Intracranial Haemorrhage

Question 1

Causes of ICH

Answer 1

• Intracerebral =15% of Stokes (Remainder are Ischaemic); Rupture of Charcot-Bouchard
Microaneurysms, Degeneration of Small deep penetrating arteries
• Associated with long term Hypertension; Typically, at Basal Ganglia, Pons, Cerebellum and
Subcortical White Matter
Normotensive patients 60+ typically have Lobar Cortical Intracranial Haemorrhage;
Associated with Cerebral Amyloid Angiopathy (rare)

Question 2

Presentation of ICH

Answer 2

• Hard to distinguish between Haemorrhage and
Thromboembolic infarction; Tends to present with more
severe Headache and more likely to lead to Coma
Seen on CT imaging immediately (unlike Thromboembolic);
Intraparenchymal, Intraventricular or Subarachnoid blood;
MRI-DW as good as CT

Question 3

Presentation of Cerebellar Haemorrhage

Answer 3

Headache, Stupor/Coma,
Cerebellar Signs (Nystagmus, Ocular Palsy, Strabismus);
Gaze deviates towards side of Haemorrhage

Question 4

Management of ICH: BP

Answer 4

Stabilise to SBP below 110mmHg;

Mannitol can reduce ICP

Question 5

Management of ICH: Other

Answer 5

Treatment of any underlying coagulopathy (FFP, Factors,
Vitamin K, Platelets)
• Anticonvulsants if any seizures or Lobar Haemorrhage
• Stress Ulcer prophylaxis (H2 antagonists, PPI)

Question 6

Management of ICH: Surgery

Answer 6

Emergency Neurosurgical Clot Evacuation by Craniotomy, especially if Deepening Coma or Coning (Pupil dilation and
failure to constrict to light, Lowered LOC, Abnormal
posturing, Vomiting due to compression of Medulla);
Especially if Haematoma >3cm

Question 7

Management of ICH: Contraindicated drugs

Answer 7

Anticoagulation and antiplatelet

Question 8

Causes of SAH

Answer 8

Spontaneous Arterial Bleeding into Subarachnoid space; 5% of all Strokes, most commonly due to rupture of Berry Aneurysms (70%); Sometimes AVM (10%); Rare
associations might be Tumours, Acute Bacterial Meningitis,
Bleeding disorders, Connective Tissue Disorders

Question 9

Berry Aneurysms: Sites of formation

Answer 9

Develop within Circle of Willis and adjacent arteries; Commonly between PComm/ICA (PComm Aneurysm), AComm/ACA (AComm Aneurysm) or Tri/Bifurcation of MCA (MCA
Aneurysm); Other sites might be Basilar, PICA, ICA and Ophthalmic

Question 10

Commonest causes of painful Oculomotor palsy

Answer 10

PComm Aneurysm on CN III is the commonest cause of painful Oculomotor Palsy)

Question 11

AVM

Answer 11

Vascular development malformation due to Arterialisation of draining Veins; Might cause Focal Epilepsy; Risk of first haemorrhage (20% Mortality, 30% Permanent Disability) is 2-3%/yr; After first bleed, Risk of rebleed at 10%/yr

Question 12

Treatment of AVM

Answer 12

Endovascular Ablation by Catheter injection of glue into Nidus, Surgery or
Stereotactic Radiotherapy

Question 13

Cavernomas

Answer 13

Cavernous Haemangiomas (Cavernomas) – Tangle of low pressure dilated vessels
without major feeding artery; Incidental findings

▪ Might cause seizure, might rupture to form small haemorrhages, but low-
pressure bleed = rarely cause deficits

▪ Surgical Resection rarely needed unless enlarging, or neurological deficits

Question 14

Presentation of SAH

Answer 14

• Sudden, Very Severe, often Occipital Headache
(mean time to peak is 3 minutes) followed by
Vomiting, often by Coma and Death; Always consider SAH in any sudden headache
• Neck Stiffness, Kernig’s Sign (Meningeal irritation),
Papilloedema might be present with Retinal/Subhyaloid Haemorrhage

Question 15

SAH: Differentials

Answer 15

Migraine Headache (less acute onset, typically no neck stiffness), Call-Fleming
Syndrome (Reversible Cerebral Vasoconstriction resulting in Thunderclap Headache), Cervical
Arterial Dissection and Acute Bacterial Meningitis

Question 16

Consequences of SAH

Answer 16

Obstructive Hydrocephalus (seen on CT); Might be asymptomatic but can cause deteriorating
consciousness; Shunting might be necessary
• Arterial Spasm might be seen on Angiography; Cause of Coma or Hemiparesis; Poor prognosis

Question 17

SAH Investigations

Answer 17

• CT Head – Subarachnoid/Intraventricular Blood readily seen (95%
sens within 24hr); LP not necessary if SAH confirmed by CT
o “Star sign” of Hyperdense blood within the Basal Cisterns
o NB: Acute blood appears Hyperdense, which becomes
Isodense and Hypodense as time progresses
• LP – CSF becomes yellow (Xanthochromic) due to Haem breakdown producing Bilirubin; May be detectable for up to 2 weeks; Spectrophotometry used to define SAH with certainty
• CT Angiography, X Ray Angiography to identify Aneurysm; Rarely
no arterial cause can be found

Question 18

Medical Management of SAH

Answer 18

Bed Rest, Supportive management; Urgent Neurosurgical consult
o Half of cases dead or moribund before reaching hospital; 10-20% of other half
rebleed and die in weeks; Delay in diagnosis contributes to inpatient deaths

Question 19

Surgical Management of SAH

Answer 19

Endovascular Treatment – Catheter coiling (Lower complication rate than surgery) is first line;
Direct Surgical Clipping if unsuitable anatomy or complicated case
o If Unruptured Aneurysm >8mm, Risk of treatment < Risk of Haemorrhage if untreated

Question 20

Subdural Haematoma

Answer 20

Accumulation of blood within Subdural space following

rupture of vein (Typically Bridging veins in the elderly); Often follows head injury; Delay between onset of symptoms

Question 21

Chronic SDH

Answer 21

Chronic, seemingly spontaneous SDH common in elderly, especially anticoagulated

Question 22

Presentation of SDH

Answer 22

Headaches, Drowsiness, Confusion; Focal deficits might develop; Epilepsy might occur; Stupor, Coma and Coning might follow

Question 23

Extradural Haematoma

Answer 23

– Typically due to MMA rupture; Characteristically presents with Lucid interval between onset of Head Injury with brief unconsciousness followed by Stupor
o Ipsilateral dilated pupil, Contralateral Hemiparesis due to rapid Tentorial Coning
o Bilateral fixed dilated pupils, Tetraplegia and Respiratory arrest follows

Question 24

Investigations of SDH and EDH

Answer 24

CT Head; MR more sensitive of small Haematomas
o T1-Weighted MRI shows bright images (Hyperdense) due to presence of Methaemoglobin if Acute bleed; Chronic bleed appears Hypodense
o SDH (Banana Sign), EDH (Lemon Sign)

Question 25

Management of EDH

Answer 25

EDH requires urgent Neurosurgery; Burrholes might be lifesaving if unavailable

Question 26

Management of SDH

Answer 26

Less urgent, Neurosurgery consult; Might even

spontaneously resolve

Question 27

Cortical Venous Thrombosis

Answer 27

Infarct leads to Headache,

Focal Neurological signs, Epilepsy often with Fever

Question 28

Dural Venous Sinus Thrombosis

Answer 28

Ocular pain, Fever, Proptosis, Chemosis; External and Internal Ophthalmoplegia with Papilloedema
o Sagittal and Lateral Sinus Thrombosis can also
cause raised ICP = Headache, Fever,
Papilloedema and often Epilepsy

Question 29

Venous Thrombosis Investigations

Answer 29

Investigated by MRI/MRA/MRV;
Treatment with Anticoagulation (Heparin, Warfarin); Anticonvulsants
given if necessary