Pediatric head injury public

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  • Infants and toddlers have
  • No universally agreed upon criteria for minor head injury exists. In addition to GCS, the AAP’s definition for minor head injury: “those who have normal mental status at the initial examination who have no abnormal or focal findings on neurologic exam and who has no physical evidence of skull fracture.”
  • History incompatible with children’s age or situation. For instance, 1 month-old rolled off the changing table. 6 month old crawled out of the crib. This can be NAT or neglect.
  • ABCDEsMake sure that the c-collar is properly fittingHead to toe assessment for trauma. Particularly in the fundoscopic exam. Look for retinal hemorrhages. This can be a clue for non-accidental trauma. Scalp hematomas in < 2 years of age is a/w increased risk of skull fx and intracranial hemorrhage. Basilar skull fracture signs- Periorbitalecchymoses, bruising behind the ears (“Battle sign”), hemotympanum, and CSF drainage from nose.
  • For Raccoon Eyes, this can be difficult to differentiate from some bruising of the eyes. In a complex trauma case, this can be difficult to find out, but typically, raccoon eyes do not involve the eyelids. It’s more of a pooling of a blood from a broken skull, so the eyelids are not involved as they do not communicate with the skull. CSF can be differential from blood from the nose by the “halo” or “double ring” sign. If you place a drop of nasal fluid onto filter paper, the CSF fluid is at a different density from the blood, so the CSF should travel at a different rate through the filter paper. I could not find much data on the utility of this sign, but some neurosurgery textbooks mention that this sign is unreliable. However, this is one sign that you can have in your back pocket.
  • One small study found a decreased incidence of vomiting in children with more severe head injuries. Also vomiting is more common in children with a history of migraine. Additionally, preverbal children cannot describe their symptoms. Behavior change by caregivers can be helpful, but again this is very common in children for any head injury.
  • Largest study
  • Largest study
  • Asymptomatic patients have less than 0.02% of ciTBI < 2 year old and 0.05% in >= 2 year old. Exact observation time is unclear. Studies have ranged from 2.5 hours to 6 hours as being safe. 4-6 hours appears to be a common number used in textbooksLess than 2 with just mechanism has 0.3% ciTBI. At least 2 years of age has 0.6% if just mechanism. 1 study showed that 0.05 and 0.6% of discharged patients and admitted patients had positive findings upon repeat head CT in those who were clinically high risk but head normal head CT, normal LOC. None required NSS intervention.
  • Etomidate has rapid onset of action (45 sec) and short duration of action (3-5 minutes) and favorable hemodynamic profile. May have adrenal suppresion but one time dose, may not have clinical significance. May also reduce ICP. Propofol is rapid onset and has anticonvulsant properties. However, have to becareful of hypotension. Short acting agents. Long acting impeded reliable neuro exam, limit ability to see seizure, and may increase risk of PNA. Succ may increase ICP in patients with brain tumors, but evidence is not definitive in humans with brain injury. Also keep in mind possible undiagnosed NM conditions in children.
  • Pediatric head injury public

    1. 1. Daniel Kwan, MD
    2. 2. Objectives  Present a case of pediatric head injury.  Examine the uniqueness of pediatric head injuries.  Discuss the clinical presentations and decision rules for minor head injury  Review the pathophysiology and treatment of moderate/severe head injury.  Review abusive head injury and other pertinent pediatric head injury types.
    3. 3. Case  CC: Stat Trauma  HPI: 11 yo boy with no PMH who presents after MVC rollover. Pt was unrestrained passenger and was ejected. EMS found pt to be GCS 4. Pt intubated at outside hospital. Pt decompensated prior going to the CT scanner. Pt also had emergent left chest thoracostomy placed. Transferred to CRMC.
    4. 4. Case  PMH: none  PSH: none  Med: None  Family hx: non-contributory  Social history: lives with mother and father
    5. 5. Physical Exam  VS: 98/52, 99, 12, 35.5, 100% (ETT)  Neuro: GCS 4T (decerebrate posturing)  Head: Open comminuted bifrontal skull fractures. Multiple contusions. 4 cm frontal laceration.  Pupils: Fixed and non-reactive (4 mm bilaterally)  Neck: Contusions/ecchymosis to right anterior neck. Carotid pulses 2+  Chest: chest contusions. L chest tube  Heart: RRR, no m/g/r
    6. 6. Physical Exam  Abd: soft, distended  Pelvis: stable, atraumatic  GU: Normal genitalia  Rectal: normal tone  Extrem  BUE: Contusions, swelling. Decerebrate posturing  RLE: Contusions, abrasions  LLE: Midshaft left femur deformity  Back: No signs of blunt or penetrating trauma.
    7. 7. Labs  ABG: 7.30/339/39/19  Chem 10:  Na: 129, K: 3.7, Bicarb- 22, BUN: 12, Cr 0.7, Glc 206  CBC: 14.7/6.6/252  PT/INR: 19.4/1.7  UA- normal
    8. 8. CXR  Small PTX  Possible pulm contusion
    9. 9. CT Chest/Abd/Pelvis  L residual PTX  Chest tube in place  Pulmonary Contusion
    10. 10. Head CT  Multiple Comminuted skull fx  Underlying L EDH with midline shift of 7 mm  IPH and DAI
    11. 11. Other Imaging  Pelvis XR- no fracture  L femur XR- midshaft femur fracture  CT C spine- no fracture  FAST- possible minimal fluid on bladder view
    12. 12. Epidemiology  650,000 to 1 million children evaluated for head trauma per year  80-90% are mild  In developed countries, TBI is the most common cause of death and disability in childhood.  Causes  Infants: Abuse  Toddlers: Abuse and falls  School-aged: Injuries (play and sports) and MVCs  Adolescents  MVCs and assault  ETOH can complicate assessments of injuries.  Across all age groups, males > females in minor head injuries.
    13. 13. Pathophysiology  Acceleration  Moving object hits stationary head  Least harmful  Deceleration  Moving head strikes stationary object.  Most severe brainstem injuries  Rotational  Vigorous shaking  Head hit at an angle  Widespread injury including large SDH  Direct blow  Direct blow fracture  EDH from either middle meningeal artery or dural venous sinuses
    14. 14. Pediatric Uniqueness  Younger children have more distensible skulls  Less protection in infants/toddlers  Infant cranial sutures are open  Toddler cranial cortex is thin.  Very young children have higher mortality than older children with the same injury.  Limited history and exam at young age  Underestimation of injuries  Reluctance to start invasive procedures
    15. 15. Pediatric Uniqueness  Increased probability of injury in infants/toddlers  Large calvaria and weak cervical muscles  Coordination and balance is poor  Dependent on caregivers  For supervision and safety equipment  Non-accidental trauma.  Stronger frontal bone  Frontal sinus develops after 8-10 years old.  Types of TBI  Less traumatic mass lesions (except SDH)  Less hemorrhagic contusion  More diffuse brain swelling and axonal injury
    16. 16. Degrees of Head Injury  Minor: GCS 13-15  Moderate: GCS 9-13  Severe: GCS <= 8
    17. 17. Pediatric GCS
    18. 18. Minor Head Injury  85% of pediatric head injuries are classified as mild.  About 400,000 ED visits per year particularly children ages 0 to 4.
    19. 19. Clinical Features  History  Mechanism from caregivers, witnesses, EMS  History incompatible with children’s age or situation.  Clinical decision rules- PECARN  Temporal changes or persistence of symptoms.  Worsening sx- intracranial injury  Persistence of HA, confusion, amnesia  concussion  Ask child directly if verbal. Ask caregiver if preverbal
    20. 20. Clinical Features  High risk  Suspicion of child abuse  Altered mental status  Persistent vomiting  Seizure following injury  Loss of consciousness (> 5 seconds)  Anticoagulated  Shunt  Intermediate risk  Vomiting that is self-limited  LOC that is brief (< 5 seconds)  Resolved lethargy or irritability  Behavior change by caregiver  High risk mechanism (fall > 3 feet, ejection, etc.)  Unwitnessed trauma of concern (e.g.: fall in another room with possible LOC)  Age < 3 months with nontrivial trauma
    21. 21. Physical Exam  ABCDE  Proper fitting C-Collar  Head to toe assessment for trauma.  Neuro  MSK  Fundoscopic: particularly retinal hemorrhages  High risk  Suspicion of child abuse  Focal neurologic findings  Acute skull fracture, including depressed or basilar skull fracture  Bulging fontanelle  Intermediate risk  Scalp hematoma (particularly nonfrontal and < 2 years old)  Skull fracture > 24 hours old (non-acute)
    22. 22. Basilar Skull Fracture Signs  Raccoon Eyes  Battle’s Sign  Hemotympanum  CSF/Blood Rhinorrhea
    23. 23. To CT or Not to CT  Benefits of CT  Early identification can reduce morbidity/mortality.  Children have atypical or vague symptoms (vomiting, behavior change).  Reassure parents.  Disadvantages  Head CT can be expensive (Avg charge ~$996)  Radiation exposure  1 head CT 1/1500 lifetime risk of death 2/2 cancer in 1 year old  1/5000 lifetime risk in 10 year old  Test threshold- no imaging was when probability of ciTBI was less than 0.9%.1 1. Hennelly, KE., et al. Pediatric Traumatic Brain Injury and Radiation Risks: A Clinical Decision Analysis. The Journal of Pediatrics. 2012;162:392-397.
    24. 24. Expert Panel Recommendations  In 1999, a study of 608 infants and children < 2 years of age. 2  5% incidence of ICH  Higher incidence in infants < 2 months old  ½ of pts with ICH had clinical symptoms or signs suggestive of brain injury.  Virtually all had scalp hematoma.  Follow-up study  Skull fx and ICH correlated with hematoma size (med to large), character (boggy), and location (non-frontal) 2. Schutzman SA, et al. Evaluation and management of children younger than two years old with apparently minor head trauma: Proposed guidelines. Pediatrics 107: 983, 2001
    25. 25. Expert Panel Recommendations High Risk Intermediate Risk for ICH Intermediate Risk for Skull Fracture Low Risk Depressed Mental status Vomiting 3-4 times Significant mechanism Low risk mech Focal Neuro Finding LOC < 1 min Large nonfrontal scalp hematoma Asymptomatic, normal exam Acute (<24h) Skull Fx Resolved lethargy or irritability Fall onto hard surface >2h since injury Basilar or depressed skull fx Caretaker concern Vague hx but signs or sx of head trauma Older age (>12 Mo) Irritability Skull fx > 24h old Vomiting > 5x in 6h Seizure LOC > 1 min Bulging Fontanelle Recommendation Recommendation Recommendation Recommendation CT Scan Obs 4-6 h or CT scan Obs 4-6h or CT or XR No imaging
    26. 26. Decision Rules  Assisting clinical decision making about neuroimaging in children with minor head trauma.  3 of the largest derived rules  Canadian Assessment of Tomography for Childhood Head injury rule (CATCH)  Children's Head Injury Algorithm for the Prediction of Important Clinical Events (CHALICE)  Pediatric Emergency Care Applied Research Network (PECARN)  Only PECARN has been derived and validated.
    27. 27. CATCH  Purpose: Identify high risk criteria 3  Study  4000 children including GCS 13  4 high risk factors and 3 medium risk factors  Sensitivity 98% for intermediate factors, 100% for high risk  Problems  Requires 52% of pts undergo CT  Not prospectively validated 3. Osmond MH, et al. CATCH: a clinical decision rule for the use of computed tomography in children with minor head injury. CMAJ 2010; 182:341.
    28. 28. CATCHCT is required only for children with minor head injury* and any of one of the following findgings: High risk (need for neurologic intervention) 1. GCS < 15 at 2 hours after injury 2. Suspected open or depressed skull fracture 3. History of worsening Headache 4. Irritability on examination Medium risk (brain injury on CT scan) 5. Any sign of basal skull fracture 6. Large, boggy hematoma of the scalp 7. Dangerous mechanism of injury (e.g.: MVC, fall from elevation > 3 ft or 5 stairs, fall from bicycle with no helmet) *Injury 24 hours associated with witnessed LOC, definite amnesia, witnessed disorientation, persistent vomiting (> 1 episode) or persistent irritability (in children < 2 years of age) in a pt with GCS 13-15
    29. 29. CHALICE  Purpose: Identify high risk criteria 4  Study  22,772 children with head injuries  10 hospitals in England  281 ICH detected on CT scan  14 high risk variables  Sensitivity 98.6% and Specificity 87% for ICH  For pts with GCS 13-15, sensitivity 97.6%  Problems  In a retrospective study, rate of head CT increased from 6.5 to 10% with very few additional skull fx found.  In another retrospective observation study, head CT rate increased from 19 to 46% and missed six with intracranial injury. 4. Dunning J, et al. Derivation of the children’s head injury algorithm for the prediction of important clinical events decision rule for head injury in children. Arch Dis Child 91: 885, 2006.
    30. 30. CHALICE History Mechanism Physical Examination Witnessed LOC > 5 min MVC > 40km/h or 25 MPH GCS < 15 for < 1 year of age Amnesia > 5 min Fall > 3 m or 10 ft GCS <14 for >1 year of age 3 or more episodes of emesis High-velocity projectile Depressed or basilar skull fracture Traumatic Seizure Penetrating injury Suspicion of NAT Tense fontanelle Drowsiness Focal Neuro Deficit Bruising, swelling, laceration > 5 cm if < 1 year of age
    31. 31. PECARN  Derived and validated prediction rule to decide when to forgo head CT. 5  Multicenter study- 25 EDs  Among enrolled children (GCS 14-15, < 18 years old)  < 2 years of age: 8502 in derivation, 2216 validation  >=2 years of age: 25,283 in derivation, 641 in validation.  ciTBI  Death from TBI  NSS intervention  Intubation >24 hrs duration  Hospital admission >= 2 nights  CTs obtained in 37% (derivation) and 35% (validation) of pts  Follow: Caregivers called at day 7 and 90 5. Kupperman, N, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet 374 (9696): 1160, 2009.
    32. 32. PECARN Age Group Low-risk Criteria Sensitivity NPV <2 years Normal Mental Status 100% (86-100%) 100% (99.7-100%) No scalp hematoma except frontal LOC < 5 sec Nonsevere mech No palpable skull fx Normal behavior >=2 years Normal mental status 96.8% (89-100%) 99.95% (99.8- 100%) No LOC No vomiting Nonsevere mech No signs of basilar skull fx No severe headache
    33. 33. PECARN  Results  Prevalence of ciTBI was approximately 1% in both derivation and validation cohorts  Defined further risk stratification  Otherwise, may increase CT usage  Intermediate risk: 0.9% (About 30% of all patients)  High risk: >4%
    34. 34. PECARN A- < 2 yrs old B- >= 2 yrs old
    35. 35. PECARN  Modified form of PECARN was externally validated 6  High clinician satisfaction (96%)  High adherence to rule (94%)  Identified all 3 children with ciTBI at first visit  Non-statistically significant increase of Head CT (7 to 8%)  Benefits  Gives physicians room for clinical judgment  A tool for physicians to risk stratify  Problems  Very low rate of clinical significant head injury  Lower bounds of 95% confidence intervals are low than other adult head CT rules. 6. Bressan, S., et al. Implementation of Adapted PECARN Decision Rule for Children with Minor Head Injury in the Pediatric Emergency Department. Academic Emergency Medicine. 19 (7); 801-807, 2012.
    36. 36. Disposition  Asymptomatic infants/children  If greater than 2-4 hrs postinjury, can d/c home.  Can discharge if no suspicion of NAT, easily aroused with normal neuro exam, return to baseline level of function, tolerating PO fluids, no extracranial injuries, reliable caretaker.  Return precautions: lethargy, irritability, focal deficits, vomiting in 24 hours.  Intermediate risk  Observation  Unclear exact time but 4-6 hours is common  Head CT  > 1 risk factors or any in < 3 months  High risk- Head CT and/or Neurosurgery  Normal Head CT: Clinical judgment for obs vs admission  Non-displaced Fracture (no ICH): NSS follow up  ICH: NSS and admission
    37. 37. Moderate/Severe Brain Injury  Moderate TBI: 10% of all head injuries  Mortality < 20%  Long term disability as high as 50%  Severe TBI  Mortality: ~40% (mostly in first 48 hours)  Moderate recovery: < 10%  75% of children with multiple trauma have TBI  ~80% of all trauma deaths a/w severe brain injury  TBI accounts for 95% of severe and fatal injuries.  Mechanisms  Children < 4 yrs old: fall accounted for 41%  Adolescents: 43% from MVC  <1 year old in ICU: 52% Assaulted
    38. 38. Pathophysiology  Brain sensitive to ischemia and hypoxia  Consumes 20% of total body oxygen and 15% of cardiac output  Changes in blood volume, pH, PO2, PCO2regulates blood flow (O2 delivery and metabolism)  Vasoconstriction occurs with hypertension, hypocarbia, and alkalosis.  Cerebral perfusion pressure  Surrogate indicator for cerebral blood flow  CPP = MAP - ICP
    39. 39. Pathophysiology  Skull is a closed space with three intracranial compartments.  Brain parenchyma, CSF, intravascular blood  When one increases, the others will decrease to maintain ICP (Monro-Kellie Hypothesis)  Normal ICP  Adult/Older children: < 10- 15 mm Hg  Children: 3-7 mm Hg  Infants: 1.5- 6 mm Hg  CPP normally > 60 mm Hg
    40. 40. Pathophysiology
    41. 41. Pathophysiology  Primary injuries  Contusions, hematomas, DAI, direct cellular damage, tearing/shearing of tissues, loss of blood-brain barrier  Secondary Injuries  Downstream effects from primary injury  Excessive glutamate released into presynaptic space activation of postsynaptic receptors  Flood of Ca2+ intracellularly  Disrupts Na and K and normal function of cells.  Mitochondria uptakes excess Ca Free radicals and more cellular dysfunction.  Leads to necrosis inflammation  apoptosis/membrane integrity  cytotoxic edema and extracellular edema  increase in ICP  compression and herniation.
    42. 42. Assessment Neurological assessment  LOC  Pupillary exam for size, reactivity, symmetry  EOM  Fundoscopic exam  Brainstem reflexes (corneal and gag reflexes)  DTR  Response to pain  Signs of herniation  CN III nerve palsy  Changes in resp pattern, pupil size, vestibuloocular reflexes, posture.  Cushing’s Triad
    43. 43. Treatment  Prevent secondary insult  Identify Treatable Mass Lesions  Identify Other Life-Threatening Injuries
    44. 44. Treatment  Secondary Insult- hypoxemia, hypotension, anemia, hyperglycemia, hyperthermia, intracranial mass  Single episode of hypotension or hypoxia a/w 150% increase in mortality.  Airway/Breathing  Intubation (GCS < 8 or deteriorating)  Cuffed tubes to prevent aspiration  No nasotracheal intubation with midface trauma or basilar skull fractures  Preinduction agents do not improve outcome.  Induction: limited effect on ICP or MAP  Etomidate, 0.3 mg/kg IV  Propofol 1-3 mg/kg IV  Ketamine 1.5-2.0 mg/kg IV 7  Paralytic  Succinylcholine 1-1.5 mg/kg IV  Rocuronium 0.6-1 mg/kg IV 7. Filanovsky, Y., et al. Myth: Ketamine should not be used as an induction agent for intubation in patients with head injury. CJEM. 12 (2):154-7. 2010.
    45. 45. Treatment  Circulation  In severe TBI, 1 hypotensive episode doubles mortality.  Aggressive fluid resuscitation (isotonic solution)  Maintain MAP > 80 mm Hg  Relative Hypotension- Normal BP but not sufficient perfusion  SBP < 100 mm Hg rarely associated with MAP > 80 mm Hg.  Fix sources of bleeding on the external head  Vasopressors to keep MAP at 80 mm Hg.  Hypertension could be a sign of cushing’s reflex.  Head positioning 30 degrees
    46. 46. Treatment  Hyperglycemia  Associated with poor outcomes  In 1 study, for children < 14 years old going for emergent craniotomy for TBI  Perioperative hyperglycemia (glc > 200 mg/dL) found in 45% of children  A/w <4 years, GCS <=8, multiple traumatic lesions  Hyperthermia- prevent and treat aggressively
    47. 47. ICP  ICP > 20 mm Hg increases morbidity and mortality.  Clinical Signs: headache, nausea, vomiting, seizure, lethargy, Cushing’s triad, agonal respirations  Herniation  Unilateral or bilateral pupillary dilatation, hemiparesis, motor posturing, and/or progressive neurological deterioration.
    48. 48. ICP- Treatment  Mannitol  lowers ICP; improves CBF, CPP and brain metabolism  Free radical scavenger  Expands plasma volume  Diuretic so maintain euvolemia  Hypertonic saline  Bolus or infusion  Reduces intracranial pressure.  Adverse effects: rebound intracranial hypertension, central pontine myelinolysis, SAH.  Hyperventilation  Not recommended as prophylactic intervention  Reduces ICP and causes vasoconstriction. Decreased CBF and hypocapnia a/w increased mortality.  Keep PaCO2 at 35-40mm Hg and O2 sat > 95%  If pending herniation, PCO2 30-35 mm Hg
    49. 49. ICP-Treatment  Barbiturate Coma  Not initiated in the ED  Treats refractory intracranial hypertension in ICU.  ICP monitoring recommended  Treat seizures  SZs raise ICP  Prophylactic anticonvulsants reduced post-traumatic seizures within first week, but do not improve long-term outcome.  Prophylaxis is controversial, but experts suggest anticonvulsant therapy for 1 week after seizure.  Steroids- no role in TBI or increased ICP  Burr hole- emergent treatment for epidural hematoma
    50. 50. Abusive Head Trauma  In US, abusive head trauma (AHT) incidence in <2 years old is 17 per 100,000 person-years  Previous abuse noted in up to 60% of cases.  Missed AHT in 31% of children  Most often: Viral GE, influenza, accidental head trauma, “rule out sepsis”  Risk factors  Infant: perinatal illness, birth defects, incessant crying, male gender  Family: Familial dysfunction (i.e.: drugs/ETOH), young maternal age, family disruption/separation, history of abuse in child or family members
    51. 51. AHT Workup  Physical exam  Retinal hemorrhages- 60-85% of abusive head injury  Facial cutaneous bruising- linear strap marks, buttocks bruising, 54% do not have bruising.  C-spine injury- 4% of abusive head injury  Evaluation  Rule out coagulopathy- CBC, Coags  Rule out other organ injury- Electrolytes, LFT, UA  Rule out meningitis- CSF RBC/Xanothochromia (83% of abusive head injury)  Skeletal Survey X-ray  Head CT  MRI- follow up CT or asymptomatic but non-cranial injuries
    52. 52. Subdural Hematoma  Blood accumulation between dura mater and the arachnoid mater  Mechanism  Sudden acceleration-deceleration of brain parenchyma tearing bridging veins  Blood collects more slowly because venous.  Classification  Acute  Subacute  Chronic (> 2 weeks)
    53. 53. Subdural Hematoma  Clinical Features  A/w other brain and parenchymal injuries  High risk populations: Elderly and alcoholics (atrophic brains) and children < 2 years old (NAT)  Acute: Severe trauma + LOC (possible lucid period)  Chronic: progressive AMS and behavior change  SDH + long bone/posterior rib fx  NAT  Strong correlation with NAT (50% of reviewed SDH cases a/w NAT)  Can be a/w perinatal birth trauma (cranial sutures tearing dural veins)  CT  Crescent shaped lesions that cross suture lines  Subacute SDH are isodense and harder to identify  MRI  Head CT IV contrast  Chronic: hypodense (dark)  Treatment: NSS  Obs vs surgery
    54. 54. Diffuse Axonal Injury  Disruption of axonal fibers in the white matter and brainstem by sudden deceleration.  Mechanism: Blunt trauma and shaken baby  Clinical Features  Edema can develop quickly.  AMS  CT  Classically: punctuate hemorrhagic injury along grey-white junction of cerebral cortex and deep structures of brain  Can be normal  Treatment  Limited  Prevent secondary injury by reducing edema and limiting increases in ICP
    55. 55. Shaken Baby Syndrome  Life threatening injury in children < 2 years of age.  Mechanism  Rapid acceleration and rotation of cranium  Impact on solid object  angular rotation  Injuries  Shearing injuries of intracranial vessels, cervical spine injury, and intraocular injury.  Clinical signs  Increased drowsiness, lethargy, decreased feeding  40% had no signs of external injury on initial evaluation
    56. 56. Case Conclusion  Taken to the OR for evacuation of L sided EDH with bone flap removed.  L femur fracture treated ORIF  Developed VAP with Acinetobacter and Enterobacter.  Thalamic storms/dysautonomia  Transferred to Children’s 3 weeks later.  Taken back to the OR with plastics and NSS for scalp wound debridement and tissue rearrangement.  Developed neutropenia 2/2 bactrim and seroquel.  Extubated but had persistent fevers and had a tracheostomy placed 2/2 to respiratory distress.  Plastics took pt to OR for completing skin graft over scalp.  Pt transferred to floor and eventually weaned off ventilator for 2 weeks.  Discharged home.
    57. 57. References  Kirsch, TD, et al. Head Trauma in Adults and Children. In: Tintinalli, JE, ed. Tintinalli’s Emergency Medicine- A Comprehensive Study Guide, 7th Edition. China. The McGraw-Hill Companies, Inc. 2011. Chapter 254  Tintinalli, JE. Minor Head Injury in Infants and Children. In: Tintinalli, JE, ed. Tintinalli’s Emergency Medicine- A Comprehensive Study Guide, 7th Edition. China. The McGraw-Hill Compaines, Inc. 2011. Chapter 132.  Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Mosby/Elsevier; 2014.  UpToDate  Bressan, S., et al. Implementation of Adapted PECARN Decision Rule for Children With Minor Head Injury in the Pediatric Emergency Department. Academic Emergency Medicine. 2012; 19:801-807.  Hennelly, KE., et al. Pediatric Traumatic Brain Injury and Radiation Risks: A Clinical Decision Analysis. The Journal of Pediatrics. 2012;162:392-397.  Schonfeld, D., et al. Effect of Duration of Emergency Department Observation on Computed Tomography Use in Children With Minor Blunt Head Trauma. Annals of Emergency Medicine. 2013;62:597-603.

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