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MD4001 Week 2 > 8. Applied physiology/The Clinical Management of Head Injury > Flashcards

8. Applied physiology/The Clinical Management of Head Injury Flashcards

1
Q

Epidemiology of head injuries

A

100000/yr in scotland
More men
Peaks in early 20s and 80s
Of all hosp visits, 15% admitted (children make up 1/3 admissions)
Trauma is leading cause of death in <45yrs (50% of head injuries)
65% adult head injuries involve alcohol
Falls, assaults, RTA (different patterns, different
countries e.g. gun shots to head)

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2
Q

World Health Organisation:
• Incidence of traumatic brain injury is ______
• Predicts by 2020 ____ ____ _____ will be the third greatest cause of global burden of disease and injury,

A

World Health Organisation
• Incidence of traumatic brain injury is increasing
• Predicts by 2020 road traffic accidents will be the third greatest cause of global burden of disease and injury,

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3
Q

Focus of medical intervention is to minimise…..

A

Focus of medical intervention is to minimise secondary brain injury

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4
Q

Focus of medical intervention is to minimise secondary brain injury. Done by?

A 
Focus of medical intervention is to minimise secondary brain injury. Done by?
• Optimise oxygenation
• Optimise cerebral perfusion
• Blood glucose
• Hypo / hypercapnia
• Body temperature?
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5
Q

Secondary processes which occur at the cell & molecular level that exacerbate neurological damage

A
  • Neurotransmitter release (glutamate)
  • Free radical generation
  • Calcium mediated damage
  • Inflammatory response
  • Mitochondrial dysfunction
  • Early gene activation
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6
Q

How does the monro-kellie doctrine demonstrate brain compensation for an expanding mass?

A

Mass= Haematoma? Clot? Hydrocephalus? Tumour?

Body compensation by squeezing out CSF and blood
Limited compensation i.e. 150ml total loss

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7
Q

How does a primary brain injury progresses to a secondary brain injury?

A

In primary brain injury the cerebral blood volume increases by:
Activation of biomolecule mediators of injury —> Neuronal damage –> Cytotoxic oedema
OR
Cerebral vessel damage –> increased interstitial fluid and tissue pressure –> Vaspgenic oedema

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8
Q

Early Management of Head Injury

A
  • Assessment and identification of the patient at risk of secondary brain injury
  • Pre-emptive investigation (CT scan)
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9
Q

Who are we going to send to hospital?

A
  • Extremes of age (<5years or >65years)
  • Amnesia for events before or after injury
  • Any loss of consciousness
  • High energy injury
  • Vomiting
  • Seizure (previous neurosurgery)
  • Bleeding /clotting disorder
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10
Q

What is the breakdown of the GCS scoring total?

A

Eyes: /4 “4 eyes)
Verbal: /5 (V= 5)
Motor: 6

E4V5M6
Degree of Head injury:
-Minimal: 15 9  (no history of unconsciousness)
- Mild: 13-15
- Moderate: 9-12
- Severe: 8 or less

Out of 15. 15 is normal score

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11
Q

How is eye opening scored in the GSC?

A 
Out of 4
Score 4= Eyes open spontaneously
Score 3= Eyes open to speech
Score 2= Eyes open in response to pain
Score 1 =Eyes do not open
Record NT = If patient is unable to open eyes due to swelling, bandages etc.
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12
Q

How is the verbal response scored in the GCS?

A

Score 5= Orientated
Score 4= Confused
Score 3= Inappropriate words
Score 2= Incomprehensible sounds
Score 1= No response despite verbal & physical stimuli
Record NT= Dysphasic, Record T if intubated

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13
Q

How is motor response scored in the GCS?

A 
Score 6= Obeys commands
Score 5= Localises to central pain
Score 4= Normal flexion towards source of pain
Score 3= Abnormal flexion
Score 2= Extension to pain
Score 1= No response to painful stimuli
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14
Q

What is the risk of opening airway in hypoxic patients with head injury?

A

REMEMBER THE CERVICAL SPINE

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15
Q

What is the risk of opening airway in hypoxic patients with head injury?

A

REMEMBER THE CERVICAL SPINE

-Check with plain x-ray (sometimes CT cervical spine)

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16
Q

What is the risk of opening airway in hypoxic patients with head injury?

A

REMEMBER THE CERVICAL SPINE

-Check with plain x-ray (sometimes CT cervical spine)

17
Q

What is ICP?

A

IntraCranial pressure

18
Q

How to control the supply and demand for oxygen in head injury patient?

A

• Optimise oxygen supply

• Minimise demand
– Convulsions occur in 15% of severe head injuries • Treat with phenytoin in early head injury
– Brain metabolic rate increases 6-9% for every degree rise in temperature
• Treat pyrexia (Is mild hypothermia a good thing?

Think about sedation (propofol / midazolam)

19
Q

Impact of CO2 in vasodilation?

A

• Cerebral vessel diameter (and CBF) changes over a wide range of PaCO2
• Target directed therapy:
PaCO2 4.5 -5.0kPa

20
Q

When assessed pre admission patients are _______ in 25% of cases

A

When assessed pre admission patients are hypotensive in 25% of cases

21
Q

Cerebral perfusion pressure?

A

CPP = MAP - ICP

MAP= Diastolic pressure + 1/3 pulse pressure

22
Q

After a severe head injury, what are the bp and ICP targets?

A

Maintain CPP above 60 - 70mmHg
Maintain systolic blood pressure higher than
90mmHg (preferably higher than 120mmHg)

ICP less than 20mmHg (invasive pressure monitor)

23
Q

What are the parameters of cerebral autoregulation?

Change in a traematised/ischaemic brain?

A

Normally autoregulation maintains a constant blood flow between MAP 50 mmHg and 150 mmHg.

Traumatised or ischaemic brain, CBF may become blood pressure dependent

24
Q

What history cases suggest risk of intracranial mass?

Examination findings that also suggest…

A

History:
high impact injury
significant retrograde amnesia
History of coagulopathy post traumatic seizure

Examination:
GCS 12/15 or less
OR
GCS 13/15 or 14/15 and failing to improve within 2 hours of injury
OR
Clinical signs of skull fracture
25
Q

What history cases suggest risk of intracranial mass?

Examination findings that also suggest…

A

History:
high impact injury
significant retrograde amnesia
History of coagulopathy post traumatic seizure

Examination:
GCS 12/15 or less
OR
GCS 13/15 or 14/15 and failing to improve within 2 hours of injury
OR
Clinical signs of skull fracture E.G.
-Pre-orbital bruising
-Battle's sign
26
Q

2 different classes of haematoma?

A

EDH (extradural haematoma)

SDH (subdural haematoma)

27
Q

Features of EDH?

A 
• Relatively uncommon
• Strongly associated with
skull fracture
• Middle meningeal artery
• 1/3 due to venous bleeding
• Classically a lucid interval
• Good outcome if treated!
28
Q

Features of SDH?

A 
• Common
• Complicates 20-30% of
head injuries
• Rupture of the veins travelling from the brain surface to the saggital sinus
• Prognosis worse
29
Q

2 classes of haemorrhage?

A

Subarachnoid Haemorrhage

Intracerebral Haemorrhage

30
Q

Causes of SAH?

A
  • Assoc.with ruptured aneurysm

* More commonly caused by head injury

31
Q

Features of intracerebal haemorrhage?

A

Intracerebral Haemorrhage
• Stretching&shearing injury
• Impactoninsideofskull
• Oftencontrecoup injury

32
Q

Features of intracerebal haemorrhage?

A

Intracerebral Haemorrhage
• Stretching &shearing injury
• Impact on inside of skull
• Often contre coup injury

33
Q

What to consider before contact neurosurgeons?

A
  • Mechanism of injury
  • Age of patient
  • Respiratory and cardiovascular status • GCS score & pupil response (due to compression of oculomotor nerve. Leads to ipsilateral dilation)
  • Alcohol/drugs
  • Associated injuries
  • Results of CT scan
34
Q

Clinical signs of herniation?

A
  • Dilatedorunreactive pupil(s)
  • Extensorposturing
  • DecreaseinGCSof2or more points
35
Q

Temporary hyperventilation can decrease ____ and “buy time”

A

Temporary hyperventilation can decrease ICP and “buy time”

36
Q

What drugs can be used to treat an increased ICP?

A
  1. 20% Mannitol (0.25-1g/kg)
    – Decreases blood viscosity
    – Osmotic diuretic
  2. Hypertonic saline
37
Q

Influence of glucose levels on outcome of patients of head injury?

A

Tight control of blood glucose has been shown to improve outcome
BUT
dangers of unrecognised hypoglycaemia…

Remember enteral nutritional support

38
Q

Why are high glucose levels avoided in head injury patients?

A

Elevated serum glucose levels have been considered deleterious based on the assumption that presentation of the ischemic brain with high levels of glucose would drive anaerobic glycolysis, resulting in the accumulation of toxic levels of lactic acid.

MD4001 Week 2 (12 decks)

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