TRAUMA IN THE PICU

Pediatric Critical Care MedicineEmory University

Children’s Healthcare of Atlanta

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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

– 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

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Resuscitation• Causes of early death in injury

– Airway compromise– Hypovolemic shock– CNS injury

• ATLS : steps in trauma eval– Primary survey– Adjuncts to primary survey– Secondary survey– Adjunct to secondary survey (investigations)– Definitive managementss

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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• Child abuse & neglect• Head injury• Spinal cord injury• Thoracic injury• Abdominal injury

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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 txs- magnesium, 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• 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

– 30 degree: dec. ICP & mean carotid pressure with no change in CPP & CBF

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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• Controlled arterial hypertension

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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

» How long» How to deliver» What fluid» Technical difficulty

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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– Airway obstruction– Tension pneumothoraces– Massive hemothoraces– Cardiac tamponade

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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

- 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

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Abdominal Trauma2- Liver: also extends below the costal margin; associated

with highest mortalityMay require surgical correction of injuries to the hepatic vein or vena cava associated with high mortality

3- Duodenum: Mostly hematoma, some with disruption of lumenObservation 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- Fracture of pancreas when crossing over vertebral colume

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Abdominal Trauma 6-Small bowel:

Disruption, mesenteric avulsion, wall contussionMore 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

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Abdominal Trauma7- 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 Trauma8- 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 Trauma8- 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 Trauma11- Pelvic fracture:

- Single fracture of pubic ramus: rarely clinical significance- Multiple fractures: associated with significant intra-abdominal injuries- Sites of silent hemorrhage