Raised ICP Flashcards
What is normal ICP?
5-15 mm Hg
How is ICP regulated?
Autoregulation = vasoconstriction, vasodilation
Chemo-regulation = vasodilation in response to low cerebral pH
When a mass is present intracranially how do constituents change?
Venous volume lost
CSF lost
Outline the pathophysiology of brain injury
Reduction of blood to the brain = lowers oxygen = Na/K ATPase stopes working = more salt inside cell = more oedema = burst = cytotoxic cellular oedema = further swelling and compression = further reduction of blood supply
Outline the signs and symptoms of raised ICP
Headache
Vomiting
Visual disturbances
Depression of conscious level
Infants = slowing increasing head size
Herniation syndrome
Outline the pathophysiology of a headache in RICP
Worse lying down = higher pressure inside the head
Breath slower when sleeping = accumulation of CO2 = vasodilation = more volume inside the head = more symptoms
Compress SVC = stagnate return of venous blood back to heart from head = more blood volume inside head
What causes vomiting in RICP?
Ishcmeia
Starts with nausea, can get projectile vomiting
Outline the causes of visual disturbances in RICP
Compression of optic nerve
Transient blindness = increased pressure = compression
Retinal haemorrhages
Why does conscious level fluctuate during RICP?
Ischaemia of reticular formation
How does the optic nerve change in response to RICP
Swelling of the optic disk = papillodema (optic disk swelling secondary to RICP)
Compression of the arteries
What is a false localising sign
Sign that is pointing to the wrong area
CN6 runs so close to the skull CN6 palsy is the first sign of RICP
What is one of the first signs of RICP?
CN6 palsy
Outline herniation syndromes
Subfalcine herniation = cingulate gyrus across midline - contralateral leg weakness if anterior cerebral A affected
Uncal herniation = uncus displaced across tentorial opening – puts pressure on midbrain, compression of CN 3 (dilated pupil)/cerebral peduncle (leg weakness)
Tonsillar herniation = herniate through foramen magnum – compression of medulla and upper spinal cord, cardiac/resp dysfunction, decreased consciousness
Outline the cushings reflex
In response to long term RICP
Triad = 1) high BP, 2) bradycardia, 3) low resp rate
Mechanism = Ischaemia at medulla –> sympathetic activation –> Rise in blood pressure + tachycardia. Baroreceptors react –> bradycardia. Ischaemia at pons/medulla at resp centres –> low resp rate.
What are the causes of RICP?
1) increased cerebral blood vol = venous outflow obstruction, venous sinus thrombosis
2) increased CSF = choroid plexus papilloma (excessive secretion), hydrocephalus (impaired absorption)
3) cerebral oedema = meningitis, encephalitis, diffuse head injury, infarction
4) space occupying lesion = abscess, tumour, haemorrhage
Discuss CSF
Clear
Hyperosmolar compared to plasma
Production = choroid plexus cells
Filtering = arachnoid vili in dural sinuses
Through aperture to subarachnoid space bathing
Discuss hydrocephalus
Accumulation of CSF is thought to be due to an imbalance between production and absorption of CSF with subsequent enlargement of brain ventricles
Obstructive = within/between ventricles, congenital or acquired
Communicating = problem outside the ventricular system, mostly post-meningitits, block arachnoid villi
Discuss how brain tumours can cause RICP
Tend to be midline or posterior
Children = astrocytomas
Adults = gliomas, meningiomas, mets from lung/breast/kidney
Outline Idiopathic intracranial hypertension
RICP without evidence of hydrocephalus or mass lesion
All scans normal
Usually obese young women after weight gain
Outline the principles of management regarding raised ICP
Increased cerebral blood vol = anticoag, tenting venous sinuses
Increased CSF = shunts, tumour resection, diuretics
Cerebral oedema = treat cause, mannitol, hypertonic saline
Space occupying lesion = surgical resection, steriods
What is the acute management of RICP?
NO lumbar puncture, nil by mouth
ABC and oxygen
Glucose – rule out other causes
Mannitol (osmotic diuretic)
