Cerebral parenchymal haemorrhage

**Definition**

Haemorrhage into the subarachnoid space between the pia and arachnoid
membranes.

**Clinical presentation**

Sudden “worst ever” headache. May have reduced GCS and may have
neurological findings.

**Pathology**

 ***\* Where it occurs***

Berry aneurysm are saccular true aneurysm that tend to occur at branch points
within or near the Circle of Willis. Thought to be due to the altered flow dynamics
and areas of wall weakening at these sites.
They are relatively common being found in 2-5% of the population. 20-30% have
multiple aneurysms. They are more common in females. There is a weak familial
risk. They are associated with various connective tissue diseases especially adult
polycystic kidney disease. Smoking is also a risk factor for aneurysmal SAH.
Where it Occurs At the common sites of Berry aneurysms but haemorrhage will spread widely
through the subarachnoid space and into ventricles with time. Most common sites
are anterior communicating artery, posterior aspect of terminal ICA either related
to posterior communication artery or anterior choroidal artery, middle cerebral
artery bifurcation, basilar tip and PICA origin from vertebral artery. Predominant
site of haemorrhage may give clue to site of aneurysm or in the case of multiple
aneurysms which one bleed.

 ***\* Complications***

Associated intraparenchymal haemorrhage, rebleed, hydrocephalus, cerebral
vasospasm.

 ***\* Differential diagnosis***

Pseudosubarachnoid hemorrhage due to cerebral edema effacing basal cisterns,
Normal structures such as calcified choroid plexus extending through foramen of
Lushka, Traumatic SAH, Vascular causes other than Berry aneurysm rupture such
as intradural vertebral dissection or AVM, Benign perimesencephalic haemorrhage
(diagnosis of exclusion, should have typical history and benign clinical course,
low pressure bleed anterior to brainstem usually limited by Lilliquist’s membrane).

**Radiology**

 ***\* Modality/Technique***

CT Brain C-, CT angiography, Conventional Angiography.

 ***\* Associated conditions***

 ***\* Features***

High attenuation acute haemorrhage within the basal subarachnoid cisterns.
Small or subtle haemorrhages may only be seen in dependent areas such as
interpeduncular cistern or occipital horns of lateral ventricles. Also evaluate
posterior fossa carefully which often suffers from beam hardening artefact. Look
for asymmetry in lateral and Sylvian fissures.

 ***\* Artefacts***

Beam hardening artefact.

 ***\* Clinical Impacts***

 ***\* Sensitivity/specificity***

Sensitivity is very good early after the onset of symptoms but will reduce will
time after this and also depends on the volume of bleed. Patients suspected of
having a SAH with a negative CT should have a lumber puncture looking for
xanthochromia.

**Management plan & communications**

1) Diagnose SAH on CT.

2) Look for complications such as hydrocephalus and if the presentation has
been delayed ischemia from vasospasm.

3) Perform a CT angiogram trying to optimise image quality and ensure good
coverage of the most likely source of hemorrhage e.g. scan higher if you think
there might be a pericallosal aneurysm.

4) Contact the clinical / neurosurgical team.

5) Look for and assess the aneurysm that caused the haemorrhage but don’t
be satisfied with that, look for the 2nd or 3rd aneurysm. Is there any obvious
vasospasm on the CTA?

**Relevant anatomy**

Cerebral arterial vasculature especially Circle of Willis, Normal cerebral structures
that can mimic haemorrhage through physiologic calcification for example.

**Further reading**