Severe Traumatic Brain Injury: Acute Treatment Based on Cerebral Perfusion Pressure

Abstract

Severe traumatic brain injury is a cause of disability with economic and social repercussions. Prehospital care is a fundamental part with important attention to avoid hypoxemia, hyperventilation, and hypotension with airway protection. During the primary evaluation, a clinical examination is performed focused on classifying according to their severity, neurological involvement, and extracranial lesions and providing a prognosis. Invasive or non-invasive intracranial pressure monitoring aims to direct management to maintain adequate cerebral perfusion pressure, which should be individualized in each patient, as this depends on the status of self-regulation.

1. Introduction

Traumatic brain injury (TBI) is defined as an injury to brain caused by an external force on the head that can be a blow, explosion, or penetrating injury [1]. It causes severe disability among young people with economic and social repercussions. Existing limitations to treatment in underdeveloped countries include inadequate prehospital care, limited advanced neuromonitoring techniques, or availability of intensive care [2, 3].

Globally, it is estimated that in 2016, there were 55 million patients diagnosed with TBI, the annual cost of the likely economic losses of productivity was $1.2 billion [4]. Approximately, 69 million people each year are affected by this clinical entity, it should be noted that in this study, it showed a threefold higher incidence in developing countries [5].

In the United States, around 1.7 million people are diagnosed with TBI per year, with the most affected population being between 15 and 19 years of age, as well as those over 65 years of age, with a 2:1 ratio with a predominance of males [6]. The mortality associated with a closed traumatic injury grows exponentially when it is associated with a brain injury, which is why prehospital rapid response emergency teams play an important role [7].

Prehospital care is a fundamental part of reducing complications in patients with TBI, there are three important pillars in prehospital care, which are avoiding hypoxemia (maintaining a saturation greater than 94%), protecting the airway by evaluating the need for endotracheal intubation, and avoiding hyperventilation and hypotension [7, 8].

TBIs accounted for approximately 2.5 million emergency department visits in the United States, of which 87% (2,213,826) were treated and discharged from the emergency room; The other 11% (283,630) were admitted to hospitalization and were discharged in the following days, and approximately 2% (52,844) died in the hospital [9]. On the other hand, this pathology has significant effects on the quality of life of those people who suffer from this disease, it is estimated that in the United States, there are 3.2 to 5.3 million people living with a disability related to TBI [10].

There is evidence that patients with moderate to severe TBI who were discharged from rehabilitation were more than twice as likely to die after 3 to 5 years compared to people in the general population who were the same age, sex, and race [11].

2. Brain physiology

2.1 Brain metabolism

The human brain weighs approximately 1350 grams, which represents 2% of the total weight of an adult [12]. It takes up more energy than any other organ. Glucose is the main source of brain energy; It does not freely diffuse the blood-brain barrier. It enters the brain by active transport via glucose transporter (GLUT) 1, it is distributed to the central nervous system by several transporters (GLUT 1, GLUT 3, GLUT 5). These transporters undergo regulation with a tendency to rise under certain conditions, such as hypoxia [13].

The generation of brain energy under conditions of oxygen and glucose at normal levels is carried out by means of glycolysis by oxidative phosphorylation of creatine phosphokinase and adenylyl cyclase. The process allows the formation of 3 molecules of adenosine triphosphate (ATP) for each nicotinamide adenine dinucleotide (NADH) and a maximum of 38 molecules of ATP is obtained for each molecule of glucose. In the absence of oxygen in astrocytes, anaerobic glucose metabolism is performed to form lactate and ATP is generated to capture glutamate. Lactate is taken up by neurons and transformed into pyruvate that initiates the citric acid cycle, in this process, hydrogen ions are released which are associated with acidosis and more brain damage. In this way, ATP generation is lower per glucose molecule, generating only 2 ATP molecules per glucose molecule, which is not enough for brain demands [13].

On the other hand, during a prolonged fast, the brain uses ketone bodies which are broken down into acetyl coenzyme A to be oxidized in the citric acid cycle, so in extreme conditions, the brain can produce low amounts of energy from gluconeogenesis using glycerol, glutamine, and glycine as substrates. With low oxygen levels, ATP generation then drops and phosphocreatine deposits are occupied until anaerobic metabolism is exhausted, resulting in the cessation of electrical activity in the brain. Maintaining normal blood glucose levels is essential for normal brain function. The brain is particularly sensitive to hypoglycemia because there are no glycogen stores [14].

2.2 Cerebral circulation

The cerebral irrigation is given by the internal carotid arteries, which branch and give rise to the anterior circulation, the vertebral arteries give rise to the basilar artery and its branches give rise to the posterior circulation [15].

The brain occupies approximately 15% of cardiac output (750 ml/min) and maintains a cerebral blood flow of 50 ml/100 g/minute. In the resting state, the brain consumes oxygen at an approximate rate of 3.5 ml/100 g/minute, which represents 20% of the body’s total consumption [16].

Cerebral perfusion pressure (CPP) is defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). Under normal conditions in adults, it ranges between 60 and 150 mmHg and the ICP around 10 mmHg [16].

2.3 Monro-Kellie theory

The skull, after the closure of the sutures and fontanelles, becomes an inextensible configuration and, therefore, maintains a constant volume regardless of the contents. Under normal conditions, this content can be separated into three components (Monro-Kellie’s theory): brain 80%, cerebrospinal fluid (CSF) 10%, and blood 10%, respectively. When there is an increase in the volume of any of the three components, the pressure exerted by that component on the other two also increases. The CSF is the main compensatory system [15].

2.4 Partial pressure of carbon dioxide (PaCO2) and its implication in cerebral blood flow

The acid-base state and its regulation have been shown to have a direct effect on cerebral blood flow (CBF), causing a series of changes that have implications for health, for years, it has been an important area of study in which CBF, PaCO2, bicarbonate (HCO-3), and pH are integrated.

The cerebral circulation varies with the levels of PaCO2, in normal situations, the CBF increases from 2 to 4% of mmHg with an increase of PaCO2, making P toCO2 the most potent physiological vasodilator [17].

The response seen in CBF to changes from PaCO2 occurs in seconds and completes equilibrium within 1 to 2 minutes due to rapid diffusion across the blood-brain barrier (BBB) to perivascular fluid and cerebral vascular smooth muscle cells.

Changes in CBF secondary to PaCO2 levels are not sustained for prolonged periods. The adaptation point in the pH of CBF is observed at 6 hours with subsequent decrease in secondary changes to PaCO2 [12, 18].

3. Clinical classifications for TBI

The primary evaluation of a patient with TBI consists of a clinical examination focused on classifying according to its severity, neurological, and even structural involvement, as well as providing prognosis.

The Glasgow Coma Scale (GCS) (score from 3 to 15 pts) and the FOUR scale (score from 0 to 16 pts) are among the most commonly used scales to assess and identify the patient’s state of consciousness and guide management [19, 20].

It is recommended to establish a single scale for the progressive evaluation of the patient at 6, 12, 24, and 72 hours of the patient and to avoid marked differences in the patient’s approach and prognosis [21, 22, 23].

3.1 Tomographic classification

Computed tomography (CT) classifications of TBI lesions are used to establish prognosis, estimate risks of intracranial hypertension (IH), and thus establish probable surgical treatment. The most commonly used classifications for these types of scenarios are Marshall and Rotterdam. Other classifications, such as Helsinki and Stockholm, have demonstrated good sensitivity and specificity in some studies for predicting decline, but it still does not exceed the previous ones mentioned in use [24].

3.1.1 Marshall’s tomographic classification

Standard method for the evaluation of CT in traumatic brain injury involves evaluating the mesencephalic cisterns, midline, presence or absence of hemorrhage and whether or not they were evacuated, as well as cerebral edema, generating a percentage risk of IH and mortality or poor clinical outcomes. Mortality and the risk of IH increase with each grade of the scale, up to 55 and 63% respectively in grade III and 100% in grade IV. In addition to these degrees, two more are described that refer to whether these hemorrhagic masses were evacuated or not; in the case of the evacuated mass, the mortality has been described between 33 and 52% and in the non-evacuated, the mortality reaches up to 80% [25, 26].

3.1.2 Rotterdam tomographic scale

A scale that values epidural hematoma and subarachnoid hemorrhage, demonstrating better performance than the Marshall classification for the 6-month prognosis, with similar results in terms of mortality. But the fact of individualizing the lesions gives you a better picture of exploration and quantification of risk. In scores 1 and 2, the mortality is 0%, in score 3, the mortality is up to 6%, in score 4, the mortality is 35%, in score 5, the mortality percentage is 54%, and in score 6, the mortality reaches 60% [25, 26, 27].

4. Neuromonitoring in the emergency room

Neuromonitoring encompasses direct and indirect techniques that help to provide early evidence of neuraxial damage and focus on reducing secondary injury by optimizing the balance between oxygen consumption and demand [28, 29]. Invasive and non-invasive surrogate PCI monitoring techniques and measurements will be addressed as a treatment guide in the emergency department.

4.1 Neurological monitoring strategies in the emergency room

4.1.1 Clinical neurological examination

The mainstay of clinical assessment is state of consciousness, such as GCS and FOUR [30, 31]. These scales should be complemented by an assessment of pupillary, cranial nerves, mobility, sensation, and limb strength.

4.1.2 Computed tomography

CT scan is the most widely used study to assess changes in the brain and can provide qualitative information on the increase in PCI [32]. It is preferred for its availability, speed, low cost, and ease of use in patients under mechanical ventilation [33].

4.2 Non-invasive intracranial pressure monitoring

4.2.1 Transcranial Doppler (TCD)

In the initial evaluation of patients with severe TBI, TCD measurements may help guide treatment and decrease mortality [34].

TCD is a non-invasive ultrasound that uses a low-frequency transducer (<2 MHz) that detects the intracranial circulation through an acoustic bony window, is based on emissions and flow receptions, the angle and position of the insonation must be adjusted to provide the best Doppler signal [35, 36].

The acoustic windows used are transorbital, temporal, submandibular, and foramen magnum. In clinical practice, the middle cerebral artery (MCA) is the most insonable due to its easy access through the temporal window above the zygomatic arch, it has a sensitivity of 38–91%, specificity of 94–100% prediction of vasospasm [37]. The TCD measures flow rates, spectral wave analysis, and various indices that vary according to the insonation window and the vessel analyzed.

• The pulsatibility index (PI) is calculated as:

$$PI=Peaksystolicflow-Peakdiastolicflow÷Meanvelocity$$E1

The normal value of PI is between 0.6 and 1.16, a PI less than 0.6 is associated with vasospasm, hyperemia, or high-grade stenosis; a PI between 1.2 and 1.6 is associated with moderate IH or microangiopathy, a PI greater than 1.7–3 with severe IH, and values greater than 3 are associated with severe IH and cerebral asystole [37]. The PCI can be estimated based on the PI with the following equation [38]:

$$ICP=\left(10.927XPI-1.284\right)+/-3.2-12mmHg$$E2

• The Resistance Index (RI) which is calculated as:

$$RI=\frac{peaksystolicflow-peakdiastolicflow}{peaksystolicflow}$$E3

It increases in the early stages of IH and in old age [16]. Anything per <0.75 is considered normal [39].

• Lindegaard Index (LI)

  It is a value that normalizes the flow velocity of the AMC with respect to internal carotid arteries (ICA), it serves to differentiate hyperemia from true vasospasm. A normal LI is considered <3, mild vasospasm 3.0–4.5, moderate 4.5–6.0, and severe >6.0 [39]. It is calculated as:

$$LI=\frac{FlowvelocityofCMA}{FlowvelocityofACI}$$E4

4.2.2 Optic nerve sheath diameter (ONSD)

The optic nerve is an extension of the central nervous system, lined by meninges and cerebrospinal fluid (Figure 1). The optic nerve sheath (ONS) is in continuity with the meninges, specifically the dura mater. It is the intraorbital segment of the optic nerve and is separated from it by cerebrospinal fluid and the arachnoid trabeculae [1, 4]. The elevation of the PCI causes the CSF to be distributed through the dura mater toward the ONS, increasing its diameter [40].

Figure 1.

ONSD measurement. Optic nerve sheath diameter (ONSD).

Several studies have validated the linear relationship between the measurement of ONS by ultrasound with invasive methods and PCI, with detection of ICP elevation in ranges of 4.8–5.6 mm with an overall sensitivity and specificity of 95 and 92%, respectively [41].

Serial measurement of the ONSD and the use of the following validated formula for inference of PCI with the ONSD [42] are recommended:

$$ICP=\left(ONSDinmmx5.69\right)-8.23$$E5

This method should not be used in patients with facial trauma, Graves’ disease, and sarcoidosis [31].

ONSD measurement is a validated non-invasive method that is easy and quick to use. Performing it together with DCT in patients with severe TBI upon admission to the emergency room can be taken as a guide for initiation of treatment and neuroprotective measures [43].

4.2.3 Other methods

Near-infrared spectroscopy (NIRS) has an uncertain sensitivity for recognizing increased PCI, yet it is considered a complementary non-invasive method in neurological monitoring, limited by its non-specificity and restricted availability [44]. Another method, such as quantitative optical pupillometry, may be useful to guide response to osmotic treatment or as a monitoring of PCI, but its use in emergency departments has not been reported [45].

4.2.4 Continuous electroencephalogram (cEEG)

cEEG provides neuronal information in response to changes in brain structure or function. It is a continuous registry, fast and easy to use, however, with a high cost. It is used for the detection of non-convulsive status epilepticus and cerebral ischemia (CBF < 25–35 mL/100 g/min, alpha and beta waves are attenuated, and if CBF <17–18 mL/100 g/min, slow delta and zeta waves are increased) [46].

4.3 Invasive intracranial pressure monitoring in the emergency room

4.3.1 Jugular bulb saturation (SjvO2)

It is a minimally invasive method of neuromonitoring. Currently, an ultrasound-guided fiber optic catheter is placed, both sides can be catheterized, however, right placement is more common [47].

SjvO2 measures the relationship between brain metabolic requirements and blood flow, being a direct determination of brain oxygen consumption (CMRO2) [48, 49].

It has a normal value of 55 to 75%, a low SjvO2 is associated with vasospasm, ischemia, or metabolic cause (fever, chills, agitation). Elevated SjvO2 is associated with hyperemia, hyperoxia, arteriovenous shunt, or extensive cerebral infarction. Although it is part of the monitoring in TBI guidelines, it is rarely used in the emergency department [49].

4.3.2 External ventricular drainage

External ventricular drainage (EVD) is globally considered the gold standard for PCI monitoring. It is used as continuous monitoring of PCI and treatment of IH for various pathologies (acute hydrocephalus, hematomas, hemorrhages, severe TBI, tumor, infection, or cerebral edema) [50]. It is associated with complications such as obstruction, improper placement, infections, and bleeding [51].

The components of the ICP wave are:

• P1 is the arterial component (percussive wave). It originates from the pulsation of the choroid plexus, it has constant amplitude.

• P2 represents intracranial compliance (tidal wave).

• P3 is associated with the closure of the aortic valve (dicrotic wave).

P2 and P3 are produced from the retrograde venous beat of the jugular veins over cortical veins, between which the dicrote cleft of the pulse occurs. The change in the P2 wave is indicative of IH and consequently loss of brain self-regulation (Figure 2) [52].

Figure 2.

Morphology of ICP waves. (A) Normal ICP curve. (B) Decreased cerebral compliance with increased P2. (C) Decreased compliance with critical increase in ICP. Intracranial pressure (ICP).

5. Treatment of severe TBI

The presence of other extracranial lesions should be considered in the management of patients with severe TBI. Post-traumatic bleeding is one of the most common causes of death in patients with TBI associated with other injuries, and is a preventable cause of death [53, 54]. Therefore, priority should be given to controlling bleeding in case of hemodynamic instability, considering medical and surgical management [54].

It is recommended that during bleeding control, a hemoglobin (Hb) greater than 7 g/dL and, in some cases, higher levels be maintained, for example, in patients with low myocardial reserve or previous heart disease and older adults. If surgical management is warranted, a platelet count greater than 50,000/mm³ and an INR of less than 1.5 should be maintained. A partial pressure oxygen (PaO2) level of 60 to 100 mmHg and a PaCO2 of 35 to 40 mmHg are maintained to ensure adequate oxygen transport [54, 55].

In hemodynamic control, a MAP greater than 80 mmHg or a systolic blood pressure (SBP) greater than 100 mmHg is sought, in case these pressure levels make it difficult to control bleeding, lower levels could be considered for short periods [55]. In addition, during the management of bleeding, consider massive transfusion protocols, as well as the use of thromboelastography (TEG) and rotational thromboelastometry (ROTEM) to guide the decision to use blood products [56].

After hemorrhage control, the severity of the brain injury should be assessed by means of pupillary evaluation, the level of consciousness with the GCS, and the performance of an imaging study [57, 58].

When performing the tomographic study, the presence of potentially surgical life-threatening intracranial lesions should be sought, and in such a case, an emergency evaluation by the neurosurgeon should be requested, who will regulate surgical management [59].

Within the management of PCI, the factors that are related to worse outcomes are values greater than 20 to 25 mmHg and the duration of the outcomes [58, 60]. The goal of management is to maintain an adequate PPC, which must be individualized in each patient, since this depends on the status of self-regulation [61], therapy should not only focus on maintaining a specific value in all patients. It is suggested in most guidelines and studies that maintaining a PPC value between 60 and 70 mmHg has better outcomes and fewer neurological sequelae [62]. PPC values above 100 mmHg are related to vasogenic edema and values below 50 mmHg are related to cerebral ischemia [61, 63].

Among the measures that can reduce PCI in order to improve PPC are osmotherapy (20% mannitol or hypertonic saline), external interventricular drainage, and hyperventilation [4, 6]. Patients with IH such as respiratory depression, bradycardia, hypertension, or signs of cerebral herniation (mydriasis or anisocoria) require immediate medical treatment with one of these options. Prophylactic use in the absence of data on increased PCI with osmotherapy over conventional therapy has not shown improvement in outcomes [62].

Mannitol and hypertonic saline (Table 1) are similar in efficacy in the control of IH [64, 65]. The decision of which osmotic therapy to use should be based on consideration of its adverse effects and the clinical scenario, as in the case of mannitol that generates osmotic diuresis and hypovolemia, which would have to be made in conjunction with volume expansion to avoid undesirable hemodynamic effects. Hypertonic saline could be considered a better option in cases of hypovolemia due to the volume expansion it generates, however, both therapies warrant monitoring of serum sodium levels and water balances [65, 66].

	Bolus dose	Mechanism of action	Disadvantages
Mannitol 20%	0.25 to 1 g/kg	Reduces ICP due to osmotic effect at the brain level plus osmotic diuresis.	Hyperosmolar hypovolemia Risk of acute tubular necrosis Hydroelectric alterations
Hypertonic solutions: 3% NaCl; 5% NaCl; 7.5% NaCl; 10% NaCl; 14.6% NaCl; 23.4% NaCl	250 mL or 2.5–5 mL/kg; 100 mL; 2–4 mL/kg or 100 mL; 75 mL; 24–48 mL; 30 mL (0.686–2.0 mL/kg)	Increase in intravascular volume. Osmotic gradient decreasing brain volume. Improved rheology of the blood.	Risk of hyperchloremic acidosis Risk of pontine myelinolysis Electrolyte disorders

Table 1.

Characteristics of the osmotherapy. Abbreviations: Sodium chloride (NaCl).

The use of hyperventilation (PaCO2 25 to 30 mmHg) is effective for the management of IH, it is considered a transient therapy in which a definitive surgical management is carried out and in cases of imminent herniation. Prolonged use of hyperventilation has deleterious effects, as well as the risk of cerebral ischemia, due to its effects on cerebral vasculature [66, 67].

The use of antiepileptic drugs prophylactically for post-traumatic seizures is not routinely recommended [68]; their use is considered only in patients with risk factors, such as skull fracture, acute subdural hematoma, initial loss of consciousness, amnesia for more than 24 hours, and age greater than 65 years [68, 69].

Other therapies for the management of TBI can be mentioned, however, there is no evidence of benefit, such as the use of high doses of glucocorticoids or the use of albumin during fluid resuscitation; In both cases, an increase in mortality was observed when compared to conventional therapy [70, 71].

Within ventilatory management, the indication for orointubation and use of mechanical ventilation depends on a combination of factors ranging from the level of consciousness (GCS less than 8 pts), loss of airway protection reflexes, severe agitation, combative state, and significant elevation of PCI [72]. Regarding the scheduling of mechanical ventilation in patients with or without IH, the parameters may be similar to those of patients without TBI, maintaining a protective ventilation strategy (tidal volume 6 to 8 mL per predicted weight, PEEP 5 cmH2O, plateau pressure less than 30 cmH2O, and a respiratory rate of 16 to 22 breaths/minute) [73].

Ventilatory management can be staggered in the case of acute respiratory failure syndrome (ARDS), with an initial protective schedule with subsequent adjustments to avoid severe hypoxemia; The tidal volume will be adjusted to maintain a conduction pressure of less than 14 cmH2O, as well as the respiratory rate for controlled hypocapnia (PaCO2 of 32 to 35 mmHG) [74].

In case of worsening of ARDS, advanced strategies such as prone position and neuromuscular blockade should be considered in conjunction with osmotherapy with optimal MAP to ensure adequate PPC [74, 75].

Every patient with severe TBI should be given measures to maintain adequate homeostasis (keep the brain happy) [62]. Multiple mnemonics have been described to ensure measures that improve and ensure cerebral oxygenation in patients with TBI.

The mnemonics of THE MANTLE (Table 2) are used at the bedside of patients with severe TBI [76]. In the following paragraphs, we will describe what is suggested to evaluate in this mnemonic.

THE MANTLE mnemonics
Temperature	36–37.5°C	Hemoglobin
7–9 gr/dl	Electrolytes your acid-basic status	Na + 140–150 mEq/L; pH: 7.35–7.45; p50 = 26–28 mmHg
Metabolism	Sedation and analgesia; SvjO2 > 55%	Arterial blood pressure
SABP >100–110 mmHg	Nutrition and glucose	Glycemia 110–180 mg/dL
Target of oxygen	PaO2 80–120 mmHg; SaO2 > 95%	Lung protective ventilation
Vt 6–10 ml/kg PBW; RR to achieve PaCO2 35–45 mmHg; PP < 14; DP < 13 cm H2O	Edema and ICP control	ICP < 22 mmHg; CPP 55–70 mmHg; ONSD <5.8 mm, PI <1.2; Serial CT scan

Table 2.

The MANTLE mnemonics.

Abbreviations: Cerebral perfusion pressure (CPP); systolic arterial blood pressure (SABP); tidal volume (Vt); respiratory rate (RR); Plateau pressure (PP); driving pressure (DP); intracranial pressure (ICP); predicted body weight (PBW); oxygen pressure at half arterial oxygen pressure (p50); optic nerve sheath diameter (ONSD); pulsatility index (PI); Computed Tomography (CT).

It is considered essential to avoid hyperthermia in these patients, this generates an increase in brain metabolism, and therefore risk of cerebral hypoxia; A temperature target of 36 to 37°C is sought [76, 77].

Maintaining adequate oxygen transport is important. A Hb between 7 and 9 g/dL is suggested for adequate oxygen transport and to avoid hypoxia [76, 78].

Serum electrolyte values and acid-base status are important for brain homeostasis; serum sodium levels of 135 to 145 mEq/L and avoiding hypotonic solutions are important to maintain an adequate osmolar gradient; in the base acid, a pH of 7.35 to 7.45 is suggested to avoid modification of the Hb dissociation curve and alteration of oxygen delivery to tissues and organs [76].

Adequate sedation, pain control, agitation, and treatment of seizures are part of bedside assessment to prevent an increase in basal metabolic rate [76, 79].

As already mentioned, the avoidance of hypotension is of utmost importance, since it is related to worse outcomes, a BPS of 100 to 110 mmHg, maintaining a normal volume, a normal peripheral perfusion, a diuresis of at least 30 ml/hr., and a central venous pressure of 6 to 10 cmH2O are suggested [76, 80].

Glucose control is crucial for proper brain metabolism. A range of 110 to 180 mg/dL is suggested, since values outside this range are related to metabolic crises and generation of neurotoxic cascades that alter homeostasis [76, 81].

In terms of oxygenation, we have a PaO2 target of 80 to 110 mmHg and a SaO2 greater than 94%, avoiding hyperoxia as well as hypoxia [76]. In case of mechanical ventilation, pulmonary protection parameters should be maintained, as mentioned above [75, 76].

Finally, cerebral edema and PCI control should be given. In case of neurological monitoring, maintain a PCI of less than 22 mmHg, SjvO2 between 50 and 75%, and non-invasively, an ONSD <5.8 mm, a PI <1.2, and a brain computed tomography scan without signs of cerebral edema [76].

Within the management of patients with severe TBI, stepwise management is sought [82]. We recommend the algorithm in Figure 3, which is based on the recommendations previously discussed, always remembering the individualization of the patient.

Figure 3.

Consensus algorithm. (1) primary assessment, (2) patient with impaired state of consciousness (GCS <8), (3) VT 6 to 8 ml, PEEP 5 cmH2O, PPLAT 30 cmH2O, RR of 16 to 22 breaths/minute, (4) bleeding with hemodynamic instability data, (5) in case of difficulty in controlling bleeding, consider lower values, (6) mydriasis or anisocoria, (7) mannitol or hypertonic saline, (8) maintain a PaCO2 of 25 to 30 mmHg, (9) follow mnemonics to maintain a happy brain, (10) consider maintaining adequate pain control, sedation, temperature, and agitation. Abbreviations: Tidal volume (VT), positive end-expiratory pressure (PEEP), plateau pressure (PPLAT), respiratory rate (RR), computed tomography (CT), Glasgow coma scale (GCS), mean arterial pressure (MAP), systolic blood pressure (SBP), hemoglobin (Hb), arterial partial pressure of oxygen (PaO2), arterial partial pressure of carbon dioxide (PaCO2), red blood cell (RBC), plasma (P), platelet (PLT), international normalized ratio (INR), thromboelastography (TEG), rotational thromboelastometry (ROTEM), intracranial pressure (ICP), cerebral perfusion pressure (CPP), intracranial hypertension (IH), optic nerve sheath diameter (ONSD), pulsatility index (PI), jugular bulb saturation (SjvO2).

6. Conclusion

The identification and appropriate approach of a patient with severe TBI, whether prehospital or Intra-hospital, requires a broad knowledge of brain physiology, in order to direct an appropriate neurological monitoring, whether invasive or non-invasive, and thus obtain information that allows us to direct a treatment in a staggered manner or controlling the ICP levels to guarantee the best CPP, taking into account variations in brain self-regulation. Regardless of the form in which the treatment is directed, the cornerstone is individualization.