Head Trauma Flashcards
Equation for intra-cranial volume
Water/brain+cerebral blood volume+CSF
Monroe-Kellie Hypothesis
Under normal physiological conditions the volume of all 3 components in the vault remains in a constant relationship
H2O/ brain tissue = 80%
Cerebral blood volume=10%
CSF=10%
As the volume of one increases there is a corresponding decrease in the others to prevent increased ICP
Venous blood is displaced into the scalp
CSF is displaced into the subarachnoid space and production is decreased
Equation for cerebral perfusion pressure
CPP=MAP-ICP
Cerebral Blood Flow
Maintained at a relatively constant level over a wide range of CPP (50-100) therefore mild BP fluctuations will not impact CBF
Chronically hypertensive patients have a higher threshold and shift to the right on a graph
Intracranial compliance
The interrelationship between the change in volume of intracranial components
High compliance -good
Increased ICP occurs when compensation is exhausted and compliance worsens
Mild increases in volume may resulting in dramatic increases in pressure and without intervention compliance fails and leads to herniation
Herniation
Displacement of brain tissue, CSP, and blood vessels outside the their compartments
Supratentorial herniations
Within the skull
Subfalcine
Uncal
Transtentorial
External herniation
Between skull plates
Infratentorial herniation
Through the foramen magnum
Tonsillar herniation
Causes of increased ICP
Increased brain tissue/H2O
Cerebral edema
Brain tumor or other lesion
Cerebral blood volume
Loss of autoregulation due to
trauma, stroke
Decreased venous outflow
Sagittal sinus thrombosis
Increased intra-abdominal pressure
Positional- head
Hematoma
CSF
Hydrocephalus
Assessment findings in worsening compliance
Decreased LOC
Decreased motor response
Decreased or unequal pupillary response
No change in vital signs
Assessment findings after herniation
Unarousable
No motor response
No pupillary response
Vital signs Cushing Triad: Increased
blood pressure, bradycardia,
abnormal respiratory patterns
Equation for cerebral perfusions pressure
CPP=MAP-ICP
Goal is to increase MAP and decrease ICP
Ways to decrease ICP
Decrease H2O on the brain with isotonic IVF, limit free water, or give osmotic solutions like mannitol
What to keep in mind with giving mannitol
With prolonged administration it may increase cerebral edema and ICP instead of lowering
Maintain euvolemia
What to keep in mind with isotonic IVF
Included hypertonic saline solutions such as 2%, 3%, and 23% saline
Establish a Na goal of 140-150
Check Na q4-6
Avoid large shifts in Na in either direction
Ways to decrease metabolic demand of the brain
Maintain normothermia
Seizure prevention
Treat agitation
Anesthesia (barbiturate therapy or propofol)
Treat paroxysmal dysautonomia (storming) with Bromocriptine, propranolol, or narcotics
How to keep excess blood off the brain to maintain CPP
Hyperventilation therapy- CO2 dilates vessels so decrease CO2
Promotes venous outflow
HOB positioning
Avoid an increase intrathroacic
pressure
Avoid trendelenburg
How to drain off excess CSF to increase CPP
Place an EVD
Surgical methods for decreasing ICP
Decompressive hemicraniotomy
Traumatic brain injury
An alteration in brain function or pathology caused by an external force
Primary brain injuries
Occur at the time of trauma
Secondary brain injury
Occurs immediately after the trauma and produces effects over the next several hours or days
Moderate to severe TBI possible physical findingins
Raccoons eyes
Battle sign
Otorrhea
Rhinorrhea
Proptosis
Periorbital edema
GSW entrance and exit wounds
Interventions for mild TBIs
Symptom management for headaches, vestibular disturbances, nausea and vomiting, and visual disturbances
May be complicated by post concussion syndrome
Post concussion syndrome
May last weeks to 3 months
Symptoms may include headaches, nausea and vomiting, personality changes, visual disturbances, vestibular issues, irritability, anxiety, memory loss, depression, or cognitive disturbances
Risks of moderate to severe TBIs
Cerebral edema
Hydrocephalus
Hypo ventilation
Seizures
Loss of airway protection
Aspiration
Loss of auto regulation
Glucose abnormalities
Loss of temp regulation
Diffuse axonal injury
Characterized by extensive generalized damage to the white matter of the brain
Produced in lateral motions of the head
Straining of tentorium and falx during high speed acceleration/deceleration
90% remain in a persistent vegetative state
Acute subdural hematoma
Immediately after injury to 72 hours after
Subacute subdural hematoma
72hours- 2 weeks
Chronic subdural hematoma
Last over 2 weeks
Medical management of subdural hematoma
Observe and watch for reabsorption
Surgical evacuation
Epidural hematoma
Arterial
Requires surgery
Classic shows as: LOC- lucid- LOC
Traumatic sub arachnoid hemorrhage
Most common kind of SAH
History is key to determining if aneurysmal or traumatic
Penetrating head injuries
Manage ICP
Usually require surgery
Life saving measures such as craniectomy may not improve quality of life
