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Nervous System & Neuropsychiatry > Head Trauma & Intracranial Events, Raised ICP > Flashcards

Head Trauma & Intracranial Events, Raised ICP Flashcards

1
Q

What is the difference, with regard to injury mechanism, between open and closed head trauma?

A

Open trauma is penetrating and causes direct injury to brain structures

Closed trauma causes a rise in ICP and shearing of intracranial structures

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2
Q

Define the term “cerebral contusion”

A

“Bruising” of brain whereby blood mixes with cortical tissue due to micro-haemorrhages and small blood vessel leaks

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3
Q

What are the most common sites of cerebral contusion?

A

Inferior frontal and anterior temporal

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4
Q

Explain the pathophysiology of cerebral contusions and how they can lead to coma/death.

A

Trauma – Micro-haemorrhages– Cerebral contusions– Cerebral oedema/ intracerebral bleed– raised ICP – Coma/death

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5
Q

Explain what is meant by the terms “coup” and “counter-coup” relating to cerebral contusion.

A

Coup- contusion at the site of impact

Counter-coup- at the opposite side to the site of impact

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6
Q

Define “concussion”

Describe its pathophysiology.

A

Head injury with a temporary loss of brain function.

Trauma–stretching/injury of axons–imparied neurotransmission–loss of ion regulation–reduced cerebral blood flow– temporary brain dysfunction

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7
Q

Describe some of the features of post-concussion syndrome.

A
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8
Q

What is meant by the term “diffuse axonal injury”

A

Shearing of the interface between grey and white matter following acceleration/decelaration or rotational injury to the brain.

Leading to damage of the intracerebral neurones and dendritic connections.

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9
Q

Describe the pathophysiology of diffuse axonal injury.

A

Trauma–shearing of grey and white matter interface–axonal death–cerebral oedema–raise ICP–coma/death

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10
Q

What is a basillar skull fracture?

Explain its pathophysiology.

A

A bony fracture within the base of the skull

Trauma–skull fractures–tear in meninges–CSF leakage

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11
Q

What are the clinical signs of basillar skull fracture?

A
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12
Q

How is a basillar skull fracture managed?

A

Traumatic brain injury management (including ICP control)

Seek and treat complications

Elevation of depressed skull fractures

Persistent CSF leak management - surgery

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13
Q

According to NICE guidance, what are the criteria for urgent CT head?

A

CGS <13 at any point

GCS <14 >2hours after injury

Focal neurological deficit, seizure, LOC WITH any of the following: age >65, coagulopathy, dangerous mechanism of injury , angigrade amnesia >30 minutes

Open/depressed skull fracture or signs of basal skull fracture

2 + discrete episodes of vomiting

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14
Q

What is an extradural haemorrhage?

What is the most common cause of this type of haemorrhage?

A

A collection of blood between the INNER SURFACE of skull and PERIOSTEAL DURA MATER

Trauma/skull fracture causing severed MMA

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15
Q

How does a patient typically present when they have suffered an extradural haemorrhage?

A
  1. Loss of consciousness
  2. Transient recovery “lucid interval”
  3. Rapid decline and loss of consciousness

CN palsies may be found on examination

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16
Q

What are the features of extradural haemorrhage on CT head?

A

Bleed is confined to the suture lines

Lemon-shaped

Pushes the hemisphere inward- midline shift and compression of the lateral ventricles

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17
Q

What is the prognosis for individuals that suffer extradural haemorrhage (both large and small)?

A

Small: generally good with early intervention, observation and conservative management, neurological follow-up

Large: referral to neurosurgery for craniotomy and clot evacuation

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18
Q

List some of the complications of extradural haemorrhage.

A

Permanent brain damage

Coma

Seizure

Weakness

Psuedoaneurysm

Arteriovenus fistula

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19
Q

What is a subdural haemorrhage?

A

A bleed between the meningeal dura matter and the arachnoid matter

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20
Q

Subdural haemorrhage can be acute, subacute or chronic.

Give the time span of these classifications.

A

Acute < 3 days

Subacute 3-12 days

Chronic >3 weeks

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21
Q

Subdural haemorrhage is caused by what?

What can increase the risk of such?

A

Trauma - shearing of briding veins

Can be spontaneous

Cerebral atrophy increases the risk

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22
Q

Acute, subacute and chronic subdural haemorrhage are usually each caused by what?

A

Acute- trauma

Subacute/Chronic-elderly with vague or absent history of head trauma

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23
Q

How do acute and chronic bleeds differ in their apperance on CT?

A

Acute- hyperdense (brighter than brain tissue)

Chronic- hypodense (darker than brain tissue)

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24
Q

How does a subdural haemorrhage look on a CT scan?

A

Banana shaped

Not confined by suture lines but stopped by falx cerebri

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25
Q

Describe the management of acute, chronic and subacute subdural haemorrhage.

How does the prognosis compare with extradural haemorrhage?

A

Acute- neurosurgical intervention to relieve raised ICP

Subacute/ Chronic- if symptomatic, via 1 or more burr holes

Poor prognosis compared to extradural haemorrhage

26
Q

What is a subarachnoid haemorrhage?

A

A collection of blood between arachnoid matter and pia matter

27
Q

In what age group do subarachnoid haemorrhages usually occur?

What is the usually cause of subarachnoid haemorrhage?

A

Middle aged (<60 years)

Usually ruptured berry aneurysm, can be trauma

28
Q

How do patients with subarachnoid haemorrhage usually present?

A

Sudden onset “thunderclap” headache

Meningism

Nausea and vomitting

Fever

Focal neurological deficits

Loss of consciousness

29
Q

The vast majority of subarachnoid haemorrhage occurs spontaneously secondary to what?

A

Berry aneurysm rupture

30
Q

Give some risk factors for subarachnoid haemorrhage

A

Hypertension

Family history

Heavy alcohol consumption

Abnormal connective tissue

31
Q

In what areas of the cerebral circulation do the majority of berry aneurysms occur?

Where, specifically, are thest most likely to occur?

A

Circle of Willis- particularly where two vessels join

Anterior cerebral artery

32
Q

What can be clinical investigation can be performed to aid the diagnosis of subarachnoid haemorrhage?

A

Lumbar puncture - presence of RBCs in CSF?

Need the same number in 3 bottles

33
Q

12 hours after symptom onset, what is the name given to the yellowish colour of CSF?

A

Xanthochromia

34
Q

What is the management of subarachnoid haemorrhage?

A

Stabilise patient

Prevent bleeding

Treat cerebral vasospasm

Correct hyponatraemia

(Neurosurgical intervention if large)

35
Q

What is the range of “normal” ICP?

In mmHg and cmH20

A

5-15mmHg

7-20cmH20

36
Q

In a healthy individual, how is blood flow to the brain regulated?

A

Autoregulation:

Vasoconstriction

Vasodilation

Chemoregulation

37
Q

From which compartments of the intracranial space does fluid drainin order to compensate for an expanding mass in the cranium?

A

Venous volume

CSF

38
Q

An uncompensated state of intracrainial pressure for expanding mass leads to what?

A

Elevated ICP- signs and symptoms

Drained off most of the CSF that we can, and cannot drain anymore

39
Q

Describe the pathophysiology of brain injury.

A

Compression by intracranial tumour/bleed

Reduction of blood supply to brain cells

Cytotoxic cellular oedema (no ATP to drive K/Na ATPase–> Na+ levels in cell increase—> fluid enters cells—> cells burst)

Further swelling and compression

40
Q

List some of the signs and symptoms of raised ICP

A

Headache (worse in the morning, bending down, coughing

Nausea/ Vomiting

Visual disturbances- diplopia on horizontal gaze, papilloedema

Depressed conscious level

41
Q

What is the most common false-localising sign of raised ICP?

How does this occur?

A

CN 6 palsy

Stretching or compression of the nerve along its corse

42
Q

What is the most common type of cerebral herniation?

What are the symptoms of this type of herniation?

A

Subfalcine herniation

Headache, contralateral leg weakness(if ACA affected)

43
Q

As uncal herniation progresses what structure is at risk?

What signs will pressure on this area cause?

A

The midbrain

Ipsilateral dilated pupil

Contralateral leg weakness

(May be false localising)

44
Q

What is tonsillar herniation?

What can this cause?

A

When the cerebellar tonsils herniate through the foramen magnum

Cardiac and respiratory dysfunction

45
Q

What is cushing’s reflex?

A

A triad of symptoms associated with raised ICP

They are: bradycardia, hypertension, low respiratory rate

(Opposite signs to sepsis)

46
Q

Explain what causes the unusual triad of symptoms seen in Cushing’s reflex

A

Ischemia at medulla–> sympathetic activation–>hypertension + tachycardia

Baroreceptors react–> bradycardia

Ischemia at pons/medulla (respiratory centres)–> low respiratory rate

47
Q

Group causes of raised ICP into 4 broad categories.

A
  1. Increased cerebral blood volume
  2. Cerebral Oedema
  3. Increased CSF
  4. Expanding mass / other SOL
48
Q

For each of the broad categories of causes of raised ICP, give some management options for them.

A

Increased cerebral blood volume:

Anticoagulation, tenting of venous sinuses (RARE)

Cerebral oedema:

Treat the cause, mannitol, hypertonic saline

Increased CSF:

Shunts, tumour resection, diuretics whilst waiting for intervention (fruosemide, CA inhibitors)

SOL:

Surgical resection- crainiotomy, steroids

49
Q

Give two mechanisms of increased cerebral blood volume that may lead to raised ICP.

A

Venous outflow obstruction

Venous sinus thrombosis

50
Q

List some causes of cerebral oedema that might lead to raised ICP

A

Meningitis

Encephalitis

Diffuse head injury

Infarction

51
Q

List the mechanisms of increased CSF which may lead to increased ICP

A
52
Q

List some space occupying lesions that may cause raised ICP

A

Tumour

Haemorrhage/ haematoma

Abscess

53
Q

What is the most common cause of raised ICP?

A
54
Q

List some of the risk factors for raised ICP

A

Use of anticoagulants

Severe infection

Immunosuppressed patients

TB infection

CV risks

Cancer

55
Q

What is the normal apperance & protein, Ig and leukocyte content of CSF?

A

Clear, colourless

Contains very little protein (15-45mg/dL)

Little Ig

1-5 leukocytes per ml

56
Q

What is hydrocephalus?

A

An imbalance between production and absorption of CSF leading to accumulation and enlargement of brain ventricles

57
Q

How is hyrdocephalus classified?

A

Non-communicating/ Obstructive- CSF is obstructed within or between the ventricles and the subarachnoid space

Communicating- IS communication between the ventricles and the subarachnoid space

The problem lies within the ventricular system (reduced abdorption/drainage or overproduction of CSF)

58
Q

Give examples of some causes of non-communicating hydrocephalus

A

Aqueduct stenosis

Tumour e.g. meningioma

59
Q

Give some examples of causes of communicating hydrocephalus

A

Post-meningitis

Subarachnoid haemorrhage

Trauma

Neoplastic infiltration of subarachois space

Choroid plexus papilloma (excess CSF production)

60
Q

At what ages are there peak incidences of brain tumours?

What kind of tumours are usually seen at these ages?

A

Children

  • Astrocytomas
  • Medulloblastomas

Middle-age

  • Gliomas
  • Meningiomas

(Mets from lung, breast, kidney)

61
Q

What is idiopathic intracrainial hypertension?

What are the treatment options?

A

Nervous System & Neuropsychiatry (17 decks)

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