Transcript 2012 Trauma in PICU - Emory University Department of Pediatrics

TRAUMA IN THE PICU
Pediatric Critical Care Medicine
Emory University
Children’s Healthcare of Atlanta
Epidemiology
• #1 cause of death in > 1yr old
• Exceeds all other deaths combined
• 20,000/yr of children & teenagers
» 65% of all death <19 yrs old – unintentional injury
• 1 death from trauma  40 hospitalized  1,120 treated in ER
• Most pediatric trauma are blunt injury (vs penetrating in
adults)
– More vulnerable to major abdominal injury from minor forces
– More immature musculoskeletal system
– Intra-abdominal organs are proportionally larger & closer together 
predisposed to multiple organ injury
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Epidemiology
• MVC – leading cause of death
– ½ are unrestrained
– 2/3 riding with drunk drivers
• Pedestrian – leading cause of death in 5-9 yrs old
• Bicycle injury increases with age – most common is head
trauma
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Physiologic Differences
• Larger head  greater inertia, movement & transfer of
energy to the head & brain
• Less soft tissue & muscle greater energy transfer to
internal organs
• Difference in center of gravity
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Infant – above umbilicus
1 yr – at the umbilicus
Adults – pubic symphysis
Jack knife effect with 2 points restraint  spinal and intestinal
injury in forward collision
Resuscitation
• Causes of early death in injury
– Airway compromise
– Hypovolemic shock
– CNS injury
• ATLS : steps in trauma eval
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Primary survey
Adjuncts to primary survey
Secondary survey
Adjunct to secondary survey (investigations)
Definitive managementss
Resuscitation – Primary Survey
• A- Large head/occiput, large oropharyngeal soft tissue,
short trachea  frequent Right stem intubation
– <12 yr: needle cricothyroidotomy because cricoid cartilage is the
major support structure of airway
– Surgical tracheostomy <12 yr
• B – Pneumothorax, tension pneumothorax, hemothorax
• C – Normal physiologic status up to 30% loss of total blood
vol; traumatic cardiac arrest or penetrating with witnessed
arrest  poor outcome
• D – Disability: CNS injury
• E – Exposure: prevent further heat loss
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Resuscitation – Secondary Survey
• Similar steps as primary survey
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Resuscitation – Investigations
• Plain X-rays
– Lateral C-spine: screen but not adequate in diagnosis
– Supine chest: pulmonary of mediastinal injuries, not good in
diagnosing small pneumothoraces
– Pelvic: major pelvic disruption
• Ultra sound
– FAST: focused abdominal sonography for trauma, not very reliable
in children as in adults
• CT:
– Chest abd. pelvis as indicated by injury
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Trauma In PICU
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Child abuse & neglect
Head injury
Spinal cord injury
Thoracic injury
Abdominal injury
Child Abuse & Neglect
• Abuse head trauma: most common in PICU causing more
long term morbidity
– Neck is weaker with larger head  larger CSF volume (move
around), larger water contents  increase in deformability
– More rotational : tear bridging veins (SDH) & axons (DAI)
– Neurons and axons – less protected due to less myelination
• Skeletal injury: posterior rib fractures, metaphyseal
fracture, spinous process fractures
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Child Abuse & Neglect
• Abdominal trauma: 2nd leading cause of fatal injury, 40%50% death rates
– Compression: crush solid viscera against anterior spine  burst
injuries to solid viscera & perforation of hollow viscera
– Deceleration forces  shear injuries at the site of fixed, ligamentous
attachment with tear & hematoma formation
• Thermal burns
– Uniformed thickness – closely replicate the objects
– Abuse scald burns – immersion pattern with circumferential &
uniform depth, well defined edges, spares body creases
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Severe Traumatic Brain Injury
• Statistic230/100,000
– 3000-4000 deaths/yr; 10-15% are severe with GCS<8 deaths or
permanent brain damage
– 0-4 yr: worse outcome probably secondary to non-accidental trauma
– 5-15 yr: favorable outcome compared to adults
• Goals: to prevent secondary injury
– Optimize substrate delivery & cerebral metabolism
– Prevent herniation
– Target specific mechanisms involved in the evolution of secondary
injuries
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TBI - Pathophysiology
• Primary – direct disruption of brain parenchyma
• Secondary – cascade of biochemicals, cellular amd molecular
events
– Ischemia/excitotoxicity, energy failure  cell deaths
– Secondary cerebral swelling
– Axonal injury
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TBI – Secondary Injury
• Post-traumatic ischemia
– Extra cerebral insults – hypotension/hypoxemia
– Early hypoperfusion are common” CBF <20ml/kg/min associated
with poor outcome
– CBF recovered usually after 24 hrs
– Delayed in normalization of CBF does not associated with poor
outcome
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TBI – Secondary Injury
• Excitotoxicity
– Glutamate & excitatory amino acid  neuronal damage
» 1st phase: Na dependent neuronal swelling
» 2nd: Ca dependent degeneration  DNA damage  DNA repair 
Deplete ATP  metabolic failure & necrotic cell deaths
– CSF glutamate increases 5 folds in TBI in adults; increase of
glutamate correlates with poor outcome
– Tx with anti-exitatory MK-801 (NMDA antagonist); other txsmagnesium, glycine site antagonists, hypothermia, pentobarb
– NMDA antagonists may induce apoptotic neurodegeneration in
children
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TBI – Secondary Injury
• Cerebral swelling: initial min to hrs of post-traumatic
hypoperfusion & hypermetabolism  metabolic depression
(CMRO2 decreases by 1/3 of normal)
• Edema
– Vasogenic & BBB disruption
– Cellular swelling: astrocytes swelling – uptake of glutamate
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TBI – ICP Monitoring
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Parenchymal fiberoptic & microtransducer system
Subarachnoid, subdural, epidural- less reliable
Ventricular- best monitoring with benefit of draining CSF
Keep ICP <20
Keep CPP 40-60
– 40-50: infants
– 50-60: Children:
– >60: adolescents
» lidocaine: decrease catechol surge with direct laryngoscopy
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TBI – Advanced Monitors
• Stable Xenon CT CBF – monitor regional CBF
• Stable Xenon technique
• Transcranial doppler: measured velocity rather than flow,
mainly MCA distribution
• Jugular venous saturation: keep >50%, lower assoc. with
mortality
• NIRS- near infrared spectroscopy: trace the oxidative state
of cytochrome, more on trends
• PO2 microelectrode implantation to frontal parenchyma:
also provide sign metabolic information: glutamate, lactic
acid, glucose, ATP
• PET: positron emission tomography
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TBI – ICH Management
• CSF drain
• Osmolar therapy
– Mannitol:
» Rapid dec. ICP by dec. viscocity  dec. bl vessel diameter. Depend on
intact viscosity autoregulation. Transient (75 min)
» Osmotic: (onset 15-30min; duration 1-6 hrs): water moves from
parenchyma to circulation; work in intact BBB. May accummulate &
worsen cerebral edema
» Excreted unchanged in urine: may precipitate ATN & renal failure in
dehydrated states. OK to use up to osmo of 365
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TBI – ICH Management
• Osmolar therapy
Hypertonic saline: same benefits as mannitol
» Other benefits: restoration of cell resting membrane potential,
stimulation of atrial natriuretic epptide release; inhibition of
inflamation; enhance cardiac performance
» Side effects: extrapontine myelinosis: demyelination of thalamus, basal
ganglia & cerebellum; SAH (tearing of bridging veins due to rapid
shrinkage); renal failure; rebound ICU
• Sedation, analgesia, NMB
• Anticonvulsion: seizures cause inc. cerebral metabolic
demands and release of excitatory amino acids
• Head position
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– 30 degree: dec. ICP & mean carotid pressure with no change in CPP
& CBF
TBI – ICH Management – 2nd tier
• Barbiturates: dec. ICP via dec. CMR & CBV; direct
neuroprotective effects by inhibiting free radical-mediated
lipid peroxidation of membraned
• Hypervent:dec. post-injury hyperemia & brain acidosis,
restore CBF autoregulation
– Prolonged hypervent: dec. brain interstitial bicarb buffering
capacity, gradual dec. local vasoconstrictor effects
• Hypothermia: 33 C
– Hyperthermia exacerbates neuronal deaths
• Decompression craniectomy
• Lumbar CSF drainage
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Acute Spinal Cord Injury
• High cervical injury
– C1-3 : infants/toddlers – MVC, trauma
– C4-7 : Adolescents/adults – sport, MVC
• Initial injury inc. in inflammatory cells & fibroblasts in
cord tissue  cellular necrosis
• Release of lysosomal enzyme  traumatic paralysis
• “Spinal Shock”: high T or C injuries  absence of
sympathetic tone  hypotension, bradycardia &
hypothermia
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Acute Spinal Cord Injury
• Treatment
– ABC
– Methylprednisolone 30mg/kg bolus then 5.4 mg/kg/hr for 23 hrs;
need to start bolus within 8 hrs of injury
– Careful fluid management with pressors to improve vasodilatation
– Osomotic diuretic to dec. secondary edema; low molecular weight of
dextran to improve microcirculation
– Hyperbaric oxygen therapy
– Spinal cord cooling: need to be done within 4 hrs to 10 C
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How long
How to deliver
What fluid
Technical difficulty
Acute Spinal Cord Injury
• Sequelae
– Respiratory failure: C3-5 innervation of diaphragm; CN IX
innvervation to accessory muscle
– UTI: neurogenic bladder, avoid overdistention and large volume
residual, inc. risk of infection
– Urolithiasis: immobility and hypercalcemia
– Acute hypercalcemia due to immobility causing vomiting,
polydipsia, polyuria, anorexia, nausea, malaise, listlessness
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Thoracic Injury
• 2:1 male to female
• 92%: blunt trauma
– 48% pulmonary contussion
– 39% Pneumo/hemothoraces
– 30% rib fractures
• 33% in pediatric trauma fatality
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Airway obstruction
Tension pneumothoraces
Massive hemothoraces
Cardiac tamponade
Thoracic Injury
• Rib fractures
– > 3 rib fx: reliable indication of intrathoracic or other organ
involvements
– Scapular or post rib fx – not associated with great vessels injury
– Thoracic spine fx – inc. suspicion of great vessel injury
• Pulmonary contussion
– Absence of external signs: chest wall abrasion, tachypnea, abn. BS
– Tx: fluid management, pulm. Toilet & respiratory support;
corticosteroid is harmful
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Thoracic Injury
• Pneumo/hemothorax
– Large bore in hemothorax to avoid fibrothorax & lung entrapment
– CT: can cause exanguinating hemorrhage (intercostal, hilar or
mediastinal vessel injuries)
– Severe tracheobronchial disruption: high energy impact injuries, sub
Q emphysema, dyspnea, sternal tenderness, hemoptysis. X-Ray:
sub Q emphysema, pneumo-mediastinum, pneumothorax, air
surrounding bronchus, abn. Appearance of ETT, collapsed of lung
toward chest wall
• Cardiac injury: 3%, most died at the scene
– Myocardial contusion: act as MI or SVT & VT; min clinical
significance, symptoms usually 12 hours post injury
– Valvular dysfunction: papillary or chordae ruptures;
– Cardiac rupture, pericarcial effusion, cardiac arrhythmias
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Thoracic Injury
• Aortic & great vessels injuries
– Traumatic aortic disruption: mid scapular back pain, UE
hypertension, dec. femoral pulses bilaterally, inc. CT output
– X-Ray: widened mediastinum, deviation of NG or CVL, blurring of
aortic knob, abn. paraspinous stripe, right tracheal deviation,
upward shift of Left stem main bronchus
• Others
– Diaphragmatic ruptures: L>R
– Esophageal rupture
– Lung cysts
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Abdominal Trauma
• 83% blunt trauma
• Solid organ injury: liver, spleen, kidneys
1- Spleen: extends below costal margin
- grade I-IV, mainly observation
- Surgical indication
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Persistent hypotension or evidence of continuous hemorrhage
>50% blood volume replacement
Other life threatening associated intra-abdominal injury
I & II healed after 4 months
III-IV: healed after 6-11 months
Abdominal Trauma
2- Liver: also extends below the costal margin; associated with
highest mortality
May require surgical correction of injuries to the hepatic
vein or vena cava  associated with high mortality
3- Duodenum:
Mostly hematoma, some with disruption of lumen
Observation with TPN, bowel rest, resolution 2-4 weeks
4- Pancreas:
- Operative repair depending on anatomy of injury &
integrity of the main pancreatic duct
- Upper abdominal pain, inc. amylase, edema of gland, fluid
in the lesser sac
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- Fracture of pancreas when crossing over vertebral colume
Abdominal Trauma
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6-Small bowel:
Disruption, mesenteric avulsion, wall contussion
More at fixation points: proximal jejunum at ligament of
Treitz, terminal Ileum
7- Renal trauma:
- Flank tenderness, mass or ecchymosis
- Hematuria
- Hematoma, laceration or vasular injury
- Isolated urinary extravasation: not an emergent surg.
Expl.
- Need Abx
- Renal pedicle injuries are rare
- Ureteral injury – surgical repair
Abdominal Trauma
7- Blunt abdominal aortic injury:
- Occur in high energy injury
- Most common at inferior mesenteric artery or at the level
of the kidneys
- Major abdominal venous injuries are usually fatal
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Abdominal Trauma
8- Bladder injury: mostly intra-abdominal
- Burst injury
- Rupture with pelvic fracture
- Cystography: extra-peritoneal bladder rupture  fluid
extending superiorly and anteriorly to the level of umbilicus
& by fluid in the retrorectal presacral space
- Tx: depends on the location of injury:
- extraperitoneal managed with catheter drainage
alone;
- penetrating or bladder neck injury or with
vaginal/rectal injury required surgical repair
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Abdominal Trauma
8- Bladder injury: mostly intra-abdominal
- Burst injury
- Rupture with pelvic fracture
- Cystography: extra-peritoneal bladder rupture  fluid
extending superiorly and anteriorly to the level of umbilicus
& by fluid in the retrorectal presacral space
- Tx: depends on the location of injury:
- extraperitoneal managed with catheter drainage
alone;
- penetrating or bladder neck injury or with
vaginal/rectal injury required surgical repair
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Abdominal Trauma
11- Pelvic fracture:
- Single fracture of pubic ramus: rarely clinical significance
- Multiple fractures: associated with significant intraabdominal injuries
- Sites of silent hemorrhage
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