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DefinitionsHead trauma can refer to any injury to the head from a superficial graze, through superficial haematoma to skull fracture, and life threatening intracranial injury. Traumatic Brain Injury (TBI) refers more specifically to
disruption of the brain tissue by an external mechanical force. This may lead to a range of presentations from minimally impaired mental status, with no neurological deficit, to profound and sustained loss of consciousness. The Glasgow Coma scale [1] has been used to classify severity of traumatic brain injury. This score designates patients as suffering from mild (GCS 13-15), moderate (GCS 9-12) or severe traumatic brain injury (GCS <8). Although originally designed for adults, the Glasgow Coma Scale has been adapted to include children and infants.[2, 3]. Other criteria used in the various classifications of head injury severity include presence of post traumatic amnesia, duration of loss of consciousness, presence of neurological changes, presence of skull fracture or intracranial lesions.[4] IntroductionHead injury in children is common. Traumatic brain injury is a leading cause of long-term disability and mortality in children. Children under 3 have the highest rates of head injury. Most are trivial or mild head injuries due to falls - around 90% will be discharged from ED[5]. The majority of head injury in young children is the result of accidental injury, however in children less than 2 years old, 80% or more of deaths from head injury are due to non-accidental trauma. [8] There is a second peak in head injuries during adolescence. This group has a greater proportion of fatal injuries, where mechanism is more commonly motor vehicle accident related.[5] In one analysis of children presenting to the Royal Children's Hospital, Melbourne, 24% of patients with
head injuries had an injury to one or more other body regions and 20 % of all children with severe head injury had an accompanying cervical spine injury. Children sustain different patterns of head injury compared to adults due to their relevant anatomical, physiological and biomechanical properties. In particular, the following differences are important[6]:
Outcomes from head injuries depend on both the severity of the initial injury (primary brain injury), as well as the extent of subsequent complications and how these are managed (secondary brain injury). A holistic approach to the management of paediatric head injury therefore includes identification of risks so that primary injuries can be prevented. This includes maintaining an increased awareness of inflicted injury, and advocating for the use of protective devices - such as seat belts, bike helmets or netting around trampolines which lessen the number of, or decrease the severity of injury following accidents. This advocacy also identifies and informs parents of those sports/activities which carry increased risks of head injuries - for example quad-biking, Aussie rules football, and horse-riding. Once a primary injury has occurred, hospital management is directed toward the prevention, identification and treatment of the secondary injuries. PathophysiologyOutcomes from head injuries depend on the severity of the initial injury (primary injury) and the extent of subsequent damage from oedema, ischaemia and inflammation (secondary injury). The initial stage of TBI is due to mechanical tissue damage from shearing or tearing forces on the neurons, glia and blood vessels. In many cases there is direct neural cell loss and necrotic cell death. The primary injury triggers secondary biochemical, metabolic and cellular changes. These include[10]:
Primary intracranial injuriesPrimary intracranial injuries include:
Secondary intracranial injuryThis refers to the injury to brain cells after the original insult. It is a major contributor to overall morbidity and mortality in traumatic brain injuries - and occurs over hours to weeks following a primary injury to the brain. Not all of this secondary brain injury is preventable. Nevertheless, the goals of patient management are aimed at:
To achieve these goals, it is important to understand cerebral haemodynamics. Cerebral haemodynamicsThere are two major principles to consider in order to understand cerebral haemodynamics - the Munro-Kellie hypothesis and autoregulation. Munro-Kellie Hypothesis This hypothesis states that the skull is a rigid compartment filled with essentially non-compressible contents - the brain, intravascular blood and CSF. An increase in volume of one of the contents should lead to a decrease in the volume of another. This can occur through displacement of CSF to the spinal subarachnoid space, or through displacement of blood by compression of the venous system. However, the degree of this compensation is limited, and once it is reached, intra-cranial pressure (ICP) can rise. Acute ICP rise can lead to:
Autoregulation. Cerebral perfusion pressure (CPP) is dependent on mean arterial pressure (MAP) and intracranial pressure (ICP). The uninjured brain is able to regulate blood flow through a range of blood pressures through autoregulation of cerebral vascular resistance. Various conditions such as hypercapnia and acidosis lead to dilation of cerebral arteries. Alkalosis, hypocapnia and hypertension lead to cerebral arterial constriction . The injured brain may lose the normal homeostatic mechanisms for blood flow and when this occurs, blood flow is dependent on the CPP. The relationship between ICP and CPP is shown below: CPP = MAP - ICP In injury, a fall in blood pressure (systemic hypotension) or a rise in ICP will lead to a reduction in the CPP. A reduction in CPP leads to cerebral ischaemia (that is a reduction in cerebral blood flow) - which leads to further neuronal death and cerebral oedema - further increasing ICP and contributing to a vicious cycle of escalating secondary brain injury. In order to prevent cerebral ischaemia, the ICP and MAP must ideally be maintained within normal limits. In healthy children, a normal ICP is typically less than 10-15 mmHg. In the head injured child, it is typical to aim to keep ICP below 20mmHg. The target MAP varies with age - but is typically kept >50-60mmHg. The goal is to achieve a CPP 40-50mmHg with infants within the lower range and adolescents in the higher range. [14] Given the concepts outlined above, the general management of traumatic brain injury focuses on minimising factors that contribute to raised intracranial pressure, cerebral edema and cerebral ischaemia. This is achieved by:
Initial management of head traumaPrimary surveyIn all aspects of trauma management the primary survey is the first priority. This should all take less than 1 minute . A Assess and ensure a patent airway, whilst maintaining C-spine immobilisation(see Airway management) B Assess and provide high-flow oxygen; Monitor oxygen saturation and respiratory rates.
(see Breathing management) C Assess adequacy of circulation
D Assess level of disability Maintain in-line cervical stabilisation at all times
AVPU Scale Use central stimuli – such as sternal pressure or pinching the trapezius
Glasgow Coma Scale
The primary survey can help guide initial management steps:
HistoryEnsure an AMPLE history has been taken (see How children are different). Also ensure to ask about the following:
Secondary surveyPerform a complete secondary survey. In all cases of head injury, pay particular attention to:
"Racoon eyes" A Racoon (see also Primary and secondary survey) Initial InvestigationsLaboratory studiesA general trauma panel is recommended including:
Imaging StudiesSkull X-RayInfants are more at risk of skull fractures than older children due to their thinner craniums. The presence or absence of a skull fracture however, does not always correlate with the severity of the underlying brain injury.
CT scanPerformance of the CT scan should only be undertaken when the patient is stable enough to be transferred to the CT scanner. They must be fully monitored and accompanied at all times. Indications for a CT head include:
There are a number of clinical decision tools to help determine the need for a head CT in children (PECARN, CATCH, CHALICE). All three tools are highly sensitive, have external validity and therefore Emergency Departments should consider instituting one tool into practice. [13] Indications for CT after the phase of initial presentation and assessment: (management directed by Consultant Neurosurgeon)
Other important considerations regarding CT and surgery
Forensic considerationsWhilst it should not interfere with emergency management documenting history and findings both descriptively and with photography and preserving clothing or other “evidence” appropriately can help the care of the child both in elucidating the nature of the mechanism particularly in the case of inflicted injury and non-verbal children. Extracranial InjuriesScalp InjuriesThe scalp, being highly vascularized, can be a source of significant bleeding. In young infants, scalp lacerations, in particular a subgaleal haematoma, can lead to haemorrhagic shock. [14] All wounds should be explored to check for underlying skull fractures. Skull FracturesSkull fractures are most common in the first year of life. They may occur in the presence or absence of external clinical signs - i.e a boggy haematoma, as these may take some time to develop. Types of skull fractures include:
It is important to evaluate children with skull fractures thoroughly and a CT scan should be included as part of the assessment. Most children should be routinely admitted for a period of observation. Where a child has injured their head, always remember to consider the potential for an associated cervical spine injury. Assess the cervical spine clinically and radiologically where indicated. (see cervical spine assessment) Management of extracranial injuriesCT scan is typically indicated in focal injuries. Discuss with neurosurgical team.
Intracranial injuriesMild traumatic brain injuries / concussion (GCS 13-15)Mild TBI and concussion are interchangeable terms. Sports concussion is a subtype of mild TBI. According to The WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury, mild TBI is defined as:
The Task Force also states the manifestations cannot be due to a penetrating head injury. [15] Others have restricted mild TBI to those with GCS 14-15 as patients with GCS 13 have a risk of intracranial lesion like those with moderate TBI. [16] In general, mild TBI does not result in in head CT or MRI changes. This finding however is not universally agreed upon and may change as new neuroimaging modalities are introduced. Management of mild TBI:The greatest risk to patients with apparent mild TBI is the delayed onset of an intracranial haematoma or brain swelling. Both are the most common causes of avoidable death in this subset of patients. The decision to perform a head CT or not in a child with apparent mild TBI is therefore critical. There are a number of clinical decision tools, with high sensitivity and external validity, to help determine the need for a head CT in children (PECARN, CATCH, CHALICE[KA1] /NICE).[13] (see Radiology). According to the 2014 National Institute for Health and Care Excellence (NICE) Guidelines (UK), factors that would prompt a head CT in children include: [17] Any one of:
Or, in the absence of any of the above, two or more of:
Observation, in hospital, for a minimum of four hours is advised where there is there is only one of the latter set of conditions. Home observation is another option for patients with normal mental status, normal neurological exam and the availability of a reliable adult parent/carer.[17] Of note, it can be difficult to have a reliable neurological exam in infants and a higher degree of suspicion is required. Prognosis of mild TBI: Typical course is resolution of confusion within 24 hours. Concussion results in an inflammatory state of the brain which is then vulnerable to second injury (second impact syndrome). Clear guidelines on rest, recovery, return to activity and return to risk activities must be given at discharge. Post-concussion symptoms are common. These include:
Some patients with mild TBI have persistent symptoms or develop neuropsychological deficits however it is difficult to predict in which patient group this occurs. A pre-morbid neuropsychiatric disorder is
strongly related to persistence of symptoms for 3 months or longer after injury. Patients with persistent symptoms for greater than 3 months may benefit from treatment guided by teams specialized in mild TBI/concussion. [15] Sports-related concussion: Post-concussion symptoms typically resolve within 7-10 days after a first concussion. [15] Patients should be counselled to have a gradual return to sport. Recommendations to families post discharge: See ‘Head Injury Handout’. (end of this chapter) Moderate traumatic brain injury (GCS 9-12)Clinical features can include:
Management of moderate TBI:Consult Neurosurgical team and consider CT scan if:
Most patients will initially rapidly recover from the effects of concussion within a 12-24 hour period. A delay or reversal of recovery suggests haemorrhage, cerebral oedema, or infection. Severe traumatic brain injury (GCS <8)Clinical features can include:
Management of severe TBIConsult neurosurgery and intensive care early. Manage as a multi-trauma patient. Goals of treatment are:
Specific management Optimise oxygenation
Optimise cerebral perfusion
Other strategies to minimise secondary injury
Imaging - Arrange urgent head CT. Management of post traumatic seizuresPost traumatic seizures are a common event following severe brain injuries. The incidence in this group (i.e. GCS <8) has been reported as between 19-39%. However, it is worth noting this risk increases further in those who are young (<2yrs), have a subdural haematoma, and those who have an inflicted injury.[18] The aggressive management and prevention of seizures in the head injured patient is required to prevent secondary brain injury. The mechanisms by which seizures worsen secondary brain injury include:[19]
Traditionally, post- traumatic seizures have been categorized into either:
However, it has been suggested that “early post-traumatic seizures” group can be further subdivided into the following groups[19]:
Risk factors for early post traumatic seizures include[19]:
Aggressive treatment of seizures is important to prevent secondary brain injury. Management includes the following:
Any early post traumatic seizure, apart from a brief (<2min) impact seizure, warrants investigation with imaging (CT or MRI brain).
Management of elevated ICPDetection of elevated ICP requires invasive monitoring – however, an acute rise in ICP can be inferred from certain clinical symptoms (described in the cerebral haemodynamics section above). Manage in consultation with neurosurgery and intensive care. Priority is to minimize ICP while awaiting surgical evaluation. In addition to the management strategies discussed above, additional therapies include: First tier therapies
Second tier therapies
Medical management may not be able to relieve elevated ICP secondary to a large haematoma or severe cerebral oedema. Emergent surgery may be required, so early consultation with neurosurgery is necessary. Localised brain injuryInjuries caused by a direct blow and confined to a focal area of the head. These injuries may cause:
Management Initial management is resuscitation, as for severe head injury (see skull fractures above).
Intracranial haemorrhageIntracranial haemorrhages will cause a rise in the ICP with the clinical features discussed above. It is essential that a neurosurgical consultation occurs as soon as possible, for advice on acute management and for definitive treatments, such as a surgical evacuation. Subdural haematomaThis is the most common type of intracranial bleed. It may occur at any age but often seen in infants. Subdural haematomas:
The CT scan above shows a subdural haematoma in the right hemisphere, associated with mass effect as evidenced by midline shift. Extradural haematomaExtradural haematomas are often associated with a skull fracture. The haematoma forms a mass and the patient may have an initial lucid period before a collapse. Typical, extradural haematomas:
Management requires urgent neurosurgical intervention with surgical evacuation of the haematoma and repair of any vessels.
The CT scan above shows an extradural haematoma overlying the right frontal lobe. Subarachnoid haemorrhageSubarachnoid haemorrhages are common in trauma. They arise as a consequence of tearing of the small vessels of the pia mater. The blood distributes within the subarachnoid space, rarely causing a mass effect and it may remain relatively focal. Subarachnoid haemorrhages are:
Cerebral contusionsThese occur from high-energy impact, when the cerebral cortex impacts against the sides of the fixed skull vault. The injuries occur at two points:
They are most likely to occur where the brain is less cushioned, i.e less CSF
Effects of cerebral contusions:
RCH head injury handoutRCH has two head injury handouts that can be given to caregivers and older children. The first covers general advice, and the second provides advice on graduated return to school and sport References and further reading
Which vital signs indicate increased pressure within the skull following head trauma?What are the symptoms of ICP?. Headache.. Blurred vision.. Feeling less alert than usual.. Vomiting.. Changes in your behavior.. Weakness or problems with moving or talking.. Lack of energy or sleepiness.. Which of the following is the result when blood accumulates between the brain and the dura mater?Blood accumulates between the dura and arachnoid maters i.e. below the dura mater resulting in a subdural haematoma. This is more common in older people as the brain shrinks with age making more room for movement within the skull.
Why does blood pressure increase with head injury?Causes of High Blood Pressure After Head Injury
The medulla can no longer detect signals from the baroreceptors telling it to dilate the arteries. Damage to the rest of the brain makes the brain stem think the body is in distress, causing it to raise blood pressure.
Which of the following signs and symptoms of increased ICP after head trauma would appear first?Which of the following signs and symptoms of increased ICP after head trauma would appear first? Question 20 Explanation: The earliest symptom of elevated ICP is a change in mental status. Bradycardia, widened pulse pressure, and bradypnea occur later.
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