Management of pediatric head injury

Managment of pediatric head injury

Prepared by: Dr. Azad S. Hatam KBMS Board TraineeShahid Doctor Aso Hosp.Sulaimany/ Kurdistán Supervised By Assisstant Prof. Dr. Ari Sami

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).

Differences between adult and pediatric head injury

1. epidemiology: A. children often have milder injuries than adultsB. lower chance of a surgical lesion in a comatose child

2. types of injury: injuries peculiar to pediatricsA. birth injuries: skull fractures, cephalhematoma ,subdural or epidural hematomas, brachial plexus injuriesB. perambulator/walker injuriesC. child abuse shaken baby syndrome ...D. injuries from skateboarding, scooters ...E. lawn dartsF. cephalhematoma:G. leptomeningeal cysts,

3. response to injuryA. responses to head injury of older adolescent are very similar to adultsB. "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

Classification of pediatric head injury

CephalhematomaAccumulation of blood under the scalp. Occur almost exclusively in children1. 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

Skull FracturesSkull 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)

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

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.

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 hematoma2- less density of hematoma due to mixture with CSF 3- Cross the dural attachments4- associated injuries

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.

Diffuse Axonal InjuryDiffuse 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

MANAGEMENT OF TRAUMATIC BRAIN INJURY

Prehospital ManagementOxygenation through bag-valve mask ventilation or endotracheal intubation, it is

essential to prevent hypoxemia in the Prehospital settingblood pressure ( fluid challenge) pupil examinationGCS

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

Fluid challengeHypertonic salineAlbumin Normale salineRingers 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

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

RESUSCITAION A IRWAB REATHING C IRCULATION D IABETIC & DRUG E PILEPSY F EVERG CSH ERNIATION I NVESTIAGTION

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

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 hyperventilationThe 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

Hyperventilationit 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

Sedation and BarbituratesBoth sedation and analgesia, as well as barbiturates, have been used to control

elevated ICPSome 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

Intracranial Pressure Monitoring Technology

There are three major groups of monitors: 1- ventricular catheters, 2- parenchymal fiberoptic transducer3- subarachnoid, subdural, or epidural monitors

In infants there are also fontanometry (less accurate) or aplanation principleThe decision of which monitor to use incorporates accuracy, safety, reliability,

and cost.They to be used for relatively short durations of 7 days or lessComplications (hematoma, infection, mal function and malposition)

Conversion factors 1 mm Hg = 1.36 cm H2O 1 cm H2O = 0.735 mm Hg

Decompressive Craniectomy

It is importantto realize that decompressive craniectomy is really only effectivewhen done before severe secondary brain injury occurs. If malignantintracranial hypertension has existed for a long period andthe brain has suffered diffuse bilateral hemispheric injury

Nutrition TBI patients found that they had180% resting oxygen consumption and 130% to 173% restingenergy expenditurepatients whodid not receive nutrition until day 5 or 7 after injury had a twofoldand fourfold increased risk for death, respectively Hyperglycemia has been correlated with worse outcomes inmany studies.

Seizure ProphylaxisPosttraumatic 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

Steroidsnot recommend the use of steroids in patients with TBI because of the

lack of evidence supporting improved outcome with steroid use