neurosurgery Flashcards
diffuse axonal injury cause
diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons
ct head within 1 hour
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
ct within 8 hours
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
SAH ix
Computed tomography (CT) head Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system. CT is negative for SAH (no blood seen) in 7% of cases. Lumbar puncture (LP) Used to confirm SAH if CT is negative. 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). Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure) Referral to neurosurgery to be made as soon as SAH is confirmed
lucid interval in which intracranial haemorrhage
Extradural
Binocular vision post-facial trauma is suggestive of
depressed fracture of the zygoma
seen prior to coning
hypertension
Fluctuating confusion/consciousness? -
subdural
complication intraventricular haemorrhage
hydrocephalus
repeat ct head if suspicious
signs of basal skull fracture
haemotympanum
, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose,
Battle’s sign bruising over mastoid process
most sensitive Ix for diffuse axonal injury
MRI brain
causes of 3rd nerve compression following trauma
extra dural bleed
transtentorial herniation
6 tests of brain death
pupillary reflex, corneal reflex, oculo-vestibular reflex, cough reflex, absent response to supraorbital pressure, and no spontaneous respiratory effort
complications of SAH
Re-bleeding (in around 30%)
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
management of SAH
Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
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
Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature) and treated with hypervolaemia, induced-hypertension and haemodilution**
Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt