Cranial Trauma Flashcards
(150 cards)
1
Q
A 78-year-old man was admitted to hospital with a 2 week history of progressive confusion and unsteadiness. His medical history included parkinsonism and a metallic mitral valve replacement. On examination his GCS was 14/15 (E4, V4, M6) and he had left-sided weakness. He was
taking warfarin, and the INR was 3.8.
DDx?
A
Progressive confusion and gait disturbance with left hemiparesis point to right hemisphere lesion.
DDx includes:
Cerebral infarction/haemorrhage
Subdural haematoma
Neoplastic lesion
Progressive symptoms suggest a slowly enlarging mass such as a tumour or chronic subdural haematoma
2
Q
Describe the CT
A
Extra-axial cresent shaped fluid collection over the right cerebral convexity (A,B) indiacting chronic SDH
As patient is supine, there is layering according to density, wthi hypodense fluid supernatant (A) above hyperdense thrombus or cellular precipitant.
This could be due to a single episode of heamorrhage or rebleeding into a chronic collection.
There is midline shift (C) with obliteration of cerebral sulci and the trigone not seen on the right
3
Q
Pathophysiology of chronic SDHs
A
Typically caused by tearing of dural bridging veins.
Cerebral atrophy (ETOH and elderly patients) causes increased tension on these veins predisposing them to tearing.
Trauma causing the initial bleed may be so mild as to be absent from hx.
Local inflammatory reaction follows the haemorrhage and results in haematoma cavity with membranes within it
Clot liquefies over time and this collection may expand.
This may be as a consequence of recurrent microbleeds from dural capillaries and haematoma membranes, secretion of fluid from haematoma membranes and osmotic fluids shifts into the haematoma cavity
4
Q
Indications for operative mx of chronic SDH
A
Presence of neurological deficit
Severe and persistent headache
5
Q
What are the surgical options for craniotomy
A
Twist-drill
Burrhole (most common)
Craniotomy
6
Q
Cx of surgery for SDH
A
Seizures
Intracranial haematoma
Pneumocephalus
Infection (including subdural empyema)
30% risk of recurrence.
Risk to life with GA
7
Q
Trauma in the hx of SDH may be absent in what proportion of cases
A
Up to 50%
8
Q
SDH recurrence rate
A
Up to 30%
9
Q
What are the challenges to treatment of chronic SDH
A
May be due to multiple bleeds- loculation of haematoma making them harder to drain via single hole.
Elderly population with multiple co-morbidites.
Elderly brains are slower to re-expand and fill the subdural space after the haematoma is evacuated, this space continues to stretch bridging veins and has tendency to fill with blood- reaccumulation.
More common in pts on anticoagulation
10
Q
Twist drill craniostomy
A
Can be done under LA.
Small-diameter drill bit and the burrhole drilled without direct vision.
Skin is closed over the burrhole without formal irrigation in the hope that a liquefied haematoma will be absorbed into the galea.
Less invasive but probably less effective
11
Q
Burrhole drainage
A
Can be performed under LA.
Operating theatre
Allows formal irrigation of the clot either in and out of a single burrhole or through two.
Burrholes are left open and the haematoma cavity communicates in the subgaleal space.
Santarius et al supports soft subdural catheter use for post-operative drainage for 2/7.
12
Q
Santarius 2009
Lancet
A
Drain vs no drain after the burrhole evacuation of chronic SDH.
RCT.
The primary endpoint was recurrence needing redrainage. Trial stopped early. Analyses on the intention to treat.
Recurrence occurred in 9.3% with drain vs 24% without.
Mortality was 8.6 vs 18.1
Medical and surgical complications were much the same.
13
Q
Craniotomy in SDH
A
Usually reserved for re-collected SDH or those with loculations that cannot be managed with burrholes alone.
Craniotomy will allow direct visulation of the subdural space and the opportunity to divide or excise the membranes that form the compartments within the haematoma cavity.
14
Q
Decision to be made in the period post-SDH evacuation
A
When to let the patient sit up
When to restart anticoagulants
15
Q
Describe this image and its issues
A
BIlateral chronic SDH with larger on the left and midline shift to the right.
There will also be vertical shift on the brain.
Bilateral burrholes are required to evacuate both haematomas.
16
Q
Recurrent chronic subdural haematoma
A
Patient who has had a chronic subdural haematoma drained returns with scan showing persisting subdural collections.
Can represent new episode
Reaccumultion of fluid
Or simply saline wash.
Can also become infected and present with sepsis +/- worsening headahce or neurological deficit
17
Q
Describe this CT
A
The arrows show septations within the collection.
There is mass effect causing effacement of the sulci with the right lateral ventricle displaced downwards out of the imaging plane indicating downward brain hernaition.
Little midline shift is evident.
18
Q
Dexamethasone in SDH
A
2mg BD may help with conservatively managed SDH- settles headache and some mild neurological deficits.
May work throguh stabilising chronic SDH membrane and protective effect on the cerebral cortex
19
Q
Mx of VTE in neurosurgical patients
A
NICE advise mechanical prophylaxis
with LMWH commenced 12-24h post op if risk of major bleeding is low.
If presentation is with cranial or spinal haemorrhage, LMWH is not recommended until the lesions is secured or condition stable
20
Q
Rates of ICH on aspirin
A
0.2-0.3%
21
Q
ICH on aspirin + clopidogrel
A
0.3-0.4% per year
22
Q
ICH on warfarin
A
0.3-1%/year vs 0.15%/year in age matched population
23
Q
Risk off thromboembolic complications when off warfarin %/year
Metallic heart valve
A
4-12
24
Q
Risk off thromboembolic complications when off warfarin %/year
AF
A
1.9-18.2%
25
Risk off thromboembolic complications when off warfarin %/year
DVT/PE
15%
26
Divisions of the cranial cavity
Divided into compartments by semirigid, densly fibrous folds of dura mater:
falx cerebri
tentorium cerebelli
27
Brain herniation
Occurs when brain is subjected to pressure gradients that cause portions of it to flow from one compartment to another.
Pressure gradients are caused by mass lesions (often surrounded by extensive oedema)
Injudicious use of hyposomolar 5% dextrose may produe abrupt increases in brain oedema and herniation
28
What is the significance of the cerebral vasculature in brain herniation
Arteries and veins are relatively fixed in space.
Herniating brain portions lose their blood supply. In lateral herniation, the hernia itself may compress or distort vessels
29
Pathophysiology of brain herniation
Disruption of vascular supply
Distortions in white matter pathways (via geometrical distortion of pathways- distension/compression), extracerebral structures, especially CN3 are also susceptible to distortion
Brain tissue is injured along the free edges of dural reflections
30
Types of brain herniation
Cingulate (subfalcine) herniation
Central (downward transtentorial herniation)
Uncal (lateral mass) herniation
Cerebellar tonsillar herniation
Transcalvarial herniation
31
1. Cingulate (subfalcine) herniation
2. Central (downward transtentorial herniation)
3. Uncal herniation
4. Cerebellar tonsillar herniation
5. Transcalvarial herniation
Types 2 and 4 may cause death through brainstem compression
32
Cushing's triad is
A respone to diminished brain stem perfusion regardless of aetiology
33
Cingulate (subfalcine) herniation
Under falx cerebri
34
Central (downward transtentorial) herniation
Through tentorial notch
35
Cerebellar tonsillar herniation
Through foramen magnum
36
Transcalvarial herniation
Swollen brain herniates through any defect in dura & skukll
37
Nonspecific symptoms of herniation syndromes
All types may have nonspecific symptoms of raised ICP (headache, vomiting, HTN, bradycardia, papilloedema, CN6 palsy, transient visual obscurations, alterations in consciousness).
Syndromes can develop over hours or minutes
38
Herniations caused by supratentorial masses
Central herniation
Uncal herniation
Cingulate (subfalcine) herniation
39
Hernitations caused by infratentorial masses
Cerebellar tonsillar herniation
Upward transtentorial herniation
40
Aetiology of central herniation
Diencephalon symmetrically moves caudally through the tentorial notch-\> whole brainstem is compressed towards foramen magnum-\> stretch on paramedian branches of the basilar artery
Diffuse brain swelling, centrally located supratentorial mass (or multiple bilateral masses)
41
Clinical features of central herniation
Rostrocaudal neurologic deterioration:
Reticular formation dysfunction
Diencephalic stage
Midbrain stage
Pontine Stage
Medullary stage
Coma may develop before eye signs appear
42
Features of retricular formation dysfunction
Progressive alteration of consciousness
43
Features of diencephalic stage
Still reversible
Pinpoint reactive pupils- loss of sympathetic output from hypothalamus.
Many individuals may have hemiparesis prior to herniation. As diencephalic stage evolves, contraleteral hemiplegia worsens with homolateral limbs developing paratonic resistance to movement-\> bilateral hyperreflexia and babinski-\> decorticate posturing
Frequent yawns and sighs-\> Cheyne-Stokes respiration
44
Features of midbrain stage
Reflects infarction rather than reversible ischaemia and compression
Pupils enlarge to midposition and become fixed, disconjugate gaze with failure to adduct-\> internuclear opthalmoplegia
Decerebrate posturing
Central neurogenic hyperventilation
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Pontine stage
Impairment of oculocephalic and oculovestibular reflexes, rapid shallow respirations, flaccid extremities with bilateral Babinski responses
46
Medullary stage
Flaccidity, Cushing's-\> pupils dilate, hypotension, slow irregular respirations-\> apnoea, death
47
Aetiiology of uncal herniation
Impaction of anterior medial temporal gyrus into anterior portion of tentorial opening (into ambient cistern surrounding midbrain)
Caused by expanding unilateral, supratentorial mass
48
Clnical features of uncal herniation
CN3 palsy
PCA compression-\> homonymous hemianopia
Diminished consciousness
Ipsilateral hemiplegia
Brainstem dysfunction
49
CN3 palsy in uncal herniation
80-85% ipsilateral- CN3 is compressed against tentorial notch by inferomedial temporal lobe,
Prominent early sign is fixed large pupil as pupillary fibres are located most peripherally in nerve
15% have contralateral or bilateral CN3 dysfunction- may relate to midbrain ischaemia.
50
Most reliable sign for determining haematoma site in CN3 palsy in uncal herniation?
Mydriasis
51
Homonymous hemianopia in uncal herniation
PCA may be compressed against tentorium, producing homonymnous hemianopia
52
Diminshed consciousness in uncal herniation
As diencepahlon beings to shift laterally away from mass, consciousness beigns to diminish. Midbrain compression causes coma.
Early depression of consciousness correlates more with lateral brain displacement than with transtentorial herniation
53
Diaschisis
Function inhibition produced by acute focal disturbance in brain portion at distance from original injury but anatomically connected with it through fibre tracts
54
Ipsilateral hemiplegia in Uncal herniation
Contralateral corticospinal tract in cerebral peduncle is compressed against tenotrium edge- Kernohan's phenomeon.
False localisation of primary lesion
55
Hemiparesis in Uncal herniation
is contralateral in 50% of cases but remember Kernohan's false localising sign
56
Brainstem dysfunction in uncal herniation
Occurs if uncal syndrome is allowed to progress.
Bilaterally fixed pupils, ophthalmoplegia, loss of brainstem reflexes. Breathing-\> ataxic.
Bilateral decerebrate posturing
Circulatory collapse and death
57
How is Uncal herniation best diagnosed on neuroimaging
By evaluating CSF spaces around midbrain (mesencephalic cisterns). absence or occlusion usually indicates dislocation of supratentorial structures below tentorial notch.
Early: enlargement of ipsilateral perimesencephalic cistern
Later: transtentorial movement of temporal lobe- uncus and hippocampus are most medial portions of temporal lobe and are thus the first structures to cross the tentorial edge.
58
Duret haemorrhages
Often accompany progression of transtentorial herniation
Linear or flame-shaped haemorrahges in midline and paramedian regions of midbrain and pons.
Occur as herniation displaces brainstem downward, stretching medial perforating branches of basilar artery which is tethered to CoW
59
Aetiology of cingulate (subfalcine) herniation
Medial frontal structures, e.g. cingulate gyrus, herniate beneath falx-\> compression on internal cerebral veins, ipsilateral anterior cerebral artery.
Caused by frontal lobe masses
60
Clinical features of cingulate herniation
SIgns related to mass itself
Signs related to raised ICP
Rarely, ischaemia in ipsilateral ACA-\> loss of function in opposite leg, loss of bladder control.
Does not affect consciousness
61
What is the significance of the infratentorial compartment
Much smaller than the 2 supratenotrial compartments, hence the compensatory mechanisms are exhausted much more quickly (tolerated volume increases are much smaller)
62
Aetiology of tonsillar herniation
Cerebellar tonsils pushed through the foramen magnum
Posterior fossa/infratentorial masses or progressive unchecked transtentorial herniation.
63
Clinical features of tonsillar herniation
```
Stiff neck (due to tension of dura mater around cerebellar pressure cone)
Flaccid quadriplegia (bilateral compression of corticospinal tracts)
```
Apnoea and circulatory collapse due to medullary imnpingement-\> secondary coma.
Mass itself may compress/destroy brainstem.
70% mortality
64
Aetiology of upward transtentorial herniation
Contents of posterior fossa herniate through tentorial opening into diencephalic region
Posterior fossa mass + ventriculostomy.
Posterior fossa masses usually herniate caudally because obstructive hydrocephalus they produce prevents retrograde pressure gradient across tentorial opening (obstructive hydrocephalus is a particularly common complication of posterior fossa mass)
Ventriculostomy allows pressure gradient to quickly build up.
Neurosurgeons prepare patient for emergent posterior fossa decompression prior to performing ventriculostomy
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Clinial features of upward transtentorial herniation
Midbrain compression
Rapid decline in level of consciousness
Upward gaze paresis, other oculomotor signs.
Superior cerebellar artery ischaemia-\> ataxia
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Herniation after lumbar puncture
CSF removal lowers lumbar spinal canal pressure leading to increased gradient between cranial and lumbar compartments-\> rostrocaudal herniation
General risk of herniation after LP is 1.2-3%
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Ix in herniation syndromes
CT- findings that suggest unequal pressure between intracranial compartments.
Angiographic signs
68
CT findings suggesting unequal pressure between intracranial compartments.
Lateral shift of midline structures.
Loss of suprachiasmatic, circum-mesencephalic, superior cerebellar and quadrigemninal plate cisterns with sparing of ambient cisterns.
Shift/obliteration of 4th ventricle
Posterior fossa mass (strong contraindication to LP)
CT may miss cerebellar tonsillar herniation
69
Angiographic signs of:
Subfalcine herniation
Displacement of ACA or internal cerebral veins across midline
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Angiographic signs of:
Transtentorial herniation
Medial displacement of anterior choroidal artery
71
Angiographic signs of:
Tonsillar herniation
Displacement of PICA branches below foramen magnum
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Treatment of herniation syndromes
Temporary measures to lower ICP:
Hyperventilation
Mannitol
Dexamethasone
Neurosurgical intervention
73
You are the neurosurgeon on call and receive a referral concerning a 20-year-old man who is admitted to the local emergency department following a road traffic accident. He was the front-seat passenger in a car travelling at approximately 70km/hour when it skidded and hit a stationary car head on. He was not wearing a seatbelt and his head hit the windscreen. According to the ambulance crew his GCS was 3 at the scene and his pupils were equal and reacting. On arrival in the local emergency department he is intubated and ventilated and his cervical spine is immobilized with a collar and blocks. His GCS is 3 and his pupils are both 5mm in diameter. The right pupil constricts to light but the left does not.
What are the priorities in the management of this patient?
High impact head injury and priorty is rapid 1o survey followed by CT head and C-spine.
Dilated unreactive pupil on one side suggests asymmetrric mass effect and mannitol should be administered.
Hypertonic saline can also be initiaed.
C-spine should be cleared rapidly as wearing tight hard collar can increase ICP by reducing venous return, for similar reasons unless the thoracolumabr spine is injured, the entire bed should be tilted to 30deg and he should be mildly hyperventilated (PCO2 4-4.5kPa)
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Why is it important to rapidly clear C-spine in ?raised ICP following trauma
Tight hard collar may increase venous congestion preventing venous return
75
From what is mannitol produced
Extracted from secretions of the flowering ash, a deciduous tree
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MOA mannitol
Hyperosmolar substance that reduceds ICP by establishing an osmotic gradient against the BBB which it does not cross, hence moving water out of the brain.
It may also reduce red cell viscosity and within the autoregulating regions of the brain, improved CBF can be accompanied by reduced cerebral blood volume and hence reduced ICP.
77
Describe the CT image.
Thin, hyperdense extra-axial collection overlying the left hemisphere indicating an acute SDH (A). This is exerting mass effect with midline shift to the right (B)
There is some beam-hardening artefact in the right frontal region which may be mistaken for a small right-sided haematoma (C)
78
You are the neurosurgeon on call and receive a referral concerning a 20-year-old man who is admitted to the local emergency department following a road traffic accident. He was the front-seat passenger in a car travelling at approximately 70km/hour when it skidded and hit a stationary car head on. He was not wearing a seatbelt and his head hit the windscreen. According to the ambulance crew his GCS was 3 at the scene and his pupils were equal and reacting. On arrival in the local emergency department he is intubated and ventilated and his cervical spine is immobilized with a collar and blocks. His GCS is 3 and his pupils are both 5mm in diameter. The right pupil constricts to light but the left does not.
Why is this unlikely to be an EDH?
Clinical presentation is more in keeping with SDH
SDH are caused by high-energy injuries which frequently result in coma from the outset.
There is a higher incidence of underlying brain injury than with extradural haematomas and a worse px overall.
There may occasionally be a lucid interval.
EDHs appear biconvex radiologically as the haematomas tend not to cross suture lines whereas SDH are concave as the blood spreads evenly over the brain.
SDH may occasionally be biconvex dependent on the location of the bleed.
79
You are the neurosurgeon on call and receive a referral concerning a 20-year-old man who is admitted to the local emergency department following a road traffic accident. He was the front-seat passenger in a car travelling at approximately 70km/hour when it skidded and hit a stationary car head on. He was not wearing a seatbelt and his head hit the windscreen. According to the ambulance crew his GCS was 3 at the scene and his pupils were equal and reacting. On arrival in the local emergency department he is intubated and ventilated and his cervical spine is immobilized with a collar and blocks. His GCS is 3 and his pupils are both 5mm in diameter. The right pupil constricts to light but the left does not.
Both pupils become reactive after mannitol and the GCS
improves to 7/15 (E1, V2, M4). He flexes to pain with the left arm
but no movement is seen on the right side of the body. How is
his motor deficit explained?
The patient has a right hemiparesis due to a mass effect from the left hemisphere, resulting in compression of the left cerebral peduncle.
Pyramidal tract fibres which traverse this area cross over in the medulla oblongata, hence compression of the left cerebral peduncle causes a right hemiparesis.
This is not cortical compression as other structures would be affected.
80
You are the neurosurgeon on call and receive a referral concerning a 20-year-old man who is admitted to the local emergency department following a road traffic accident. He was the front-seat passenger in a car travelling at approximately 70km/hour when it skidded and hit a stationary car head on. He was not wearing a seatbelt and his head hit the windscreen. According to the ambulance crew his GCS was 3 at the scene and his pupils were equal and reacting. On arrival in the local emergency department he is intubated and ventilated and his cervical spine is immobilized with a collar and blocks. His GCS is 3 and his pupils are both 5mm in diameter. The right pupil constricts to light but the left does not.
What is the definitive mx of this case?
This patient requires urgent craniotomy and evacuation of the haematoma.
The timing in acute SDH is critical.
30% mortality if the surgery takes place within 4h of injury but 90% after 4h
81
You are the neurosurgeon on call and receive a referral concerning a 20-year-old man who is admitted to the local emergency department following a road traffic accident. He was the front-seat passenger in a car travelling at approximately 70km/hour when it skidded and hit a stationary car head on. He was not wearing a seatbelt and his head hit the windscreen. According to the ambulance crew his GCS was 3 at the scene and his pupils were equal and reacting. On arrival in the local emergency department he is intubated and ventilated and his cervical spine is immobilized with a collar and blocks. His GCS is 3 and his pupils are both 5mm in diameter. The right pupil constricts to light but the left does not.
What practical steps need to be taken to transfer the patient to your hospital for urgent surgery.
Check with ICU for bed availability after which the referring hospital should be advised to transfer the patient, possibly directly to theatre without delay.
The anaesthetic and theatre staff should be informed to prepare the operating theatre and the consultant neurosurgeon notified
82
You are the neurosurgeon on call and receive a referral concerning a 20-year-old man who is admitted to the local emergency department following a road traffic accident. He was the front-seat passenger in a car travelling at approximately 70km/hour when it skidded and hit a stationary car head on. He was not wearing a seatbelt and his head hit the windscreen. According to the ambulance crew his GCS was 3 at the scene and his pupils were equal and reacting. On arrival in the local emergency department he is intubated and ventilated and his cervical spine is immobilized with a collar and blocks. His GCS is 3 and his pupils are both 5mm in diameter. The right pupil constricts to light but the left does not.
The ITU is full, what are the other options?
One option would be to redirect the patient to the next nearest neurosurgical unit, though this may result in further delay.
Another would be to transfer the patient directly to theatre so that the search for an ICU bed can continue, possibly at an alternative centre. This is not ideal may be needed if the indication is severe.
If the patient is to be transferred to another hospital post-operatively, a CT scan may be performed before the transfer to check post-operative appearances in order to reassure the transferring team.
83
Describe the iamge
The patient has undergone craniectomy with evacuation of subdural haematoma.
An intraparenchymal ICP has been placed in the left frontal lobe.
The patient should have a cranioplasty at a later date usually, 3-4/12 to cover the cranial defect if the recovery is satisfactory.
84
What factors determine when a patient should be extubated
Depends on whether the patient is likely to achieve a sufficient conscious state to maintain his airway when woken. ICP must also be acceptable.
Premorbid state, nature of injury and the effect of surgery all factor in to this decision.
It is desirable to wake the patient as soon as possible.
In the case of the acute SDH as described the patient is radiologically cured but his pre-operative state was dire.
85
Indications for conservative Mx of acute SDH
The operation generally required in the presence of neurological deficit, large haematoma or significant mass effect.
Small acute SDH without neurological deficits may be managed conservatively.
Elderly patients may also be managed conservatively even with the neurological deficit if mild.
This is generally because acute SDH requires large craniectomy which is poorly tolerated by the elderly.
If the haematoma is left to turn chronic, the liquefied chronic SDH may be washed out through burrholes.
86
Conservative mx of acute SDH
Regular neuro-obs
Monitoring Na
CT scan should be repeated if any neurological deterioration or symptoms of raised ICP caused by expanding haeamatoma
87
62y/o woman who fell of horse and sustained head injury
The two images are separated by 5days, when she became nauseous.
Describe the CT scan
A- there is a right sided acute subdural haematoma, there is mass effect.
B- the haematoma has enlarged in size and is now of lower density as the thrombus is being degraded. there is some residual blood posteriorly.
There is more severe midline shift.
The right lateral ventricle is compressed and contalateral hydrocephalus has developed (distortion of the foramen of Monro by midline shift obstructs the left lateral ventricle, which has enlarged, exacerbating the overall mass effect on the brain)
The SDH shown in B was eventually evacuated through burrholes with the patient making an excellent recovery.
88
Features of the dura mater
Tough connective tissue which consists of two layers- outer periosteal layer and inner meningeal layer.
The two layers separate in defined locations to form the intracranial venous sinuses.
The falx cerebi, tentorium cerebelli, falx cerebelli and diaphragma sellae are double folds of dura that form partitions within the cranium.
89
Periosteal dura at the foramina of the skull
Continuous with the periosteum of the skull through the cranial foraminae and the foramen magnum
90
What happens to the meningeal dura at the foramen magnum?
Continues down the spinal canal as the thecal sac.
91
Why do EDH not usually cross suture lines?
Dura is firmly adherent to bone at the conxity suture lines. EDHs form between the bone and perisoteal dura and do not usually cross these lines.
92
What is the only haematoma crossing the midline?
EDH. Dura is firmly attached to the base of the skull and a fracture here has the propensity to tear the dura resulting in CSF leak.
93
Featues of the arachnoid mater
Thin avascular membrane covered with mesothelial cells.
Adheres to the inner aspect of the meningeal dura. The subarachnoid space below it contains CSF.
Major nerves and blood vessels traverse the subarachnoid space.
Some spaces are larger than others and these are called cisterns.
94
Basal cisterns
Refers to the subarachnoid cisterns around the brainstem. Effacement of the basal cisterns occurs in raised ICP and is a bad prognostic sign
95
Superior= quadrigeminal cistern
96
What is the signfiicance of the cisterna magna or cerebellomedullary cistern?
Lies between the inferior surface of the cerebellum and the back of the medulla.
CSF flows out of the fourth ventricle at this cistern
97
Features of the pia mater
Thin membrane composed of mesodermal cells. Closely adherent to the brain and invaginates into fissures and sulci
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101
An 18-year-old man attends the emergency department 30 minutes after being hit on the head with a champagne bottle at a party. There was no loss of consciousness. He had vomited several times and complains of a severe headache over the left side of his head. On examination, his GCS is 15/15, his pupils are equal and reactive, and there are no focal neurological deficits.
Are there any evidence based guidelines on whether this patient requires a CT scan of the brain?
Immediate CT brain is recommended by NICE if any of the following factors are present post HI
GCS \<13 at initial assessment or \<15 2h after injury
Focal neurological deficit
Seizure
Suspected open or depressed skull fracture
Vomiting more than once in an adult
Amnesia of more than 30 minutes before incident.
LOC or any amnesia in the presence of age, coagulopathy dangerous MOI.
This patient merits a scan as he has vomited more than once
102
An 18-year-old man attends the emergency department 30 minutes after being hit on the head with a champagne bottle at a party. There was no loss of consciousness. He had vomited several times and complains of a severe headache over the left side of his head. On examination, his GCS is 15/15, his pupils are equal and reactive, and there are no focal neurological deficits.
The CTH is shown below.
Describe the apperances
There is an extra-axial biconvex high-density lesion overlying the right frontal lobe, typical of an extradural haematoma. There is a midline shift with distortion of the ventricles. There is a scalp haematoma on the right.
103
Why do extradural haematomas typically appear biconvex?
The periosteal layer of the dura mater is tightly bound to the skull and folds into the cranial sutures.
An extradural haematoma lies between the bone and the periosteal dura. As it enlarges, it strips the dura from the bone but is restrained at the sutures and hence appears convex.
Enlargement typcially does not traverse sutures lines
104
The rupture of which vessels usually leads to an extradural haematoma?
Extradural haemtomas are usually caused by arterial bleeding classically from the MMA. They can also be caused by bleeding from an overlying skull fracture (these tend to be smaller) or from venous haemorrhage if the dura is breached over a venous sinus
105
An 18-year-old man attends the emergency department 30 minutes after being hit on the head with a champagne bottle at a party. There was no loss of consciousness. He had vomited several times and complains of a severe headache over the left side of his head. On examination, his GCS is 15/15, his pupils are equal and reactive, and there are no focal neurological deficits.
CTH shows extradural haematoma
What is the management of this case?
Conservative or operative management
Expanding extradural haematoma can cause rapid neurological deterioration and immediate surgery is indicated if there is significant or ongoing neurological deficit.
Conservative Mx may be appropriate if the haematoma is small and the patient neurologically intact.
In this case, the haematoma is large but the patient is neurologically intact. The risks of surgery must be balanced against the risks of further deterioration if managed conservatively.
Additional factors of consideration include: midline shift, mass effect, likely arterial bleed.
106
What is the significance of an extradural haematoma caused by an arterial bleed
Arterial bleeding will not stop due to tamponade, unlike bleeding from fracture or venous bleeding
107
An 18-year-old man attends the emergency department 30 minutes after being hit on the head with a champagne bottle at a party. There was no loss of consciousness. He had vomited several times and complains of a severe headache over the left side of his head. On examination, his GCS is 15/15, his pupils are equal and reactive, and there are no focal neurological deficits.
CTH shows extradural haematoma
He underwent craniotomy and evacuation of haematoma, his post-operative scan is shown. Describe it
The post-operative scan shows complete evacuation of the haematoma.
The arrow shows an area of low density indicating a contusion
108
An 18-year-old man attends the emergency department 30 minutes after being hit on the head with a champagne bottle at a party. There was no loss of consciousness. He had vomited several times and complains of a severe headache over the left side of his head. On examination, his GCS is 15/15, his pupils are equal and reactive, and there are no focal neurological deficits.
CTH shows extradural haematoma which is surgically evacuated.
The patient works as a delivery driver and asks if his license will be affected
Must report the condition to DVLA
There is a document specifying driving restrictions is available on DVLA website.
Significant HI usually requires 6-12/12 off driving for group 1 license, may result in refusal or revocation of a group 2 license
109
A 54-year-old man sustained a head injury in a bicycle accident. On arrival, his GCS is 13/15 (E4, V4, M5) and he is agitated and combative. A CT scan is performed and is shown in Fig. 3.3. What does it show?
There is a posterior fossa EDH (A).
Locules of air are present and there is opacification of the right mastoid cells. This is due to a fracture through the occipital bone extending into the petrous temporal bone.
There is some mass effect with compression of the fourth ventricle (B) and the prepontine cistern (C).
110
A 54-year-old man sustained a head injury in a bicycle accident. On arrival, his GCS is 13/15 (E4, V4, M5) and he is agitated and combative.
CT scan shows posterior fossa EDH likely related to occipital bone fracture.
What are the options for mx?
Conservative or surgical.
The major risk of surgery is heavy haemorrhage from the transverse sinus from which this venous extradural haematoma has probably arisen.
Risk of conservative management is brainstem compression from an enlarging haematoma.
As the neurological deficit is relatively mild it may be reasonable to opt for conservative Mx.
Venous EDHs are less likely to enlarge than their arterial counterparts.
Very close observation is required as rapid cardiorespiratory deterioration can occur with posterior fossa EDHs as a result of brainstem compression without neurological deterioration.
Many surgeons would advocate early repeat CT scan, especially if initial scan is within 4h of injury.
Surgery would be indicated if there were further neurological deterioration
111
A 62-year-old woman presents to the emergency department. Last night, when intoxicated, she fell down a full flight of stairs at home but does not remember exactly how she fell and whether she hit her head. She has developed a worsen- ing headache, and her husband called an ambulance as she appeared confused the next morning. On arrival she is confused and drowsy, only eye opening to pain. She goes for a CT scan (Fig. 3.4); on returning from the radiology depart- ment she is no longer obeying commands. What does the CT show?
The axial view shows a midline mass which is both hyper and hypodense. Exact nature is difficult to determine but in the context of trauma likely represents blood. The mixed density of the clot indicating solid and liquid componenets likely signifying active haemorrhage.
The coronal view demonstrates a haematoma crossing the mid-line which is therefore an EDH.
Given its location, the aetiology is likely to be a torn sagittal sinus caused by an associated skull fracture.
The venous aetiology would account for the slightly delayed (12h) presentation
112
A 62-year-old woman presents to the emergency department. Last night, when intoxicated, she fell down a full flight of stairs at home but does not remember exactly how she fell and whether she hit her head. She has developed a worsen- ing headache, and her husband called an ambulance as she appeared confused the next morning. On arrival she is confused and drowsy, only eye opening to pain. She goes for a CT scan (Fig. 3.4); on returning from the radiology depart- ment she is no longer obeying commands.
CT scan shows haematoma crossing the midline, likely secondary to torn sagittal sinus.
How would you manage the patient and what concerns would you have?
Conservative Mx is generally preferred because extension is unlikely due to low-pressure venous blood and the considerable risk of intraoperative haemorrhage.
Surgical Mx is indicated in the case due to her deteriorating neurological state.
In the process of evacuating the haematoma, the sagittal sinus is likely to be encountered and cannot simply be coagulated but must be repaired or at least tamponaded whilst maintaining patency.
The patient's haematoma was evacuated through bilateral craniotomies which left a midline strip of bone over the sagittal sinus.
The dura was stitched up to the bone to tamponade the dura against haemostatic material which was left in situ.
Intraoperative blood loss was 1500mL
113
What is a significant consideration when operating with an open major venous sinus during surgery?
Risks negative venous pressure if the opening is appreciably high than the right atrium and air consequently being sucked into the open sinus causing air embolism
114
A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.
What are the priorities in the management of this patient?
1o survey- ATLS guidelines
Followed by CTB to exclude IC pathology +/- CT C-spine if indicated.
He will need a 2o survey to ensure no other injury has been missed.
115
A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.
How should his agitation be managed?
The use of sedatives masks neurological degeneration and is not recommended in the acute setting.
Specialist nurses are required to manage agitated patients with HIs.
Treat simple causes e.g. analgesia, reduction of #, catheterisation of full bladder.
Small dose of promazine is often helpful
116
When is intubation indicated in a patient with reduced GCS
If unable to maintain airway or agitation renders essential supportive therapy (O2, IVF) or Ix (CTB) impossible.
Decision should be made on a case by case basis with a post-ictal patient with GCS 7/15 may not require airway whereas GCS 13/15 agitated patient requiring CT scan may
117
A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.
CT scan is shown, describe findings
Extensive bifrontal contusions (A).
The hypodense areas surrounding the blood are indicative of oedema (B).
Traumatic SAH is also present (C).
118
A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.
CTH shown below.
How should this patient be managed?
Requires admission for close observation, Na levels, clotting and liver function.
Anticonvulsants are recommended for one week after severe TBI and then discontinued if there has not been a seizure
119
A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.
One day after admission, he is no longer disorientated and feels well. He has no focal neurological deficits. He asks how long he needs to stay in hospital and whether any more tests are required. How would
you answer his question?
The scan showed sizable contusions with surrounding oedema.
Cerebral oedema around evolving contusions is maximal 24-48h after injury but can also manifest several days after injury and lead to neurological decline.
A further period of hospital observation would be recommended at least a few days with repeat CT scan and serum eletrolytes prior to discharge
120
What are the risks associated with hyponatraemia
Altered mental state, seizures, cerebral oedema, death
121
A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.
There are extensive bifrontal contusions (A). The hypodense areas surrounding the blood (B) are indicative of oedema. Traumatic subarachnoid haemorrhage is also present (C).
The patient has a blood test prior to discharge (6 days into his admission) and his sodium level is 116mmol/L. He is alert and orientated.
What is the likely diagnosis
Hyponatremia in neurosurgery is commonly due to SIADH or CSW
Other causes of hyponatraemia should be checked
122
Bloods to Ix hyponatraemia in neurosurgery
Paired plasma and urine osmolality
Urine sodium concentration
123
What can differentiate between SIADH and CSW in hyponatraemia in neurosurgical patients?
Clinical Ax
SIADH- hyper or euvolaemia
CSW- hypovolaemic
124
A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.
The patient has a blood test prior to discharge (6 days into his admission) and his sodium level is 116mmol/L. He is alert and orientated.
plasma osmolality 265mmol/kg, urine osmolality 218mmol/kg, urine sodium 40mmol/L. He is clinically euvolaemic. How should
he be managed?
Management of a patient with a clinical picture in keeping with both SIADH/CSW is controversial.
This patient was managed with fluid restriction in the HDU
125
Characteristics of Ix in both SIADH and CSW
Low plasma osmolality
High urine osmolality
High urine sodium concentration
Volume status Ax can differentiate between the two but is not always reliable
126
How to differentiate between SIADH and CSW
SIADH is relatively more common in head injury
CSW in SAH.
Extracellular volume, patients with CSW are expected to be dehydrated
127
An additional cause of hyponatraemia in neurosurgery?
Cortisol deficiency following pituitary surgery
128
Mx of hyponatraemia in neurosurgery
Magnitude of hyponatraemia, underlying diagnosis, clinical symptoms.
If symptomatic, immediate salt and water replacement with IV hypertonic saline.
If asymptomatic, either salt and water replacement or fluid restriction.
Though fluid restriction is not advised in SAH due to risk of precipitating cerebral ischaemia
129
Rate of correction of hyponatraemia
No more than 8mmol/L/24h.
130
Why should Na be raised cautiously?
Due to risk of central pontine myelinolysis
131
Na \<131
High plasma osmolality
Lab error
Pseudohyponatraemia
132
Na \<131
Low plasma osmolality
Low urine osmolality
Polydipsia
133
Na \<131
Low plasma osmolality
High urine osmolality
Low urinary sodium conenctration (\<25mmol)
Extrarenal: diarrhoea, nausea/vomiting/sweating
Trying to renally conserve Na
134
Na \<131
Low plasma osmolality
High urine osmolality
High urine Na concentration (\>25)
?SIADH
?CSW
Assess volume
135
Pathophysiology of SIADH
Hypothalamic osmoreceptors detect changes in plasma osmolality and secrete ADH in response.
ADH alters the water permeability of the collecting ducts in the kidney.
More ADH results in more aquaporins in the collecting ducts, leading to increased water reabsorption independent of sodium reabsorption.
In SIADH there is excess water reabsorption, leading to a low-volume, concentrated urine and relatively increased plasma volume.
The plasma sodium and osmolality are low due to dilution and the urine osmolality is high.
Urinary sodium is normal but concentration is increased due to low volume
136
Mx of SIADH
Limit or decrease plasma volume with fluid restriction or diuretics.
If the patient is symptomatic, the priority is to increase the plasma sodium level and IV salt supplementation is indcated
137
Pathophysiology of CSW
Not completely understood.
Thought to result from impaired sodium reabsorption in the kidney leading to net sodium loss and therefore water loss.
This leads to hyponatraemia with low plasma osmolality and high (or normal) urine osmolality.
138
When is CSW of considerable concern
In SAH where, along with DCI, it is a major cause of delayed neurological deterioration after the haemorrhage
139
Seizure risk:
Brain tumour
Depends on tumours type and location.
Up to 100% for Dysembryoplastic neuroepithelial tumour. 75% for low grade astrocytomas. 50-60% for high-grade astrocytomas
140
Treatment of seizure in known brain tumour
Treat as epilepsy
Non-enzyme inducers e.g. levetiracetam do not affect the efficacy of corticosteroids and CTx
Continue for as long as tumour is present and may taper after resection
141
Seizure risk in TBI
Depends on severity
15% with severe TBI
Risk increased \>20% in penetrating injury, depressed skull fracture, early seizure, SDH
142
What factors increase the risk of seizures in TBI and by how much?
Penetrating injury
Depressed skull fracture
Early seizure
SDH
20%
143
Prophylactic seizure therapy in TBI
Phenytoin for 1/52
Though has no effect on outcome
144
Treatment of seizure after TBI
Treat as epilepsy
145
Seizure risk after SAH
5-8%
146
Seizure prophylaxis in SAH
Not recommended (phenytoin use has been associated with worse outcomes)
147
Seizure treatment in SAH
Treat as per epilepsy with drug other than phenytoin
148
Seizure risk, spontaneous ICH
3-17%
149
Seizure prophlyaxis, spontaneous ICH
Not recommended as prophylactic anticonvulsants have been associated with worse outcomes
150
Seizure treatment, spontaneous ICH
As epilepsy
