Monro-Kellie hypothesis
Understanding how our patients progress with TBI
3 brain components: brain csf blood
Any increase of one component requires a decrease in another
the total volume of the brain, cerebrospinal fluid (CSF), and blood within the skull is constant. If the volume of one component increases, the volume of another must decrease to maintain equilibrium
ICP
Normal 0-15mmHg
Estimate 20 when you don’t know
Cerebral Blood Flow
Requires 15-30% of cardiac output to meet metabolic demands
Maintained by cerebral auto regulation, despite changes in cerebral perfusion pressure CPP
CPP (cerebral perfusion pressure)
Normal 60-70 optimal CBF, <50 infarction
CPP= MAP - ICP (est 20 when don’t know)
MAP= [(Diastolic BP X 2) + SBP) / 3
Min map 90 in trauma pt, 80 in peds
Causes of secondary TBI
3 H’s: hypoxia, hypo hypertension, hypo hypercapnia
Ischemia
Edema
Increased ICP
Vasodilation – maintain ETCO2 35-40
Signs Inc ICP
Change in LOC
Sighs of herniation: decirticate decerebrate, blown pupil
** Cushing’s Triad***
Widened pulse pressure (HTN)
Bradycardia
Cheyne Stokes resp
CT
Subdural- concave- looks like a banana
Epidural- convex- looks like a lemon
Subdural hematoma Tx
Between dura mater and arachnoid membrane
Always venous
Acute: < 4 days, subacute 4 to 21 days, chronic greater than 21 days
Tx: reduce stim, osmotherapy (mannitol 3%), Na+ upper limit of 155, higher serum osmolality (less volume more solute- cell shrinks down), anticonvulsant keppra or Dilantin
Epidural hematoma
Always from trauma
Occurs between the cranium and Dura matter often associated with skull fracture
Usually arterial bleeding from the middle meningeal artery, but can be Venus in some case
Causes rapid compression of the brain stem
Classic presentation, LOC, lucid, interval, neurological deterioration 
They initially lose LOC, wake back up, and then the second loss of consciousness is when herniation starts 
Subarachnoid hemorrhage
A lot of times caused from AVM but can be caused by trauma or aneurysm occurs mostly in circle of Willis inside brain
Signs: decreased mental status, seizure, sudden onset of severe headache, nausea, vomiting
Tx: SBP<140, Dec ICP
Big thing: don’t allow re-bleading
Give nicardipine for BP
Intraventricular hemorrhage
Trauma, aneurysm
Found in frontal and temporal lobe injuries
Treatment maximize CPP greater than 70 maintain SVP less than 160, control ICP
More serious injury, bad outcomes 
Diffuse axonal injuries DAI
Occurs when nerve fibers are shown torn or stretched as a result of head impact (frontal-occipital impacts)
MRI preferred for diagnosis
Often diagnosed by ruling out, other injuries, difficult to diagnose bc doesn’t show up on CT
Patients don’t do well
Treatment: prevent secondary injuries, avoid hypotension, hypoxia, cerebral edema, and elevated ICP 
Hypoxic ischemic encephalopathy
Inclusion criteria: Neonate’s greater than 35 weeks presenting on the first day of life with evidence of HIE
Exclusion criteria: in infants, less than 35 weeks, encephalopathic infants due to causes other than ischemic encephalopathy
is there any evidence of intrapartum hypoxia. Most often caused from shoulder dystocia
Therapeutic hypothermia: 33-34C, EEG and supportive care
Seizure
75% of pediatrics will have first seizure activity as status seizures
Causes: hyperthermia, hypoglycemia, hyperglycemia, electrolyte, imbalances
Management: airway, intubation, mechanical ventilation,
First line: Ativan .1mg/kg, Valium .15-.2mg/kg
Second line: phenytoin 20mg/kg, valproic acid 20-40mg/kg phenobarbital 15-20mg/kg
Anterior cord syndrome
Iatrogenic, not common in trauma
Anterior spinal artery embolus
Aortic dissection
Hyperflexion injury of the cervical spine
Signs: injury below T10, urinary incontinence, spastic, paralysis, loss of pain, pressure, temp, crude touch
Brown-Sequard Syndrome
***TQ
Results from an injury to 1/2 of the spinal column
Causes: penetrating trauma, like stabbing or GSW, spinal cord tumor
Signs: ipsilateral loss of fine touch, ipsilateral UMN lesion, contralateral loss of pain/temp
Central cord syndrome
Causes: hyper extension, injury, parentheses MVA, diving), syringomyelia (chiari malformation)
These are cervical – thoracic injuries, upper motor neuron, upper extremities affected more than lower*TQ**
Sciwora
Neurological symptoms of a spinal cord injury despite normal imaging. Often associated as swelling of the spinal cord
Spin
Cord
Injury
Without
Radiograph
Abnormality
2 assessment findings that are important in spinal cord injury patient
1) Are they hot or cold? True spinal cord injuries will say they are hot.
2) can they lift their legs?
Spinal shock versus neurogenic shock 
Spinal shock is acute spinal cord injury, loss of voluntary reflexes below level of injury, last days two months
Neurogenic shock is an acute spinal cord injury C1 to T5, loss of vasomotor and sympathetic, nervous system tone below level of injury, hypotension, bradycardia, temperature regulation, last up to six weeks. Norepi first line med when they start to diurese
Spinal shock is a temporary neurological state of depressed reflexes that resolves, neurogenic shock is a persistent circulatory problem from loss of sympathetic tone
Autonomic dysreflexia
Side effects of spinal cord injury. Lesions t6 and above. Any pain stimuli induced this- spiked BP
Ex: kinked foley cath, too small shoes. Pt can’t register pain but body responds w spike in BP
What can increase mortality by 50% in spinal cord injuries?
One episode of hypoxia or hypotension 
What happens with hypocarbia?
Leads to decrease cerebral blood flow and possible cerebral ischemia
A patient suffering from brown Sequard syndrome presents how?
Greater weakness and upper extremities and lower extremities
Ipsilateral motors, contralateral pain loss
Complete motor pain and temperature loss below the level of the injury
Complete flaccidity below the level of the injury 
Ipsilateral motor loss, contralateral pain loss