Head Injury Flashcards
CT features of Extradural haematoma
Biconvex shape
?midline shift and ventricle compression - sign of impending herniation
When to consider CT head for trauma?
High risk criteria
- GCS <15 2 hours post injury
- Suspected open or dperessed skull fracture
- any sign of base of skull fracture
- >2 epsidoes of vomiting
>65 years old
anticogaulated
Medium risk
retrograde amnesia >30mins
dangerous mechanism
- pedestrian struck by motor vehicle
- ejected from vehicle
- fall from >3ft or 5 stairs
Normal ICP
supine 7-15 mmHg
standing -10 (never less than -15)
Ways to measure ICP
intraventricular catheter is the gold standard as it allows drainage to lower ICP but it is the most invasive method and carries a risk of infection.
An intraparenchymal prpobe has a lower infection risk but only meausres local pressure and zero cand rift, and cannot be reset which it can in an intraventricular catheter
subarachnoid and epidural probes have lower infection rate and epidural doesn’t require dura puncture but both have limited reliability
Lumbar CSF measure is inaccurate and may be dangerous if there is brain oedema
what is the danger of LP in increased ICP
herniation and coning
what is the cushing reflex
physiologic nervous system response to an elevated ICP that results in cushings triad - hypertension, bradycardia, and irregular respirations.
hypertension occurs to ensure adequate CPP.
pathophysiology of increased ICP
monro-kellie hypothesis
the skull is a fixed box containing 3 components
brain (80%) blood (10%) and CSF (10%)
These 3 component govern ICP/volume relationship
increase volume in one will cause a compensatory fall in another to prevent rise in ICP
however whenICP has reached 25mmHg, small increases in volume may cause marked elevation in ICP due to failure of intracranial compliance leading to herniation
what is a lucid interval
a temporal improvement in condition after TBI after which the condition deteriorates with rapid decline in GCS
during this period blood accumulated in extradural space leadinf to an inceased ICP and coerebral oedema
CPP equation
CPP = MAP - ICP
MAP equation
MAP = Diastolic + 1/3( systolic-diastolic)
MAP autoregulation
between 50-150mmHg
to maintain constant cerebral blood flow. Disruption in MAP autoregulation can cause cerebral ischaemia
clinical picture of raised ICP
haedache
nausea/vomiting
papilloedema
fall in GCS
dilated pupil (CNIII palsy)
defect in lateral gaze ( CNVI palsy)
cushings triad - hypertension, bradycaria, irregular resps
management of raised ICP
ABC approach
A - Assess the airway consider intubation if reduced GCS
B - ensure adequate oxygenation and ventilation. Can hyperventilate as a temporary measure to reduce ICP. Hyperventilation causes cerebral vasoconstriction and decreasing cerebral blood flow.
C - ensure adequate blood volume, reduced cerebral perfusion worsens ischaemia so aim for a MAP 60-80.
D - assess GCS, pupillary response, neurology
E - fully expose to look for further injuries, prevent hypothermia
Improve venous drainage from the brain
- elevate the head to 30 degrees
- head in neutral position
- do not compress neck veins with ET tube ties
- imbolisation with sandbags and tape as opposed to collar
Reduce cerebral oedema
- mannitol (0.5-1mg/kg)
- hypertonic saline is an alternative
- monitor NA levels maintain 140-145
- furosemdie (0.5-1mg.kg
reduction of metabolic rate for oxygen
- adequate sedation and analgesia - agitation, pain, coughing will increase ICP
- close temperature regulation (avoid hyperthermia but don’t actively cause hypothermia)
- if witnessed sezure, load with anticonvulsant
- burst suppression on EGG - thiopentone infusion
reduce blood volume
- hyperventilate to induce vasoconstriction temporarily but can cause ischaemia if prolonged
- definitive is depressive craniectomy
reduce CSF volume
- in a neurosurgical centre, external ventricular drain allows drainage of CSF
CT head findings SDH
crescentic hyperdense lesion
loss of grey-white matter
studies have shown that injury to grey matter, the areas of the brain with neural cell bodies, can cause long-term cognitive disability
What is GCS
neurological scale aimed to be a reliable objective way of recording the conscious state of a perso for initial and subsequent assessment
M6 - oberys commands
M5 - localise to pain
M4 - withdraw from pain
M3 - abnormal flexion in response to pain
M2 - extending to pain
M1 - no response
V5 - oritentated
V4 - confused
V3 - words
V2 - sounds
V1 - none
E4 - spontaneous
E3 - speech
E2 - pain
E1 - none
Management if acute SDH
Active SDH +/- coma, signs of raised ICP or neurological deterioration since the injury with potential for recovery should have urgent surgaical evacuation of the haematoma. Or patiets with a clot thickness of >10mm or midline shift >5mm on CT regardless of GCS
Nonsurgical patients need close nerological monitoring, ideally in ITU with ICP monitoring and serial head CTs. Any sign of neurological deterioration or maintained raised CICP (?20mmHg) shoud have urgent surgical evacuation
indications for intubation
GCS <8
risk of raised ICP due t agitation
inability to control/protect the airway or loss of laryngeal reflexes (M4 or less)
to opitimise ventilation and oxgygenation
seizures
compromised airway
severe facial injuries
advantages of tracheostomy
hygeine
reduced cahnce of aspiration
les dead space
long-term option
ventilator weaning
may allow swallowing and eating and drinking
Extradural haematoma vs subdural haematoma
*Extradural haematoma (EDH) appears as a biconvex or lenticular hyperdense collection on CT, often associated with a middle meningeal artery rupture. It typically causes a rapid deterioration after a lucid interval and is confined by the sutures.
Subdural haematoma (SDH) presents as a crescentic or banana-shaped hyperdense collection, usually along the convexity of the brain. It is often caused by venous bleeding, typically from bridging veins, and may cause slower deterioration. SDH can cross suture lines and is often associated with shearing injuries. The mass effect may be less abrupt than in EDH, and it can cause gradual or progressive worsening of symptoms
