1. Description of the problem

What every clinician should know

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in children. The injury can be caused by both a primary insult to the brain itself or by a secondary injury (such as secondary ischemia). Certainly known trauma, such as motor vehicle collisions, falls and sports-related injuries are common causes of TBI in children; however, in the infant, child abuse, or shaken baby syndrome, must also be considered. If a child presents with an altered level of consciousness, TBI should be considered in the differential diagnosis.

TBI can be stratified into mild, moderate or severe injury based on the Glasgow Coma Scale (GCS). An initial GCS of 13 to 15 with either no loss of consciousness or a brief loss of consciousness is classified as a mild head injury. GCS of 9 to 12 is classified as a moderate injury and a GCS of 3 to 8, a severe Injury. This chapter will concentrate on the child with severe TBI.

Key management points

The initial management and stabilization of the child with severe TBI is the same as any injured child. The first priority is making sure the airway is patent, the patient is breathing adequately, and the circulation is acceptable.

There is a growing body of literature that supports hypotension and hypoxia worsen outcomes in TBI. While there is limited evidence-based medicine for the treatment of TBI in children, in 2003 consensus guidelines were established for the treatment of severe TBI. These principles concentrate on avoiding hypoxia and hypotension as well as management of increased intracranial pressure (ICP) and maintaining cerebral perfusion pressure (CPP).

2. Emergency Management

The child with a severe TBI must be monitored closely. If the child has an altered sensorium one needs to consider intubation to ensure airway protection. Certainly in a child with a GCS of 8 or less or a waxing and waning level of consciousness, intubation should be undertaken. Particular attention should be made to ensuring adequate oxygenation and ventilation. Both hypoxia and abnormal partial pressures of carbon dioxide (PCO₂) can impact cerebral blood flow (CBF) and contribute to secondary injury.

Management points not to be missed

Consult a neurosurgeon and if unable to treat patient at your facility, initiate the transport process
Keep oxygen saturations above 92
If GCS less than 8 or waxing and waning sensorium, secure the airway
Maintain a normal to slightly elevated MAP for age; fluid resuscitation or vasopressors as needed
Maintain a PCO₂ within normal range (35–45 mmHg)
Elevate head of bed to 30 degrees if possible
Keep head midline
Maintain normothermia
Ensure adequate analgesia and anxiolysis
If intracranial monitor in place attempt to maintain ICP less than 20 and CPP greater than 40 for infant, 50 for toddler and 60 for adolescent
Hypertonic saline (10cc/kg) or mannitol 0.5 to 1 g/kg for signs/symptoms of increased ICP

3. Diagnosis

Diagnostic criteria

The diagnosis is initially based on history and physical examination if there is a known history of trauma. In the altered child without a clear history of trauma there must be a high index of suspicion especially in the neonate who presents altered or with seizures. The diagnosis is then confirmed by radiologic imaging, generally a non-contrast head computed tomography (CT) scan. The scan can delineate intracranial bleeding, cerebral edema, fractures, etc.

Normal lab values

Radiologic findings can include skull fractures, intracranial hemorrhages (epidural, subdural and subarachnoid bleeds), intraparenchymal hemorrhages and cerebral edema. The patient can also have significant injury related to ischemia or diffuse axonal injury that may not be apparent on initial scans and may only be found on follow-up imaging.

While most laboratory data may be relatively normal, It is important to check and follow the patient’s prothrombin and partial thromboplastin time, as patients with severe TBI often have an associated coagulopathy that is believed to be caused by tissue activation factors. Additionally it is important to maintain normocarbia; therefore the PCO₂should be followed.

If the provider is using hyperosmolar therapy utilizing mannitol, then serum osmolality should be followed to maintain levels within acceptable limits; most target a level around 320, but some centers will drive levels as high as 340. If hypertonic saline is used then serum sodium levels should be monitored and targeted to the 150 to 160 range.

Additionally hypoglycemia, and many believe hyperglycemia, can cause further injury. Therefore we recommend keeping glucose levels within normal ranges. Other laboratory values may be essentially normal unless there are coexisting injuries related to trauma.

How do I know this is what the patient has?

In a patient with a history of trauma, the diagnosis is initially made based on history and physical findings and then confirmed based on imaging. However, the diagnosis may not be as apparent in the infant with no known history of trauma. In fact the infants who are victims of child abuse can present with a wide variety of symptoms ranging from mild irritability or vomiting to full arrest.

There may be a story that is inconsistent with the child’s capability or severity of presentation, such as the 2-week-old infant who “rolled” off the bed; or If the child presents in the early stages, the diagnosis can be difficult to make as the symptoms may be vague. It is not uncommon for these children to be sent home upon initial presentation with a diagnosis of colic, reflux or a viral illness only to represent later with apnea or seizures.

In any child whose signs and symptoms do not correlate with the history or the story is suspicious, the provider must keep nonaccidental trauma in mind and consider radiologic imaging.

Differential diagnosis

With a known history of trauma the differential is fairly limited. If the head CT is normal one should consider diffuse axonal injury or nonconvulsant status epilepticus as a cause of prolonged altered mental status—or if the child had a prolonged down time, hypoxic ischemic encephalopathy.

In the child with no known history of trauma, the differential is fairly broad. Altered mental status can be caused by infectious etiologies such as meningitis or abscesses. It can be caused by metabolic derangements such as hyperglycemia in diabetic ketoacidosis or hyperammonemia seen in liver failure. Further it may be related to ingestions, either accidental or intentional. A good history and physical examination as well as further laboratory testing may narrow the differential.

Confirmatory tests

Aside from a thorough physical examination, a noncontrasted head CT is likely the one test that will provide the most immediate information. If there is concern for increased ICP then an ICP monitor (either a bolt or an EVD) will be valuable to guide further therapy. (An EVD is an external ventricula drain. Its advantage over a bolt is the ability to drain CSF as well as measure ICP.)

4. Specific Treatment

As discussed previously, treatment starts with making sure the airway is secure. If the GCS is significantly altered the patient should be intubated. While the specific sedative used can vary, most advocate the use of lidocaine to blunt an increase in ICP and avoidance of ketamine as it may increase ICP. One must be careful to avoid hypotension; therefore doses may need to be adjusted and volume should be on hand.

Once the patient is intubated it is important to monitor PCO₂. It is ideal to keep the PCO₂ 35 to 45 mmHg. While ventilator management is beyond the scope of this chapter, PCO₂ can be adjusted by changing minute ventilation. Therefore adjustments in ventilator rate or tidal volume (peak inspiratory pressures if in pressure mode or tidal volume if in volume mode) can be used to make adjustments in PCO₂.

Remember both hyper- and hypoventilation can alter CBF and cause secondary injury. Lowering PCO₂ less than the normal range should only be used briefly for acute herniation and long term only when other treatments have been exhausted.

Likewise, maintaining adequate oxygenation is also important. Hypoxia will lead to alterations in CBF if autoregulation is disrupted. Ideally the oxygen saturation should be maintained above 92%. If one is having difficulty, oxygenating the FIO₂ on the ventilator can be increased. However, if the patient is on greater than 60% FIO₂ for an extended period, one should consider increasing positive end-expiratory pressure (PEEP).

Keep in mind that increases in PEEP will decrease venous return and may result in hypotension; so careful attention must be paid to MAP when increasing PEEP, especially once the PEEP is raised to above the 8 to 10 range.

Once airway and breathing have been assured, attention should be turned to circulation. Hypotension can result in secondary injury and should be avoided. The provider should target normal to slightly high blood pressures for age. One can estimate a MAP in a child 1 to 10 years as (50 + 2x age in years); in the child 10 or older, a MAP of 70 should be used. This is initially achieved through volume administration but may require the addition of vasoactive drugs such as dopamine or norepinepherine. This should be done until an ICP is in place.

Once a pressure monitor is in place and an ICP can be measured, the provider should aim to maintain a CPP rather than a MAP. The CPP is calculated as MAP minus ICP and generally a level of 40 is target in infants, 50 in children and 60 in adolescents.

Once the ABCs have been taken care of, further treatment is targeted at improving ICP and reducing secondary injury. There are a few simple measures one can employ that may help decrease ICP even without knowing the exact number. First the head of the bed should be placed midline and the head of the bed elevated to 30 degrees. This helps with venous drainage and may help reduce ICP.

Additionally, care should be made to avoid and aggressively treat hyperthermia. Increased temperature will increase cerebral metabolic demands, which in turn increase CBF and therefore ICP. While there is some suggestion that decreasing temperatures below the normal range may be helpful, there is currently no evidence to suggest this as a first-line therapy. Certainly in refractory cases mild hypothermia may be initiated.

Ideally an ICP monitor should be placed to help guide therapy. If a draining device is placed, cerebral spinal fluid (CSF) removal may also help reduce ICP and therefore the monitor may provide therapeutic as well as diagnostic benefits. If CSF removal is utilized it is important to measure the output. This can be a significant fluid loss in small children and if left unchecked can lead to dehydration. Likewise CSF is a sodium-rich solution and if losses are significant and not being replaced, hyponatremia can occur.

It is important to make sure the patient is treated adequately for pain and agitation. Anxiety, stress and pain can all lead to increase metabolic demands and thus increase CBF and ICP. In refractory cases this may entail paralytic drips or pentobarbital comas.

Finally, hyperosmolar therapy can be utilized. Both mannitol and hypertonic saline have been proven to be effective and therefore preference is up to the provider. Both agents will cause alteration in the osmolar gradient across the blood brain barrier and lead to fluid shifts. The dose of mannitol is 0.5-1 gram per Kilogram and for hypertonic saline if 3% saline is used 5-10c/kg can be given over 10-15 minutes. When using hypertonic saline a serum sodium in the high 150s to mid-160s is generally targeted. If mannitol is being used the aim is to keep the serum osmolality around 320.

Drugs and dosages

Mannitol: 0.5–1g/kg
3% saline: 5–10cc/kg
lidocaine 1mg/kg
pentobarbitol load with 5mg/kg and then place on a drip at 1mg/kg/h and adjust as needed to maintain burst suppression

Refractory cases

In particularly refractory cases the neurosurgeon may decide to perform a decompressive craniotomy. Medical management in refractory cases may include lowering PCO₂ into the high 20s or low 30s and instituting mild hypothermia (maintaining the patient’s core temperature around 34 degrees).

5. Disease monitoring, follow-up and disposition

Expected response to treatment

Monitoring of pediatric patients with severe TBI should occur in an intensive care setting. Often these children will have intracranial monitors placed and will require placement of central venous catheters as well as arterial access for treatment and monitoring capabilities. Management can be complex, especially in the child with refractory ICP, and a multidisciplinary approach is beneficial.

Depending on the degree of injury the initial hospitalization can be prolonged and the child that survives often requires extended stays in rehabilitation facilities. Obviously the degree of primary injury will impact prognosis and survival the most. However, location and secondary injury related to hypoxia, hypotension and cerebral edema will also impact outcomes. Likewise other co-morbidities or injuries to other organ systems may affect outcomes.

Incorrect diagnosis

In the child with known trauma, diagnosis should be fairly simple. One needs to assure that in resuscitating the critically ill child no other injuries are overlooked. Ensuring a primary trauma survey is completed quickly and a secondary survey once the child is stabilized will help.

It is the infant who presents with vomiting, lethargy or irritability who can be missed during the initial presentation. Maintaining a high index of suspicion, in the infant or small child whose story keeps changing or whose symptoms do not seem to fit, the history is important.

Follow-up

The child with severe TBI often requires extensive rehabilitation. Referral to a facility with expertise in TBI is recommended. Even after a mild to moderate TBI, children will require cognitive testing.

Pathophysiology

TBI can be broken down into two categories: Primary injury and secondary injury. Primary injury is directly related to the initial trauma and includes such things as skull fractures, intracranial hemorrhages or contusions and diffuse axonal injury (DAI). The hemorrhage is related to acceleration–deceleration forces, which can cause shear injury to the arteries or veins. DAI is more often related to a rotational acceleration injury, which causes damage to the axons. DIA may not be apparent on the initial CT.

The secondary injury is not directly related to the trauma but more to the aftereffects. It is the injury that results secondary to hypotension, hypoxia or cerebral edema. The injury may result from poor CBF or the cascade of effects related to cell death.

The treatment of TBI is based on the premise that the brain is encased in a fixed space and any increase in volume will result in an increase in pressure if not counterbalanced by a reduction in volume of one of the other components. This principle is known as the Monroe Kelly doctrine. The three key components in the fixed compartment are blood, brain and CSF. Therefore the treatment of TBI aims to control one or more of the three components.

In the uninjured brain the body is able to compensate for brief small changes in pressure by regulating blood flow or shifts of CSF. However, when the volume becomes too high or the ability to autoregulate is lost, there is a significant increase in pressure for a relatively small change in volume. The primary injury itself can lead to increases in compartmental volume related to hemorrhage and therefore increased ICP. Likewise cerebral edema can cause further increases in brain volume and therefore increases in ICP.

When targeting treatments for increased ICP the aim is reduce the volume of one of the components to try to reestablish homeostasis. For example, hyperventilation reduces CBF, as do treatments that are aimed at decreasing cerebral metabolic demands (analgesia, sedation, paralytics and drug-induced comas).

Epidemiology

TBI is a very serious problem in children. Approximately 500,000 children are affected in the United States alone. It is a leading cause of trauma-related morbidity and mortality in children and accounts for several thousand pediatric deaths per year.

The most common causes of TBI tend to be motor vehicle accidents (whether pedestrian versus auto or motor vehicle to motor vehicle), falls, sports-related injuries and in the very young nonaccidental trauma. There tends to be a bimodal age distribution with a predilection to the very young (0–4 years) and the late adolescents (15–19). Males have a higher propensity, almost twice the risk, of severe injury than do females.

Prognosis

Prognosis is very difficult to predict in TBI as outcomes are affected by many overlapping factors. Generally, the more severe the primary insult the poorer the prognosis. A low initial GCS that has not significantly improved upon arrival to the emergency room tends to indicate a more severe injury and therefore a higher likelihood of a poor prognosis.

Additionally, the location and degree of primary injury are important factors. One must remember, however, that there are two causes of injury in TBI and secondary injury also plays a major role in outcomes. For example, periods of significant hypotension or hypoxia can lead to significant secondary injury and turn a relatively small primary injury into a very severe TBI.

What's the evidence?

“"Paediatric Intensive Care Society UK; Society for Neuroscience in Anesthesiology and Critical Care; World Federation of Pediatric Intensive and Critical Care Societies. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents—."”. Pediatr Crit Care Med. vol. 13. 2012. pp. S1-82.

Agrawal, Shruti, Ricardo, Garcia Branco. “"Neuroprotective measures in children with traumatic brain injury."”. World journal of critical care medicine. vol. 5.1. 2016. pp. 36

Curry, R, Hollingworth, W, Ellbogen, RG. “Incidence of hypo- and hypercarbia in severe traumatic brain injury before and after 2003 pediatric guidelines”. Pediatr Crit Care Med. vol. 9. 2008. pp. 141-6. (Provides rationale for limiting significant hyperventilation in TBI.)

Carney, NA, Chestnut, R, Kochanek, P. “Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents”. Pediatr Crit Care Med. vol. 4. 2003. pp. S1-S75. (This excellent reference goes over the rationale for TBI treatment and the recommended guidelines.)

Pigula, FA, Wald, SL, Shackfor, SR. “The effect of hypotension and hypoxemia on children with severe head injury”. J Pediatr Surg. vol. 28. 1993. pp. 310-4. (This study elucidates the secondary injury that can occur with uncontrolled hypotension and to a lesser degree hypoxia.)

Coates, BM, Vavilala, MS, Mack, CD. “Influence of definition and location of hypotension on outcome following severe pediatric traumatic brain injury”. Crit Care Med. vol. 33. 2005. pp. 2645-50. (This article examines at outcomes in children with TBI based on degree of hypotension and location [field/ER/ICU].)

Michaud, LJ, Rivara, FP, Grady, MS. “Predictors of survival and disability after severe brain injury in children”. Eurosurgery. vol. 31. 1992. pp. 254-64.

Ong, L, Selladurai, BM, Dhillon, MK. “The prognostic value of the Glascow coma scale, hypoxia, and computerized tomography in outcome prediction of pediatric head injury”. Pediatr Neurosurg. vol. 24. 1996. pp. 285-90.

Mansfield, RT. “Severe traumatic brain injuries in children”. Clin Pediatr Emerg Med. vol. 8. 2007. pp. 156-64.

“Pediatric advanced life support provider manual. Dallas (Tex): American Heart Association”. 2002.

Marion, DW, Obrisr, DW, Carlier, PM. “The use of moderate therapeutic hypothermia for patients with severe head injuries: a preliminary report”. J Neurosurg. vol. 79. 1993. pp. 354-62.

Biswas, AK, Bruce, DA, Sklar, FH. “Treatment of acute traumatic brain injury with moderate hypothermia improves intracranial hypertension”. Crit Care Med. vol. 30. 2002. pp. 2742-51.

Shiozaki, T, Hisashi, S, Taneda, M. “Effect of mild hypothermia on uncontrollable intracranial hypertension after severe head injury”. J Neurosurg. vol. 79. 1993. pp. 363-8.

Muizelaar, JP, Lutz, HA, Becker, DP. “Effect of mannitol on ICP and CBP and correlation with pressure autoregulation in several head injured patients”. J Neurosurg. vol. 61. 1984. pp. 700-6.

Khanna, S, Davis, D, Peterson, B. “Use of hypertonic saline solutions in the treatment of cerebral edema and intracranial hypertension”. Crit Care Med. vol. 28. 2000. pp. 1144-51.

Qureshi, AI, Suarez, JI. “Use of hypertonic saline solutions in the treatment of cerebral edema and intracranial hypertension”. Crit Care Med. vol. 28. 2000. pp. 3301-13.

Nathens, AB, Johnson, JL, Minei, JP. “Guidelines for mechanical ventilation of the trauma patient”. J Trauma. vol. 59. 2005. pp. 764-76.

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Traumatic brain injury and intracranial hypertension in the child