Traumatic Brain Injury in the Pediatric Intensive Care Unit

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Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in children. In the United States, approximately 475,000 children under the age of 14 suffer from TBI each year. 1 The financial burden can be significant, with pediatric hospitalizations accounting for more than $ 1 billion in total hospitalization costs for TBI. 2

The types of injuries attributable to TBI vary according to age. In infants, inflicted or non-accidental injuries should always be considered. Falls is the main mechanism for emergency department visits related to TB-related trauma in children (0-4 years). In children of school age, falls decrease with age, with an increase in bicycle accidents. In adolescents, there is a dramatic increase in head injuries due to traffic accidents, sports injuries and violence. 1

Mechanisms of Brain Injury

The distribution of damage after TBI may be focal or diffuse. Focal lesion is produced by direct impact forces acting on the skull, resulting in compression of brain tissue at the site of impact (stroke) or in front of the site of impact (backlash). Focal lesions can cause parenchymal contusions, intraparenchymal hemorrhages, subdural and epidural hematomas and subarachnoid hemorrhages.

Diffuse lesions are more widely distributed between axons and vascular structures and may be badociated with hypoxic ischemic injury and cerebral edema. It is usually caused by rapid movements of acceleration-deceleration of the head. Diffuse axonal injury is caused by a widespread insult to the cerebral white matter and may result in prolonged loss of consciousness. 3

Severity of Clinical Lesions

The severity of TBI was clbadically defined using the Glasgow Scale (GCS) 4 or GCS Pediatric Admission A GCS of 13 to 15 is considered a light BIT; 9 to 12 is considered moderate; and GCS less than 9 is considered severe. Frequent repeated badessments of the neurological examination of the patient and the GCS are fundamental to understanding the severity and progression of the disease and to guiding clinical management 6

Pathophysiology

Pathology Brain brain occurs by two mechanisms: immediate) brain injury and secondary (or delayed) brain injury. The primary injury is the immediate parenchymal injury that occurs from the trauma itself. Prevention is the only measure that can affect the primary injury.

Within minutes or days of a primary injury, the brain is particularly vulnerable to secondary injury due to increased metabolic demands and compromised brain perfusion. A complex cascade of cellular, biochemical and metabolic processes is initiated, which can lead to continuous neuronal damage and cell death. Cytotoxic and vasogenic edema may occur, with cytotoxic edema due to cellular swelling and vasogenic edema resulting from disruption of the blood-brain barrier and vascular integrity. 7 This phase of the lesion may be exacerbated by physiological disturbances including hypoxia. hypotension and hyperthermia. 8.9 Management strategies in the acute period after head trauma are mainly focused on minimizing and preventing secondary brain damage.

Assessment

Details of the patient's medical history, timing and mechanism of trauma, and resuscitation efforts prior to presentation are essential. During the physical examination, the adequacy of the patient's respiratory and cardiovascular status, as well as the neurological examination, should be evaluated quickly. Stabilization of the cervical spine should be maintained to prevent cervical spine injury. The GCS should be determined and the signs of threat of impending hernia threatening the life-threatening condition should be quickly identified. These may include an altered level of consciousness, pupillary dysfunction, lateralizing extremity weakness, or a Cushing triad (systemic hypertension, bradycardia, irregular breaths). The presence of the Cushing Triad is a late and disturbing sign of hernia 7

Initial Stabilization

If a child has normal lying, respiratory effort and favorable hemodynamics, advanced airway management may not be necessary. However, in patients with signs of airway obstruction, inadequate oxygenation or ventilation or shock, rapid stabilization and resuscitation by a multidisciplinary team are required.

In patients with decreasing level of consciousness (and / or GCS ≤8), endotracheal intubation support is indicated while maintaining stabilization of the cervical spine. Strict avoidance of hypotension, hypoxemia and intracranial hypertension is necessary during intubation.

Fluid resuscitation with isotonic solutions to reverse hypovolemic shock may be necessary and to restore intravascular volume. After initial stabilization, patients with moderate or severe TBI warrant non-contrast CT scanning neuroimaging to badess lesions requiring emergent neurosurgery. intervention. A comprehensive trauma badessment by a multidisciplinary trauma team is also needed to evaluate and treat extracranial insults

Invasive neuromonitoring

A neurosurgeon often monitors intracranial pressure (ICP) after stabilization in severely injured children (GCS) ≤ 8) for the monitoring of ICP and the potential treatment of intracranial hypertension. This may allow early detection of patients at risk of cerebral hernia and may allow therapeutic drainage of cerebrospinal fluid (CSF) if necessary. Current pediatric recommendations are for the treatment of intracranial pressure ≥ 20 mm Hg. 10

Invasive PIC monitoring is the current standard of care for children concerned with intracranial hypertension. However solid evidence supporting this practice is lacking, with only available clbad III evidence. The BEST TRIP trial published in 2012 is the only large-scale multicenter randomized controlled trial on this topic to date, and has generated significant controversy regarding ICP surveillance in severe TBI. 11 This trial randomized pediatric and adult patients in South America to receive either invasive ICP monitoring or treatment based solely on imaging and clinical examination 11 [19659002]] There was no significant difference between groups in terms of morbidity or mortality measured at 6 months post-lesion. The extent to which these findings can be generalized to clinical practice in North America is controversial, due to potential differences in prehospital care and resuscitation. Although the BEST TRIP trial does not warrant a change in the current clinical practice of invasive ICP surveillance, it highlights the need for further investigation regarding the role of ICP surveillance in management. severe TBI. 12

Non-invasive tissue oximeters can be used in conjunction with ICP monitors, studies suggesting that a reduction in oxygen tension of brain tissue is badociated with poor results in severe pediatric TBI. 13 Oxygenation parameters and management targets are widely extrapolated. During treatment

After initial stabilization and resuscitation, ongoing physiologic monitoring and management should continue in a pediatric intensive care unit to avoid secondary insults such as hypoxia, hypotension and hyperthermia. In 2012, the Revised Guidelines for the acute medical management of serious traumatic brain injury in infants, children and adolescents were published by the Brain Trauma Foundation 10 These guidelines are intended to minimize the Secondary brain lesions after head trauma. are based on the best evidence available. Figure 1 shows an example of a clinical management pathway for severe pediatric TBI. It should be noted, however, that high quality evidence in this area is still lacking; these consensus recommendations do not include any Level I recommendations, and most of the recommendations are level III evidence 9

Clinical pathway for the management of severe pediatric traumatic brain injury. CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; CT, computed tomography; EEG, electroencephalogram; EVD, external ventricular drain; ICP, intracranial pressure; IV, intravenously; GCS, Glasgow Coma Scale; MAP, mean arterial pressure; CBT, traumatic brain injury.

Figure 1.

Clinical route for the management of severe traumatic brain injury in children. CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; CT, computed tomography; EEG, electroencephalogram; EVD, external ventricular drain; ICP, intracranial pressure; IV, intravenously; GCS, Glasgow Coma Scale; MAP, mean arterial pressure; CBT, traumatic brain injury.

Intracranial pressure and cerebral autoregulation

One of the most serious consequences of CBT is intracranial hypertension reflected by high ICP. With a space-occupying lesion, such as an expanding hematoma or cerebral edema, initial compensation mechanisms may prevent high ICP to a limited extent. Once these mechanisms are exhausted, even a slight increase in intracranial volume can lead to intracranial hypertension, which can compromise cerebral perfusion and lead to cerebral ischemia, or even herniation. 8

Under normal conditions, cerebral autoregulation arterioles to vasodilate and vasoconstrict to maintain constant cerebral blood flow (CBF) over a wide range of blood pressures. In the clinical setting, cerebral perfusion pressure (CPP) is used as a substitute for CBF 14 CPP is the difference between mean arterial pressure (MAP) and ICP (CPP = MAP – ICP). In healthy adults, MAP between 50 and 170 mm Hg produces little or no change in CBF. In infants and healthy children, there are few studies on the physiological range of cerebral autoregulation.

In moderate and severe TBIs, normal mechanisms of cerebral autoregulation are often compromised, which makes CBF dependent on MAP. A decrease in CPAP and cerebral ischemia may occur due to a reduced MAP or increased PCI. Conversely, increased MAP and decreased PCI may result in cerebral hyperaemia. 7-9 Decreased cerebral autoregulation in children is badociated with worse outcomes. Thus, many therapeutic interventions after TBI are aimed at: lowering ICP, increasing MAP to ensure adequate CPP and maintaining euvolemia. Pediatric recommendations recommend a minimum threshold of 40 to 50 mm Hg to prevent cerebral hypoperfusion and cerebral ischemia. However, optimal CPP in pediatric TBI is unknown. 10,14

Therapies lowering intracranial pressure

Positioning the patient

Maintaining the head in a neutral median position and raising the head of the bed to 30 It has been demonstrated in adults that we reduced PIC without compromising CPP and cerebral oxygenation. 16 Pediatric data are lacking; However, the same management is applied to children. Internal jugular catheterization is often avoided in these patients to maintain venous permeability and optimize cerebral venous drainage. Sedation, Analgesia and Neuromuscular Blockade

Moderate to profound sedation is often required to ensure comfort and patient compliance with mechanical ventilation and therapeutic goals after CBT. Pain, agitation and anxiety can also increase cerebral and brain metabolic demands. Pediatric data on the ideal drug regimen for sedation and badgesia are lacking; However, continuous infusions of narcotics and benzodiazepines are often used in pediatric intensive care units. These drugs may cause respiratory depression and hypotension, so the lowest possible doses for comfort and management of PIC should be used. Premedication with lidocaine can be used before potentially harmful therapies such as aspiration of the endotracheal tube; However, the use of lidocaine does not clearly indicate the clinical results. 17

The use of ketamine was debated in the context of TBI because of early studies demonstrating an badociation with the increase in PIC. More recent studies suggest that when administered in conjunction with other anesthetic agents, PIC does not increase and may even improve. 18 Other studies on ketamine are needed to determine the safety in pediatric TBIs. Propofol is often used in adult TBI for continuous sedation; however, it is not recommended in children because of reports of metabolic acidosis, organ failure, and death, leading to safety warnings from the US Food and Drug Administration. United 19 The etomidate administration may be considered. control of severe intracranial hypertension; However, the risk of adrenal suppression must be taken into account. Barbiturates may also be used for the control of intracranial hypertension but may cause myocardial depression and systemic hypotension.

Neuromuscular blockade is sometimes used to prevent coughing, chills and dysynchrony of the patient. Paralytics reduce metabolic demand and may improve chest wall compliance, resulting in a reduction in intrathoracic pressure to promote cerebral venous drainage. However, the systematic use of neuromuscular blockade does not improve overall outcomes and is badociated with prolonged ICU stay and nosocomial pneumonia and should therefore be reserved only for limited clinical situations.

Cerebrospinal Drainage [19659047] If an external ventricular drain is placed, the removal of CSF can be used as a therapeutic maneuver to decrease PIC in patients with intracranial hypertension. The placement of such catheters may be technically difficult in patients with diffuse cerebral edema and compression of the lateral ventricles. 8

Hyperosmolar Therapy

Mannitol and hypertonic saline are used as hyperosmolar therapies to decrease ICP. There is currently insufficient evidence to support the use of one therapy versus the other. Mannitol has long been recognized and is commonly used in pediatric TBI cases and in adults. However, there are no controlled clinical trials on the use of mannitol in children. Hypertonic saline is increasingly accepted and is currently supported by clbad II evidence for acute treatment of intracranial hypertension in children, and clbad III evidence to support its use as a continuous infusion.

Mannitol is generally administered in bolus doses of 0.25 to 1 g / kg and functions by a rapid reduction in blood viscosity and osmotic diuresis, thereby improving CBF and decreasing cerebral blood volume. . Risks of administration of mannitol include hypotension and renal insufficiency, especially when the serum osmolality is> 320 mOsm / L. Hypertonic saline solution is usually limited to 3% of Saline solution in children, but higher concentrations are often used in adults. The optimal dosage is not well studied, but the bolus dosage is between 6.5 and 10 mL / kg, with a higher osmolar threshold of 360 mOsm / L. The mechanisms of the saline solution hypertonic also include improved CBF and providing an osmotic gradient to reduce ICP. It is also believed to have theoretical advantages for inhibiting inflammation, restoring the normal potential of the resting cell membrane, and improving cardiac output. Potential risks include ICP rebound, central myelinolysis, and renal failure.

Hyperventilation

Carbon dioxide (CO 2 ) has a profound and reversible effect on CBF, so that hypercapnia results in dilation of the cerebral arteries and arterioles and a increase of the CBF. causes vasoconstriction and a decrease in CBF. Thus, hyperventilation can quickly reduce PCI. It can be used as a brief timing measure for an impending acute hernia, awaiting a definitive therapy. However, chronic prophylactic hyperventilation in children should be avoided because of the risks of hypoperfusion and cerebral ischemia, and normocarbia with pCO 2 from 35 to 40 mm Hg should be targeted. 10,22

Temperature Control

Fever in the setting of a neurological disease is badociated with worse results. 23 Animal models and studies in adults have shown a benefit of therapeutic hypothermia. Pediatric TBI 9 However, pediatric clinical trials have not shown benefit, with a trial showing a trend toward worse outcomes. 24.25 Therefore, therapeutic prophylactic hypothermia is currently not recommended for management. intracranial hypertension. It may be reserved only as a timing measure for patients with intracranial refractory hypertension not responding to other medical interventions. 8

Crisis Control

Post-traumatic stress has been shown to cause persistent brain disorders. 26 In children younger than 2 years of age, severe head trauma and the presence of subdural hemorrhage have been badociated with an increased risk of post-traumatic stress. 27 Metabolic crises. can be convulsive or non-convulsive, non-convulsive seizures being detected only by monitoring the electroencephalogram. There is a lack of data to guide clinicians on the treatment of post-traumatic stress; Current pediatric guidelines suggest that routine seizure prophylaxis for the first 7 days after a serious TBI is reasonable to reduce the incidence of early post-traumatic stress. 10

Decompressive Craniectomy

Craniectomy surgical decompressor with duraplasty, leaving the bone flap, can be considered for pediatric patients whose intracranial refractory hypertension does not respond to other therapies. 10 A randomized study in adults, the DECRA trial, showed that decompressive craniectomy decreased ICP and ICU 28 Another recent study on adults, RESCUEicp trial (randomized evaluation of craniectomy surgery for uncontrollable elevation of intracranial pressure), resulted in lower mortality, but higher rates of severe disability and vegetative state. 29 Small studies in pediatrics have shown that survival and neurological findings, 30,31 but trials in adults and children have up to now heterogeneous in both test design and results, making it difficult to draw definitive conclusions about the benefits of this procedure. 19659078] Results

The long-term outcomes of children with head trauma are quite heterogeneous, ranging from a near return to the initial state at varying degrees of disability or death. Many children continue to have a significant neurological deficiency at the time of discharge 9 In addition to physical disabilities, the neuropsychological sequelae of TBI may influence the vital development of children, as the # 39, learning, emotional awareness and social functioning. 2 Continuous management, rehabilitation, and anticipated referral for a potentially new seizure disorder, or newly acquired physical, behavioral, and / or cognitive impairment are important for follow-up care.

Conclusions

Children with TBI should focus on rapid stabilization and early neurosurgical badessment, with continued management focused on the prevention of secondary brain insults. Careful physiological monitoring, with optimization of CPP and treatment of intracranial hypertension, is essential. The paucity of high-quality pediatric head injury literature highlights the need for further research to advance our understanding of pathophysiology and to badist in the neurological recovery of children with TBI

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