Pediatric Brain Injury Key considerations to ensure best outcomes. S de Ribaupierre Pediatric Neurosurgeon Talk Trauma London 2010

Transcription

1 Pediatric Brain Injury Key considerations to ensure best outcomes S de Ribaupierre Pediatric Neurosurgeon Talk Trauma London 2010

2 Objectives Pediatric TBI the difference with adult TBI Etiology / Mechanism Pathology 2 categories: Severe TBI and concussion Severe TBI: On-site Emergency department In hospital Concussion Return to sports, avoid catastrophes

3 Most common: MVA Epidemiology Pediatric head injury incidence <15 yo: 2/ yo:3.4/1000 Neurological injuries account for 18% of all pediatric injuries and 23% of traumatic deaths Except for <4yo with combination of non-accidental injury and falls 10% is a severe TBI Leading to 50% mortality

4 Pediatric vs adult Large head, thinner bones Less myelinated brain -> more vulnerable Higher incidence of raised ICP in children (8-% vs 50%) Diffuse TBI is the most common Brain vs body New born: 12.5% 6 mo: 10% 5 yo: 7.5% 10 yo: 4% Adult: 2%

5 Pediatric range Change in cerebral metabolic rate with aging Increased metabolic rate in children Oxygen 5.8ml/100mg (vs 3.5ml/100mg) Glucose 6.8ml/100mg (vs 5.5ml/100mg) Variation of Cerebral Blood Flow with age ICP Infants: 2-4mmHg Older children and adults: 5-15mmHg

6 Avoid

7 Pathophysiology Primary lesion Other factors Secondary lesion Herniation Intracranial hypertension

8 Children more prone to secondary insults than adults

9 Initial management (on-site) ABCs Initial assessment Modified GCS Cervical spine immobilization 60-80% of spinal injuries are cervical in children vs 30-40% in adults Airway management GCS<9 require airway protection, but NO evidence of advantage of prehospital tracheal intubation vs bag-mask ventilation Intravenous access Children can become hypovolemic from a scalp or an isolated brain injury Isotonic crystalloids (colloid controversial adult study showing worse outcome) ICP control If signs of raised ICP -> Mannitol or 3%

10 In the emergency department Stabilize the patient Monitoring Blood pressure iv fluids ICP (clinically) Imaging

11 In hospital ABC s and supportive therapy. Controlling Blood pressure (CPP > 40-50mmHg, if no ICP monitor, keep SBP >5 th percentile for age) Glycemia (controversial threshold varies from institutions, but studies showing worse outcome in patients with glycemia >200mg/dl) Hyperthermia No advantage (controversial Cochrane study showed benefit, Hutchison worse outcome) of hypothermia, but normothermia 37 C (Cool Kids study underway) ICP: Depending of GCS and CT-scan

12 ICP monitoring Criteria not as well defined as in adults Study in UK: only 60% of severe TBI have ICP monitoring Less in toddlers and infants Threshold for treatment? Most keep >20mmHg as target Monitor CPP or ICP?

13 Management Hyperventilate only for signs of impending herniation (moderate 30-35mmHg). Mannitol (0.5 1 g/kg) or 3% NaCl (3 cc/kg) intravenously. Patient may require neuromuscular blockade and paralysis. Goal to keep intracranial pressure below 20mmHg. Intracranial pressure monitoring will help guide ICP management. Decompressive craniectomy

14 Outcome from head injury related to age Luerssen, J Neurosurg 68:409, 1988 prospective analysis of 8814 head injured patients 1906 pediatric patients (14 years or less) Decrease mortality for every equivalent GCS motor score, for equivalent pupillary abnormalities, for associated injuries, for hypotension fewer mass lesions different mechanisms 60% of children with EDHs obey commands vs. 30% adults (4% childhood mortality vs 21% adult) SDH mortality 40% in children and adults

15 Pediatric Sport Related Injury

16 Concussion Definition: Caused by a direct blow to the head or body with an impulsive force transmitted to the head Rapid onset of short-lived neurological impairment resolving spontaneously Symptoms reflect a functional disturbance rather than a structural injury Postconcussion symptoms might be prolonged No imaging abnormality No need for LOC

17 Different theories -concussion Vascular Reticular Centriped Cholinergic (pontine) Convulsive Shaw N, Progr Neurobiol 2002, 67:

18 Convulsive theory

19 On the field Medical evaluation onsite (! cervical spine injury) If no healthcare provider is available, the player should be safely removed from practice or play and referral to a physician arranged. Assessment of the concussive injury should be made using the SCAT2 or other similar tool. Don t leave the injured alone and serial monitoring for deterioration is essential over the initial few hours following injury. If there is a diagnosed concussion: no return to play on the day of injury

20 Post-concussive syndrome: Headaches, dizziness, nausea, fatigue, poor balance. Anxiety, depression. Impaired memory, poor concentration, slow processing. Second impact syndrome: Second (even trivial) head injury during the postconcussive symptomatic period which causes increased morbidity / mortality

21 Second impact syndrome Malignant brain oedema 2 nd minor brain trauma occuring during recovery period after the 1 st trauma Morbidity 100%, mortality 50% Males McCrory et al., Neurology 1998, 50:

22 Second impact syndrome Loss of autoregulation

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24 Return to play (steps of 24h each) McCrory P, Meeuwisse W, et al: Consensus Statement on Concussion in Sport. Clin J Sport Med 2009: 19:

25 Return to play Wait until all symptoms have resolved(at rest and with exertion) Progressive return to play (practice then games) CT- abnormalities (such as contusion): Out for the season, consider stopping contact sports - 6 months: no contact sports If permanent neurologicaldeficit, diffuse axonal injury or hematoma requiring surgery: No more contact sports Neuropsychological testing may be helpful.

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27 Pediatric ImPACT test

28 in General

29 CLINICAL PEARLS: DO Perform quick neurological exam after ABCs. Children are not small adults Sudden bradycardia in awake patient may precede herniation Isolated head injuries can lead to low BP or anemia In moderate and severe TBI long term follow-up is important since there might be some development delay, and neuropsychological

30 CLINICAL PEARLS: DON T Sedate and paralyze before quick neurological assessment Treat increased intracranial pressure at the expense of ABCs Remove a penetrating object without prior imaging Hesitate to involve neurosurgery if needed Send a player back on the field after a concussion

31 Future Biomarkers Vascular cell adhesion molecule, IL-6, IL-12, intracellular adhesion molecule, TNF-2, fibrinogen, matrix metallopeptidase 9, hepatocyte growth factor, Neuronal Specific Enoslase, S100B, myelin basic protein

32 Ca homeostasis Excitotoxic cell death Calcium overload => mitochondrial swelling, opening of membrane permeability pores and release of factors active in programmed cell death