Head injury
Dr Torsten Lauritsen, Copenhagen, Denmark
Severe traumatic brain injury (TBI) in children is a life-threatening circumstance that requires specific
management beginning as early as possible. This management requires a precise assessment of the brain
lesions, as well as of any associated injuries. The primary brain damage is a direct result of the injury and
unfortunately nothing can be done about it. Secondary brain injury (SBI) can however be prevented. One of
the major goals of critical care management in these children is aimed at protecting against secondary brain
injury which represents a major cause of worsening in neurological outcome. A systematically approach to
the clinical examination as well as the treatment of the child with TBI has to be followed in order to prevent
further damage. SBI is mainly due to systemic hypotension, hypoxia, hypercarbnia, anemia and
hyperglycemia. A systematical approach using the ABCDE principles is recommended.
Management of any airway problems in a child with severe TBI requires early intubation to be able to control
oxygenation and ventilation. A rapid sequence induction modified for the paediatric patients is
recommended. Normoventilation with a PaCO2 in the normal range is optimal and hyperventilation should in
general be avoided since it worsens the outcome due to vasoconstriction and ischemia in the already injured
areas of the brain. Likewise hypoxemia or hyperoxemia should be avoided and oxygen treatment should be
guided by continuous monitoring and oxygen saturation or oxygen tension should be kept in the normal
range.
Global or regional cerebral ischemia is an important secondary insult to the acutely injured brain. Cerebral
perfusion pressure (CPP), as defined by mean arterial pressure (MAP) minus the mean intracranial pressure
(ICP), is the pressure gradient driving cerebral blood flow. Volume management of multiple trauma patients
with concomitant brain injury is challenging. In the presence of TBI, the potential benefits of permissive
hypotension and limited fluid resuscitation have to be weighed against the adverse consequences of
cerebral hypoperfusion. Hypotension has to be identified and treated. Blood pressure monitoring as well as
ICP monitoring should guide the fluid and inotropic treatment after the initial resuscitation.
Hypothermia initiated early after TBI in children has been widely debated. Hyperthermia (body temperature
>38 ͦC) is a known factor that may worsen outcome through several mechanisms (increasing metabolic
demand, lipid peroxidation, cell death, and acute seizure) and must be avoided. The concept of hypothermia
for brain protection is based on the principle that cooling reduces the cerebral metabolic rate and thereby
reducing cellular damage. Data from the neonatal population and animal studies indicate a favor of cooling.
Published clinical data are however controversial. There is no clear recommendation of hypothermia as
treatment after TBI in children, but it seems that only moderate (32-33 ͦC) cooling for 24 hours should be
avoided. Moderate cooling for 48 hours and slow rewarming can be considered for treatment of raised
intracranial pressure.
Transport to a specialized center and early neurosurgical consultation should be obtained. Evidence of the
benefit of ICP monitoring, cerebrospinal fluid drainage and decompressive cranictomy is sparse. However
neurosurgical evaluation of the clinical condition and the CT-scan is important for triage and decision of
specific treatment of raised ICP.
Hyperosmolar fluid therapy mainly consists of hypertonic saline and mannitol. Use of hypertonic saline or
mannitol reduces ICP by reducing blood viscosity (within minutes) and by an osmotic effect (hours).The
effect is transient and requires an intact blood brain barrier. Due to accumulation of mannitol or sodium in
injured brain a reverse osmotic shift may occur and possibly increasing ICP. There is class 2 evidence for
the use of hyperosmolar fluid therapy in the treatment of severe TBI in children with intracranial hyprtension.
Sedation and analgesia should be administered in children with TBI. They can minimize the stress
associated with necessary interventions such as airway management, ventilation, other invasive procedures
and transport. Other proposed benefits of sedatives include anticonvulsant and antiemetic actions, the
prevention of shivering, and reducing pain and stress. Pain and stress markedly increase cerebral metabolic
demands and can pathologically increase cerebral blood volume and raise ICP. No specific drug is superior
to another and in general it is advised to use well known drugs in order to minimize the side effects of
sedation.
Algorithm for early treatment in TBI
Fig: Algorithm for resuscitation of children with TBI
Conclusion
Traumatic brain injury in children is a leading cause of death and disability. Guidelines have been
established to prevent secondary brain injury caused by mainly hypotension or hypoxia. Initial resuscitation
follows the ABCDE principles with adequate airway handling, ventilation and fluid resuscitation to prevent
hypoxia, hyperoxemia, hypo- or hyperventilation and inadequate cerebral perfusion pressure. Specific
treatment of raised intracranial pressure must be initiated.
References
Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and
Adolescents-Second Edition. Pediatr Crit Care Med 2012 Vol. 13, No. 1 (Suppl.)