Head trauma Flashcards
Primary goal of treatment for patients with suspected traumatic brain injury
Prevent secondary brain injury
Via ABCDE and controlling BP etc
Cushing’s triad
(Aka Cushing’s response)
Hypertension
Bradycardia
Irregular breathing
Implication of Cushing’s triad
Impending uncal herniation (coning)
Uncus
Medial part of temporal lobe
Compartments of the intracranial cavity
Supratentorial compartment
Infratentorial compartment
Through which structure does the uncus herniate
Tentorial notch
Consequence of uncal herniation
Compression of midbrain
Compression of CN III
Contralateral hemiparesis
Implication of a blown pupil
Midline shift and impeding uncal herniation
eg from subdural haematoma
Classical signs of (impending) uncal herniation
Ipsilateral blown pupil
Contralateral hemiparesis
Cushing’s response
Monro-Kellie Doctrine
Total volume of intracranial contents must remain constant as it is a closed space
When intracranial volume increases, ICP rises
CSF and venous blood compressed out first
Once this compression has reached capacity, brain matter becomes compressed
Leads to herniation / hemispheric shift
Cerebral perfusion pressure
Cerebral perfusion pressure = Mean arterial pressure - Intracranial pressure
Intracranial consequence of low MAP
Ischaemia / infarct of brain tissue
Intracranial consequence of high MAP
Brain swelling
Layers of the meninges including vessels
Skull
Meningeal arteries
Dura mater (encloses large venous sinuses)
Arachnoid mater
Blood vessels and CSF
Pia mater
Grey matter
White matter
Parts of the brainstem
Midbrain
Pons
Medulla
Ventricular system in brain
Filled with and constantly produce CSF
CSF absorbed over brain surface
Consequence of blood in CSF
Can impair reabsorption of CSF and increase intracranial pressure
Normal intracranial pressure
10 mmHg
Raised intracranial pressure associated with poor outcomes
20 mmHg
Methods of classifying Traumatic brain injury
Severity
Morphology
Severity of traumatic brain injury classification
Mild = GCS 13 - 15
Moderate = GCS 9 - 12
Severe (/ coma)= GCS 8 or less
Morphology of traumatic brain injury classification
Skull fractures:
- Vault
- Basilar
Intracranial lesions:
- Focal
- Diffuse
Signs of basilar skull fracture
Panda eyes
Battle’s sign
Oto/rhinorrhoea of blood or CSF
Facial paralysis
Hearing loss
Focal intracranial lesion examples
Epidural haemorrhage
Subdural haemorrhage
Intracranial haemorrhage
Diffuse intracranial lesion examples
Concussion
Multiple contusions
Hypoxic / ischaemic injury
Axonal injury
Axonal injury mechanism of injury
High velocity impact or deceleration impact
Multiple punctate haemorrhages throughout cerebral hemispheres
Often poor outcome
Concussion definition
Transient, non-focal neurological disturbance
Often LOC
No CT changes
Classic presentation of extra-dural haematome
Lucid interval between injury and neurological deterioration
Concern with cerebral contusions
In hours to days can evolve to form intracerebral haematomas and may require surgery
Repeat CT scans to assess progressive changes
Management of mild TBI (traumatic brain injury)
Often associated with concussion
Usually make uneventful recovery
Indications for CT head
Initial GCS <13
GCS <15 after 2 hours
Suspected open or depressed skull fracture
Sign of basilar skull fracture
Vomiting > 2 episodes
LOC / amnesia and >65 yrs age
LOC > 5 mins
Amnesia > 30 mins prior to HI
Anticoagulant use
Dangerous mechanism of injury
Management of moderate TBI
CT head with follow up scan within 24 hours
D/W neurosurgery
Admit for observation in ITU
Management of severe TBI
Urgent Neurosurgical consult
Intubate
Treat hypotension and hypoxia
Maintain pCO2 around 4.7 kPa (35 mmHg)
Consider mannitol, pCO2 28-32 for deterioration
Avoid pCO2 <28
Target for systolic BP in TBI
Age 50 to 69: SBP > 100 mmHg
Age 15 to 49 or >70: SBP > 110 mmHg
Replacement of choice to manage hypovolaemia in TBI and why?
Isotonic fluids
Intracranial haemorrhage cannot cause haemorrhagic shock
Best prognostic indicator in patients with variable response to stimulation
Best motor response
Focussed neurological examination in primary survey
Level of consciousness
Pupil size and response
Lateralising signs to each limb
Signs of spinal cord injury when pt alert
Secondary survey neuro exam
Complete neurological examination
Reversal of antiplatelets (eg Aspirin, clopidogrel)
Platelets
Consider Deamino-Delta-D-Arginine Vasopressin (Desmopressin acetate)
Reversal of warfarin
FFP
Vitamin K
Reversal of unfractionated heparin
Protamine sulfate
Monitor APTT
Reversal of low molecular weight heparin
Protamine sulfate
Reversal of direct thrombin inhibitors (Dabigatran)
Idarucizumab (Praxbind)
May benefit from prothrombin complex concentrate
Reversal of rivaroxaban
No reversal agent
May benefit from prothrombin complex concentrate
Use of mannitol
Reduces raised intracranial pressure in euvolaemic patients with raised ICP
Contraindication to mannitol
Systemic hypotension SBP < 90
Dose of mannitol
0.25 - 1 g/kg
Use as bolus
Monitoring with mannitol use
ICP monitor (unless evidence of herniation)
Maintain serum osmolality <320
Maintain euvolaemia
Mechanism of action of mannitol
Acts as osmotic diuretic
Use of hypertonic saline
Reduces raised ICP in euvolaemic patients
Concentration of hypertonic saline used
3% to 23.4%
When is hypertonic saline preferred to mannitol
With systemic hypotension
Both provide equivocal effects to reduce ICP in euvolaemic patients
When to use anticonvulsants in TBI
Only when absolutely necessary to cease seizure activity
Anticonvulsants can inhibit brain recovery
Which anticonvulsants are used in TBI and when
Phenytoin and Fosphenytoin in acute phase
Benzodiazepines added if necessary until seizure stops
Management of intracranial mass lesions
Neurosurgery
Rapidly expanding life threatening haematomas may warrant emergency craniotomy
Management of penetrating brain injury
CT head +/- angiography
Prophylactic abx
Leave partially exteriorised objects in place until definitive neurosurgical management
Determination of death by neurological criteria
(Brain death)
1) GCS 3
2) Non reactive pupils
3) Absent brainstem reflexes
4) No spontaneous ventilatory effort on formal apnoea testing
5) No confounding factors eg EtOH, drugs, hypothermia
Brainstem reflexes
Oculocephalic (Doll’s eyes)
Corneal
Gag reflex
