Neuro18 - Raised Intracranial Pressure Flashcards
Volumes inside the skull
Brain, Blood, CSF
1.) Brain - 1300-1750ml
- intracellular fluid is 900-1000 mls
- extracellular fluid is 100-150mls
- tissue is 300-400mls
2.) Blood and CSF - 100-150mls each
5 general features of intracranial pressure (ICP)
Normal ICP/CSF Pressure
Relationship Between ICV (volume) and ICP
Risk Factors for raised ICP x5
Compensatory Mechanisms for Raised ICP x4
Cerebral Perfusion Pressure (CPP)
1.) Normal ICP/CSF Pressure (mmHg)
- adults: <10-15, children: 3-7, term infants: 1.5-6
2.) Relationship Between ICV and ICP - exponential
- ↑ICV leads to exponential (not linear) ↑ in ICP
3.) Risk Factors for Raised ICP
- severity of head injury, abnormal CT scan
- age >40, BP <90, abnormal motor posturing
4.) Compensatory Mechanisms for Raised ICP
- ↓CSF volume by movement of CSF into spinal cord
- ↓CSF production
- ↓blood volume as blood is squeezed out the sinuses
- ↓ in extracellular fluid (delayed compensation)
5.) Cerebral Perfusion Pressure
- CPP = mean arterial pressure (MAP) - ICP
- ↑ICP –> ↓CPP which will lead to brain ischaemia
4 features of an ICP waveform
Pulses x2
P1, P2, P3
Peaks During Raised ICP
Lundberg Waves (ABC)
1.) Pulses - arterial/vascular and respiratory pulses
- respiratory cycle forms most of the amplitude
- arterial pulse forms the a smaller, peak, amplitude
2.) P1, P2, P3 - peaks in an ICP waveform
- P1 represents the arterial pulse, P2 is the brain tissue compliance, P1 is normally the highest peak (P1>P2)
- P3 is the dicrotic notch (closure of the aortic valve)
3.) Peaks During Raised ICP
- acute brain injury causes compliance to decrease, causing P2 to become the highest peak (P2>P1)
4.) Lundberg Waves - ICP waveform trend over time
- A/Plateau: steep ↑ICP lasting 5-10 mins, always pathological and suggests early brain herniation
- B: rhythmic oscillations every 1-2mins, associated with unstable ICP
- C: oscillations every 4-8 months, normal
Cushing Reflex
Raised Intracranial Pressure
Hypercapnia
Reflex Bradycardia
1.) Raised Intracranial Pressure
- leads to a fall in cerebral blood flow/CPP
- reduced blood flow leads to a build up of CO2
2) Hypercapnia - triggers sympathetic nervous system
- vasoconstriction –> ↑MAP –> ↑CPP
3.) Reflex Bradycardia - ↓HR as a response to the ↑BP detected by baroreceptors in aortic arch and carotids
Symptoms and signs of raised ICP
Symptoms x4
Signs x8
Pupil Reactions
1.) Symptoms
- headache, N+V, diplopia, other neurological changes
2.) Signs
- Cushing’s: ↓HR, ↑systolic BP, irregular respirations
- confusion, ↓mental ability, loss of consciousness
- non-reactive pupils, papilledema
3.) Pupil Reactions
- normal –> constricted and slightly reactive –>
- normal size, unreactive –> fixed and dilated
- contralateral eye lags behind ipsilateral eye
4 types of brain herniation
Cingulate/Subfalcine
Central/Transtentorial
Uncal
Tonsillar/Coning
1.) Cingulate/Subfalcine - part of the frontal lobe (cingulate gyrus) is scraped under the falx cerebri
- often a precursor to other types of herniation
2.) Central/Transtentorial - brain moves upwards or downwards across the tentorium cerebelli
3.) Uncal - uncus moves towards the tentorium, putting pressure on the midbrain/brainstem
- can compress the oculomotor nerve
4.) Tonsillar/Coning - cerebellar tonsils move down through the foramen magnum
- this can compress the lower brainstem or the upper cervical spinal cord
Pathophysiology of anoxic brain injury
Reduced ATP
Failure of the Sodium Pump
Influx of Na+ into Cells
Mitochondiral Anoxia
1.) Reduced ATP - ↓in cerebral blood flow –> ↓oxygen
2.) Failure of the Sodium Pump - due to ↓ in ATP
3.) Influx of Na+ into Cells - reverse of the Na pump
- causes depolariastion
- also brings water which causes oedema
4.) Mitochondrial Anoxia - causes metabolic failure
- activates nitric oxide synthase (NOS) –> ↑NO radicals
- toxic oxygen radicals are also produced
6 main causes of raised ICP
Localised Mass Lesions x3
Disturbances in CSF Circulation
Obstruction to Venous Sinuses x2
Diffuse Brain Oedema/Swelling x4
Craniosynostosis
Idiopathic
1.) Localised Mass Lesions
- haematomas: extradural, subdural, intracranial
- abscess, focal oedema
2.) Disturbances in CSF Circulation
- hydrocephalus (obstructive and communicating)
3.) Obstruction to Venous Sinuses
- depressed fractures overlying major venous sinuses
- cerebral venous thrombosis
4.) Diffuse Brain Oedema/Swelling
- infection: encephalitis, meningitis
- injury: subarachnoid or diffuse head injury
- water intoxication/drowning, lead encephalopathy
5.) Craniosynostosis - premature fusion of parts of the skull. As brain grows, skull becomes more misshapen
- features: prominent forehead (contralateral) and temporal region (ipsilateral), deviated nose
6.) Idiopathic (IIH)- benign intracranial hypertension
- demographic: obese, young-middle aged woman
- diagnostic: lumbar puncture if no blockage of CSF, must exclude venous sinus thrombosis
5 obstructions in non-communicating hydrocephalus
Interventricular Foramen/Foramen of Monro
Cerebral Aqueduct/Aqueduct of Sylvius
Fourth Ventricle
Median and Lateral Apertures
1.) Interventricular Foramen/Foramen of Monro
- may lead to dilation of one/both lateral ventricles
2.) Cerebral Aqueduct/Aqueduct of Sylvius
- causes: atresia, ependymitis, tumour, haemorrhage
- dilation of both lateral and 3rd ventricle
3.) Fourth Ventricle
- caused by tonsillar herniation (Chiari malformation)
- dilation of the aqueduct, lateral, and 3rd ventricles
4.) Median and Lateral Apertures
- foramen of Magendie and foramen of Luschka
- obstruction: Dandy-Walker (congenital) malformation
General management/Tier 0 for raised ICP
Assess ABCs
Blood Pressure
Fluids
Other x3
1.) Assess ABCs - airway, breathing, circulation
- hypoxia ↑ICP due to vasodilation and oedema
- CO2 is also a potent cerebral vasodilator
- sedatives can be used if intubation is required
2.) Blood Pressure - prevent hypotension
- hypotension ↓ cerebral perfusion which exacerbates secondary brain injury
- hypertension is a compensatory mechanism
3.) Fluids - rehydrate using oral route in stable patients
- avoid hypo-osmolar solutions and hyponatraemia and albumin
4.) Other - other ways to prevent a spike in ICP
- sedation and analgesia to reduce/prevent pain
- control any fevers to prevent a spike in ICP
- facilitate cerebral venous drainage (elevate bed)
3 features of communicating hydrocephalus
What is it?
Arachnoid Granulations
Causes x3
1.) What is it? - accumulation of CSF due to impaired CSF reabsorption and without obstruction of CSF flow
2.) Arachnoid Granulations - often impaired
- site of CSF reabsorption back into the venous system
- this is located along the superior sagittal sinus
3.) Causes
- subarachnoid/intraventricular haemorrhage
- infections/inflammation of the subarachnoid space
- congenital abscence of arachnoid villi
Criteria for an urgent CT head
Consciousness x2
Neurological Abnormality x3
Other x2
1.) Consciousness
- GCS < 13 at any point
- GCS < 14 2 hours after injury
2.) Neurological Abnormality
- focal neurological deficit, seizure
- LOC w/ any of: age >65, coagulopathy, dangerous mechanism of injury, anterograde amnesia > 30mins
3.) Other - fracture or vomiting
- open/depressed or basal skull fracture
- 2+ discrete episodes of vomiting
Advanged management for raised ICP
Tier 1 x2
Tier 3 x3
1.) Tier 1 - hyperosmolar therapy and CSF diversion
- hypertonic saline or mannitol, diuretics
- CSF drainage, hyperventilation (↓CO2)
2.) Tier 3
- barbiturate induced coma, optimised hyperventilation, decompressive craniectomy
