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Y4 final checklist_ SURGERY > Neurosurgery > Flashcards

Neurosurgery Flashcards

1
Q

Pathophysiology of disc prolapse

A

Herniation of nucleus pulposus through annulus fibrosus

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2
Q

What’s spinal cord compression?

a common group of patients

A

Spinal cord compression

  • an oncological emergency
  • affects up to 5% of cancer patients
  • Extradural compression accounts for the majority of cases, usually due to vertebral body metastases
  • It is more common in patients with lung, breast and prostate cancer
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3
Q

Features of spinal cord compression

A
  • back pain - the earliest and most common symptom - may be worse on lying down and coughing
  • lower limb weakness
  • sensory changes: sensory loss and numbness
  • neurological signs depend on the level of the lesion

*Lesions above L1 usually result in upper motor neuron signs in the legs and a sensory level

*Lesions below L1 usually cause lower motor neuron signs in the legs and perianal numbness. Tendon reflexes tend to be increased below the level of the lesion and absent at the level of the lesion

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4
Q

Mx of spinal cord compression

A
  • high-dose oral dexamethasone
  • urgent oncological assessment for consideration of radiotherapy or surgery
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5
Q

Presentation of disc prolapse

A
  • L5 and S1 roots most commonly compressed by prolapse of L4/5 and L5/S1 discs
  • May present as severe pain on sneezing, coughing or twisting a few days after low back strain
  • Lumbago: low back pain
  • Sciatica: shooting radicular pain down buttock and thigh
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6
Q

Signs of L4/L5 root compression

A

L4/5 → L5 Root Compression

• Weak hallux extension ± foot drop

  • In foot drop due to L5 radiculopathy, weak

inversion (tib. post.) helps distinguish from peroneal N. palsy

• ↓ sensation on inner dorsum of foot

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7
Q

Signs of L5/S1 root compresison

A

L5/S1 → S1 Root Compression

  • Weak foot plantarflexion and eversion
  • Loss of ankle-jerk
  • Calf pain
  • ↓ sensation over sole of foot and back of calf
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8
Q

Management of disc prolapse

A
  • Conservative: Brief rest, analgesia and mobilisation effective in ≥90%; physio
  • Medical: analgesia, transforaminal steroid injection
  • Surgical: discectomy or laminectomy may be needed in cauda-equina syndrome, continuing pain or muscle weakness
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9
Q

Indications for surgery in disc prolapse (3)

A

Surgical: discectomy or laminectomy may be needed in:

  • cauda-equina syndrome
  • continuing pain
  • muscle weakness
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10
Q

Signs of Acute Cord Compression

A

Acute Cord Compression = emergency!

  • Bilateral pain: back and radicular
  • LMN signs at compression level
  • UMN signs and sensory level below compression
  • Sphincter disturbance
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11
Q

Signs of Cauda Equina

A

Acute Cauda Equina Compression

  • Alternating or bilateral radicular pain in the legs
  • Saddle anaesthesia
  • Loss of anal tone
  • Bladder ± bowel incontinence
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12
Q

Treatment of different causes (3) of acute cord compression

A

Acute cord compression = EMERGENCY

  • Large prolapse: laminectomy / discectomy
  • Tumours: radiotherapy and steroids
  • Abscesses: decompression
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13
Q

What’s extradural haematoma

A

An extradural (or ‘epidural’) haematoma is a collection of blood that is between the skull and the dura

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14
Q

What’s that?

A

Extradural haemorrhage

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15
Q

Cause of extradural haemorrhage

A

It is almost always caused by trauma and most typically by ‘low-impact’ trauma (e.g. a blow to the head or a fall)

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16
Q

The most common artery affected in extradural haemorrhage

A
  • often in the temporal region since the thin skull at the pterion overlies the middle meningeal artery and is therefore vulnerable to injury.
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17
Q

The classical presentation of extradural haemorrhage

(2 signs and why)

A
  • Luicid interval
  • Apatient 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.
  • Fixed and dileted pupils

-​As the haematoma expands the uncus of the temporal lobe herniates around the tentorium cerebelli

-the patient develops a fixed and dilated pupil due to the compression of the parasympathetic fibers of the third cranial nerve

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18
Q

Ix and characteristic appearance in Extradural Haemorrhage

A

CT head

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

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19
Q

Management of extradural haematoma

A
  • close clinical and radiological observation → in patients who have no neurological deficit
  • craniotomy and evacuation of the haematoma → definitive treatment
20
Q

What’s subdural haematoma?

A

A subdural haematoma

  • a collection of blood deep to the dural layer of the meninges
  • the blood is not within the substance of the brain and is therefore called an ‘extra-axial’ or ‘extrinsic’ lesion
  • they can be unilateral or bilateral
21
Q

Classification of subdural haematoma (3)

A

Subdural haematomas can be classified in terms of their age:

  • Acute
  • Subacute
  • Chronic
22
Q

Causes of acute subdural haematoma

A

An acute subdural haematoma → a collection of fresh blood within the subdural space

  • most commonly caused by high-impact trauma
  • Since it is associated with high-impact injuries, there is often other brain underlying brain injuries
23
Q

The severity of symptoms in acute subdural haematoma

A
  • There is a spectrum of severity of symptoms and presentation depending on the size of the compressive acute subdural haematoma and the associated injuries
  • Presentation ranges from an incidental finding in trauma to severe coma and coning due to herniation
24
Q
A
25
Q

Ix in acute subdural haematoma

A

CT imaging → first-line investigation

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.

26
Q

Management of acute subdural haematoma

A
  • Conservative observation → small or incidental acute subdurals
  • Surgical options: monitoring of intracranial pressure and decompressive craniectomy
27
Q

What’s chronic subdural haematoma?

A

A chronic subdural haematoma is

  • a collection of blood within the subdural space that has been present for weeks to months
28
Q

Groups of patients at risk of chronic subdural haematoma?

A
  • Rupture of the small bridging veins within the subdural space → 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
  • Infants also have fragile bridging veins and can rupture in shaken baby syndrome
29
Q

Presentation of chronic subdural haematoma

A
  • typically a several week to month
  • progressive history of either confusion, reduced consciousness or neurological deficit
30
Q

Ix of chronic subdural haematoma

A
  • On CT imaging they similarly are crescentic in shape, not restricted by suture lines and compress the brain (‘mass effect’
  • In contrast to acute subdurals, chronic subdurals are hypodense (dark) compared to the substance of the brain.
31
Q

Management of chronic subdural haematoma

A
  • Conservative management → if it’s an incidental finding or if it is small in size with no associated neurological deficit
  • Surgical decompression with burr holes is required if the patient is confused, has an associated neurological deficit or has severe imaging findings
32
Q

What’s a subarachnoid haemorrhage

  • location
A

A subarachnoid haemorrhage (SAH)

  • intracranial haemorrhage
  • defined as the presence of blood within the subarachnoid space, i.e. deep to the subarachnoid layer of the meninges
33
Q

Causes of subarachnoid haemorrhage

A

Causes of spontaneous (non-traumatic) SAH include:

  • Intracranial aneurysm* (saccular ‘berry’ aneurysms) → around 85% of cases.
  • Arteriovenous malformation
  • Pituitary apoplexy
  • Arterial dissection
  • Mycotic (infective) aneurysms
  • Perimesencephalic (an idiopathic venous bleed)
34
Q

(2) types of SAH

A
  • 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
35
Q

Conditions associated with Berry-aneurysm

A
  • adult polycystic kidney disease
  • Ehlers-Danlos syndrome
  • coarctation of the aorta
36
Q

Presentation of SAH

A
  • 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
37
Q

Ix used to confirm SAH (2)

A
  • Computed tomography (CT) head Acute blood (hyperdense/bright on CT) *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 if SAH is confirmed

38
Q

What Ix are needed after SAH is confirmed?

A

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)
39
Q

Management of SAH (caused by intracranial aneurysm)

A

The treatment in spontaneous SAH is in accordance with the causative pathology

  • 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
  • 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
40
Q

Complications of aneurysm caused SAH

A

Complications of aneurysmal 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
41
Q

(3) predictive factors in SAH

A

Important predictive factors in SAH:

  • conscious level on admission
  • age
  • amount of blood visible on CT head
42
Q

What’s an intracerebral haematoma?

A

An intracerebral (or intraparenchymal) haemorrhage is a collection of blood within the substance of the brain

43
Q

Causes/ risk factors for intraparenchymal haemorrhage

A

Causes / risk factors include:

  • hypertension
  • vascular lesion (e.g. aneurysm or arteriovenous malformation)
  • cerebral amyloid angiopathy
  • brain tumour
  • infarct (particularly in stroke patients undergoing thrombolysis)
44
Q

Presentation of a patient with intraparenchymal haemorrhage

A

Patients will present similarly to an ischaemic stroke (which is why it is crucial to obtain a CT in head in all stroke patients prior to thrombolysis) or with a decrease in consciousness

45
Q

Ix of intraparenchymal haemorrhage

A

CT imaging will show a hyperdensity (bright lesion) within the substance of the brain

46
Q

Treatment of intraparenchymal haemorrhage

A

Treatment is often conservative under the care of stroke physicians, but large clots in patients with impaired consciousness may warrant surgical evacuation

Y4 final checklist_ SURGERY (25 decks)

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