Intracranial Bleeds Flashcards

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1
Q

What are risk factors to intra-cranial bleeds?

A
  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke → can progress to haemorrhage
  • Brain tumours
  • Anticoagulants i.e. warfarin, DOACs
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2
Q

What are the four main types of Intracranial bleeds?

A
  • Extradural haemorrhage
  • Subdural haemorrhage
  • Subarachnoid haemorrhage
  • Intra-cerebral haemorrhage
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3
Q

What symptoms would make you suspect a patient could be having an intracranial bleed?

A
  • Sudden onset headache
  • Weakness
  • Vomiting
  • Reduced / Loss of consciousness
  • Sudden onset neurological signs
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4
Q

GLASGOW COMA SCALE:

  1. What are the elements of the GCS score?
  2. How much does each element score maximally?
  3. What is the maximum and minimum GCS?
  4. At what score should you think about securing airway?
  5. Discuss each score for the Eye element
  6. Discuss each score for the Verbal element
  7. Discuss each score for the Motor element
A
  1. EVM = Eyes, Motor, Verbal
  2. Eyes = 4 maximum, Verbal = 5 maximum, Motor = 6 maximum
  3. Maximum = 15, Minimum, 3
  4. Secure airway when GCS = 8
  5. Spontaneous, To speech, To pain, No response
  6. Orientated in time place person, Confused, Inappropriate words, Incomprehensible sounds, No response
  7. Obeys to command, Moves to localised pain, Flexion withdrawal from pain, Abnormal flexion, Abnormal extension, No response
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5
Q

What is Cushing’s triad?

A
  • Physiological response to raised ICP, whereby there is:
    1. Bradycardia
    2. Hypertension
    3. Deep, irregular breathing
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6
Q
  • What is a subdural haemorrhage? How can they be classified?
A
  • A collection of blood beneath the dura mater, the outermost layer of the meninges
  • Can be classified based on age; acute, subacute, chronic
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7
Q

What is the presentation of a subdural haemorrhage?

A
  • Fluctuating level of consciousness, insidious physical / intellectual slowing
  • Sleepiness
  • Headache
  • Personality change
  • Unsteadiness
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8
Q
  • What is the pathophysiology of an acute or chronic subdural haemorrhage?
A
  • Due to rupture of small bridging veins BETWEEN CORTEX AND VENOUS SINUS within the subdural space, causing a slow bleed over weeks to months (if chronic subdural) or due to high impact trauma (if acute subdural)
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9
Q
  • What is the first-line investigation for a suspected Subdural Haemorrhage?
A

CT

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10
Q

What does an Subdural hemorrhage appear like on CT? What about Acute SDH vs. a Chronic SDH?

A
  • Appears crescentic in shape, not limited by the suture lines (can cross over it)
  • Acute Subdural Haemorrhage (< 3 days): hyperdense, lighter relative to brain tissue
  • Chronic Subdural Haemorrhage (>15 days): hypodense, darker relative to brain tissue
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11
Q

What patients are at risk of Subdural haemorrhage and why?

A
  • Alcoholics and elderly patients, due to brain atrophy and fragile bridging veins → more likely to fall
  • Epileptics → more likely to fall
  • Babies, due to fragile bridging veins (Shaken baby syndrome)
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12
Q

How are acute subdural haemorrhages managed?

A
  • Reverse clotting abnormalities if any
  • Small / incidental ones → managed conservatively
  • Larger ones → Monitor ICP, decompressive craniectomy
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13
Q

How are chronic subdural haemorrhages managed?

A
  • Reverse clotting abnormalities if any
  • Small / incidental → managed conservatively
  • Larger ones → Surgical decompression with burr holes
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14
Q

What are some differentials to a subdural haemorrhage?

A
  • Dementia, stroke, CNS mass
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15
Q

What is an extradural haemorrhage? In what patients is it most commonly seen and why?

A
  • An acute bleed between the dura mater and the inner surface of the skull
  • Commonly seen in young adults aged 20-30, due to low impact trauma
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16
Q

What is the presentation of an extradural haemorrhage?

A
  • History of head trauma
  • Patient initially loses consciousness, then briefly regains consciousness “lucid interval”, then loses it again
    • Lucid interval usually lasts 6-8 hours, but can last a few days
    • During this phase, may have an increasingly severe headache, vomiting, confusion, seizures, may have hemiparesis with brisk reflexes, Babinski+
  • The final loss of consciousness is due to expanding haematoma and brain herniation
  • If bleeding continues → ipsilateral pupil dilates (CN3 palsy, “blown pupil”, bilateral limb weakness, breathing becomes deep and irregular
17
Q
  1. What is the most common cause of an extra-dural haemorrhage?
  2. What may be other causes?
  3. What is a pterion?
A
  1. Most commonly caused by rupture of the middle meningeal artery, due to trauma at the temporoparietal region (pterion)
  2. Can also occur due to middle meningeal vein or dural sinuses
  3. An anatomical landmark and is where the parietal, frontal, sphenoid and temporal bones fuse
18
Q
  1. What is the first-line investigation for a suspected extradural haemorrhage? Other investigations?
  2. What investigation is contraindicated?
  3. What does an extradural haemorrhage appear like on CT?
A
    • Non-contrast head CT → First line
    • X-Ray → Not first line because CT is better
    • Angiography → When assessing a non traumatic aetiology i.e. AVMs
  1. LP is contraindicated
  2. Appears as a biconvex, lentiform hyperdense (lighter) collection limited by the suture lines of the skull
19
Q

What is the management of an Extra-dural haemorrhage?

A
  1. ABCDE assessment
  2. If needed, high flow O2, C-spine protection, intubation / ventilation
  3. Referral to neurosurgical team
    • Urgent decompression and evacuation to reduce ICP by burr hole to relieve pressure where thickest
    • Craniectomy
  4. Medical management
    • Diuretics i.e. Mannitol → reduce ICP
    • Anti-convulsants → reduce post-trauma seizures
    • Prophylactic ABX → reduce meningitis
    • Barbiturates → reduce ICP, to protect brain from anoxia / ischaemia
20
Q

What are poor prognostic factors of an Extra-dural haemorrhage?

A
  • Low Glasgow Coma Scale
  • Lack of lucid interval
  • Pupil abnormalities
  • Decerebrate rigidity (extensor posture)
21
Q

What is a subarachnoid haemorrhage?

A
  • An intracranial haemorrhage defined as bleeding within the subarachnoid space (between pia mater and arachnoid mater)
22
Q

What are the clinical features of a Subarachnoid Haemorrhage?

A
  • Sudden onset, occipital, thunderclap headache “worse of my life”
  • Nausea and vomiting
  • Symptoms of meningism → photophobia, neck stiffness
  • Seizures
  • COMA, SUDDEN DEATH
23
Q

What is the most common cause of a Subarachnoid Haemorrhage? What conditions are associated with this?
What drugs are associated with Subarachnoid Haemorrhage?

A
85% of cases → commonly caused by saccular "berry" aneurysms
- Acute polycystic kidney disease
- Ehler-Danlos Syndrome
- Coarctation of the Aorta
- Sickle cell Anaemia
Drugs associated are cocaine
24
Q

Aside from intracerebral aneurysms, what are less common causes of Subarachnoid haemorrhage?

A
  • Arteriovenous malformation
  • Pituitary apoplexy
  • Arterial dissection
  • Mycotic (infective) aneurysms
  • Perimesencephalic (idiopathic venous bleed)
25
Q

What is the first-line investigation to diagnose a Subarachnoid Haemorrhage? What is seen?

A
  • CT of the head → Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system
26
Q

If the primary investigation for a Subarachnoid Haemorrhage is negative, what can be ordered? When is it done and why? What is seen?

A
  • Lumbar puncture, usually performed 12 hours following onset of symptoms for development of Xanthochromia
  • On LP may see raised Xanthochromia (broken down RBC) and a normal / raised opening pressure
27
Q

Once a subarachnoid haemorrhage is confirmed by CT / LP, how is the underlying course identified?

A
  • CT intracranial angiogram→ To identify a vascular lesion e.g. aneurysm or AVM
  • +/- digital subtraction angiogram (catheter angiogram)
28
Q

What ECG changes are associated with Subarachnoid Haemorrhage?

A

ST elevation

29
Q

What is the management of a Subarachnoid Haemorrhage?

A
  • Referral to neurosurgery
  • IF DUE TO ANEURYSM → Coil, or craniotomy + clips, must also be under bed rest, well-controlled BP and no straining
  • IF DUE TO VASOSPASM → 21 days of Nimodipine
30
Q

What are complications of a Aneurysmal Subarachnoid Haemorrhage?

A
  • Re-bleeding (30%)
  • Vasospasm → 1-2 weeks later
  • Hyponatremia → due to SIADH
  • Seizures
  • Hydrocephalus
  • Death
31
Q

What are the indications for a Head CT within 1 hour of A&E presentation?

A
  • GCS < 13 on initial assessment
  • GCS < 15 at 2 hours post-injury
  • Suspected open or depressed skull fracture.
  • Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
  • Post traumatic seizure
  • Focal neurological deficit
  • More than 1 episode of vomiting
32
Q

What are the indications for a Head CT within 8 hours of A&E presentation?

A
  • Patient with head injury + Warfarin
  • Patient with head injury + LOC or amnesia + …
    • Age 65 years or older
    • Any history of bleeding or clotting disorders
    • Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
    • More than 30 minutes’ retrograde amnesia of events immediately before the head injury
33
Q
  1. What is an Intracerebral Haemorrhage?
  2. What is an Intracerebral Haemorrhage aka?
  3. What are the risk factors for developing an Intracerebral Haemorrhage?
  4. What are the different types of Intracerebral Haemorrhage?
  5. What is the main investigation, what would you see?
  6. What is the main treatment?
A
  1. An intracerebral haemorrhage is a collection bleeding within the brain tissue
  2. Also known as an Intraparenchymal haemorrhage
  3. Hypertension, Vascular lesions i.e. AVMs, aneurysms, Cerebral amyloid angiopathy, Brain tumours, Previous infarct
  4. Lobar, deep, intraventricular, basal ganglia, cerebellar
  5. CT head, you will see hyperdense (white areas) in brain
  6. Conversative care under stroke physicians, but if large clots then surgery