Brain Injury I Flashcards
Describe what is meant by the Monro-Kellie doctrine [1]
Inside the skull is:
- Brain 80%, CSF 10%, blood (venous 6-7%, arterial 3-4%) + (SOL, oedema)
- An increase in one should cause a decrease in one or both of the remaining two.
How do you calculate CPP / cerebral perfusion pressure? [1]
What is normal CPP? [1]
CPP = MAP – ICP
- CPP normally 60-80 (150) mmHg
Intracranial haemorrhage refers to bleeding within the skull. There are four types.
What are they? [4]
Extradural haemorrhage (bleeding between the skull and dura mater)
Subdural haemorrhage (bleeding between the dura mater and arachnoid mater)
Intracerebral haemorrhage (bleeding into brain tissue)
Subarachnoid haemorrhage (bleeding in the subarachnoid space)
Describe the different patterns of haemorrhages inside the brain
Describe the clinical features and investigations for EDH [4]
patient who initially loses, briefly regains and then loses again consciousness after a low-impact head injury.
- The brief regain in consciousness is termed the ‘lucid interval’ and is lost eventually due to the expanding haematoma and brain herniation.
- As the haematoma expands the uncus of the temporal lobe herniates around the tentorium cerebelli and the patient develops a fixed and dilated pupil due to the compression of the parasympathetic fibers of the third cranial nerve.
On imaging:
- An extradural haematoma appears as a biconvex (or lentiform), hyperdense collection around the surface of the brain. They are limited by the suture lines of the skull.
- AKA bannaa
What is the definitve mx of EDH? [1]
The definitive treatment is craniotomy and evacuation of the haematoma.
Subdural haemorrhage occurs between the [2]
Subdural haemorrhage occurs between the dura mater and arachnoid mater
SDH is caused by damage to which blood vessels in the brain? [1]
Subdural haemorrhage occurs between the dura mater and arachnoid mater and is caused by a rupture of the bridging veins in the outermost meningeal layer. On a CT scan, they have a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).
Describe the differences in clinical features between acute and chronic SDH
An acute subdural haematoma is a collection of fresh blood within the subdural space and is most commonly caused by high-impact trauma.
- Since it is associated with high-impact injuries, there is often other brain underlying brain injuries.
A chronic subdural haematoma is a collection of blood within the subdural space that has been present for weeks to months.
- Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding. Elderly and alcoholic patients are particularly at risk of subdural haematomas since they have brain atrophy and therefore fragile or taught bridging veins.
- Presentation is typically a several week to month progressive history of either confusion, reduced consciousness or neurological deficit.
Describe the investigation finding of SDH [1]
CT imaging is the first-line investigation and will show a crescentic collection, not limited by suture lines. They will appear hyperdense (bright) in comparison to the brain. Large acute subdural haematomas will push on the brain (‘mass effect’) and cause midline shift or herniation.
Acute and chronic SDH Mx? [2]
Acute subdural haematoma
- Small or incidental acute subdurals can be observed conservatively.
- Surgical options include monitoring of intracranial pressure and decompressive craniectomy.
Chronic subdural haematoma
- If the chronic subdural is an incidental finding or if it is small in size with no associated neurological deficit then it can be managed conservatively with the hope that it will dissolve with time.
- If the patient is confused, has an associated neurological deficit or has severe imaging findings then surgical decompression with burr holes is required.
What are the most common complications of SDH? [3]
- What are their sx? [+]
Increased intracranial pressure (IICP):
- This is the most common complication and can lead to cerebral herniation if not managed promptly. Symptoms may include headache, vomiting, altered mental status, and papilloedema.
Cerebral oedema:
- Swelling of the brain tissue can occur due to the accumulation of blood in the subdural space.
- This can further exacerbate IICP and worsen neurological outcomes.
Herniation syndromes:
- Increased IICP can lead to displacement of brain tissues into regions they normally do not occupy. These may include uncal herniation, central herniation or tonsillar herniation, each with its own characteristic clinical features
What are the two types of SAH? [2]
What causes them? [+]
The most common cause of SAH is head injury and this is called traumatic SAH
In the absence of trauma, SAH is termed spontaneous SAH . The rest of this note focuses on spontaneous SAH.
* Intracranial aneurysm (saccular ‘berry’ aneurysms) accounts for around 85% of cases
* conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
* arteriovenous malformation
* pituitary apoplexy
* mycotic (infective) aneurysms
Describe the clinical features of SAH [+]
headache
* usually of sudden-onset (‘thunderclap’ or ‘hit with a baseball bat’)
* severe (‘worst of my life’)
* occipital
* typically peaking in intensity within 1 to 5 minutes
* there may be a history of a less severe ‘sentinel’ headache in the weeks prior to the presentation
nausea and vomiting
meningism (photophobia, neck stiffness)
altered consciousness: Levels can range from slight drowsiness to coma, indicative of the severity of the haemorrhage or associated complications like hydrocephalus
focal neurological signs
* cranial nerve palsies: particularly affecting the third, fourth, and sixth cranial nerves, leading to visual disturbances or diplopia
* hemiparesis or hemiplegia: indicative of extensive bleeding or secondary ischaemia
speech disturbances: aphasia may occur if the dominant hemisphere is affected.
seizures
Examination fndings of SAH? [4]
ECG Changes? [2]
fundoscopy:
- subhyaloid haemorrhages may be visible
meningeal signs: positive Kernig’s or Brudzinski’s signs may be elicited
papilloedema: though uncommon, may be present indicating raised intracranial pressure
vital signs: hypertension is commonly observed; however, hypotension is a poor prognostic sign
ECG changes:
* transient ECG changes including ST elevation may be seen
* this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines
Ix for SAH? [3]
non-contrast CT head is the first-line investigation of choice
- if CT head is done within 6 hours of symptom onset and is normal: consider an alternative diagnosis (DON’T do an LP)
- if CT head is done MORE than 6 hours after symptom onset and is normal: DO an LP (should occur within 12hrs)
if the CT shows evidence of a SAH
* referral to neurosurgery to be made as soon as SAH is confirmed
After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:
* CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
* +/- digital subtraction angiogram (catheter angiogram)
What results on an LP would indicate SAH? [2]
xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).
- as well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure
Describe the Mx of a confirmed aneurysmal subarachnoid haemorrhage [3]
supportive
* bed rest
* analgesia
* venous thromboembolism prophylaxis
* discontinuation of antithrombotics (reversal of anticoagulation if present)
vasospasm is prevented using a course of oral nimodipine
intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
* most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
Complications of aneurysmal SAH? [5]
re-bleeding
* happens in around 10% of cases and most common in the first 12 hours
* if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
* associated with a high mortality (up to 70%)
hydrocephalus
* hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt
vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
* ensure euvolaemia (normal blood volume)
* consider treatment with a vasopressor if symptoms persist
hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
seizures
Describe the current NICE guidelines on CT imaging for head trauma [+]
Head trauma comes to A&E.
What would be an alarming sign and why?
Unequal pupils —> Alarming sign , indicates increased ICP & asymmetric mass effect.
A patient with head trauma comes in with unequal pupils.
What would be next immediate appropriate steps? [5]
Measures to lower high ICP:
* Head elevation (30 degrees)
* Remove neck restrains (unless unstable spine injury)
* Hyperventilation (pCO2: 4-4.5 kpa) for cerebral vasoconstriction
* Mannitol, hypertonic saline
What are the possible neurosurgical tx of brain bleeds? [3]
Surgical treatment:
* Evacuation of haematoma
* Decompressive craniectomy
* ICP monitoring
What type of brain bleeds would the following cause? [4]
Aneurysms
Arteriovenos malformations
Cavernomas
Hemorrhagic stroke
Aneurysms – SAH
Arteriovenos malformations – rupture/bleed
Cavernomas – bleed
Hemorrhagic stroke – ICH/IVH
Ischemic stroke (+post fossa stroke)
