We will get a first impression by observing the following: 1) general appearance; 2) respiratory effort; and 3) peripheral perfusion, as well as obvious lesions and bleeding.21

The ABCDE sequence is recommended over C-ABCDE, unless massive hemorrhage is suspected.22

• A

  Alertness-airway control-definitive cervical control

After determining whether the patient is conscious, presents diminished consciousness, or is comatose, the airway is evaluated. If endotracheal intubation is required, sedoanalgesia increases the risk of hemodynamic collapse and cardiorespiratory arrest (CRA). Administering volume and using ketamine as the sedoanalgesic of first choice (0.5−1 mg/kg in the presence of hemodynamic instability) is advisable, since ketamine produces less cardiovascular and respiratory depression when used with a neuromuscular blocker in a rapid induction sequence. For very unstable patients, intubation can be performed while maintaining spontaneous breathing with ketamine alone (without neuromuscular blockade).23 Atropine is only indicated if reflex bradycardia occurs in response to stimulation during laryngoscopy, which is more common in children. Cuffed tubes are currently the first choice at any age. Devices for difficult airway management, such as videolaryngoscopy, Frova-type introducers, and laryngeal masks, are available for all ages.24 In the "non-intubable, non-ventilatable" scenario, there are no percutaneous devices for children under 5 years of age; therefore, angiocatheters must be used in these cases. For patients between 5 and 10 years of age, such devices are available, but they have a narrow caliber that only allows oxygenation.25 Cervical control is preferably manual, as it is more comfortable, although the indications are increasingly restrictive (Appendix B Table 2 of the Supplementary material).

• B

  Ventilation and oxygenation

The FiO2 required to achieve target saturations of 93–97% is administered to avoid hyperoxia. The smallest self-inflating bag (250 ml) should be excluded. It is essential to observe correct thoracic excursion and to auscultate good air entry. The tidal volume administered in invasive mechanical ventilation (IMV) should be 6−8 ml/kg of ideal body weight to achieve normal ventilation. Despite its variable correlation with arterial pCO2, capnography is useful. Among the possible NFRIs, tension or open pneumothorax, massive hemothorax, flail chest, and pulmonary contusion should be mentioned.26 Thoracic drainage is performed in the fourth or fifth intercostal space (mid- and anterior axillary line) or the second space on the midclavicular line. In cases of CRA, thoracotomy should be considered, especially for penetrating trauma, provided that experienced personnel are available.27,28

• C

  Evaluation of circulation and bleeding

The hemodynamic situation is evaluated based on the heart rate, arterial pressure, perfusion, and other factors. The evaluation should include a diagnosis of the source of the hemorrhage. Although resuscitation will be discussed in depth later (in the "Hemorrhagic shock" section), it is important to note that venous access should be established within the first five minutes (the peripheral route in the antecubital fossa being the preferred choice). There are different types of shock: hypovolemic-hemorrhagic (the most common type, which will be discussed below), obstructive (pneumothorax or cardiac tamponade), distributive, and cardiogenic (due to thoracic contusion or electrocution). Traumatic shock is described as a dynamic combination of these mechanisms. For cardiac tamponade, the safest approach is the echo-assisted anterior intercostal approach.29 In CRA, reversible causes should be treated immediately, even before adrenaline is administered, and in parallel with compressions.28

• D

  Neurological deficit

Neurological deficits are assessed using the Glasgow Coma Scale (GCS), which has been adapted for children under 2–3 years of age (Appendix B Table 3 of the Supplementary material). A motor GCS score of less than 4 implies loss of airway protection.27 Seizures in the early hours after traumatic brain injury (TBI) can occur without intracranial damage.30 They should be treated with benzodiazepines and, unless they persist, should not result in intubation. Pain and agitation should be treated aggressively, and non-pharmacological measures should be considered (e.g., presence of parents, toys, or videos). An NFRI is characterized by endocranial hypertension, pupillary abnormality, and bradycardia. The appearance of an erythematous rash on the upper part of the body is infrequent but characteristic.31 Hyperosmolar therapy with hypertonic saline (2−5 ml/kg at a concentration of 3% in 10−20 min) can be used for immediate treatment during crises. At present, the use of hypertonic saline is preferable to avoid the osmotic diuresis of mannitol. Hyperventilation is limited to a rescue maneuver until definitive measures are put in place.32

• E

  Exposure and prevention of hypothermia

The patient should be exposed to proactively look for external injuries and then be quickly covered again. The temperature should be determined, and the patient should be actively warmed in case of hypothermia (temperature < 35 °C).33

Establishing a vascular access in pediatric patients with vasoconstriction can be complicated. Peripheral access should be achieved within 5 min (60 s in CRA) or within two attempts in accessible areas and with the largest possible caliber. The most recommended locations are the antecubital fossa and saphenous route.38 Intraosseous access is the first alternative and may be the primary option if difficulty is anticipated. It is easy to place and can be performed in the proximal tibia (most frequently), with alternatives being the proximal humerus (in larger patients) and the distal femur.39

Ideally, no more than 20 ml/kg of crystalloids should be administered; excess administration is associated with a poorer course.40 Blood products should be prioritized, even in an out-of-hospital setting. The preferred ratio of red blood cell concentrates, plasma, and platelets is close to 1:1:1.41 The transfusion of group O whole blood with low titers of anti-A and anti-B IgG (LTOWB: Low-Titer Group O Whole Blood) has been proposed as a safe and fast alternative. However, further studies are needed to demonstrate its superiority.42

If hypotension persists despite volume resuscitation, vasoactive support should be administered. Noradrenaline is the drug of choice despite scarce supporting evidence.43 In cases of cardiac dysfunction, adrenaline or dobutamine should be considered. These drugs can be administered conveniently diluted via the peripheral route.44

The goal of permissive hypotension in cases of uncontrolled bleeding is to administer the least amount of volume possible until the bleeding is controlled. If there is no central nervous system (CNS) involvement, a minimum blood pressure should be maintained at p5; if there is CNS involvement, it should reach at least p50. The chosen resuscitation target should be the minimum needed to ensure adequate tissue perfusion and oxygen supply.45 The Shock Index (heart rate divided by systolic blood pressure) is an early indicator that identifies patients at a higher risk for severe hemorrhaging and the need for intervention. In pediatrics, the Shock Index, Pediatric Age-Adjusted, is more appropriate. The reference values are: 1.22 for ages 4–6, 1 for ages 7–12, and 0.9 for ages 13–16 years.46 Less widespread and validated are the reverse shock index multiplied by the GCS and the ABC-D, which includes lactate and base excess (BE), though with promising results.47,48 Lactate, BE, and hemoglobin evolution over time are also useful.

The initial clinical examination is essential to classify and establish a prognosis. Thus, a motor GCS ≤ 3 is strongly predictive of a poor prognosis.66 Anisocoria is suggestive of increased intracranial pressure (ICP) and uncal herniation, requiring urgent treatment. Bilateral mydriasis is associated with high mortality. Automated pupillometry provides greater precision, and some of the derived indices may be of prognostic value.59

ICP is the pressure exerted by the sum of the intracranial volumes (parenchymal tissue, blood, and cerebrospinal fluid). An increased intracranial volume that overcomes compensatory mechanisms (decreased compliance) can raise ICP, leading to cerebral compression, ischemia, herniation, and death. There are different methods available for measuring ICP; each method has different advantages and limitations (Table 5).67 ICP monitoring should be performed in patients with severe TBI (GCS ≤ 8) and injuries identified by brain CT (e.g., hematomas, contusions, swelling, herniation, or basal cistern compressions). Monitoring is also indicated in severe TBI without lesions, but with evidence in the examination of unilateral or bilateral decorticate posturing or arterial hypotension. Finally, ICP monitoring is also indicated in severe polytrauma and TBI when correct neurological monitoring is impossible due to other reasons, such as lung injury or hemodynamic instability. For patients without clear indications (e.g., moderate TBI with risk injuries), or in the early stages of care, noninvasive techniques (e.g., optic nerve sheath diameter or Doppler ultrasound) may be useful for follow-up and making decisions about invasive monitoring. In patients undergoing invasive monitoring, these techniques remain relevant, as they provide supplementary information.68

ICP monitoring allows the calculation of cerebral perfusion pressure (CPP): CPP = mean arterial pressure (MAP)-ICP. Clinicians can act on CPP by lowering ICP, increasing MAP, or both. It is important to adjust the CPP target according to patient age: under 2 years > 45 mm Hg, between 2–8 years > 60 mm Hg, and over 8 years > 70 mm Hg.69

There is a consensus that complementary parameters, such as autoregulation, oxygenation, and cerebral metabolism, should be incorporated alongside ICP. Loss of cerebral autoregulation (CA) is common after TBI, which makes the brain more vulnerable. Management guided by fixed CPP targets is insufficient. For example, loss of CA increases the risk of cerebral edema. Conversely, patients with preserved CA may benefit from higher CPP, which decreases ICP.70 CA assessment is based primarily on the reactivity index (PRx). This is a moving correlation coefficient between spontaneous slow wave changes between MAP and ICP during a 5-min window. PRx can take values from −1 to +1. Negative values represent an inverse relationship and intact CA, indicating a better clinical outcome, whereas positive values indicate altered CA.71 By constructing the CPP-PRx curve, one can calculate the optimal CPP, which is the area of the curve that makes PRx more negative. This curve also allows for the treatment of endocranial hypertension by increasing CPP, provided that CA is preserved (PRx < 0). Though evidence is limited in children, pending trials, there are promising results in adults.65 Transcranial Doppler ultrasound measures cerebral blood flow velocity and is used to calculate the pulsatility index to estimate ICP and CPP. In pediatrics, a good correlation has been described in the determination of CPP, although the evidence on the usefulness of the formulas for estimating ICP is not conclusive.62

Cerebral oximetry with near-infrared spectroscopy provides information on global oxygenation in all the vascular compartments. While the absolute value has not been shown to be useful, changes over time may help in monitoring cerebral perfusion.61 Cerebral tissue oxygenation (PTiO2) and cerebral microdialysis provide information on perfusion and cellular metabolism. PTiO2 helps prevent tissue hypoxia and adjust therapies to lower ICP. In pediatrics, values < 10−20 mm Hg are associated with ischemia and a poorer prognosis.58 Microdialysis allows for the analysis of brain metabolites such as glucose and lactate/pyruvate, which serve as indicators of ischemia or mitochondrial dysfunction.72