasma barbiturate concentration by administering them using an automatic perfusion pump at a dose of 1 mg/kg per hour. The duration of infusion is at least 48 hours.

The use of barbiturates for elevated ICP in children with severe TBI has been practiced since the 1970s. One of the first publications was by Marshall et al., who reported that the use of barbiturates in patients with refractory intracranial hypertension improves outcomes in severe TBI.

Clinical studies on the use of barbiturates in children are limited to two case reports, which precludes definitive conclusions. Based on these data, it can only be hypothesized that barbiturates are effective in treating persistent intracranial hypertension in children; however, their effect on survival or neurological outcome improvement has not been established. High-dose barbiturate therapy leads to arterial hypotension in both children and adults, which requires appropriate hemodynamic monitoring [3, 11, 17-20].

Hyperventilation

Comments:

When using hyperventilation, it is advisable to monitor the adequacy of brain oxygen supply by measuring SvjO2 and/or PbrO2. SvjO2 values between 55% and 75% are considered normal, provided there is adequate arterial blood oxygenation. The normal PbrO2 is 25-35 mmHg at an arterial oxygen tension of 80-100 mmHg [11].

Comments:

The reduction of intracranial pressure during hyperventilation is due to vasoconstriction (induced by hypocapnia) and a decrease in cerebral blood flow (CBF). Recent studies involving adults and children have shown that hyperventilation reduces brain oxygenation and leads to ischemia [3, 7]. In a study by Stringer et al. [10], the authors demonstrated that hyperventilation caused a simultaneous decrease in CBF in both damaged and presumably intact brain areas. The authors showed a correlation between the degree of hypocapnia and the incidence of cerebral ischemia. The incidence of regional ischemia was 28.9% during normocapnia and increased to 59.4% and 73.1% at PaCO2 of 25-35 mmHg and <25 mmHg, respectively. Experimental studies have shown that prophylactic hypocapnia, in addition to reducing CBF, alters the buffering capacity of cerebrospinal fluid, and the significance of this effect may outweigh its impact on CBF [5].

Despite the lack of published data on the benefits of hyperventilation in children with severe TBI, it continues to be widely used. No randomized controlled trials have been conducted on the effect of hyperventilation on various aspects of severe TBI in children, such as refractory intracranial hypertension or the development of herniation syndrome.

Hypothermia

Comments:

Cooling the patient to the target temperature must be done very rapidly (within 30-60 minutes), while rewarming should be very slow (0.2-0.3°C per hour). Patient cooling may be accompanied by serious complications: hypocoagulation, increased diuresis, electrolyte disturbances, impaired humidification of respiratory gases, and infectious complications (adapted from adult guidelines).

There are significant doubts regarding the prophylactic use of hypothermia in children with TBI. Several studies, including two class II evidence studies, have shown that mild or moderate hypothermia compared to normothermia helps reduce intracranial hypertension. However, the efficacy of this therapy compared to other treatment modalities, including first-line drugs or targeted therapy for refractory intracranial hypertension, remains unclear. Furthermore, conflicting results have been reported regarding the effect of hypothermia on mortality and/or outcomes.

3.1.2.8. Prevention and treatment of pulmonary complications

Comments:

Indications for tracheostomy:

a) Facial skeletal injuries

b) Sinusitis

c) Prolonged intubation exceeding one month

d) Bulbar disorders

Comments:

Thorough reprocessing of mechanical ventilators and flexible bronchoscopes must be carried out, alongside regular monitoring of bacterial contamination of ventilators post-sterilization.

Maintain individual use protocols for suction devices and prohibit the reuse of suction catheters. Whenever possible, specialized closed tracheobronchial suction systems and combined breathing filters should be used. Tracheobronchial suctioning must be performed wearing sterile gloves. Hands and gloves must be treated with special alcohol-based disinfectants after any manipulation involving the patient. Disposable paper towels or wipes should be used for drying hands after washing with running water.

• When prescribing antibacterial therapy in children to achieve maximum efficacy, it is recommended to consider the pharmacokinetic properties of antibiotics, select doses based on their minimum inhibitory concentrations, and implement scheduled drug rotation [124].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

3.1.2.9. Prevention and treatment of intracranial suppurative complications

Comments:

When intracranial suppurative complications develop, intrathecal administration via lumbar puncture, lumbar drain, or ventricular catheter may be used. A lumbar drain should be placed when the cell count exceeds 400-500 cells per mm³. To prevent brain herniation, lumbar puncture and lumbar drain placement should not be performed if there are signs of axial or significant transverse shift on brain computed tomography.

If there are clinical and CT signs of ventriculitis, catheters are inserted into the anterior horns of both lateral ventricles. Antibiotic therapy is prescribed according to cerebrospinal fluid culture results. Antibacterial drugs are administered through the drain 2-6 times a day. Antibiotic administration is performed by a neurosurgeon. Intrathecal administration of systemic antibacterial drugs is carried out after dilution with normal saline** (ATX code B05XA). Vancomycin** 5 mg intrathecally is preferred (ATX code J01XA01, glycopeptide antibiotics) [125, 151, 154]. At all other times, the drain is set to passive drainage.

During ventricular or lumbar drainage, cerebrospinal fluid hyperdrainage should be avoided by positioning the drainage system's 'knee' level with the foramen of Monro or by using special closed systems that allow simultaneous measurement of CSF pressure and controlled CSF drainage. Parenteral antibiotic therapy should be discontinued 3–4 days after the complete regression of symptoms of meningitis or ventriculitis (recommendations).

3.1.2.10 Post-traumatic seizures

• Phenytoin** (ATC code N03AB02) may be recommended for children from three years of age, taking into account the dosage form, for the prevention of early post-traumatic seizures (PTS) [17–19]. Given the high probability of metabolic disorders in patients with severe traumatic brain injury, monitoring the drug level is recommended. [147]

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

Comments:

Post-traumatic seizures are defined as seizure episodes developing within 7 days after trauma, or later, 8 days or more after emerging from a coma (1). Risk factors for the development of post-traumatic seizures include injury severity, localization and nature of the injury, presence of bone fragments or foreign bodies in the brain parenchyma, depressed skull fracture, focal neurological deficit, loss of consciousness, decreased Glasgow Coma Scale score <10, duration of post-traumatic amnesia, presence of subdural or epidural hematoma, penetrating injury, chronic alcoholism, and age. The incidence of PTS in children with TBI is approximately 10%. In infants and young children, the seizure threshold is lower.

Pathophysiological changes in the hippocampus are considered as mechanisms for the development of post-traumatic epilepsy, including axonal sprouting, impaired potassium depolarization of glial cell plasma membranes, dysfunction of Schaffer collaterals, apoptosis of neurons adjacent to the lesion, and activation of the TrkB-ERK1/2-CREB/ELK-1 signaling pathway in the hippocampus. Recent studies suggest a role for albumin-induced changes in the electrophysiological properties of astrocytes, mediated by the transforming growth factor-beta receptor and leading to extracellular potassium accumulation (27, 28).

Computed tomography, electroencephalography, and magnetic resonance imaging are the most significant methods for diagnosing post-traumatic epilepsy. These neuroimaging methods in the acute period of traumatic brain injury allow for the identification of lesion foci corresponding to risk factors for the development of post-traumatic epilepsy.

During the EEG examination, attention is paid to the presence of epileptiform activity patterns or epileptic seizures according to the criteria for identifying epileptiform activity. At the same time, it is important to note that the development of epileptic seizures necessitates brain CT (MRI) and an EEG examination.

3.1.2.11. Nutrition for patients with severe TBI

The acute and early periods of severe TBI are characterized by the development of hypermetabolism and hypercatabolism, which causes malnutrition and the loss of a significant portion of muscle mass in this category of patients. A direct correlation has been established between malnutrition in critically ill patients and their mortality—the higher the energy deficit, the more frequently they experience severe multiple organ failure and death. As early as 1936, H.O. Studley noted that when patients lost more than 20% of their body weight, postoperative mortality reached 33%, whereas with adequate nutrition it was no more than 3.5%.

Over recent decades, our understanding of the role of molecular and biological effects of nutrients in maintaining homeostasis in critically ill patients has advanced significantly. The main tasks of nutritional support in the complex therapy of severe TBI are: preserving body muscle mass, maintaining an adequate immune response, and preventing metabolic complications [3, 7, 11, 13].

Initiation of enteral feeding

Comments:

EN helps preserve the barrier and immunological functions of the intestine through microbiome normalization and the synthesis of secretory IgA (GALT). It is important to reach 80% of the calculated protein and calorie requirements by 5–7 days after the initiation of EN

• To assess the patient's nutritional status in routine practice, anthropometric evaluation should be performed, including measurement of height, weight, and body mass index (BMI), as well as the dynamics of these indicators [97, 126].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

Comments:

Traditional laboratory tools for nutritional assessment (total protein, serum albumin, prealbumin, retinol-binding protein, and anthropometry) have not proven their reliability as markers of muscle mass status.

Choice of feeding method

• EN is recommended as the preferred feeding method for critically ill patients in the absence of contraindications [97, 127].

GPP CLOE 4Level of Evidence C (Level of Likeness/Evidence — 4)

• If there are signs of protein-energy malnutrition upon admission and EN is impossible, it is recommended to start PN as soon as possible after admission and adequate resuscitation measures [102, 138].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

Dosing of enteral nutrition

Comments:

In the absence of indirect calorimetry, predictive equations can be used. Predictive equations should be used with caution as they provide a less accurate estimate of energy expenditure than indirect calorimetry. In obese patients, energy requirements calculated using predictive equations should be based on ideal body weight, and in malnourished patients, on actual body weight

Comments:

The use of additional modular protein supplements or high-protein enteral formulas helps reduce nitrogen losses, thereby helping to minimize muscle mass loss

Patient positioning during feeding.

Improving tolerance to enteral nutrition

Comments:

Regular monitoring of EN tolerance allows for the early detection of intolerance signs and the timely correction of emerging disorders by changing the enteral formula, feeding regimen, administration rate, and/or feeding volume.

To accurately assess patients' energy expenditure, the method of indirect calorimetry should be used. In the absence of a metabolograph, patients' energy requirements are calculated using formulas.

Nutrition can be administered both enterally and parenterally. The advantages of enteral nutrition over parenteral nutrition include a lower risk of hyperglycemia and infectious complications. For enteral nutrition, a nasogastric/orogastric tube is placed. If gastric feeding is ineffective for more than 2 days, an intestinal tube is placed. In this case, special semi-elemental formulas should be used for feeding patients. If long-term enteral tube feeding for more than 4 weeks is required, gastrostomy placement is possible (recommendation). Whenever possible, preference should be given to enteral nutrition. In children, 130 to 160% of metabolic expenditure should be provided [15].

The use of parenteral nutrition in children with traumatic brain injury (TBI) is of great importance. Just like adults, children with severe TBI need to have their energy requirements met for the effective recovery from injuries, body functioning, and prevention of other pathological conditions initiated by trauma. In children, energy requirements necessary for normal growth and development are higher than in adults. The decision to use parenteral nutrition, including timing, amount, route, and composition of such support, can significantly affect short- and long-term outcomes.

The results of a phase II randomized controlled trial showed no difference in outcomes in children receiving standard nutrition versus nutrition including immunomodulators.

3.2. Surgical treatment of TBI

3.2.1. Decompressive craniectomy

• Decompressive craniectomy with duraplasty may be recommended in the event of a threat/progression of herniation syndrome or the development of refractory intracranial hypertension in children with severe TBI [3, 4, 10, 11, 17–21, 67, 68].

GCR BLOE 1Grade of Recommendation B (Level of Evidence - 1)

Comments:

Decompressive craniectomy can be used as an adjunctive procedure during the removal of mass-effect lesions (intracranial hematomas, contusions) when there is a threat of progressive brain edema (secondary decompressive craniectomy).

Decompressive craniectomy is used as a last resort when conservative therapy measures are ineffective. The main goal of decompressive craniectomy is to increase intracranial volume, thereby reducing intracranial pressure and improving the functional state of the brain. The timing of decompression is determined by the results of clinical examination, the dynamics of neurological disorders, the level of ICP elevation, or the resistance of this elevation to various conservative treatment options. Primary decompressive craniectomy as a surgical method for controlling intracranial pressure remains a subject of debate. Two randomized trials have focused on the use of decompressive craniectomy for ICP control in adults: the DECRA trial (1), the results of which showed a decrease in ICP after decompressive craniectomy without improved outcomes (2), and the RescueICP trial (3). In the pediatric population, such studies have not been conducted, and the evidence base is lacking.

There are several types of decompressive craniectomy. It may consist of unilateral and bilateral subtemporal decompression, hemispheric craniectomies, circular craniectomy, or bifrontal craniectomy. The choice of method depends on CT findings.

Contraindications to decompressive craniotomy:

Atonic coma (GCS score of 3 + bilateral mydriasis + muscle atonia and areflexia) without subsequent improvement during resuscitation measures and associated with:

– primary brainstem contusion according to CT (MRI) with clinical features of irreversible permanent damage (GCS score of 3 from the moment of injury);

– secondary ischemic brainstem injury against the background of herniation syndrome with clinical features of permanent irreversible damage (GCS score of 3 + bilateral mydriasis + muscle atonia and areflexia);

– reverberating blood flow (or absence of blood flow) in the main cerebral arteries of the base of the brain bilaterally on transcranial Doppler ultrasonography combined with the clinical presentation of atonic coma;

– absence of blood flow in the four basins of the main cerebral arteries according to MR angiography combined with the clinical presentation of atonic coma;

– absence of bilateral auditory brainstem evoked potentials combined with reverberating (or absent) cerebral blood flow

3.2.2. Surgical treatment of acute epidural hematomas

Comments:

1. With a smaller hematoma volume, indications for removal include a total volume of the pathological lesion greater than 60 cm³, compression of the ambient cistern, and a decrease in the patient's level of consciousness from the time of injury to surgery.

2. An epidural hematoma with a volume of less than 30 cm³, a thickness of less than 15 mm, and a midline shift of less than 3 mm in conscious patients with no focal neurological symptoms may be managed conservatively (with careful neurological and CT monitoring in a neurosurgical inpatient unit) [11, 18, 21].

There is no consensus regarding surgical intervention techniques, but it is believed that craniotomy provides more complete evacuation of the hematoma [1, 3, 4, 10, 21].

3.2.3. Surgical treatment of acute subdural hematomas

• Surgical intervention in the scope of primary decompressive craniectomy and removal of subdural hematoma is recommended for patients with a hematoma thickness of less than 10 mm and a midline shift of less than 5 mm, when there is a decrease in the level of consciousness by 2 or more points on the GCS from the time of injury to admission to the hospital, progression of herniation syndrome, and an increase in ICP above 20 mm Hg [11, 17, 18, 21].

GCR CLOE 5Grade of Recommendation C (Level of Evidence - 5)

3.2.4. Surgical treatment of brain contusions

Comments:

Indications for surgical removal of contusions include a decrease in consciousness to coma with contusions in the frontal and temporal lobes with a volume greater than 20 cm³, if the midline shift is greater than 5 mm and/or there are signs of compression of the brain cisterns on computed tomography scans, as well as if the volume of the contusion exceeds 50 cm² [Note: keeping original tag placement as requested, standardizing text superscript].

Patients with cerebral contusions without signs of neurological deterioration, as well as with controlled ICP and a minor mass effect on computed tomography, may be treated conservatively provided that monitoring and serial CT are performed [21, 105].

3.2.5. Indications for surgery in posterior cranial fossa lesions

Comments:

Conservative treatment in patients with posterior fossa structural injuries can be performed for epidural hematomas with a volume of less than 10 cm³, lateral cerebellar lesions of less than 10 cm³, absence of fourth ventricle shift, and brainstem symptoms.

A wait-and-see approach in patients with posterior fossa structural injuries is possible for epidural hematomas with a volume of 10 to 20 cm³ and cerebellar lesions of 10 to 20 cm³ in a lateral location [21].

3.2.6. Surgical treatment of depressed skull fractures

Comments:

Indications for surgical treatment are:

• bone fragment depression greater than the thickness of the bone,

• dural tear,

• damage to the paranasal sinuses, pneumocephalus,

• presence of a hematoma,

• cosmetic defect,

• wound contamination.

Elevation of the depression and surgical debridement of the wound are the core elements of the surgery. Management of open depressed fractures should include the use of systemic antibacterial drugs.

Patients with a depressed skull fracture are recommended to be managed conservatively if the depression is less than the bone thickness and there are no signs of dural tear. Pediatric patients under 1 year of age with "ping-pong" ball skull fractures and a depression of less than 5 mm may also be managed conservatively [11,21]

• Conservative treatment of a closed depressed fracture is recommended to be decided on an individual basis for each pediatric TBI patient (0–18 years) [18,20].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

3.3. Other treatment. Other treatment methods are not used for traumatic brain injury in children

4. Medical Rehabilitation and Sanatorium-Resort Treatment

The goal of rehabilitation is the fastest possible recovery of lost functions and the improvement of the quality of life for both the child and their family members [69,70].

As part of early rehabilitation, it is fundamentally important to identify the primary pathogenetic link hindering further recovery [26, 71]. The age aspect is of critical importance. The younger the child, the more differences there are in the complex of rehabilitative measures, where an extremely complex task comes to the fore: restoring conditions for the further development of motor and cognitive functions.

The pathogenetic impact of the damaging factor on the body of a growing child must be constantly re-evaluated, and the goals and objectives of rehabilitation must be continually refined in order to facilitate progress through the corresponding stages of development and recovery. This necessitates regular multidisciplinary discussions during the rehabilitation process, especially in the early period when spontaneous recovery processes are most pronounced [6,8,12,26].

Rehabilitation must be based on the patient's preserved functions (M. Dimitrijevic, 2012). It is mandatory in the rehabilitation of children with the consequences of severe TBI to use the International Classification of Functioning to assess the degree of impaired functions, determine the recovery prognosis, and formulate a rehabilitation diagnosis [6].

• Rehabilitation is recommended for pediatric patients (0–18 years) to begin as early as possible in the acute and hyperacute periods of TBI in the intensive care unit, continue in the intensive care ward of the neurosurgical/traumatological department, and on the beds of a specialized department (first-early rehabilitation stage at V-IV supervision levels) involving a multidisciplinary team of specialists [6,8,26, 74-79].

GPP BLOE 2Level of Evidence B (Level of Likeness/Evidence — 2)

Comments:

After discharge from the primary hospital, rehabilitation continues at the second stage in a 24-hour department/center for patients with central nervous system injuries (second stage of rehabilitation – at III-IV supervision levels). The third stage of rehabilitation is carried out in an outpatient rehabilitation department, a rehabilitation day hospital, or in the form of tele-rehabilitation. Each stage has its own goals, objectives, and composition of the multidisciplinary team [6, 8].

5. Prevention and Dispensary Observation

Pediatric TBI patients of varying severity are at risk of developing post-traumatic complications. The probability of developing complications is directly proportional to the severity of brain damage. Complications include post-traumatic epilepsy, hydrocephalus, cerebrospinal fluid leakage (CSF leak), cranial vault defects, chronic hematomas, and subdural collections [81-83].

Comments:

The examination during the first year of dispensary follow-up includes brain CT/MRI, electroencephalography, consultation with a neurologist, ophthalmologist, and otolaryngologist.

6. Organization of Medical Care

6.1. Prehospital stage:

- medical care is provided by a paramedic or an emergency medical team, with a preference for specialized pediatric teams

- restoration and stabilization of vital functions are performed

- assessment of the severity of the condition

- immediate transfer to a specialized pediatric hospital

- during the transportation of a moderately severe/severe patient with a threat of vital disorders (GCS <12 points), the paramedic/emergency physician is obliged to notify the hospital about the transported patient.

6.2. Admission department

Hospitalization of pediatric patients with vital disorders or with the threat of their development is recommended through the shock room, where resuscitation measures must be continued/initiated. Resuscitation measures accompany the diagnostic stage and are continuous in nature. The main goal is to identify and eliminate the primary pathophysiological mechanism posing a threat to life.

Patients exhibiting the following symptoms are directed to the shock room

1. Hemodynamic instability

2. Respiratory disorders

3. GCS <13 points

4. Paresis, paralysis

5. Suspected (presence of) spinal and spinal cord injury

6. Seizures

7. Suspected/presence of chest injury

8. Open fractures

9. Suspected unstable pelvic bone fractures

Comments:

If necessary, taking into account the location and nature of injuries, pediatric specialists of other fields are involved: ophthalmologists, otolaryngologists, maxillofacial surgeons, urologists, etc.

The purpose of the consilium is to diagnose all injuries, identify the leading life-threatening injury, and determine the stages and scope of specialized care delivery.

In the absence of a shock room, patients can be hospitalized directly into the intensive care unit, bypassing the admission department.

6.3. Inpatient stage

Patients with mild and moderate TBI (GCS 15-13 points) are hospitalized in the neurosurgery department.

Patients with moderate and severe TBI (GCS 12-3 points) are hospitalized in the intensive care unit.

Patients who do not require emergency surgical interventions during the recovery and stabilization of vital functions undergo advanced neuromonitoring, including intracranial pressure (ICP) and cerebral perfusion pressure monitoring.

Patients requiring emergency surgical interventions must be transferred to the operating room.

After the stabilization of the injured child's condition, the patient is transferred to the neurosurgery department.

6.4. Rehabilitation stage. Rehabilitation measures begin in the intensive care unit and continue at all stages of specialized care delivery (stages I–II of rehabilitation).

7. Additional Information

Prognosis and Outcomes

• The Glasgow Coma Scale (Appendices G1, G2) is recommended as one of the earliest and most highly reliable predictors of TBI prognosis and outcomes in children [1-3, 9, 11, 17-19, 22, 23, 25].

GPP CLOE 5Level of Evidence C (Level of Likeness/Evidence — 5)

Comments:

The probability of a favorable outcome is directly proportional to the GCS score. Favorable outcomes are reliably more frequent (66%) at a higher level of consciousness (7-8 points). All outcomes in children with a consciousness level of 3-4 points are unfavorable, and mortality reaches 82% [25,26].

Outcomes depending on the level of consciousness

The prognostic significance of the child's age as a predictor of severe TBI outcome remains uncertain, as evidenced by ongoing discrepancies in recent studies [21,23,26,28]. The child's age rather determines the mechanism of injury, which in turn determines the pattern of brain damage. Infants are more frequently subjected to abusive head trauma. Younger children more commonly sustain injuries from falls from a height and road traffic accidents (RTAs). RTAs remain the leading cause of trauma in preschool, school-age children, and adolescents, followed less frequently by falls from a height. [28]

7.1 Pupil reactivity

Pupil diameter and the presence of the pupillary light reflex are among the early and highly reliable predictors of prognosis and outcomes in pediatric TBI [1-4]. Pupil diameter and the light reflex can be easily and reliably assessed at any time post-injury. This parameter remains an independent and highly reliable predictor of severe TBI outcome in children and is widely used in clinical practice.

Injury to the orbit or oculomotor nerve accompanied by pupillary dilation limits the use of this predictor in prognosis.

Favorable outcomes are significantly more frequent in patients with normal pupil size and preserved light reflex (62%), whereas unfavorable outcomes occur in children with mydriasis and absent light reflex (89%), Table 4.

7.2 Arterial hypotension

Arterial hypotension impairs cerebral perfusion, leads to secondary strokes, increases ICP, causes brain edema, and ultimately significantly worsens the outcome of severe TBI in children.

Arterial hypotension in children older than 10 years is conventionally defined as a drop in systolic blood pressure below 90 mm Hg. For children under 10 years old, arterial hypotension is defined as a drop in systolic blood pressure below 70 + (2 × age) mm Hg, and for infants in the first year of life, less than 70 mm Hg [11,19].

7.3 Associated injuries

The severity of polytrauma >50 scores is a risk factor for an adverse outcome of severe TBI. Associated injuries contribute to the development of pathophysiological processes that can lead to secondary brain injury. Acute blood loss, traumatic shock, and acute respiratory failure are accompanied by hemodynamic impairment, decreased cerebral perfusion, and brain hypoxia. All of these are factors of secondary brain injury and are considered independent predictors of severe TBI outcome [1,3,11,19].

In patients with a GCS consciousness level of 6 scores and higher, favorable injury outcomes are significantly more frequent at an ISS value below 32 scores (ISS ≤32), whereas unfavorable outcomes are significantly more frequent at an ISS value greater than 40 scores (ISS >40) [22].

7.4 Neuroimaging findings

Comments: Mortality with open basal cisterns is 22%, and in the absence of cisterns, 77%. The "state of the basal cisterns" sign shows the highest sensitivity in predicting a favorable outcome in patients with a level of consciousness of 6–8 GCS scores. In addition, compression or absence of basal cisterns is a sign of intracranial hypertension. The risk of developing intracranial hypertension with compression or absence of cisterns increases threefold, and the risk of mortality doubles [2,3,11,18,21,23].

Traumatic subarachnoid hemorrhage (tSAH) occurs in an average of 40% of severe TBI cases and also has prognostic value. Patients with subarachnoid hemorrhage are at risk for developing acute subdural hematomas, intraventricular hemorrhages, and intracranial hypertension. Traumatic SAH, in addition to the state of the ambient cisterns, the presence of mass effects, and midline shift, increases the prognostic value of CT findings.

Midline shift of the brain is also a predictor of severe TBI outcome. In most domestic and international studies, a shift of more than 10 mm is considered an extremely unfavorable factor, with a mortality rate exceeding 80% with such a shift. The volume of the mass effect also has prognostic value; the risk of an adverse outcome increases with an increasing volume of the intracranial hematoma and the magnitude of the midline shift.

Computed tomography findings such as the degree of ambient cistern compression, the presence of a mass effect and traumatic SAH, and midline shift formed the basis of the Rotterdam prognostic CT score. The probability of mortality in children increases in direct proportion to the score assessed by the Rotterdam prognostic CT score. Its prognostic accuracy is low for diffuse injuries [22].

7.5 Marshall CT prognostic scale

It is based on the evaluation of a combination of data: the presence of a contusion volume greater than 25 ml, the degree of ambient cistern compression, the presence of midline shift, and the presence of a mass effect requiring surgical evacuation [21]. The Marshall classification proved useful not only for determining treatment tactics but also demonstrated itself as a reliable predictor of outcome. Favorable outcomes are significantly more frequent in diffuse injuries I–II and in situations with an evacuated mass effect, whereas unfavorable outcomes are more frequent in diffuse injuries III–IV and in the presence of a mass effect requiring surgical evacuation.

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

1. Semyonova Zhanna Borisovna, MD, PhD, Head of the Department of Neurosurgery and Neurotrauma at the Research Institute of Emergency Pediatric Surgery and Traumatology of the Moscow Healthcare Department, Professor at the Department of Pediatric Neurosurgery of RMACPE, Chief freelance pediatric neurosurgeon of the Moscow Healthcare Department and the Central Federal District of the Russian Ministry of Health

2. Melnikov Andrey Viktorovich, PhD, Leading Researcher at the Department of Neurosurgery and Neurotrauma at the Research Institute of Emergency Pediatric Surgery and Traumatology of the Moscow Healthcare Department

3. Meshcheryakov Semyon Vladimirovich, Candidate of Medical Sciences, Leading Researcher, Department of Neurosurgery and Neurotrauma, Research Institute of Emergency Pediatric Surgery and Traumatology, Moscow Healthcare Department

4. Akhadov Tolibdzhon Abdullaevich, Doctor of Medical Sciences, Professor, Head of the Department of Diagnostic Radiology, Research Institute of Emergency Pediatric Surgery and Traumatology, Moscow Healthcare Department, Honored Doctor of the Russian Federation, Honored Scientist of the Russian Federation.

5. Savvina Irina Aleksandrovna, Doctor of Medical Sciences, Professor, Chief Researcher, Head of the Neurosurgical Anesthesiology and Intensive Care Department No. 12, Almazov National Medical Research Centre of the Russian Ministry of Health, Professor at the V.L. Vanevsky Department of Anesthesiology and Reanimatology, North-Western State Medical University named after I.I. Mechnikov of the Russian Ministry of Health

6. Lekmanov Andrey Ustinovich, Doctor of Medical Sciences, Professor, Chief Researcher, Research Institute of Pediatric Surgery, Pirogov Russian National Research Medical University of the Russian Ministry of Health.

7. Valiullina Svetlana Albertovna, Doctor of Medical Sciences, Professor, Deputy Director of the Research Institute of Emergency Pediatric Surgery and Traumatology of the Moscow Healthcare Department, Head of the Department of Restorative Treatment, Chief freelance pediatric rehabilitation specialist of the Moscow Healthcare Department.

8. Ponina Irina Vitalyevna, Pediatrician, Rehabilitation Department, Research Institute of Emergency Pediatric Surgery and Traumatology of the Moscow Healthcare Department

9. Gorelyshev Sergey Kirillovich, Doctor of Medical Sciences, Professor, Head of the Department of Pediatric Neurosurgery, National Medical Research Center for Neurosurgery named after Academician N.N. Burdenko of the Russian Ministry of Health, Chief freelance pediatric neurosurgeon of the Russian Ministry of Health

10. Khachatryan Vilyam Aramovich, Doctor of Medical Sciences, Professor, Head of the Pediatric Neurosurgery Department, Almazov National Medical Research Centre of the Russian Ministry of Health

There is no conflict of interest.

Appendix A2. Methodology for Developing Clinical Guidelines

In these clinical guidelines, all data are ranked by level of reliability (evidence) depending on the quantity and quality of studies on the issue.

Table 1. Levels of Evidence (LoE) grading scale for diagnostic methods (diagnostic interventions)

Table 2. Scale for grading levels of evidence certainty (LEC) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, and rehabilitative interventions)

Table 3. Scale for grading grades of recommendation (GR) for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions)

The methods used to formulate the recommendations were expert consensus. Cost analysis was not performed, and pharmacoeconomic publications were not analyzed.

Clinical guidelines are updated every 3 years.

Appendix A3. Reference Materials

These clinical guidelines were developed taking into account the following regulatory legal documents:

1. Order of the Ministry of Health of the Russian Federation No. 931n dated November 15, 2012, "On Approval of the Procedure for Providing Medical Care to the Adult Population in the Profile 'Neurosurgery'."

2. Order of the Ministry of Health of the Russian Federation No. 927n dated November 15, 2012, "On Approval ofതം the Procedure for Providing Medical Care to Victims with Associated, Multiple, and Isolated Traumas Accompanied by Shock."

3. Order of the Ministry of Health of the Russian Federation No. 388n dated June 20, 2013, "On Approval of the Procedure for Providing Ambulance, Including Specialized Ambulance, Medical Care."

4. Decree of the Government of the Russian Federation No. 554 of July 24, 2000, "On Approval of the Regulation on the State Sanitary and Epidemiological Service of the Russian Federation and the Regulation on State Sanitary and Epidemiological Standardization" (Collected Legislation of the Russian Federation, 2000, No. 31, Art. 3295; 2004, No. 8, Art. 663; No. 47, Art. 4666; 2005, No. 39, Art. 3953)

5. Order of the Ministry of Health of the Russian Federation No. 788n of July 31, 2020, "On Approval of the Procedure for Organizing Medical Rehabilitation for Adults" (registered by the Ministry of Justice of the Russian Federation on September 25, 2020, registration No. 60039).

6. Order of the Ministry of Labor and Social Protection of the Russian Federation No. 572n of September 3, 2018, "On Approval of the Professional Standard 'Medical Rehabilitation Specialist'" (registered by the Ministry of Justice of the Russian Federation on September 17, 2018, registration No. 52162).

Appendix B. Physician Action Algorithms

Examination algorithm for pediatric patients with mild and moderate traumatic brain injury in the emergency department setting.

• Follow the pulse sequence order.

• The 2DFLAIR and 2DT2 sequences are performed with a rectangular field of view.

• Prescan normalization filters and distortion correction are disabled in all sequences.

Table 4

MRI protocol for traumatic brain injury on a 3.0 T scanner.

• Follow the pulse sequence order.

• The 2DFLAIR and 2DT2 sequences are performed with a rectangular field of view.

• Prescan normalization filters and distortion correction are disabled in all sequences.

Table 5.

Algorithm for basic and ICP-directed therapy in children with severe traumatic brain injury

Algorithm for decision-making and performance of decompressive craniectomy

Appendix C. Patient Information

TBI complications and TBI sequelae should be differentiated. TBI complications include pathological processes, primarily purulent-inflammatory ones. The development of complications in patients with traumatic brain injury can cause mortality, profound disability with an increased duration of treatment, and the need for repeated hospital admission. Various complications occur in 5-10% of pediatric TBI patients. Knowledge of these complications and the applied preventive and therapeutic measures help improve the prognosis and outcome of traumatic brain disease. To monitor complications, patients must remain under medical supervision until their condition is completely stabilized.

TBI sequelae are directly related to the injury itself and neuronal death at the moment of impact. The severity of sequelae directly depends on the severity of the injury. This is an evolutionarily predetermined and genetically fixed complex of processes in response to damage to the brain and its coverings. Sequelae also include persistent disruptions of the anatomical integrity of the brain, its meninges, and the bones of the cranial vault and skull base resulting from traumatic brain injury. In some cases, traumatic brain injury sequelae require surgical treatment only. Timely performed surgical intervention helps optimize the prognosis and outcome of the injury.

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

Appendix G1. Glasgow Coma Scale

Russian name: Glasgow Coma Scale

Original title (if available): Glasgow Coma Scale

Source (official developer website, validation publication): Buyukcam F. et al. Predicting the outcome in children with head trauma: comparison of FOUR score and Glasgow Coma Scale // Ulusal Travma Ve Acil Cerrahi Dergisi-Turkish Journal Of Trauma & Emergency Surgery. – 2012. – Vol. 18. – No. 6.

Type: rating scale

Purpose: To assess the level of consciousness

Content (template):

Key (interpretation):

Scores are summed up. Possible result from 3 to 15.

15 points – alert

13-14 points – mild obtundation

11-12 points – moderate obtundation

9-10 points – stupor

7-8 points – moderate coma

4-6 points – deep coma

3 points – terminal coma

Appendix G2. Pediatric Glasgow Coma Scale

Russian title: Pediatric Glasgow Coma Scale (for children under 4 years of age)

Original title (if applicable):

Source

Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974,

Morray JP et al: Coma scale for use in brain-injured children. CriticalCareMedicine 12:1018, 1984. doi: 10.1097/00003246-198412000-00002 [152, 153]

Type: rating scale

Purpose: To assess the level of consciousness

Content (template):

Key (interpretation):

Scores are summed up. Possible result from 3 to 15.

15 points – alert

13-14 points – mild obtundation

11-12 points – moderate obtundation

9-10 points – stupor

7–8 points – moderate coma

4–6 points – deep coma

3 points – terminal coma

Appendix G3. Marshall CT classification

Russian name:

Original name (if applicable): Marshall computed tomographic classification

Source (official developer website, validation study): Marshall L. F. et al. The diagnosis of head injury requires a classification based on computed axial tomography // J Neurotrauma. – 1992. – Vol. 9. – №. Suppl 1. – P. S287-S292.

Type: rating scale

Purpose: to assess injury severity and determine management strategy.

Content (template) and Key (interpretation):

Appendix G4. CT prognostic scoring scale

Russian name: Rotterdam computed tomography score

Original name (if applicable): Rotterdam CT score

Source (official developer website, validation study): Maas AI, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery. 57 (6): 1173-82; discussion 1173-82.

Type: rating scale

Purpose: assessment of injury severity and prognosis

Content (template):

Basal cisterns: 0 – normal, 1 – compressed, 2 – absent

Midline shift: 0 – none or ≤5 mm, 1 – >5 mm

Epidural hematoma ≥25 ml: 0 – present, 1 – absent

IVH or SAH: 0 – absent, 1 – present

Key (interpretation):

Instructions: add 1 point to the calculated sum. 6-month mortality after injury

• 1 point: 0%

• 2 points: 7%

• 3 points: 16%

• 4 points: 26%

• 5 points: 53%

• 6 points: 61%

Appendix G5. R. Firsching brainstem injury classification

Russian name: R. Firsching brainstem injury classification

Original name (if applicable): Classification of Severe Head Injury Based on Magnetic Resonance Imaging

Source (official developer website, validation study): Firsching R. et al. Classification of severe head injury based on magnetic resonance imaging // Acta Neurochir. – 2001. – Vol. 143. – №. 3. – P. 263-271.

Type: rating scale

Purpose: assessment of injury severity, prognosis

Content (template) and key (interpretation):

Appendix G6. Glasgow Outcome Scale

Russian name: Glasgow Outcome Scale

Original name (if applicable): Glasgow Outcome Scale

Source (official developer website, validation study): Crouchman M. et al. A practical outcome scale for paediatric head injury // Arch Dis Child. – 2001. – Vol. 84. – №. 2. – P. 120-124.

Type: rating scale

Purpose: assessment of patient outcomes

Content (template) and key (interpretation):

Appendix G7. Glasgow Outcome Scale-Extended

Russian name: Extended Glasgow Outcome Scale

Original name (if applicable): Glasgow Outcome Scale–Extended

Source (official developer website, validation study): Beers S. R. et al. Validity of a pediatric version of the Glasgow Outcome Scale–Extended // J Neurotrauma. – 2012. – Vol. 29. – №. 6. – P. 1126-1139.

Type: rating scale

Purpose: status assessment

Content (template) and key (interpretation):

Note: assessment is performed within 1 month after trauma

Appendix G8. FOUR Score (Full Outline of UnResponsiveness)

Russian name: FOUR Coma Scale

Original name (if any): FOUR (Full Outline of UnResponsiveness)

Source (official developer website, validation publication): Buyukcam F. et al. Predicting the outcome in children with head trauma: comparison of FOUR score and Glasgow Coma Scale //Ulusal Travma Ve Acil Cerrahi Dergisi-Turkish Journal Of Trauma & Emergency Surgery. – 2012. – Vol. 18. – No. 6.

Type: rating scale

Purpose: details neurological status, identifies locked-in syndrome, assesses brainstem reflexes, assesses breathing pattern, and detects various stages of brain herniation (dislocation). The FOUR Coma Scale provides additional prognostic information in patients with low Glasgow Coma Scale scores

Content (template): The FOUR Coma Scale includes 4 parameters with a maximum score of "4" for each: eye responses (eye opening and tracking), motor responses (pain response and execution of simple commands), brainstem reflexes (pupillary, corneal, and cough), and breathing patterns (respiratory rhythm and breathing attempts in mechanically ventilated patients).

1. Eye responses (E)

Eyes open, tracks, and blinks to command 4 points

Eyes open, but does not track 3 points

Eyes closed, open to loud voice, but no tracking 2 points

Eyes closed, open to pain, but no tracking 1 point

Eyes remain closed in response to pain 0 points

2. Motor responses (M)

Obeys commands (thumbs up, fist, peace sign) 4 points

Localizes pain 3 points

Flexion response to pain 2 points

Extension posture to pain 1 point

No response to pain or generalized myoclonic status epilepticus 0 points

3. Brainstem reflexes (B)

Pupillary and corneal reflexes present 4 points

One pupil wide and fixed to light 3 points

Pupillary or corneal reflex absent 2 points

Pupillary and corneal reflexes absent 1 point

Absent pupillary, corneal, and cough reflexes 0 points

4. Breathing pattern (R)

Not intubated, regular breathing 4 points

Not intubated, Cheyne-Stokes breathing 3 points

Not intubated, irregular breathing 2 points

Responds/resists to ventilator 1 point

Fully synchronous with ventilator or apnea 0 points

Key (interpretation):

The maximum FOUR score is 16, and the minimum is 0.

16 – Clear consciousness

15 – Moderate obtundation

13-14 – Deep obtundation

9-12 – Stupor

7-8 – Coma I

1-6 – Coma II

0 – Coma III

Note: The FOUR Coma Scale was developed at the Mayo Clinic and presented by E.F. Wijdicks et al. in 2005. Numerous studies have confirmed the validity of this scale in neurointensive care settings.

Appendix G9. Injury Severity Score (ISS)

Russian name: Injury Severity Score (ISS)

Original title (if applicable):

Source (official developer website, validation publication): Brown J. B. et al. The value of the injury severity score in pediatric trauma: time for a new definition of severe injury? //The journal of trauma and acute care surgery. – 2017. – Vol. 82. – No. 6. – P. 995.

Type (underline): rating scale

Purpose: Assessment of injury severity

Content (template) and key (interpretation):

(conversion of AIS scores to ISS scores)

Mild (minor) <=8

Moderate 9-15

Severe 16-24

Critical >=25