Pediatric head trauma is a major public health issue that can cause long-term physical, cognitive, and behavioral impairments. Boys are at higher risk than girls generally until age 10. Children with moderate to severe head injuries have high rates of behavioral and cognitive problems. Management of pediatric head injuries differs from adults due to differences in epidemiology, injury types, and responses to injury. Intensive care focuses on controlling intracranial pressure and maintaining adequate cerebral perfusion pressure to prevent secondary brain injury.

1. Managment of pediatric head injury
Prepared by: Dr. Azad S. Hatam
KBMS Board Trainee
Shahid Doctor Aso Hosp.
Sulaimany/ Kurdistán
Supervised By Assisstant Prof. Dr. Ari Sami

2. BACKGROUND
Pediatric head trauma is an important public health issue with both high
mortality and lifelong physical, cognitive, behavioral, and social
implications.
The incidence of TBI is an overall male-to-female ratio of about 2:1
This gender difference does not start until after the age of 5; boys’
risk for TBI increases as they reach their teens, whereas girls’ risk
declines after the age of 10.
children with moderate (GCS score of 9 to 12) to severe (GCS score or
8 or less) head injuries are at significant risk for long-term problems
with behavior and cognition. 40% of children have a persistent
change in personality after severe head injury, and the incidence of
behavioral problems correlates with increasing severity of head
injury (36% in those with severe injury and 22% in those with
moderate injury).

3. Differences between adult and pediatric head injury
1. epidemiology:
A. children often have milder injuries than adults
B. lower chance of a surgical lesion in a comatose child
2. types of injury: injuries peculiar to pediatrics
A. birth injuries: skull fractures, cephalhematoma ,subdural or epidural hematomas, brachial
plexus injuries
B. perambulator/walker injuries
C. child abuse shaken baby syndrome ...
D. injuries from skateboarding, scooters ...
E. lawn darts
F. cephalhematoma:
G. leptomeningeal cysts,
3. response to injury
A. responses to head injury of older adolescent are very similar to adults
B. "malignant cerebral edema": acute onset of severe cerebral swelling (probably due to)
following some head injuries, especially in young children (may not be as common as previously
thought)
C. posttraumatic seizures: more likely to occur within the 1st 24 hrs in children than in adults

4. Classification of pediatric head injury
Cephalhematoma
Accumulation of blood under the scalp. Occur almost exclusively in children
1. subgaleal hematoma: may occur without bony trauma, or may be associated with
linear nondisplaced skull fracture (especially in age< 1 yr). Bleeding into loose
connective tissue separates galea from periosteum. May cross sutures. Usually starts
as a small localized hematoma, and may become huge (with significant loss of
circulating blood volume in age < 1 year, transfusion may be necessary).
Inexperienced clinicians may suspect CSF collection under the scalp which does not
occur. Usually presents as a soft, fluctuant mass. These do not calcify
2. subperiosteal hematoma (some refer to this as cephalhematoma): most commonly
seen in the newborn (associated with parturition, may also be associated with
neonatal scalp monitor . Bleeding elevates periosteum, extent is limited by sutures.
Firmer and less ballotable than subgaleal hematoma scalp moves freely over the
mass. 80% reabsorb, usually within 2-3 weeks. Occasionally may calcify

5. Skull Fractures
Skull fractures are very common in pediatric patients and are often very minor injuries
without associated brain injury.
They can be
- linear,
- comminuted
- diastatic along a suture line.
They can also be classified as either closed or open ( dura injury or brain laceration)
Depressed skull fractures occur in about 11% of patients with TBI, and basilar skull
fractures, which require more force than cranial vault fractures, are seen in 4% of all
patients with severe brain injuries.
basilar fractures may be an indication for some sort of vascular study, such as computed
tomography angiography or magnetic resonance angiography
Growing skull fractures are most commonly seen when the initial injury is in a child younger
than 2 years. Bilateral or multiple skull fractures should alert the provider to the
possibility of nonaccidental trauma (NAT)

6. Hematomas
Epidural Hematoma (EDH)
Accumulation of blood out side dura, it more common after age of 2 years commonly
caused by skull fractures often in the pterional point when middle meningeal artery
exists an cause rapid grow of the hematoma in 6-8 hours, or in 10% the source is
veounos bleeding that may present as delay epidural hematoma ( DEDH) usually
between 6- 15 days of truama
Classical presentation 10-27% ( lucid interval)
Unlike other head injuries, patients with poor GCS scores can have good outcomes
postoperatively if there is no major concomitant brain injury

7. Subdural hematomas (SDHs)
collections of blood in the subdural space caused by both direct brain injury and shearing
of small bridging veins that cross that space.
SDH results from rotational or linear shearing forces. When seen in infants, it should
raise concern for NAT, especially if retinal hemorrhages are also noted.
Acute SDH has a significantly higher mortality rate than EDH because there is a much
greater degree of associated brain Injury.

8. Differentiate between EDH and acute SDH
Five percent of Epidural hematoma has similar radiological feature to Acute
subdural hematoma but they can be differentiated by
1- diffuse subdural hematoma
2- less density of hematoma due to mixture with CSF
3- Cross the dural attachments
4- associated injuries

9. Subarachnoid hemorrhage (SAH)
is bleeding into the subarachnoid space between the arachnoid membrane and the pia
mater. Although often associated with aneurysms in adults, the most common cause
of SAH is trauma, and it can be seen in up to 60% of patients with TBI.
Intraventricular hemorrhage (IVH) has been found in 35% with
moderate to severe TBI and is usually associated with either intracerebral
hemorrhage, contusions, or SAH. As with SAH, hydrocephalus is a potential
complication after IVH.
Intracerebral hemorrhages or contusions occur within the
parenchyma itself and are caused by damage to the parenchymal vessels or
contusion of the tissue. The amount of neurological deficit associated with these
injuries can vary widely depending on the location and associated edema.

10. Diffuse Axonal Injury
Diffuse axonal injury (DAI) is a diffuse injury to the white matter caused
by severe rotational or deceleration forces that shear the white
matter tracts. Two thirds of DAI occur at the gray-white matter
junction.
DAI is difficult to detect on computed tomography (CT), but small
hemorrhages in the corpus callosum or scattered diffusely in the
hemispheres are an indication. Magnetic resonance imaging (MRI)
can reliably show the classic findings of DAI

11. MANAGEMENT OF TRAUMATIC BRAIN INJURY
Prehospital Management
Oxygenation through bag-valve mask ventilation or endotracheal intubation, it is
essential to prevent hypoxemia in the Prehospital setting
blood pressure ( fluid challenge)
pupil examination
GCS

13. Oxygenation
Hypoxemia has been shown to have a significant impact on the survival and
outcome of patients with TBI.
worsening outcomes and mortality being associated with worsening hypoxemia
at an arterial oxygen saturation (Sao2) of greater than 90%
(mortality,14.3%), 60% to 90% (mortality, 27.3%), and less than 60%
(mortality, 50%)
Another consideration in Prehospital management of the airway is prevention of
significant hypocapnia or hypercapnia. Physiologically, there are clear links
between Pco2 and cerebral blood flow (CBF), and currently, it is thought
best to maintain normocapnia because in pediatric TBI its associated with
secondary brain injury and further brain ischemia

14. Fluid challenge
Hypertonic saline
Albumin
Normale saline
Ringers lactate
The Saline versus Albumin Fluid Evaluation (SAFE) study compared normal saline and
albumin for resuscitation and found significantly worse outcomes in patients who
received albumin
Hypertonic saline compared with normal saline for the Prehospital treatment of
hypotension and found an initial survival advantage with hypertonic saline but no
significant difference in long-term survival
hypertonic saline versus lactated Ringer’s solution and found no difference in survival or
outcome

15. The primary goals of prehospital treatment are to prevent
hypoxia and hypotension en route to an appropriate
trauma facility. A mortality rate of 55% can occur if
hypoxia, hypotension, or hypercapnia is present in the
setting of severe TBI; the rate is reduced to just 7.7%
when none of these risk factors are present

16. RESUSCITAION
A IRWA
B REATHING
C IRCULATION
D IABETIC & DRUG
E PILEPSY
F EVER
G CS
H ERNIATION
I NVESTIAGTION

17. Clinical and Radiographic Examination
Clinical examination can be unreliable in patients with TBI as 33% of
the patients with abnormal head CT findings had normal results on
neuro logical examination
Therefore, almost all children who have sustained a significant injury or
are suspected of having TBI should undergo imaging
the initial GCS score and pupil response have been significantly
correlated with long-term outcomes. If a child is initially seen with
bilateral fixed and dilated pupils, multiple studies have shown 100%
mortality

18. Intensive Care Unit Management
Guidelines for Management of Intracranial Pressure and Cerebral
Perfusion Pressure
AIM : Lowering ICP and maximizing cerebral perfusion pressure (CPP)
Association of persistently elevated ICP (usually ICP > 20 mm Hg) with
poor outcome or increased mortality (or both) in comparison to patients with well-
controlled ICP.
modalities to control ICP, including early decompressive craniectomy, hypertonic saline,
barbiturates, and hyperventilation
The presence of an open fontanelle or sutures does not preclude the development of
intracranial hypertension, and the fontanelle should not be used as a guideline by
which to judge ICP.
cerebral perfusion pressure (CPP)s it’s a the difference between mean arterial pressure
and intracranial pressure and it is more outstanding than ICP
the CPP must be maintained above 40 mm Hg and no patient survived with CCP below
40 mm Hg

19. Hyperventilation
it has been found that hyperemia is less common in pediatric TBI
patients than formerly believed, which has led to concern that
hyperventilation could lead to worse outcomes by depriving the
brain of needed blood flow
prophylactic hyperventilation (Paco2 < 35 mm Hg) should be avoided
but that mild hyperventilation (Paco2 of 30 to 35 mm Hg) may be
considered as a treatment option for patients with elevated ICP
refractory to other treatments, including sedation, hyperosmolar
therapy, and CSF diversion

20. Sedation and Barbiturates
Both sedation and analgesia, as well as barbiturates, have been used to control
elevated ICP
Some data suggest that sedation can decrease secondary damage by reducing
metabolic demand, especially since routine ICU care such as suctioning has
been shown to increase ICP and decrease cerebral oxygenation
The benefits of barbiturates suppression of metabolism, alter vascular tone to
improve the blood supply to brain regions that need it most, and provide
neuroprotection both through inhibition of lipid peroxidation and membrane
stabilization

21. Intracranial Pressure Monitoring Technology
There are three major groups of monitors:
1- ventricular catheters,
2- parenchymal fiberoptic transducer
3- subarachnoid, subdural, or epidural monitors
In infants there are also fontanometry (less accurate) or aplanation principle
The decision of which monitor to use incorporates accuracy, safety, reliability,
and cost.
They to be used for relatively short durations of 7 days or less
Complications (hematoma, infection, mal function and malposition)
Conversion factors
1 mm Hg = 1.36 cm H2O
1 cm H2O = 0.735 mm Hg

22. Decompressive Craniectomy
It is important
to realize that decompressive craniectomy is really only effective
when done before severe secondary brain injury occurs. If malignant
intracranial hypertension has existed for a long period and
the brain has suffered diffuse bilateral hemispheric injury

23. Nutrition
TBI patients found that they had
180% resting oxygen consumption and 130% to 173% resting
energy expenditure
patients who
did not receive nutrition until day 5 or 7 after injury had a twofold
and fourfold increased risk for death, respectively
Hyperglycemia has been correlated with worse outcomes in
many studies.

24. Seizure Prophylaxis
Posttraumatic epilepsy is reported to have developed in 15% of patients with severe TBI,
and the prophylactic use of antiseizure medication has been shown to improve
Survival
One third of TBI patients have seizures within the first 3 to 4 months, and two thirds have
had seizures by 2 years, with anywhere from 58% to 95% of pediatric patients
reported as having a seizure within the first 24 hours after injury
the risk for seizures: depressed skull fractures, SDH, an early (provoked) seizure, or
severe head injury, with posttraumatic epilepsy developing in 20% to 35% of this
patient population.
The current pediatric guidelines recommend a 7-day course of prophylactic antiepileptic
after head injury to decrease the risk for early seizures

25. Steroids
not recommend the use of steroids in patients with TBI because of the
lack of evidence supporting improved outcome with steroid use