From
StayCurrentMD
Traumatic Brain Injury
With Dr. Pramod Pulaamba · hosted by Dr. Em Gootee & Dr. Ray Hankey
Part of
Traumatic Brain Injury 3 items
Chapter 1 of 7 · Case-Based Learning
Initial management
Case presentation and initial management
Expert statements on this page
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Host summaries · secondary, not cited in answers
Educational content from recorded physician discussions — not medical advice. Talk to your (or your child's) care team about your situation.
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What the experts said
For a patient with small epidural hematoma, immediate neurosurgical consultation is needed to determine if surgical evacuation is required.
Small epidurals may be managed with repeat CT scan in several hours or clinical observation for deterioration rather than immediate surgery.
ICP monitoring should be discussed with neurosurgeons for patients being managed for potential intracranial pressure issues.
Invasive blood pressure monitoring is needed for accurate blood pressure identification in patients with intracranial hypertension.
Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure.
Most guidelines suggest keeping cerebral perfusion pressure greater than 45 mmHg as minimal acceptable, sometimes 55 mmHg in children.
ICP above 20 may require ongoing treatment and/or reevaluation with imaging.
Acute intracranial hypertension may first manifest as dilation of the ipsilateral pupil or progressive bradycardia with hypertension.
Acute ICP management includes raising head of bed to improve venous drainage, providing oxygen, and bag valve masking.
Hyperventilation to PCO2 of around 35 helps vasoconstrict the brain and reduce ICP.
Opening an ICP drain is one of the first interventions to evacuate fluid and reduce pressure.
3% normal saline at 5 mL per kilogram will generally increase serum sodium by 3 to 5 mEq per liter.
3% normal saline has a higher osmolarity limit (360 millimoles) compared to Mannitol (320 millimoles).
Hypotension in the context of closed head injury is a very poor prognosticator and should be avoided at all costs.
In older children and teenagers, systolic blood pressure should be kept above 90 or 95 mmHg; younger children should use age-appropriate norms.
Norepinephrine can be used to drive up blood pressure to maintain cerebral perfusion.
Based on the most recent guidelines published in Pediatric Critical Care Medicine, there is no evidence that 3% saline is better than Mannitol or vice versa.
Mannitol's diuretic effect can lead to difficult-to-control diuresis and potential hypotension.
Mannitol's first effect within 15 to 20 minutes is changing blood vessel rheology to allow freer passage through cerebral circulation and improve oxygen delivery, not diuresis.
The dose of Mannitol is 0.5 to 1 gram per kilogram.
There is no role for steroids in pediatric traumatic brain injury.
Steroids are no longer considered effective therapy for suspected spinal cord injury and may cause detriment.
Neurosurgical options after failed conservative treatment include simple evacuation of surgical lesions like epidurals.
Decompressive craniectomy is an emerging option for diffuse axonal injury with difficult-to-control ICP when there is no true surgical lesion to decompress.
In decompressive craniectomy, the bone is preserved and can be replaced after things settle down.
For persistently elevated ICP above 20 with higher spikes, the patient will slowly deteriorate to the point of being unsalvageable without intervention.
Based on the third iteration of Management of Traumatic Brain Injury in Children published in Pediatric Critical Care Medicine, there is no clear consensus that decompressive craniectomy improves outcomes.
Major trauma centers across North America are using decompressive craniectomy more frequently for severe TBI.
CT scan is preferred in acute situations with acute ICP presentation because it provides the best information for determining need for OR or drain placement.
MRI is used after the first 48 hours once the patient is stable and ICP spikes are controlled, primarily as a prognosticator.
MRI is useful in severe cases for counseling families and directing care plans, and can be repeated in a week to determine true extent of injury and level of disability.
CT head scan can be completed in 5 minutes versus 20-30 minutes for MRI, making it preferable for critical patients.
Sympathetic storming occurs due to imbalance of sympathetic and parasympathetic nervous systems as a result of head injury.
Untreated sympathetic storming can lead to secondary brain injury or potentiate ongoing injury.
Hyperventilation during sympathetic storming leads to vasoconstriction which could cause cerebral hypoxia and further cellular injury.
Hypertension during sympathetic storming can lead to hemorrhage within the brain.
Arrhythmias during sympathetic storming can lead to hemodynamic instability and hypoperfusion.
Neurogenic pulmonary edema is sometimes common in TBI patients and can cause hypoxia and difficult ventilation.
The cornerstone of sympathetic storming treatment is sedation and pain control, usually with narcotics and/or benzodiazepines as first-line medications.
Bromocriptine acts on the hypothalamus to reduce hyperthermia, diaphoresis, and blood pressure in sympathetic storming.
Oxycodone has been used for its longer-acting effect for pain control in sympathetic storming.
Propranolol can help control arrhythmias and lower blood pressure in sympathetic storming.
Clonidine is an alpha-2 agonist that can reduce levels of catecholamines throughout the body and reduce ongoing sympathetic storm.
Traumatic brain injury caused over 837,000 visits, hospitalizations, and deaths in children in 2014.