Intracranial Haemorrhage Flashcards
(37 cards)
Categories of causes of intracranial haemorrhage?
Traumatic
Spontaneous (main focus here):
• Vascular pathologies (aneurysms, AVMs, hypertension)
• Other causes (bleeding diatheses / disorders, tumours, drugs like warfarin and heparin)
Types of spontaneous intracranial haemorrhage?
Subarachnoid haemorrhage
Intracerebral haemorrhage
Intraventricular haemorrhage
What is a subarachnoid haemorrhage (SAH)?
Bleeding into the subarachnoid space
Potentially fatal if diagnosis is missed; mortality is high, even with treatment
Causes of spontaneous SAH?
Main causes are vascular pathologies:
• Usually, an underlying BERRY ANEURYSM (small, berry-like aneurysms; most individuals with these have 1/2)
• AVM (arteriovenous malformation)
Sometimes, no underlying cause is found
Presentation of SAH?
SUDDEN-ONSET SEVERE HEADACHE (AKA thunder-clap headache), like being “hit on the back of the head with an axe); occurs due to extreme rise in ICP
Collapse and decreased conscious level (or sudden death)
Blood in the CSF space results in a chemical meningitis:
• Vomiting
• Neck pain/stiffness
• Photophobia
Focal neurological deficit
Signs of focal neurological deficit that can appear in SAH?
Depends on where the aneurysm is:
• Dysphasia (deficiency in the generation of speech)
• Hemiparesis (unilateral weakness of 1 side of the body)
• CN III palsy - ipsilateral blown pupil with an eye that is averted outwards and downwards (only the lateral rectus and superior oblique extraocular muscles operate)
Fundoscopy in SAH?
May be able to see a retinal or vitreous haemorrhage
NOTE - fundoscopy is difficult due to photophobia
Differential diagnosis of sudden-onset headache?
SAH
Migraine (typically, these patients have experienced this before)
Benign coital cephalgia - a benign stress headache that occurs post-orgasm; a diagnosis of exclusion, as sex and increased BP can also rupture Berry aneurysms
Diagnostic Ix for SAH?
CT scan
If this is done immediately, it is diagnostic
However, if >3 days post-ictus, it may be negative, despite the patient having had an SAH; this is because the CSF has recirculated
Appearance of SAH on a CT scan?
CSF is typically black on CT scan (as it is of low-density / hypodense); for this reason, on a normal CT, the ventricles should appear black
However, fresh blood is hyperdense and appears white on a CT scan
What should be done if the CT scan is -ve but the suspicion of SAH remains?
LP - safe in an alert patient with no focal neurological deficit, no papilloedema OR after a normal CT scan
Signs of SAH on LP?
LP may have bloodstained CSF; this must be differentiated form a traumatic tap, which is blood due to injury of epidural veins during the LP
Xanthochromic CSF (yellow CSF, due to blood breakdown products) occurs 6-48 hours after the SAH; the guidelines recommend waiting to do an LP, so that this can be observed and there is no risk of confusing with a traumatic tap However, in practice, it may be more prudent to ensure LP is safe for the patient and then take 3 CSF sample
Use of cerebral angiography in diagnosis of SAH?
Gold standard but there is the occasional risk of missing an aneurysm, due to vasospasm
Contrast injected into femoral artery, which goes into the carotid vertebral arteries; can be used to diagnose Berry aneurysms
Other Ix for SAH diagnosis?
CT angiogram
MR angiogram
Complications of SAH?
Death
In those who survive the initial bleed, there is a major risk of RE-BLEEDING (often fatal)
Delayed Ischaemic Neurological Deficit (DIND)
Hydrocephalus
Hyponatraemia
Seizures
Many patients develop a major disability and many successful survivors never return to work
Treatment of re-bleeding in patients who have had a SAH?
Endovascular techniques (presently the main technique)
Surgical clipping (occasionally used)
When does DIND occur after a SAH?
Days 3-12, i.e: delayed
Occurs due to vasospasm
Signs of DIND?
Altered conscious level
Focal neurological deficits, depending on where the ischaemia occurs, e.g: hemiparesis, dysphasia, etc
Prevention of DIND?
Nimodipine (CCB) is used to prevent DIND, by protecting against vasospasm
Patient must be well-hydrated, so high fluid intake ‘Triple H therapy’ is used; this induces hypertension, hypervolaemia and haemodilation to protect against vasospasm
What is hydrocephalus?
Increased intracranial CSF pressure; most patients with SAH will have a degree of hydrocephalus, due to blood in the CSF space preventing reabsorption at the arachnoid granulation
Signs of hydrocephalus in a patient who has had a SAH?
INCREASING headache OR altered conscious level
These symptoms are often transient
NOTE - typically, patients who survive SAH will usually find that their headache decreases; it increases with hydrocephalus
Treatment of hydrocephalus in a patient who has had a SAH?
CSF drainage via either:
• LP
• External ventricular drain (EVD)
A more permanent solution is a CSF diversion shunt
Mechanisms by which hyponatraemia occurs in patients who have had a SAH?
- Most common cause is Syndrome of Inappropriate ADH production (SIADH) - various traumatic or ischaemic factors stimulate the hypothalamus, leading to excessive ADH release
- Minority due to Cerebral Salt Wasting (CSW) syndrome - too much urinary sodium excretion by the kidneys but normal ADH secretion; this excessive natriuresis may be contributed to by the abnormal release of natriuretic hormones (from the brain and atria)
Treatment of hyponatraemia in patients who have had a SAH?
Often transient
NOTE - in most cases of hyponatraemia, patients are fluid restricted
However, when SAH is the cause, FLUID IS NOT RESTRICTED, as this may cause vasospasm and DIND; instead, sodium intake is supplemented
Fludrocortisone (reduce natriuresis to maintain plasma volume and prevent DIND and cerebral infarction)
NOTE - this is not generally used for hyponatraemia; it is however used when SAH is the cause
