Intracranial Haemorrhage Flashcards

1
Q

What is the pathophysiology behind subarachnoid haemorrhage?

A
  • 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.
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2
Q

What is the epidemiology of SAH?

A
  • 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.

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3
Q

Which signs and symptoms are commonly seen in SAH?

A
  • 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.
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4
Q

What are the risk factors for SAH?

A
  • Smoking
    • HTN
    • Family history
    • ↑Cholesterol
    • Autosomal dominant polycystic kidney disease.
    • Coagulopathy
    • Ehlers Danlos and Marfan’s.
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5
Q

Which investigations are important in suspected SAH?

A
  • 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.
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6
Q

What medical management can be implemented in SAH?

A
  • 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.
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7
Q

Which neurosurgical options are available for patients suitable for surgery?

A
  • Clipping

* Endovascular coil embolisation.

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8
Q

What complications can arise in patients with SAH? What does the prognosis look like for SAH patients?

A
  • 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.
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9
Q

Which different head injury types can a person sustain?

A
  • 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.
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10
Q

What is a traumatic brain injury?

A
  • 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.
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11
Q

What are the pathological consequences of a head injury?

A
  • Pathological consequences of head injury:
    • ↑ICP
    • Focal neurological deficits.
    • Secondary brain injury: ↓perfusion from ↑ICP, vascular damage, or hypovolaemia.
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12
Q

What is the Cushing reflex in terms of cerebral perfusion pressure?

A
  • 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.
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13
Q

How is concussion defined?

A

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.

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14
Q

What are the symptoms of concussion?

A
  • 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.
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15
Q

What is the commonest type of bleed in a traumatic head injury?

A

A subdural haematoma

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16
Q

Which signs and symtoms are seen in subdural haematoma?

A
  • Drowsy
    • Physical or cognitive slowing, personality changes.
    • Nausea and vomiting
    • ↑Signs of ICP.
    • Urine incontinence (also suggests normal pressure hydrocephalus).
    • Can be acute or chronic, the latter not presenting until weeks or months post trauma.
17
Q

What are the risk factors for subdural haematoma?

A
  • 3As:
    • Age
    • Anticoagulation
    • Alcohol
18
Q

What is the pathophysiology behind epidural haematoma/herniation (AKA extradural haematoma/haemorrhage)?

A
  • Bleed from vessels supplying skull or dura, causing dura to separate from skull. Commonly the middle meningeal artery beneath the temple, and may have associated parietal or temporal fracture.
    • Rare but carries high mortality.
19
Q

What are the signs and symptoms of an extradural haematoma?

A
  • Loss of consciousness or concussion – from the initial impact – then lucid period as haematoma expands and is initially accommodated.
    • Eventually, expanding mass no longer accommodated, and ↑ICP leads to further loss of consciousness and uncal herniation through tentorium.
    • Compression of CN3 as it passes through tentorium leads to constricted then dilated pupil on affected side, with contralateral hemiparesis.
    • Eventually other pupil affected, followed by coning as brain stem is pushed through foramen magnum.
20
Q

Which investigations are carried out in initial assessment of suspected extradural haematoma?

A
  • nitial assessment:
    • Glasgow coma scale (GCS).
    • The extent of amnesia, both retrograde (before the accident) and anterograde (can’t form new memories), is an indication of severity.
    • Consider cervical-spine injuries. X-ray ± CT if suspected.
21
Q

Which information might you use to decide whether or not to perform a CT?

A
  • Use guidelines or a clinical decision rule to decide whether or not to CT: NICE, Canadian CT head, or New Orleans.
Common criteria for scanning are any one of CSF NOT BAD:
    • Comatose: GCS <13 on arrival or <15 2 hours post-accident.
    • Seizure
    • Suspected skull Fracture, including signs of basal fracture: panda eyes (periorbital ecchymosis), Battle’s sign (mastoid ecchymosis), hemotympanum, or CSF leak from ear/nose.
    • Focal Neurological deficit.
    • Old i.e. age ≥65 plus amnesia, LOC, or dangerous mechanism.
    • Two or more vomiting episodes.
    • Blood thinners or bleeding disorder.
    • Amnesia (retrograde) of ≥30 mins pre-event.
    • Dangerous mechanism plus amnesia, LOC, or age ≥65: cyclist/pedestrian vs. car without helmet, MVC with ejection/rollover/other fatality, fall >1 m or >5 stairs.
22
Q

How might you decide whether or not to perform a head CT in a child?

A
  • n kids, use PECARN and/or clinician judgement (CATCH and CHALICE are less validated alternatives). Basic approach:
    • Scan if GCS <15 or signs of skull fracture.
    • Observe if transient altered mental status (LOC >5 seconds, amnesia >5 minutes), severe symptoms (vomiting ≥3 times or severe headache), non-frontal scalp hematoma, or dangerous mechanism (as for adult plus struck by high-speed projectile).
23
Q

Which CT head findings may be seen with different types of head injury?

A
  • Extra-dural haemorrhage: lentiform shape, skull fracture.
    • Sub-dural haematoma: banana shape all along one side, midline shift, shrunken ventricles.
    • Sub-arachnoid haemorrhage: hyperdense (white) areas in the basal cisterns and sulci, highlighting their shape.
    • Ischaemic stoke: hypoattenuation in a vascular distribution.
    • Abscess and brain tumour: ring-enhancing lesion, as the walls are vascularised but the core isn’t.
24
Q

What is the initial management for head injury and how might you decide whether a patient is safe for discharge?

A
  • Initial management:
    • Analgesia. Pain can increase ICP.
    • Neurosurgical referral if there are (a) persistent symptoms after initial management, (b) focal neurological deficits, or (c) significant findings on CT. Consider urgent referral – before CT – if GCS ≤8 and/or open fracture.
  • Safe discharge:
    • Criteria: GCS 15, eating and drinking (not vomiting), neuro signs largely resolved.
    • Give verbal and written post-discharge advice. For concussion, avoid activities with risk of recurrent injury while still symptomatic. However, traditional advice of complete and prolonged rest from all activities now replaced by advising brief rest then early, controlled return to normal daily activities.
    • Need someone at home to monitor them for initial 24 hours.