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Neurology and psychiatry > Neurotrauma & raised ICP > Flashcards

Neurotrauma & raised ICP Flashcards

1
Q

Describe the classification of primary head injuries

A

Grouped into focal and diffuse. There are two types of diffuse- concussion and diffuse axonal injury. There are two subtypes of focal- haematoma (epidural, subdural or intracerebral) and contusion (site of impact (coup) and opposite site (contracoup))

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2
Q

What is a cerebral contusion?

A

Bruising of the brain where by the blood mixes with the cortical tissue due to micro-haemorrhages and small blood vessel leaks.

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3
Q

Describe the pathophys of a cerebral contusion?

A

Trauma-> microhaemorhages-> cerebral contusion-> cerebral odema/ intracranial bleed-> raised ICP-> coma

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4
Q

Which lobes tend to be most affected by cerebral contusions? What does this lead to?

A

Parietal lobes, leading to attention, memory and emotion problems

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5
Q

What is a concussion?

A

Head injury with temporary loss of brain function

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6
Q

Describe the pathophys of a concussion

A

Trauma-> stretching and injury to axons-> impaired neurotransmission + loss of axonal iron regulation and reduced cerebral blood flow-> temporary brain dysfunction until they recover

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7
Q

What is post concussion syndrome?

A

Difficulty thinking/ remembering/ concentrating, headaches, N+V, dizziness, tiredness, irritability, sadness, sleeping more or less than normal for days to weeks to months after a concusssion. Not sure why it occurs, think it due to structural brain damage needing to repair.

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8
Q

What is diffuse axonal injury?

A

Shearing of interface between grey and whit matter following traumatic acceleration/ de-acceleration or rotational injury. This tends to lead to axonal death-> cerebral odema-> coma and death.

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9
Q

How does diffuse axonal injury appear on CT?

A

Hyperdense (white) spots on CT

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10
Q

Give 5 basilar skull fracture signs

A

Racoon eyes, CSF rhinorrhea, CSF otorrhea, battle sign, haemotympanum, bump

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11
Q

How are basilar skull fractures managed?

A

ICP control, seek and treat complications, elevation of depressed skull fractures, if persistent CSF leak they need surgery to reattach meninges

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12
Q

What 3 measures are used to asses severity of brain injuries?

A

GCS, post traumatic anmesia duration, loss of consciousness duration

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13
Q

When should an urgent head CT be ordered? (4)

A

GCS <13 at any point or <15 more than 2 hrs after injury.
Neurological abnormality (focal neurological deficit, seizure, loss of consciousness.
Suspected basilar skull fracture.
2+ discrete episodes of vomiting.

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14
Q

Describe the presentation of someone with an epidural haemorrhage?

A

Loss of consciousness due to brain injury, followed by lucid interval and then rapid decline in consciousness due to bleed expanding.

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15
Q

Describe the CT appearance of a chronic vs an acute subdural haemorrhage?

A

Acute: hyperdense (white) banana
Chronic: hypodense (black) banana
Neither will cross midline due to falx cerebri

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16
Q

How are epidural haemorrhages managed?

A

Urgent craniotomy to relieve increased ICP, or observation of only small.

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17
Q

How are acute and chronic subdural haemorrhages managed?

A

Acute: surgery (burr holes) to relieve increased ICP
Chronic: neurological surgery to remove haematoma, not often done as pts are old and wouldn’t survive surgery.

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18
Q

How are subarachnoid haemorrhages managed?

A

ITU, prevent rebleeding, manage short and long term complications, high mortality.

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19
Q

What is normal ICP?

A

5-15mmhg

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20
Q

How is ICP controled in body?

A

Vasodilation and constriction in response to BP changes.CSF production and removal can also change.

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21
Q

How do brain injuries caused raised ICP?

A

Drop in blood flow or cell damage leads to stopping of ATP production and reversal of Na/K/ATPase. Na+ increases in cell leading to swelling as water moves in. Swelling of cells increases ICP. Some cells burst and release components. Increase in ICP further reduces blood supply to brain cells as vessels are constricted.

22
Q

Give and explain 4 signs and symptoms of raised ICP?

A
  • headache: firing of pain receptors in blood vessels and meninges as they get compressed. Its worse in mornings as lying down all night, and hypoventilation= vasodilation. Also worse on bending down, coughing, sneezing.
  • vomiting: ischaemia of vomiting center (postrema) and compression of medulla stimulates postrema
  • Visual disturbances: burring due to papillodema, diplopia on horizontal gaze due to CNVI compression also retinal haemorrhages.
  • Reduced consciousness: compression of brain stem-> compression of reticular formation
23
Q

Describe how the optic disc changes due to papillodema?

A

The boundaries/ outline of the optic disc becomes more blurred

24
Q

What is a subfalcine herniation, how can it be seen on CT and what could be complication of it?

A

Hernation of cingulate gryus under free edge of falx cerebri. Seen as midline shift on CT.
Can compress anterior cerebral artery leading to headache and ischaemia of medial motor homonculus (leads to contralateral leg weakness), sensory homunculus and corpus callosum.

25
Q

What is a uncinate herniation? Describe its complications?

A

Uncus is displaced across the tentorial opening. It 1st compresses CNIII -> ipsilateral dilated pupil. As it progresses it puts pressure on midbrain, reducing consciousness. It can compress the cerebral peduncle leading to contralateral leg weakness. A later CNIII palsy will led to a down and out pupil.

26
Q

What is a tonsillar herniation and describe the complications

A

Cerebellar tonsils herniate through foramen magnum. Leads to compression of medulla and upper spinal cord. Medulla compression-> decreased cardiac and resp function and decreased consciousness.

27
Q

Give an explanation for the cushings reflex?

A

Hypertension, bradycardia and low resp rate due to ischaemia at medulla causing sympathetic activation causing rise in BP and tachycardia. However baroreceptors detect rise in BP causing bradycardia. Ischaemia at pons and medulla resp centers-> low resp rate. This is late sign of raised ICP so untreated will lead to death.

28
Q

Give 3 causes of raised ICP other than space occupying lesions (abcesses, tumours, haemorrhages)

A
  • increased cerebral blood volume (venous outflow obstruction, venous sinus thrombus)
  • cerebral odema (meningitis, encephalitis, diffuse head injury, infarction)
  • increased CSF (impaired absorbtion (hydrocephalus, benign intracranial hypertension), excessive secretion (choroid plexus papilloma)
29
Q

Where is CSF reabsorbed?

A

By arachnoid villi into dural venous sinuses, where it enters venous system.

30
Q

What is hydrocephalus?

A

Accumulation of CSF due to imbalance between production and absorption of CSF with subsequent enlargement of the ventricles.

31
Q

What are the two types of hydrocephalus?

A
  • noncommunicating/ obstructive- CSF not getting from ventricles to subarachnoid space: usually aqueduct stenosis
  • Communicating: problem lies outside ventricular system. may be due to choroid papilloma increasing production, reduced absorption or blockage of venous drainage. Mostly post meningitis, subarachnoid haemorrhage or trauma.
32
Q

What is idiopathic intracranial hypertension and how is it managed?

A

Raised ICP without hydrocephalus or mass lesion. Investigations are normal and other causes ruled out. Usually seen in obese women after weight gain.
Treatment options: lose weight, carbonic anhydrase inhibitors/ mannitol, csf drainage and shunts.

33
Q

How is raised ICP managed?

A
  • ABC and oxygen
  • measure glucose
  • mannitol bolus or 3% saline over 5 mins
  • treat shock if present
  • call anaesthetist for incubation and ventilation
  • NG tube and urinary catheter
  • CT when stabilised
  • Call neurology
34
Q

Why is a lumbar puncture not done if raised ICP is suspected?

A

It will raise ICP further as needle is inserted, possibly causing herniation etc

35
Q

Which part of the spinal cord can be injured in hyperflexion injuries (eg in car crash, rugby, falls onto head)

A

Anterior cord and/ or central cord syndromes (usually younger pts) can be present

36
Q

Give 3 non spinal cord injuries associated with hyperflexion injuries?

A
  • anterior wedge
  • flexion teardrop
  • anterior sublaxations
  • bilateral interfacet dislocations
  • atlanto- occipital dislocations
37
Q

Which spinal cord syndromes associated with extension injuries of the elderly?

A

Central cord syndrome

38
Q

Which fractures are associated with hyperextension injuries?

A

hangmans and teardrop fractures also atlanto occpital dislocations

39
Q

What can cause complete cord transection syndrome?

A

trauma, infection, transverse myelitis, abscess, tumour

40
Q

Why is hypotension and priapism present in complete cord transections?

A

Loss of sympathetic input from spinal cord but maintenance of parasympathetics from vagus nerve

41
Q

Describe the urinary consequences of complete spinal cord transections above T12?

A

Get reflex bladder- sympathetics and parasympathetics intact but somatic sensation not. Sympathetics can still inhibit contraction when bladder empty but loss of descending inhibition means parasympathetics (and so voiding) is dominant

42
Q

Describe the urinary consequences of complete spinal cord transection at S2-S4?

A

Loss of parasympathetic input. So loss of ability to sense filling and cause contraction. Will fill until leaks out.

43
Q

Give 3 causes of anterior cord syndrome?

A

flexion injury, vasular/ atherosclortic disease of anterior spinal artery, iatrogenic secondary to cross clamping of aorta in operations.

44
Q

Describe the consequence of an anterior cord syndrome?

A
  • ipsilateral/ bilateral paralysis below lesion
  • contralateral/ bilateral loss of pain, crude touch and proprioception below lesion
  • dorsal column intact
45
Q

Give 3 causes of central cord syndrome?

A

Syringomyelia, hyperflexion in young, hyperextension in elderly, cervical spinal stenosis, degenerative spinal disease, syringomyelia, central canal ependymoma (rare tumour), blood flow distruption

46
Q

Describe the consequence of central cord syndrome?

A
  • Decussating fibres of spinothalamic hit first-> bilateral/ipsilateral loss of pain and temp sensation in that dermatome
  • Then medial part of spinothalamic tract hit-> loss of pain and temp sensation in upper limb dermatomes (assuming cervical lesion)
  • If wide enough, corticospinal tract affected - again affecting cervical myotomes 1st and spreading down body as lesion enlarges
  • Also get bladder dysfunction as ventral horns affected
47
Q

What may cause a posterior cord syndrome and which tract is affected?

A

Spondylosis, spinal stenosis, infections, B12 deficiency, occlusion of paired posterior spinal arteries.
Dorsal column affected

48
Q

How should spinal cord injuries be managed initially?

A
  • ABCDE
  • stabilise head manually until rigid C collar given
  • consider incubation for injuries above C5
  • sympathetic NS loss may lead to hypoxia (so give O2 +/- airway adjuncts), hypotension (give fluids and vasopressors), hypothermia (bair hugger), bladder dysfunction (catheterise)
49
Q

When is spinal cord injury assumed?

A
  • head injury
  • unconscious of confused
  • spinal tenderness
  • extremity weakness
  • loss of sensatinon
50
Q

How do you clear a spine as being ok?

A
  • alert and oriented
  • no lang barrier
  • no intoxication
  • no midline or posterior tenderness
  • no focal neuro deficit
  • no painful distracting injuries

Neurology and psychiatry (8 decks)

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