Intracranial bleed Flashcards
First line for subarrach
CT head
Presentation of subarrachnoid haemorrhage
Sudden explosive headache 10/10 pain in back of head - thunderclap
Nausea and vomitting
Photophobia
What is seen on lumbar puncture in a subarrachnoid haemorrhage?
Xanthachromia
What is a subarrahcnoid haemorrhage?
Bleed into subarachnoid space between arachnoid and pia mater meningeal layers
Complications of SAH
Brain damage - hypoxia, raised ICP, direct cranial injury
Neurological disabilities
Coma
Death
Causes of SAH
Traumatic injury or spontaneous
Intracranial aneurysms
Arteriovenous malformation
Unknown
Rare disorders
Risk factors for spontaneous SAH
HPTN
Smoking
FH
Autosomal dominant PCKD
Over 50
Female
Clinical findings in SAH
reduced LOC due to raised ICP
Neck stiff - meningeal irritation
Kerniges sign
What is kerniges sign caused by?
Irritiation of motor nerve roots pass through innflamed meninges as under tension
Non specific
Lab investigations for SAH
FBC and U+Es to obtain a baseline
Coag studies - before LP/surgery
Imaging investiations SAH
Plain CT head - blood in SA space, hydrocephalus
CT angiogram - arterial vessel highlights - aneurysm
When is an LP necessary in SAH?
When SAH suspected but CT scan does not show evidence of bleeding or raised ICP
How quickly does an LP need to be performed after onset?
12 hours
What is xanthochromia?
CSF stained yellow - infiltration of blood
jbilirubin, oxyhaemoglobin from haemolysis RNCs
Management SAG
A to E
Airway - reduced LOC
B - hypoxia - oxygen
C - BP - IV fluids, electrolyte replacement - Na
CCBs MUST be given
D - intracranial pressure monitoring. Pupils dilated = blown = brainstem damage
Why are CCBs given in SAH?
eg nimodipine
To reduce cerebral artery spasm and secondary cerebral ischaemia
General cpmplications ICH
Obstructive hydrocephalus - ventricular drain
Arterial vasospasm
Re-bleeding of aneurysms
Neurological deficits
Cerebral ischaemia
What is an epidural haemotoma?
Haemorrhage between dura mater and inner surface of skull
Subarrach on CT
white in ventricles
Epidural on CT
Lemon on CT
Midline shift
Tentorial/brainstem herniation
Subdural on CT
Moon
How can an Epidural haemotoma cause brainstem death?
Raised ICP can cause cerebellar herniation -> brainstem death
Causes of epidural haemotoma
Skull traum and temporparietal region
eg fall, assault, sporting injury
Rupture of a vein - MMV or dural sinus
Arteriovenous abnormalities, bleeding disorders
Which part of the sull is espicially vulnerable to fracture?
Pterion = pariteal, sphenoid and temporal bones fuse
What artery does a fracture to the pterion dmaage?
Middle meningeal artery
Symptoms of epidural haemotoma
Headache
N+V
Confusion
LOC followed by period of lucidity, progressively decreasing LOC after several
Clinical findings in EDH
Tender skull
Confusion
Reduced GCS
Cranial nerve deficits
Motor or sensory deficits of upper and lower limbs
Hyperreflexia and spasticity
Upgoing plantar reflex - babainskis sign
Cushings triad
What is cushings triad?
Raised ICP to attmept to improve perfusion
-HPTN
-Bradycardia
Irrefular breathing pattern
Bedside investigationsEDH
Cap blood glucose - rule out hypoglycaemia
ECG - heart block - bradycardia cause
Lab investigationsEDH
FBC
U+Es
GCS
CRP
Coagulation
Group and save
Imaging investigations for intracranial bleed gold standard
CT head
When do you do a skull x ray?
When skull fracture to assess for evidence of EDH
Management of EDH
Conservative - bleed is small with miinimal mass effect
Medical - Reversal of anitcoagulation, Prophylatctic antibiotics - in context of open skull fracture, mannitol, barbituates
Surgical - Burr hole craniotomy, trauma craniotomy, hemicranectomy
Coagulopathy
Thrombocytopenia
Porlonged PT
Agents to reduce ICP
Mannitol - IV - osmotic effect prior to surgery
Barbituates - reduce ICP and protect brain from anoxia
Burr hole craniotomy
evacuation of the haematoma.
When is trauma craniotomy used?
Significant mass effect - evacuate blood, treat cause of bleeding (litigation) + reduced ICP
When do hemicraniectomy?
Prevent brain stem herniation + death due to raising ICP in SDH
Post surgical management EDH
ICP monitoring and repeat CT scans
Complications of EDH
Infection
Cerebral ischaemia (adjacent to haemotoma)
Seizures
Cognitive impairment
Hemiparesis
Hydrocephalus (ventricle obstruction)
Brainstem injury (raised ICP)
Types of subdural haematoma
Acute < 3 dyas
Subacute 3 - 21 days
Chronic > 21 days
sIMPLE OR COMPLICATED - PARENCHYMAL injury or not
Types of subdural haematoma
Acute < 3 dyas
Subacute 3 - 21 days
Chronic > 21 days
Cause of subdural haematoma
Trauma
Rupture of cerebral aneurysm
Cerebral hypotension
Malignancy - rare
Spontaneous
Risk factors for developing subdural haemotama
History of trauma
Co-morbidities that make patient vulnerable to falls
Age over 65
Anticoagulant
History of coagulopathy
History of LOC
Fctors that stretch bridging veins eg cerebral atrophy, low CSF pressure after shunt
Alcoholism
Symptoms of subdural haematoma
Headache
Nausea and vomitting
Fluctuating consciousness level:
Confusion, drowsiness, personality change, memory loss
Intervening lucid periods
Poor balance
Weakness
Paraesthesia or numbness
Aphasia if on L side
Findings on exam for subdural haematoma
Neurological exam of CNs, upper limb and lower limb
Limb weakness or sensory disturbance
Cranial nerve abnormalities
Ataxia
Seizures
Reduced LOC
Lab investgiations
FBC
U+Es
LFTs
Coag studies
Group and save - crossmatch
What do you need FBC, U+Es, LFTs and coag studies for in subdural haematoma?
FBC - identify anaemia - raised WCC
U+Es - assess pre-op renal function and electrolyte abnormalities
LFTs = baseline + synthetic function of liver (vit K dependent clotting factors)
Coag studies - identify coagulopathy needing correction to reduce haematoma extension and allow for surgical intervention
Imaging investigations
Non contrast CT head - required for all intracranial bleeding sus
Crescent shaped collection blood overlying one of cerebral hemispheres
CT appearances of SDH acute
Crescent - banana shaped
Acute - hyperdense
Chronic - hypodense - dissolution of liquified blood
Not limited by suture lines
Management of subdural haematoma - medical
Correct coagulation studies - reversal agents, haematology
Anticonvulsants - eg levetiracetam, phenytoin
Complications of SDH
Seizures
Neurological deficits
Recurrent haemorrhage
Infection
ECG subarrach
Peaked P and T waves
Short PR interval
Prolonged QT interval
tall U waves
When do you not perform an LP?
Sus raised ICP
When are CT/MRI angiographyies done in bleed?
TO find sourve of bleed in those fit for surgery
Classification for SAH
Hunt and HEss
1-5
Grades in Hunt and HEss classification for SAH
1 - asymptomatic
2 - moderate - severe headache, nuchal rigidity, CN palsy
3 - drowsy, confused, mild neurological deficit
4 - stupor, moderate to severe hemiparesis
5 - Coma, decerebrate posturing
Risk factors SAH
HPTN
Smoking
Cocaine
Alcohol exceess
Genetic disorders - marfans, ehlers dhanlos, NF type I, polycystuc disease
1st degree relatives
How does trauma cause a SDH
Teearing of bridging veins from tortex to one drainging venous sinuses - rapid acceleration decelration of head
Damaged cortical artery
Blunt head trauma
Investgiations SDH
Bloods - FBCs, U+Es, LFTs, coag screen, grouo and save/crossmatch
CT head = 1st line
Skull X ray
MRI head
Chronic subdural haematoma on CT head
hypodense (dark), crescentic collection around the convexity of the brain
Acute to chronic subdural haematoma
Acute: Symptoms usually develop within 48 hours of injury, characterised by rapid neurological deterioration
Subacute: Symptoms manifest within days to weeks post-injury, with a more gradual progression.
Chronic: Common in the elderly, developing over weeks to months. Patients may not recall a specific head injury.
Neuro symptoms of subdural haematoma
Altered Mental Status: Ranging from mild confusion to deep coma. Fluctuations in the level of consciousness are common.
Focal Neurological Deficits: Weakness on one side of the body, aphasia, or visual field defects, depending on the haematoma’s location.
Headache: Often localised to one side, worsening over time.
Seizures: May occur, particularly in acute or expanding hematomas.
ESP memory loss in elderly
Cushings triad raised ICP
Bradycardia
HPTN
resp irregularities
