Pediatric Critical Care Medicine Children’s Healthcare of Atlanta 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

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

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

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

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

Resuscitation – Secondary Survey Similar steps as primary survey

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

Trauma In PICU 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thoracic Injury Rib fractures Pulmonary contussion > 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

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

Thoracic Injury Aortic & great vessels injuries Others 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

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

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 - Fracture of pancreas when crossing over vertebral colume

Abdominal Trauma 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

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

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

Abdominal Trauma 11- Pelvic fracture: - Single fracture of pubic ramus: rarely clinical significance - Multiple fractures: associated with significant intra-abdominal injuries - Sites of silent hemorrhage