Intracranial Haemorrhage Flashcards
What is the pathophysiology behind subarachnoid haemorrhage?
- Bleeding in the subarachnoid space, causing brain injury through local pressure, toxicity from bleeding, and global ↑ICP.
- 80% are due to the rupture of a berry (aka saccular) aneurysm in the circle of Willis.
- Most of the rest are due to arteriovenous malformations.
- If it results in a neurological deficit lasting ≥24 hours, can be considered a type of haemorrhagic stroke, though in clinical practice this term is rarely applied to SAH.
What is the epidemiology of SAH?
- Peak onset 40-60 years old. Onset in men slightly earlier.
* 1/200 lifetime risk. 1/5000 if no risk factors, 1/15 if several major risk factors present.
Which signs and symptoms are commonly seen in SAH?
- Symptoms:
- Thunderclap headache: sudden, devastating, occipital. Though the cardinal symptom of SAH, it is absent in 25%.
- Sentinel headache (30%). Milder headache in the preceding days to weeks, reflecting small aneurysmal leaks.
- Vomiting, seizures.
- Collapse, loss of consciousness (40% at onset), coma.
- Onset timing: ⅓ during daily activities, ⅓ during sleep, ⅓ during exertion.
- Signs:
- Meningism: stiff neck, Kernig’s (after 6 hours).
- Retinal and subhyoid haemorrhage.
- Focal neurological signs.
What are the risk factors for SAH?
- Smoking
- HTN
- Family history
- ↑Cholesterol
- Autosomal dominant polycystic kidney disease.
- Coagulopathy
- Ehlers Danlos and Marfan’s.
Which investigations are important in suspected SAH?
- Initial
- FBC
- Clotting: may show coagulopathy.
- U&E: may show ↓Na+ due to cerebral salt wasting.
- Glucose may be elevated.
- ECG: SAH can cause cardiac abnormalities e.g. long QT.
- Diagnosis
Non-contrast CT head:
- Most sensitive in first 6 hours.
- LP after 12 hours if CT -ve:
- Allows time for development of xanthochromia, a yellowing of the CSF from Hb breakdown.
- Xanthochromia is detected with spectrophotometry of the last (of 4) CSF bottles, as there may be RBCs in the first bottle(s) from a traumatic tap.
- Take simultaneous venous blood to check serum BR, protein, and glucose for comparison.
- Will detect SAH in only 1 in 500 patients who’ve had a -ve CT in first 6 hours.
- If CT or LP +ve, confirm diagnosis with digital subtraction angiography (DSA) or CT angiogram.
What medical management can be implemented in SAH?
- Medical:
- Requires close specialist care, often ITU.
- Regular neuro obs: GCS, pupils, neurological signs.
- Aim SBP <180.
- Nimodipine: calcium channel blocker to reduce vasospasm.
- Analgesia for headache.
Which neurosurgical options are available for patients suitable for surgery?
- Clipping
* Endovascular coil embolisation.
What complications can arise in patients with SAH? What does the prognosis look like for SAH patients?
- Acute complications:
- Neuro: obstructive hydrocephalus, rebleed, vasospasm in the circle of Willis (after 3-15 days).
- Others: arrhythmias, pulmonary oedema.
- Outcomes:
- 25% die, usually within 1 month. Due to initial bleed, rebleed, or vasospasm.
- 50% left with long-term disability or neurological impairment.
Which different head injury types can a person sustain?
- Skull fractures: linear, depressed, open, or basal.
- Intracranial bleeds: acute extradural (aka epidural), acute subdural, subarachnoid, or intracerebral.
- Diffuse brain injury: concussion (mild TBI), diffuse axonal injury.
- Contusions: areas of focal brain injury, either coup – direct damage by impacted skull – or contre coup – brain squashed remotely from area of impact.
What is a traumatic brain injury?
- Describes any head or neck injury which results in disruption of brain function.
- Classified as mild (GCS 13-15 at 30 mins post-injury), moderate (GCS 9-12), or severe (GCS ≤8), with mild TBI (concussion) accounting for the vast majority of cases.
What are the pathological consequences of a head injury?
- Pathological consequences of head injury:
- ↑ICP
- Focal neurological deficits.
- Secondary brain injury: ↓perfusion from ↑ICP, vascular damage, or hypovolaemia.
What is the Cushing reflex in terms of cerebral perfusion pressure?
- Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) – intracranial pressure (ICP).
- A CPP of ≥70 mmHg is usually sufficient, and as ICP is usually ~10 mmHg, there is sufficient cerebral perfusion within normal MAP ranges.
- As ICP rises, MAP may rise in response to maintain CPP. The Cushing reflex is a combination of ↑BP, irregular breathing, and ↓HR in response to ↑ICP.
How is concussion defined?
Concussion is often synonymous with mild traumatic brain injury (GCS 13-15 at 30 mins post-injury), though some use it specifically to refer to the symptoms that results from mild TBI.
What are the symptoms of concussion?
- Mild behavioural or cognitive changes, including confusion.
- Amnesia, which may include both the event (retrograde) and following (anterograde).
- Loss of consciousness (up to 30 minutes).
- Focal neurological deficits can occur, though should raise suspicion for more severe injury.
- Initial symptoms often resolve within minutes, but others – headache, nausea, dizziness, imbalance, fatigue, irritability – may persist for hours, days, or even weeks. 90% recover within 1-2 weeks, but persistence beyond this is possible and is known as postconcussion syndrome.
What is the commonest type of bleed in a traumatic head injury?
A subdural haematoma