Keywords: TBI prehospital management, TBI hospital management, prognosis
Introduction | How to tackle the management of TBI patients?
Traumatic brain injury (TBI) represents a significant problem all over the world which leads to a decrease in the life expectancy of affected patients and high costs for society. In low- and middle-income countries, road traffic accidents represent the main cause of TBI. Their number is rising due to increased motorization without appropriate traffic safety regulations. On the contrary, in high-income countries, TBI incidence due to road traffic incidents is decreasing, but the elderly remain the vulnerable population due to the increased risk of falls [1, 2].
The current management of the traumatic brain injury patient is carried out according to the ‘Guidelines for the Management of Severe Traumatic Brain Injury’, which provides essential information to ensure quality medical services associated with improvements in the prognosis. In addition, in a study conducted by Dash HH and Chavali S in 2018, a brief presentation was made of the approach to the patient with head trauma from the scene of the accident to the care received during the hospitalization period [2].
The pathophysiological mechanisms of TBI
The authors included a brief description of the changes that occur in the human body during traumatic brain injury. The cascade of pathologic modifications begins with direct tissue damage due to primary or secondary brain injury. Primary lesions occur during the impact (e.g., traffic accident, fall) due to mechanical forces. Secondary lesions occur after a variable period due to the biochemical, cellular, and physiological changes in the damaged tissues [2, 3].
The primary stage after a TBI starts from tissue damage, leading to a compromised cerebral blood supply and disordered metabolism. The main changes in the brain are represented by the accumulation of lactic acid and the increase in cell permeability with the appearance of edema. These changes cause cellular ischemia and the depletion of adenosine triphosphate (ATP) reserves, representing cells` energy source (Figure 1) [2].
The second stage is represented by changes in membrane permeability with the release of excitatory neurotransmitters (such as aspartate and glutamate) and the activation of voltage-dependent Ca++ and Na+ channels. The process of apoptosis (programmed cell death) is triggered by the activation of catabolic enzymes (proteases, phospholipases, lipid peroxidases), followed by cell death due to the destruction of the membrane. TBI causes systemic inflammation in the affected individuals leading to organ dysfunction without a pre-existing impairment.
Common manifestations following TBI are presented in Figure 2 [2, 4].
The management of TBI in the prehospital phase
The prehospital management of TBIs aims to prevent secondary injuries through an appropriate approach from the site of the injury and the quick transport of the patient to the nearest hospital. However, the aggravation of the traumas can appear in a few minutes or hours as a result of factors such as hypotension, hypoxemia, hypo- or hyperglycemia, and hypo- or hyperthermia. Studies have shown that a single episode of hypotension is associated with increased morbidity risk and doubled mortality risk [5].
The initial approach to a TBI patient involves ensuring the airway, adequate ventilation, and blood circulation. For patients with moderate or severe TBI, access to a neurosurgery hospital must be ensured as quickly as possible to carry out the appropriate treatment. It is vital to maintain O2 saturation over 90%, and all TBI potential patients should receive continuous high-flow O2 to avoid hypoxia associated with a poor prognosis [2].
Endotracheal tube intubation (ET) was recommended for a GCS≤ 8 points, but current studies have shown that intubation performed in the pre-hospital setting can do more harm due to the lack of experience of the prehospital providers, the transient hypoxia during the procedure or the prolonged duration of the procedure. In addition, hyperventilation to reduce intracerebral pressure is no longer recommended, except for patients with definite signs of impending cerebral herniation, because it has been observed that excessive ventilation leads to a worse prognosis. The signs of impending cerebral herniation are showcased in Figure 3 [2, 6].
Systolic blood pressure (SBP) should be maintained above 90 mmHg by intravenous administration of isotonic substances, such as normal saline or Ringer`s lactate. Hypertension after a trauma occurs due to the release of catecholamines and is not recommended to be treated with medication [2, 6].
Hospital management of TBI
The assessment of the patient arriving in the emergency department must be carried out quickly using the ABCDE algorithm described in Figure 4.
A (airway and oxygenation)
To ensure adequate oxygenation in patients with persistent hypoxia despite supplemental oxygen, GCS≤ 8 points, or with signs of cerebral herniation, endotracheal tube intubation must be performed under safe conditions. Intubation at the site of the accident by inexperienced medical providers is associated with a higher mortality rate and worse functional outcomes [2, 6].
A cervical spine fracture is suspected in victims of road accidents or falls and should be carefully examined until the radiological evaluation of the cervical region. Intubation must be performed with the stabilization of the head in the axis to avoid the appearance of new spinal cord injuries. Using neuromuscular blockers is recommended because it facilitates the intubation process, reducing the risk of hypoxia and airway trauma [2, 6].
B (breathing and ventilation)
Maintaining normocarbia (PaCO2 values between 34 and 38 mmHg) is essential to ensure cerebral blood flow and prevent neurologic complications. Hypoventilation ensures increased values of PaCO2 that cause the dilation of cerebral blood vessels and the increase of intracranial pressure (ICP). Conversely, hyperventilation causes vasoconstriction with worsening hypoxia in the penumbra area and decreases the ICP [2, 6].
Hypoventilation and hyperventilation are associated with poor outcomes. Therefore, hyperventilation is accepted for a short period only if the cerebral herniation is imminent until hyperosmolar therapy or surgical decompression [2, 6]. Recent studies have shown that patients with tracheostomy require fewer ventilation days, so early tracheostomy is recommended when the benefits outweigh the risks [2].
C (circulation and fluid management)
Maintaining blood pressure within normal limits is imperative to ensure cerebral perfusion pressure and avoid the occurrence of secondary brain lesions. Current guidelines recommend maintaining systolic blood pressure ≥100 mmHg for patients between 50 to 69 years old and ≥110 mmHg for patients 15 to 46 or over 70 years old [2].
The cerebral perfusion pressure (CPP) target is between 60 and 70 mmHg. High CPP values are associated with hyperemia and high, unlike low values of PPC that are associated with hypoxia and cerebral ischemia. Vasopressors can be used to augment CPP in patients with severe TBI. [2, 6]
Restoration of intravascular volume is essential in managing TBI patients and can be achieved by using colloidal, crystalloid substances or, in selected cases, blood products. The crystalloid substances recommended for resuscitation are isotonic, such as saline and Ringer`s lactate. However, administering large amounts of saline solutions leads to hyperchloremic metabolic acidosis, which has harmful consequences for TBI patients. To avoid these complications, renal function must be considered when calculating the doses of administered infusion substances [2].
D (disability)
All patients with TBI must be evaluated neurologically with the follow-up of pupillary anomalies, signs of neurologic laterality, and the calculation of the GCS score. In addition, special attention must be paid to the signs of cerebral herniation, such as decerebrate or decorticate posturing, anisocoria, and Cushing`s triad. In this case, administering hypertonic substances or mannitol will lower the intracranial pressure by reducing blood viscosity and promoting osmotic diuresis [2, 7].
For each patient, the Glasgow Coma Score (GCS) should be evaluated to establish the state of consciousness and the severity of the TBI. However, some studies have shown that the GCS score has limited utility in establishing TBI patients’ prognoses. Rancho Los Amigos Scale is a newer scale used to evaluate cognitive and behavioral patterns in TBI victims. This scale is divided into 8 levels, from level I, where the patients have no response, to level VIII, where the responses are almost normal. These scales are used for dynamic assessment of the recovery in TBI patients [2].
E (exposure and examination)
Maintaining body temperature within normal limits is vital because hypothermia aggravates coagulopathy and is associated with a worse prognosis. Also, hyperthermia is associated with more extended periods of hospitalization due to the appearance of edema and the promotion of inflammation [2, 6].
Decompressive Craniectomy
In some cases, intracerebral pressure remains elevated despite medical treatment, leading to brain herniation, a complication associated with an increased risk of morbidity and mortality. Decompressive craniectomy involves removing a part of the skull, thus creating additional space for the swelling of the brain and helping to lower intracranial pressure. This intervention is associated with a decrease in the risk of mortality but with increased chances of permanent disability [2].
Other Considerations
Seizure prevention
The risk of seizures is higher after brain trauma due to increased intracerebral pressure and alteration of cellular oxygenation. Therefore, anticonvulsant therapy is recommended to prevent and treat post-traumatic seizures in TBI patients. Current studies recommend the preventive administration of anticonvulsants in the first 7 days after the trauma, levetiracetam being the most used drug. Unfortunately, there are not enough studies to determine the most suitable antiepileptic drug for patients with TBI, considering both the benefits and the side effects [2, 7].
Glycemic control
Hyperglycemia occurs after a traumatic brain injury due to the release of catecholamines and cortisol, leading to the appearance of oxidative stress and insulin resistance. In addition, high blood sugar levels cause acidosis at the cerebral level and neuronal dysfunction, factors that are associated with a poor prognosis. Therefore, in the first days after a TBI, it is recommended to avoid very high or very low blood glucose values and administer fluids rich in glucose [2].
Antibiotic therapy
Patients with severe TBI are more prone to infections due to the need for mechanical ventilation and intracerebral pressure monitoring. However, prophylactic antibiotic administration is not recommended because no significant differences were observed between patients who received antibiotics and those who did not. Still, an increase in bacterial resistance to the usual drugs was observed. Therefore, current guidelines recommend using antibiotic-impregnated catheters to reduce the risk of infection [2, 7].
Venous thromboembolism prophylaxis
Patients with TBI are more prone to thromboembolic complications due to the blood hypercoagulability associated with the trauma, and its complications, such as prolonged immobilization and motor deficit. These complications can be prevented by using mechanical means (gradual compression stockings or intermittent pneumatic compression) and pharmacological (low molecular weight heparin) [2, 7].
Nutrition
Ensuring early nutritional support after TBI is associated with a better prognosis, and it is necessary to ensure a basal caloric replacement no later than 5-7 days after the trauma. Transgastric jejunal feeding has been observed to decrease the risk of pneumonia. Increased intracranial pressure and opioid treatment affect gastric emptying, leading to digestive intolerance. The administration of prokinetic drugs helps to increase digestive tolerance [2].
Head trauma for pediatric patients
TBI is the most frequent cause of mortality and morbidity in the pediatric population. In 2014, at the level of the European pediatric population (0-19 years), there were 2303 deaths and 441,368 hospitalizations due to TBI. The main cause of TBI was traffic accidents (63%), followed by falls, suicides, and violence [8].
In the case of children, brain trauma can manifest differently with the appearance or maintenance of symptoms in adult life. Their skull is incompletely developed with open sutures that allow the increase of intracranial pressure (ICP) without specific symptoms of increased ICP, such as crying, excessive irritability, vomiting, headaches, and visual disturbances (diplopia, blurred vision). Sometimes the only manifestation of elevated ICP is the bulging of the anterior fontanel without an alteration of the neurological status. Therefore, the assessment of ICP must be carried out by evaluating the child’s clinical condition and by non-invasive methods (computed tomography, magnetic resonance imaging) in the absence of specific symptoms with the aim of early neurosurgical intervention when it is necessary [2, 8].
Assessing the prognosis of pediatric patients with TBI is difficult due to the immaturity of the nervous tissue. Still, the following factors are responsible for the poor prognosis:
- age
- severe TBI
- surgical intervention
- subdural hemorrhage.
Future studies are needed to identify some biomarkers with a role in stratifying the prognosis of TBI pediatric patients [2].
Conclusion
TBI remains a fundamental problem in today’s world, despite the established prevention measures and the provision of adequate treatment in specialized centers. Patients with TBI have a higher morbidity and mortality rate than the general population, implying high costs for society and a decreased quality of life [2].
The current guideline by Dash HH and Chavali S was created from the need to standardize the treatment of traumatic brain injury in all countries and improve functional outcomes. Early therapeutic intervention is necessary to avoid the occurrence of secondary cranial lesions that are associated with poor functional status. TBI management recommendations are constantly evolving due to new clinical studies that seek to improve the prognosis of patients with TBI [2].
For more information about the impact of TBI visit:
- Immune response post-TBI
- How does TBI affect the functions of patients?
- Advances in TBI care and therapies
We kindly invite you to browse our Interview category https://brain-amn.org/category/interviews/. You will surely find a cluster of informative discussions with different specialists in the field of neurotrauma.
Bibliography
- Roozenbeek B, Maas AIR, Menon DK. Changing patterns in the epidemiology of traumatic brain injury. Nat Rev Neurol. 2013;9(4):231–6; doi: 10.1038/nrneurol.2013.22.
- Dash HH, Chavali S. Management of traumatic brain injury patients. Korean J Anesthesiol. 2018;71(1):12; doi: 10.4097/kjae.2018.71.1.12.
- Ng SY, Lee AYW. Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets. Front Cell Neurosci. 2019;13:528; doi: 10.3389/fncel.2019.00528.
- Gaddam SSK, Buell T, Robertson CS. Systemic manifestations of traumatic brain injury. In: Handbook of Clinical Neurology. Elsevier; 2015. p. 205–18. Available at: https://pubmed.ncbi.nlm.nih.gov/25702219/
- Gravesteijn BY, Sewalt CA, Stocchetti N, Citerio G, Ercole A, Lingsma HF, et al. Prehospital Management of Traumatic Brain Injury across Europe: A CENTER-TBI Study. Prehospital Emergency Care. 2021; 25(5):629–43; doi: 10.1080/10903127.2020.1817210.
- Rakhit S, Nordness MF, Lombardo SR, Cook M, Smith L, Patel MB. Management and Challenges of Severe Traumatic Brain Injury. Semin Respir Crit Care Med. 2021; 42(01):127–44; doi: 10.1055/s-0040-1716493.
- Hawryluk GWJ, Rubiano AM, Totten AM, O’Reilly C, Ullman JS, Bratton SL, et al. Guidelines for the Management of Severe Traumatic Brain Injury. 4th ed; United States; Neurosurgery. 2017;87(3):427–34; doi: 10.1227/NEU.0000000000001432.
- Majdan M, Melichova J, Plancikova D, Sivco P, Maas AIR, Feigin VL, et al. Burden of Traumatic Brain Injuries in Children and Adolescents in Europe: Hospital Discharges, Deaths and Years of Life Lost. Children (Basel). 2022;9(1):105; doi: 10.3390/children9010105.
