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Management of Head Injury and Increased ICP
Nicole Baier, MD
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Objectives Review the: Epidemiology of head injury
Various intracranial lesions Pathophysiology of increased ICP Management of head injury
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Epidemiology 2 cases per 1000 children per year Mild TBI: 82%
Moderate to severe TBI: 14% Fatal TBI: 5% (7000 deaths per year)
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Etiology Motor vehicle accidents Falls Non-accidental trauma
Sports injuries
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Mechanisms of injury Coup contusion Contrecoup contusion
Adjacent to the site of injury Brain accelerates against the fixed skull Injury to parenchyma and blood vessels Contrecoup contusion Deceleration and recoil of the brain Contralateral lesions
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Epidural Hematoma Classic: arterial origin, blood collects between skull and dura
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Subdural Hematoma Due to tearing of bridging veins, blood collects between dura and cortex
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Subarachnoid hemorrhage
Disruption of small vessels on the cortex, occur along the falx, tentorium, or outer cortical surface
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Intraventricular Hemorrhage
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Mechanisms of Injury Axonal injury: Areas affected:
Etiology: deceleration and shearing forces Axonal swelling and degeneration CT findings: Normal initially Delayed edema and petechial hemorrhages Areas affected: Basal ganglia Thalamus Deep hemispheric nuclei Corpus callosum
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Mechanisms of Injury
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Diffuse Axonal Injury
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Cerebral Edema Cytotoxic Edema Vasogenic Edema Interstitial Edema
Intracellular swelling Due to cellular injury (DAI, hypoxia-ichemia) Irreversible Vasogenic Edema Increased endothelial permeability Therapy may prevent secondary injury Seen with tumors, hematomas, infarcts, CNS infections Interstitial Edema Increased fluid in periventricular white matter Etiology - hydrostatic CSF pressure
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Monro-Kellie Doctrine
Intracranial Volume = Brain + CSF + Blood Normal: Brain 80% CSF 10% Blood 10%
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Monro-Kellie Doctrine
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ICP and intracranial volume
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Secondary injury Bleed/edema increases intracranial volume →
Compress intracranial vessels → Impairs blood flow → Ischemia
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Cerebral perfusion pressure
CPP = MAP – ICP > 70 in adults Children ????
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What is Cushing’s Triad?
Hypertension, tachycardia, and dilated pupils Hypotension, bradycardia, and posturing Hypertension, bradycardia, and dilated pupils Hypertension, bradycardia, and irregular respirations Hypotension, tachycardia, and posturing
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Cushing’s Triad Hypertension Bradycardia Irregular respirations
Etiology: When MAP < ICP, the hypothalamus stimulates sympathetic output Increase in BP stimulates carotid baroreceptors and leads to a vagal response and bradycardia
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A 2 year old boy is brought in by EMS
A 2 year old boy is brought in by EMS. He was playing outside at home when a van backed into the driveway and ran over him. He was minimally responsive at the scene required bag-mask ventilation on the way in. You cannot elicit any response from him with painful stimulation. What is his GCS? 2 3 4 5 6 GCS = 3
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Glasgow Coma Score Eyes: Motor: Verbal: - 2 decerebrate
4 opens spontaneously follows commands 3 opens to verbal command - 5 localizes pain 2 opens to pain withdraws to pain 1 no response decorticate Verbal: decerebrate 5 oriented no response 4 confused conversation 3 inappropriate words 2 incomprehensible sounds 1 no response
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Head Injury - grading Mild: GCS ≥ 13 Moderate: 9-12 Severe: ≤8
Battle’s sign
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You decide to intubate the child
You decide to intubate the child. Which of the following medications would be contraindicated in the given scenario? Etomidate Lidocaine Fentanyl Succinylcholine Rocuronium Given the crush injury, succinylcholine would be contraindicated in this scenario
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Management - Airway Indications for intubation: GCS ≤ 8 Hypoxia
Loss of airway protective reflexes Hypoventilation
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Management - Airway Rapid sequence intubation: C-spine stabilization
Preoxygenation Cricoid pressure Induction Meds: Thiopental – ICP ( cerebral metabolic rate) (may lower BP) or Etomidate – ICP or Benzodiazepine (may lower BP) + Opiate for analgesia for injuries/ laryngoscopy +/- Lidocaine (may blunt ICP assoc. with laryngoscopy) Neuromuscular blockade
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Insertion of an ICP monitor 3% normal saline bolus Mannitol
The child was successfully intubated after premedication with lidocaine, fentanyl, etomidate, and rocuronium. None of his labs are back yet. However, you decide to institute therapy for increased ICP. Which of the following therapies is indicated at this point? Insertion of an ICP monitor 3% normal saline bolus Mannitol Hyperventilation to CO2 of 25-30 Therapeutic hypothermia Mannitol is readily available in the ER and should be given. Another alternative is 3% NaCl bolus, although not as readily available and preferred route is via central line. Hyperventilation indicated only if signs of herniation (eg, pupil assymmetry).
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Management - Breathing
Try to keep CO2 normal (35-40) in patients with ICP Risk of ischemia with hyperventilation Hyperventilation used only for acute herniation
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Management - Circulation
Maintain CPP to avoid secondary injury Hypoxemia and hypotension each occur in 1/3 of patients 1 episode of hypotension mortality 2x Eval source of shock: Internal bleeding? Spinal cord injury?
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Monitoring ICP Indications: Types: GCS ≤ 8
Neuro exam impossible (sedated, needs to go to OR for other injuries Types: Ventriculostomy most reliable, also therapeutic Intraparenchymal – measurement drift Subarachnoid, subdural, epidural – less reliable
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Head positioning Head midline Head of bed to 30 degrees
Promote venous drainage
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Sedation/ Analgesia Benefits:
Decrease cerebral metabolic demands associated with pain and stress Prevent spikes in ICP that may occur with suctioning, etc. Facilitate mechanical ventilation Anticonvulsant and antiemetic actions Prevent shivering
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Neuromuscular blockade
Benefits: airway and intrathoracic pressure – facilitate cerebral venous outflow Prevent shivering and posturing Facilitate mechanical ventilation
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Can only be given through a central venous line
Which of the following statements about the use of 3% normal saline is true? Can only be given through a central venous line Does not cause hypotension Can only be used if serum osmolarity < 320 Dose is 10 mL/kg Can only be used if serum sodium is < 160 Dose is 5-10 mL/kg bolus
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Hyperosmolar Therapy 3% normal saline Creates osmotic gradient
Decreases ICP and increases CPP Used as boluses and/or continuous infusion Goal: serum sodium > 150 Max serum osm: 360 ??
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Hyperosmolar Therapy Mannitol Mechanisms: 0.25-1 g/kg doses
blood viscosity creates osmotic gradient between plasma and brain g/kg doses May repeat every 6-8 hours Max serum osm: 320 Adverse effects: ATN Hypovolemia
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CSF Drainage Ventriculostomy catheter
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The hallmark of pentobarbital coma is burst suppression
Which of the following statements regarding the use of pentobarbital is false? Continuous EEG monitoring should be present when a pentobarbital coma is induced The hallmark of pentobarbital coma is burst suppression Pentobarbital causes profound myocardial depression Pentobarbital use requires the approval of a neurologist Pentobarbital reduces cerebral blood flow #4
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Barbiturate Coma Consider in: Mechanisms:
Patients with refractory intracranial hypertension Mechanisms: Lowers resting cerebral metabolic rate by 50% Decreases cerebral blood flow and cerebral blood volume Neuroprotective: inhibits free radical-mediated lipid peroxidation, stabilizes membranes
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Barbiturate Coma Monitoring: Adverse effects: Burst suppression on EEG
Myocardial depression
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Thermoregulation Avoid hyperthermia Increase cerebral metabolism
Inflammation Lipid peroxidation Excitotoxicity Seizures
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Surgical management Decompressive craniectomy
Favorable surgical outcomes: Within 48hrs of injury Secondary GCS Herniation Unfavorable: Unimproved GCS of 3 Extensive secondary brain insults
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Nutrition Begin by 72 hours Full replacement by 7 days
Patients with injury have increased resting metabolism expenditure Increased mortality when head injured patients not fed within 1 week
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Antiepileptic medications decrease the incidence of late seizures
Which of the following statements is true regarding the incidence of seizures in traumatic brain injury? Antiepileptic medications decrease the incidence of late seizures Children < 2yo have a lower risk of seizures Most early seizures occur in the first 24 hours Seizures do not affect the outcome of traumatic brain injury All children with traumatic brain injury should be treated with antiepileptic medications until 1 week post-injury #3
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Antiseizure prophylaxis
Posttraumatic seizures Early: within 7 days Late: after 7 days Adverse effects: Increase brain metabolic demands Increase ICP Lead to secondary brain injury
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Antiseizure prophylaxis
Risk of seizures: Early: 20-39% incidence in severe TBI risk if low GCS < 2 yrs have 3x greater risk Majority occur within first 24 hours
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Antiseizure medications
Risk of seizures Late: 7-12% incidence in severe TBI Increased incidence in depressed skull fracture Relation to early seizures? Prophylactic anticonvulsants do not affect incidence
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