Disease and Clinical Features of Coma Flashcards

1
Q

What is the definition of a coma?

A

State of unrousable unconsciousness

GCS of 8 or less

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2
Q

What is included in the GCS?

A

Eye opening /4

Motor response /6

Verbal response /5

Total: 15

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3
Q

What is the definition of arousal?

A

Level of consciousness/alertness

Function of the reticular activating system in pons and midbrain and its interaction with the thalamus

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4
Q

What is the definition of awareness?

A

Content of consciousness

Awareness of self environmnet

Function of multiple cortical areas

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5
Q

What is a unilateral cause for cortical damage leading to coma?

A

Large expanding mass lesions → raised ICP

e.g. haemorrhage, large MCA infarct

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6
Q

How can a single hemisphere or cerebellar lesion produce a coma?

A

Compression of the brainstem

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7
Q

What are the causes of coma?

A

Massive cortical damage

Brainstem lesion

Brainstem compression

Diffuse physiological brain dysfunction

Metabolic disorders, drugs and toxins, mass leasions, trauma, stroke and CNS disorders

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8
Q

How may brainstem compression lead to a coma?

A

Supratentorial mass lesion within the brain → inhibition of ARAS

Coning from brain tumour or haemorrage

Mass lesions within the posterior fossa are particularly prone to cause brainstem compression and hydrocephalus

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9
Q

How does diffuse physiological brain dysfunction arise to cause comas?

A

Generalised severe metabolic/toxic disorders depress cortical and ARAS function

Hypothermia/sudden hypertension, prolonged status epilepticus

Drugs, toxins, poisoning: Alcohol, sedatives, opiates, anaesthetics, uraemia, hypercapnia

Psychiatric

Metabolic - deranged Na/glucose, raised Ca, renal/hepatic failure

Endocrine: hypothyroidism, Addison’s, pan-hypopituitarism

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10
Q

What are two important coma mimics?

A

Locked in syndrome - de-efferented motor tracts

  • complete paralysis except blinking and vertical eye movements intact in ventral pontine infarction (basilary artery)
  • awareness and arousal retained (functioning cerebral cortex)

Psychogenic coma

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11
Q

What is the immediate management of coma?

A

ABC - intubate? oxygenation? correct hypotension/hypertension?

Blood glucose - if hypo, give glucose

Treat seizures with buccal medazolam

IV Abx for fever and meningism

IV naloxone if opiate OD, Flumazenil if benzo OD

Thiamine if Wernicke’s encephalopathy

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12
Q

How do the following give clues to the cause of coma?

Temperature

Odour of breath

Skin

RR

Pulse

BP

A

Temperature ↓: Cold, hypothyroid, alcohol, drugs, Addison’s; ↑: Infection/drugs

Odour of breath: Alcohol, Ketosis, Uraemia

Skin: Rash, Signs of liver disease, needle tracts, bruising (head injury)

RR - ↓: optiates; ↑: uraemia, pneumonia

Pulse - ↓: Hypothyroid, drugs, cold, Raised ICP; ↑:Infection, drugs

BP - ↓: Trauma, Shock, Cardiac failure, Drugs; ↑:Stroke, SAH, Raised ICP, Stimulants, Hypertensive encephalopathy

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13
Q

What should a neurological examination include for a patient in a coma?

A

Meningism - (neck stiffness, photophobia, headache) - SAH, meningitis

Fundi - look for papilloedema and retinal haemorrhages - raised ICP and SAH

Brainstem function - Pupils, Eye movements, Brainstem reflexes

Lateralising signs - Asymmetry of response to visual threat, face, tone, decerebrate and decorticate posturing, response to pain, tendon and plantar reflexes

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14
Q

What can the pupils show in a patient in a coma?

A

Dilation of one pupil that’s fixed → compression of CNIII (neurosurgical emergency)

Bilateral mid-point reactive pupils (normal) - metabolic/sedative drug coma

Bilateral light-fixed, dilated pupils → sign of brain death, deep coma

Bilateral light-fixed, pinpoint pupils → pontine lesions (pointine)/opiates

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15
Q

What can eye movements show in a patient in a coma?

A

Dysconjugate eyes - divergent ocular axes - brainstem lesion

Conjugate gaze deviation

  • Towards lesion in frontal lobe (intact side pushing eyes away)
  • Away from lesion in brainstem - PPRF in pons controls lateral gaze ipsilaterally

VOR - passive head turning produced conjugate ocular deviation away from direction of rotation - reflex disappears in coma, brainstem lesions, brain death

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16
Q

What are the other brainstem reflexes?

A

Corneal Reflex

Gag/cough reflex

Respiratory drive

17
Q

What will the following scans show in the case of a coma?

CT

MRI

MRA/CTA

A

CT - blood/large hemisphere lesions

MRI - midbrain/brainstem lesions, white matter disease, encephalitis

MRA/CTA - basilar artery thrombosis

18
Q

What is persistent vegetative state?

A

Recovery of arousal, not awareness

  • no awarenss of self or surroundings
  • no language/comprehension
  • roving eye movements
  • brainstem reflexes intact
  • maintains respiration and circulation
19
Q

When is a persistent vegetative state deemed to be permanent?

A

> 6 months in non-traumatic coma

> 12 months in traumatic coma

20
Q

What is minimally conscious state?

A
  • Make eye contact/turn head when spoken to
  • grasp object when asked
  • mouth words
  • track objects with eyes
  • have some intelligent verbilisation
21
Q

What is brain death?

A

Patients maintained by artificial ventilation and persistent heart beat, but brain recovery is impossible

Patient cannot be hypothermic, metabolically deranged, suffer from endocrine disturbance, under the influence of sedative/NM blocking agents