SEVERE PEDIATRIC TRAUMATIC BRAIN INJURY by sammyc2007

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									SEVERE PEDIATRIC TRAUMATIC
BRAIN INJURY – PATHOPHYSIOLOGY
& GUIDELINES FOR THE ACUTE
MEDICAL MANAGEMENT

Michael Halberthal, MD           Ido Yatsiv, MD
Pediatric Critical Care Unit     Pediatric CCM
Meyer – Children’s Hospital      Hadassah University Hospitals
Rambam Medical Center            Jerusalem
Haifa
Based in part on the Society of CCM’s June 2003 Guidelines and on
the www.picucourse.org website
              EPIDEMIOLOGY


•   200 per 100,000 children per year
•   Mild (GCS > 12) 82%
•   Moderate to severe (GCS <12) 14%
•   Fatal 5%, 7000 deaths per year (1987)
•   200,000 children hospitalized/year
•   1-2 % of all ED presentations in children
                EPIDEMIOLOGY


• Children with severe head injuries have a lower
  rate of mass lesions requiring intervention than
  adults (25 vs 46%).
• Even those with low GCS generally survive and
  achieve social rehabilitation.
   – (Lieh-Lai, 1992) GCS 3-5, 55% “satisfactory”
   – (Bruce 1978) GCS 3-4, 80% good recovery or
     moderate disability
 HOW DO PATIENTS PRESENT ?

• Obvious--motor vehicle accident, car vs
  pedestrian, fall from height, etc
• Less obvious--sports injuries (football),
  delayed deterioration (epidural)
• Hidden--shaken baby syndrome, older
  child maltreatment
    CAVEATS IN BRAIN INJURY

• Neurologic examination - the most
  important information you have
• Accurate history is often unavailable or
  inaccurate
• Potential for associated injuries or
  illness (cardiovascular, respiratory,
  cervical spine)
   CEREBRAL RESUSCITATION

• Primary survey - airway, breathing, and
  circulation
• Neurologic evaluation
• Secondary survey - “head to toe”
• Neuroradiologic evaluation
• Ongoing evaluation and transport
MECHANISMS OF INJURY-PRIMARY

• Impact: epidural, subdural, contusion,
  intracerebral hemorrhage, skull
  fractures
• Inertial: concussion, diffuse axonal
  injury
• Hypoxic\ Ischemic
   MECHANISMS OF 2nd INJURY

• Global
  – Hypoxia and ischemia of brain
  – Decreased cerebral blood flow due to
    increased intracranial pressure
• Local
  – impairment of cerebral blood flow or extra
    cellular milieu due to the presence of
    injured brain
        PATHOPHYSIOLOGY

• Primary damage – the only treatment is
  by prevention.
• Secondary damage – multifactorial and
  time dependent.
SOME of the SECONDARY EVENTS IN TRAUMATIC BRAIN INJURY

                                             diffuse axonal
     BBB                        inflammation      injury
  disruption                                                                    apoptosis

                                                                                necrosis
        edema
       formation
                                              Brain trauma                      ischemia

                                                                          energy failure
 cytokines

Eicosanoids
                                      Acetyl                       polyamines     Calcium
endocannabinoids                      Choline         ROS
                                                                                Shohami, 2000
Green – pathophysiological processes; Yellow – various mediators
Dynamic Changes Following Stroke/Trauma
                  Hours          Days            Weeks / Months
                                              Weeks/Mont
          2           8 hrs       7        14         hs
           Ca , Na+
         Glut, ROS
     I
     N         Necrosis Apoptosis
     J
     U                Inflammation
     R                          Repair
                              Remodeling
     Y

                                                Plasticity
                                               Functional
                                               Recovery



                                           Barone &Feuerstein JCBF, 1999
        MONRO-KELLIE DOCTRINE
Vintracranial vault=Vbrain+Vblood +Vcsf
        BRAIN: CEREBRAL EDEMA-VASOGENIC
(Caused mainly by activation of NMDA receptors by glutamate)
      BRAIN: CEREBRAL EDEMA-CYTOTOXIC
(Caused mainly by activation of cytokines, ROS and other
            pro-inflammatory mediators)
BLOOD: CEREBRAL BLOOD FLOW

             o The brain has the ability
               to control its blood
               supply to match its
               metabolic requirements
             o Chemical or metabolic
               byproducts of cerebral
               metabolism can alter
               blood vessel caliber and
               behavior
BLOOD: CEREBRAL BLOOD FLOW
         (VOLUME)
• Increases in cerebral metabolic rate
  – Hyperthermia
  – Seizures
  – Pain, anxiety
   CSF: CEREBROSPINAL FLUID

• 10% of intracranial volume
• Initial displacement of CSF from
  ventricles
• Ventriculostomy to drain CSF
Free at www.pccmjournal.com
GUIDELINES – GENERAL ASPECTS
• 18 key topics
   – There are insufficient data to support treatment
     standards for any of the key topics
• Medline search 1966-2001 for pediatric
  studies / data, if no data  adult guidelines
   GUIDELINES – GENERAL ASPECTS

• Standards: accepted principles of patient
  management that reflect a high degree of
  clinical certainty
• Guidelines: strategies that reflect moderate
  clinical certainty
• Options: unclear clinical certainty
 EBM - CLASSIFICATION of EVIDENCE

• Classification in Evidence Based Medicine:
 Class I – Randomized Controlled Trials
  (RCT) = THE GOLD STANDARD.
 Class II – Data collected prospectively
  (better) or retrospectively (based on reliable
  carefully selected data).
 Class III – Most of the retrospective studies.
  Includes series, database data, case reviews
  and “expert opinion”.
TRAUMA SYSTEMS, PEDIATRIC TRAUMA CENTERS, AND THE
   NEUROSURGEON – LET’S AGREE ON VOCABULARY


• Pediatric STBI – severe traumatic brain injury.
• PTC – Pediatric trauma center:
• PTCs in Israel: Rambam (Haifa), Sheba / Ichilov /
  Rabin (not Schneider) [all in Tel Aviv], Hadassah EK
  (Jerusalem), Soroka (Beer Sheba).
• ATC AQ – Adult trauma center with added
  qualifications for treating children.
• ATC - Adult trauma center
• S – standards; G – guidelines; O - Options
.

Johnson DL, Krishnamurthy S. Send severely head-injured
children to a pediatric trauma center. Pediatric Neurosurg. 1996
Dec;25(6):309-14

    •   Between 1985 and 1988, a total of 1,320 head-injured children were seen by the
        neurosurgical service at the Children's Hospital in Washington, D.C. (CHOW).
        This included 1,095 minor injuries, 127 moderate injuries, and 98 severe
        injuries. Children brought from the scene of an accident were considered direct
        transports, whereas those taken to another hospital prior to transfer to CHOW
        were indirect. Of the children that suffered severe head injuries, 56 were
        admitted directly to the hospital and 42 indirectly. The indirect group had a
        higher percentage of children with lower coma scores and abused children. The
        trauma score was significantly higher in the direct group (9 vs. 7). The mortality
        rate for severe injuries referred directly from the scene of the accident was
        26.8%, and the mortality rate for children referred indirectly was 50.0%. The
        higher number of abused children in the indirect group did not account for the
        increase in mortality rate (p = 0.021) in this group. This is the first study to
        show that children brought directly from the scene of an accident to a
        well-established pediatric trauma center have a significantly better chance
        of survival than children transported first to the nearest available hospital.
 CH. 2: TRAUMA SYSTEMS, PEDIATRIC TRAUMA
     CENTERS, AND THE NEUROSURGEON

• In a metropolitan area, pediatric patients with
  STBI should be transported directly to a PTC 
  better outcome. Mort. D 1.9% Vs. ID 4.7%
  PTC / ATCAQ > ATC I / II (G)
• Recent research suggests that survival in
  certain subgroups may not be improved (e.g-
  rural areas, transfer time increased after the
  trauma system was established, not stable)
CH. 3 - PREHOSPITAL AIRWAY MANAGEMENT

• Hypoxia must be avoided, and correct
  immediately (G). 13%-27% O2
• Supplemental oxygen should be administered
• No advantage of ETI (ET intubation) Vs. BVM
  (Bag / valve / mask) ventilation for the pre-
  hospital airway in pediatric TBI
  420 TBI; 115 BVM; 177 ETIno change (Gausche,
  JAMA 2000)
• TBI + ETI  ETCO2
CH. 4 - RESUSCITATION OF BP AND O2 AND PREHOSPITAL
        BRAIN-SPECIFIC TX’S FOR SPTBI PATIENTS


 • Hypotension should be identified and corrected
   as rapidly as possible with fluid resuscitation.
   (G)
 • Hypotension on arrival to ER (Pigula, J Ped Surg 1993)
   18% ER: mortality 61% Vs. 22%, ↓BP+↓O2 –
   mortality  85% !
 • Levine (Neurosurg 1992): TBI 0-4y ↓BP – 32% poor
   outcome.
 • Laurssen (J Neurosurg 1988):↑BP ↓EX; White (CCM
   2001): syst BP > 135  X19 in survival !
          BLOOD PRESSURE

• In children, hypotension is defined as
  systolic blood pressure below the fifth
  percentile for age or by clinical signs of
  shock.
• Tables depicting normal values for
  pediatric blood pressure by age are
  available (Horan MJ, pediatrics
  1987;79:1).
         BLOOD PRESSURE

• The lower limit of systolic blood
  pressure (5th percentile) for age may be
  estimated by the formula:
      70 mm hg + (2 × age in years)
• Evaluation for associated extra cranial
  injuries is indicated in the setting of
  hypotension.
   PREHOSPITAL TREATMENTS

• No evidence of efficacy: sedation, NMB,
  Mannitol, saline 3%, hyperventilation.
• The prophylactic administration of
  mannitol is not recommended.
• Mannitol may be considered for use in
  euvolemic patients who show signs of
  cerebral herniation or acute neurological
  deterioration.
   PREHOSPITAL TREATMENTS

• Mild prophylactic hyperventilation is not
  recommended.
• Hyperventilation may be considered in
  patients who show signs of
  – Imminent cerebral herniation or
  – acute neurological deterioration
• After correcting hypotension or hypoxemia
CH. 5 - INDICATIONS FOR ICP MONITORING IN
  PEDIATRIC PATIENTS WITH SEVERE TBI

• ↑ICP ≡↓Outcome; Aggressive Tx ≡↑Outcome
• Intra-cranial pressure monitoring (ICP) is
  appropriate in infants and children with severe
  traumatic brain injury (TBI) (Glasgow Coma
  [GCS] score ≤8) (O).
• The presence of open fontanels and/or sutures
  in an infant with severe TBI does not preclude
  the development of intracranial hypertension or
  negate the utility of ICP monitoring.
 INTRACRANIAL PRESSURE MONITORING


• STBI (GCS≤8) + Abnormal CT ≡ 53-63% ↑ICP
  (adult data).
• Intra-cranial pressure monitoring is not routinely
  indicated in infants and children with mild or
  moderate head injury.
• However, a physician may choose to monitor
  ICP in certain conscious patients with
   – traumatic mass lesions or
   – serial neurological examination is precluded by
     sedation, neuromuscular blockade, or anesthesia.
    CH. 6 - THRESHOLD FOR TREATMENT OF
         INTRA-CRANIAL HYPERTENSION

• ICP>20-40mmHg ≡ Mort. 28%; ICP>40mmHg ≡ 100%
• Treatment for intracranial hypertension, defined as a
  pathologic elevation in intracranial pressure (ICP), should
  begin at an ICP ≥20 mm Hg. (O)
• Patients may herniate at ICP < 20-25mmHg.
• Is there a lower ICP threshold for younger children ?
• Interpretation and treatment of ↑ICP based on any ICP
  threshold should be corroborated by frequent
   – clinical examination
   – monitoring of physiologic variables (CPP, Compliance)
   – cranial imaging.
       Ch. 7 - INTRACRANIAL PRESSURE
         MONITORING TECHNOLOGY



• ICP monitoring: a ventricular catheter; external
  strain gauge transducer (??); catheter tip pressure
  transducer device  All accurate & reliable (O)
• Ventricular cath. device most accurate, reliable,
  low cost + enables therapeutic (CSF) drainage.
• No report of meningitis  ICP monitoring.
  Jensen: 7% tip; positive > 7.5 days
ICP Monitoring
       CH. 8 - CEREBRAL PERFUSION
               PRESSURE (CPP)
• A cerebral perfusion pressure (CPP) >40 mm
  Hg in children with traumatic brain injury (TBI)
  should be maintained (G)
   CEREBRAL PERFUSION PRESSURE

• A CPP between 40 and 65 mm Hg probably
  represents an age-related continuum for the
  optimal treatment threshold. (O)
• There may be exceptions to this range in some
  infants and neonates.
• Advanced cerebral physiologic monitoring may
  be useful to define the optimal CPP in individual
  instances.
• Hypotension should be avoided.
CH. 9 – THE USE OF SEDATION AND NEUROMUSCULAR
         BLOCKADE IN TX OF PEDIATRIC STBI


 • In the absence of outcome data, the choice
   and dosing of sedatives, analgesics, and
   neuromuscular blocking agents should be left
   to the treating physician.
 • However, the effect of individual sedatives
   and analgesics on ICP in infants and children
   with severe TBI can be variable and
   unpredictable
CH. 10 - THE ROLE OF CSF DRAINAGE IN THE TX OF
                 PEDIATRIC STBI




• Cerebrospinal fluid (CSF) drainage can
  be considered as an option in the
  management of elevated ICP in children
  with severe closed head injury (O)
• Drainage: Ventriculostomy ± Lumber
  puncture.
CSF Drainage
   CH. 11 - USE OF HYPEROSMOLAR THERAPY IN THE
            MANAGEMENT OF PEDIATRIC STBI

• Mannitol (2 X Class III) Vs. Hypertonic Saline (3 X Class II;
  1 X Class III). (O)

• Mannitol is effective.
• Euvolemia + Folly catheter
• Accepted osmolarity: Mannitol < 320mOsm/L;
  Hyper NS < 360mOsm/L
• Mannitol blood viscosity  arteriolar diameter
  and  osmotic effect.
• Hyper NS  Osmolar grad; membrane pot.;
  cellular volume; ANP; Inflammation; C.O.
         HYPEROSMOLAR THERAPY



• Hypertonic saline is effective for control of
  increased ICP after severe head injury
• Effective doses: cont. infusion of 3% saline
  0.1 - 1.0 ml/kg/h, a sliding scale.
• Goal minimum dose maintain ICP <20
  mmHg.
• Mannitol bolus dose: 0.25g/Kg – 1g/Kg.
    CH. 12 - USE OF HYPERVENTILATION in the
    ACUTE MANAGEMENT of PEDIATRIC STBI

• Mild or prophylactic hyperventilation (paco2 <35
  mm hg) in children should be avoided.
• Mild hyperventilation (paco2 30-35 mm hg) may
  be considered for longer periods for intra-
  cranial hypertension refractory to
  – Sedation and analgesia
  – Neuromuscular blockade
  – Cerebrospinal fluid drainage
  – hyperosmolar therapy
           HYPERVENTILATION

• Aggressive hyperventilation (Paco2 < 30 mm Hg)
  may be considered as a second tier option in the
  setting of refractory hypertension (O).
• Cerebral blood flow (CBF), jugular venous oxygen
  saturation, or brain tissue oxygen monitoring is
  suggested to help identify cerebral ischemia in this
  setting.
• Aggressive hyperventilation therapy titrated to
  clinical effect may be necessary for BRIEF
  PERIODS in cases of cerebral herniation or
  acute neurologic deterioration.
              Hyperventilation




Freq. regional ischemia {CBF<18ml/100gr/min}
Normocapnia - 28.9%; paCO2<25mmHg – 73%
 CH. 13 - THE USE of BARBITURATES in the CONTROL of
   INTRA-CRANIAL HYPERTENSION in PEDIATRIC STBI


• High-dose barbiturate therapy may be considered
  in hemodynamically stable patients with
  salvageable severe head injury and refractory
  intracranial hypertension.

• If high-dose barbiturate therapy is used, then
  appropriate hemodynamic monitoring (CVP, Swan-
  Ganz, repeated ECHOs) and cardiovascular
  support (Dopamine, Adrenaline) are essential.
CH. 13 - THE USE of BARBITURATES in the CONTROL of
 INTRA-CRANIAL HYPERTENSION in PEDIATRIC STBI


  • Gold standard – continuous EEG to
    achieve a state of burst suppression.
  • Serum barbiturate levels are NOT GOOD
    for monitoring that therapy.
  • Prophylactic therapy is not recommended
    (side effects).
  CH. 14 - THE ROLE OF TEMPERATURE CONTROL
            FOLLOWING PEDIATRIC STBI


• Extrapolated from the adult data,
  hyperthermia should be avoided in children
  with severe traumatic brain injury (TBI) (O).
• Despite the lack of clinical data in children,
  hypothermia may be considered in the
  setting of refractory intracranial
  hypertension
 Ch. 15 - SURGICAL TREATMENT OF PEDIATRIC

        INTRA-CRANIAL HYPERTENSION


Decompressive craniectomy should be
 considered in pediatric patients with severe
 TBI, diffuse cerebral swelling, and intra-
 cranial hypertension refractory to
  – intensive medical management, or
  – infants and young children with abusive head
    trauma, or
  – who have a potentially recoverable brain injury.
   DECOMPRESSIVE CRANIECTOMY

• Decompressive craniectomy appears to be less
  effective in patients who have experienced
  extensive secondary brain insults
• Patients who experience
  – Secondary deterioration on the Glasgow coma scale
    (GCS) and/or evolving cerebral herniation syndrome
    within the first 48 hrs after injury may represent a
    favorable group
  – Unimproved GCS of 3 may represent an unfavorable
    group
DECOMPRESSIVE CRANIECTOMY
CH. 16 - THE USE OF CORTICOSTEROIDS IN THE
    TREATMENT OF SEVERE PEDIATRIC TBI



• With the lack of sufficient evidence for
  beneficial effect and the potential for
  increased complications and suppression
  of adrenal production of cortisol, the routine
  use of steroids is not recommended for
  children following severe traumatic brain
  injury.
     CH. 18 - NUTRITIONAL SUPPORT

• Replace 130-160% of resting metabolism
  expenditure after TBI in pediatric patients.
  Weight-specific resting metabolic
  expenditure guidelines can be found in
  Talbot's tables.
• Based on the adult guidelines, nutritional
  support should
  – begin by 72 hrs
  – with full replacement by 7 days.
Ch. 18 - NUTRITIONAL SUPPORT
      Ch. 19 - THE ROLE of ANTI-SEIZURE
   PROPHYLAXIS FOLLOWING PEDIATRIC STBI



• Prophylactic anti-seizure therapy may
  be considered as a treatment option to
  prevent early PTS in young pediatric
  patients and infants at high risk for
  seizures following head injury.
ANTI-SEIZURE PROPHYLAXIS
Critical Pathway for the
Treatment of Established
      Intracranial
      Hypertension
Thank You

								
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