Neurosurgery Flashcards
Criteria for brain stem death testing
Deep coma of known aetiology
Reversible causes excluded
No sedation
Normal electrolytes
Testing for brain death should be undertaken by whom?
two appropriately experienced doctors on two separate occasions
other should be experienced in performing brain stem death testing and have at least 5 years post-graduate experience. One of them must be a consultant.
members of transplant team cannot confirm brain stem death
true
Testing for brain death - eyes
Fixed pupils which do not respond to sharp changes in the intensity of incident light
No corneal reflex
Absent oculo-vestibular reflexes
No response to supraorbital pressure
Testing for brain death - breathing/pharynx
No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
No observed respiratory effort in response to disconnection of the ventilator
oculo-vestibular reflexes are tested how?
slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric test)
- no eye movements = absent reflexes
Describe the following type of herniation: Subfalcine
Displacement of the cingulate gyrus under the falx cerebri
Describe the following type of herniation: Central
Downwards displacement of the brain
Describe the following type of herniation: Transtentorial / uncal herniation
Displacement of the uncus of the temporal lobe under the tentorium cerebelli.
Describe the clinical consequences of uncal/transtentorial herniation
parasympathetic compression of the third cranial nerve - ipsilateral dilated pupil
ompression of the cerebral peduncle - contralateral paralysis
Describe the following type of herniation: Tonsillar
Displacement of the cerebellar tonsils through the foramen magnum
Tonsillar herniation is also called coning
true
tonsillar herniation/coning in raised ICP results in?
compression of the cardiorespiratory centre
tonsillar herniation/coning in chiari 1 malformation is seen without raised ICP
true
Describe the following type of herniation: Transcalvarial
Occurs when brain is displaced through a defect in the skull (e.g. a fracture or craniotomy site)
The brain autoregulates its blood supply
true
as ICP rises you get increasingly hypotensive systemically
false
systemic circulation will display changes to try and meet the perfusion needs of the brain. Usually this will involve hypertension.
if ICP compresses the brain what are the consequences?
cranial nerve palsies
compression of essential centres in the brain stem will occur. When the cardiac centre is involved bradycardia will often develop.
Extradural haematoma Often results from
acceleration-deceleration trauma or a blow to the side of the head
The majority of extradural haematomas occur where?
The majority of extradural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.
Extradural haematoma may have a lucid interval
true
Subdural haematoma Most commonly occur around the
frontal and parietal lobes
subdural has a slower/faster onset of symptoms compared to extrafural haematoma
slower
Subarachnoid haemorrhage Usually occurs spontaneously in the context of
ruptured cerebral aneurysm, but may be seen in association with other injuries when a patient has sustained a traumatic brain injury.
Pathophysiology of haematoma?
Primary brain injury may be focal (contusion/ haematoma) or diffuse (diffuse axonal injury)
Diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons
Intra-cranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact
Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury. The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia
The Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event
Where there is life threatening rising ICP such as in extradural haematoma and whilst theatre is prepared or transfer arranged use of IV ? may be required.
mannitol/ frusemide
Diffuse cerebral oedema may require
decompressive craniotomy
in head injury Hyponatraemia is most likely to be due to the syndrome of inappropriate ADH secretion.
true
Minimum cerebral perfusion pressure in adults and children?
Minimum of cerebral perfusion pressure of 70mmHg in adults.
Minimum cerebral perfusion pressure of between 40 and 70 mmHg in children.
ICP monitoring is indicated when?
ICP monitoring is appropriate in those who have GCS 3-8 and normal CT scan.
ICP monitoring is mandatory in those who have GCS 3-8 and abnormal CT scan.
Interpretation of pupillary findings in head injuries:
Unilaterally dilated Light response - Sluggish or fixed
3rd nerve compression secondary to tentorial herniation
Interpretation of pupillary findings in head injuries:
Bilaterally dilated Light response - Sluggish or fixed
Poor CNS perfusion
Bilateral 3rd nerve palsy
Interpretation of pupillary findings in head injuries:
Unilaterally dilated or equal
Light response: Cross reactive (Marcus - Gunn)
Optic nerve injury
Interpretation of pupillary findings in head injuries:
Bilaterally constricted
Opiates
Pontine lesions
Metabolic encephalopathy
Interpretation of pupillary findings in head injuries:
Unilaterally constricted
Light response preserved
Sympathetic pathway disruption
Head injury - NICE guidance on investigation:
CT head immediately
which GCS scores?
GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
Head injury - NICE guidance on investigation:
CT head immediately
which fractures?
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).
Head injury - NICE guidance on investigation:
CT head immediately
how many episodes of vomitings?
MORE than 1 episode of vomiting
Head injury - NICE guidance on investigation:
CT head immediately if they have a seizure
true
Head injury - NICE guidance on investigation:
CT head immediately if they have focal eurological deficit
true
CT head scan within 8 hours of the head injury - for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:
age 65 years or older
any history of bleeding or clotting disorders
dangerous mechanism of injur
more than 30 minutes’ retrograde amnesia of events immediately before the head injury
If a patient is on warfarin who have sustained a head injury with no other indications for a CT head scan, perform a CT head scan within ?hours of the injury.
8 hours
Intracerebral haematoma CT imaging will show
hyperdensity (bright lesion) within the substance of the brain.
Hydrocephalus is defined as
excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain and is caused by an imbalance between CSF production and absorption.
Patients with hydrocephalus present with symptoms due to raised intracranial pressure, which include:
Headache (typically worse in the morning, when lying down and during valsalva)
Nausea and vomiting
Papilloedema
Coma (in severe cases)
Children with severe hydrocephalus also classically present with
failure of upward gaze (‘sunsetting’ eyes)
Hydrocephalus can be broadly divided into two categories
Obstructive (‘non-communicating’) hydrocephalus
Non-obstructive (‘communicating’) hydrocephalus
Obstructive hydrocephalus is
due to a structural pathology blocking the flow of cerebrospinal fluid. Dilatation of the ventricular system is seen superior to site of obstruction.
Obstructive hydrocephalus causes?
tumours, acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage) and developmental abnormalities (e.g. aqueduct stenosis).
Non-obstructive hydrocephalus is
due to an imbalance of CSF production absorption. It is either caused by an increased production of CSF (e.g. choroid plexus tumour (very rare)) or more commonly a failure of reabsorption at the arachnoid granulations (e.g. meningitis or post-haemorrhagic).
Normal pressure hydrocephalus is
unique form of non-obstructive hydrocephalus characterised by large ventricles but normal intracranial pressure. The classic triad of symptoms is dementia, incontinence and disturbed gait.
Hydrocephalus first line ix?
CT head
MRI may be used to investigate hydrocephalus in more detail
Hydrocephalus what is both diagnostic and therapeutic
Lumbar puncture
Treatment hydrocephalus
external ventricular drain (EVD) is used in acute, severe hydrocephalus
ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique
most common cause of SAH is head injury and this is called traumatic SAH . In the absence of trauma, SAH is termed
spontaneous SAH
Causes of spontaneous SAH include:
Intracranial aneurysm 85% Arteriovenous malformation Pituitary apoplexy Arterial dissection Mycotic (infective) aneurysms Perimesencephalic (an idiopathic venous bleed)
Conditions associated with berry aneurysms include
adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
Classical presenting features include: SAH
Headache: typically sudden-onset (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’) and occipital
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death
ECG changes including ST elevation may be seen
Computed tomography (CT) head shows what in SAH
Acute blood (hyperdense/bright on CT) CT is negative for SAH (no blood seen) in 7% of cases.
What is Used to confirm SAH if CT is negative?
Lumbar puncture
CSF findings consistent with subarachnoid haemorrhage include ?
normal or raised opening pressure
xanthochromia
LP should be performed when in SAH?
LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).
Referral to neurosurgery to be made as soon as SAH is confirmed
TRUE
After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:
FURTHER IX?
CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
+/- digital subtraction angiogram (catheter angiogram)
Most intracranial aneurysms are now treated with a
coil
Until the aneurysm is treated, the patient should be kept on strict bed rest, well-controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm
true
anuerysmal SAH - Vasospasm is prevented using
21-day course of nimodipine
aneurysmal SAH vasospasm mx
hypervolaemia, induced-hypertension and haemodilution
Complications of aneurysmal SAH:
Re-bleeding
happens in around 10% of cases and most common in the first 12 hours
Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
Seizures
Hydrocephalus
Death
Important predictive factors in SAH:
conscious level on admission
age
amount of blood visible on CT head
