This document discusses coma, including its definition, causes, and approach to assessment and management. Coma is the deepest state of impaired consciousness where a patient cannot be aroused. Causes include structural brain injuries, infections, metabolic derangements, and drugs. Evaluation of a comatose patient involves assessing vital signs, neurological exam including pupil response and eye movements, investigations like blood tests and imaging, and treatment of reversible causes. Brain death is the complete and irreversible loss of brain function while cardiac and respiratory functions may be maintained artificially.

1. Omaido Blair Andrew

2.  Definition
 Epedimiology
 Aetiology
 Approach to a comatose patient
 Brain death

3. Coma is a deep sleeplike state from which the
patient cannot be aroused.
Its is the most severe form on the continuum
of reduced levels of alertness.
-Vegetative state(awake bt unresponsive from
coma)
-Stupor(transiently awakened by vigorous
stimuli)
-Drowsiness(light sleep)

4. 1. Lesions that damage the RAS in the upper
midbrain or its projections.
2. Destruction of large portions of both
cerebral hemispheres.
3. Suppression of reticulocerebral function by
drugs, toxins, or metabolic derangements
such as hypoglycemia, anoxia, uremia, and
hepatic failure.

5. Outline of causes of coma Body
A. Functional Lack of substrate Hypoglycaemia
 Hypoxia
 Hypotension
 Stroke
 Depression of function Hypothermia
 Drugs (including alcohol)
 Abnormal function Epilepsy
 Metabolic
 Diabetes mellitus
 Renal failure
 Hepatic failure
 Hypothyroidism
B. Structural Diffuse Meningitis
 Encephalitis
 Other infections (e.g. cerebral malaria)
 Subarachnoid haemorrhage
 Head injury
 Hypertensive encephalopathy
 Focal
Supratentorial lesions Cerebral haemorrhage
 Cerebral infarction with oedema
 Subdural haematoma
 Extradural haematoma
 Tumour
 Cerebral abscess
 Pituitary apoplexy
 Subtentorial lesions Cerebellar haemorrhage
 Pontine haemorrhage
 Brainstem infarction
 Tumour
 Cerebellar abscess
 Secondary effects of transtentorial herniation of brain due to cerebral mass lesions

6.  ABC,high flow Oxygen,IV cannula,RBS,pulse
oximeter,No fits,GCS
 Signs of Trauma
 Swelling of soft tissues
 Racoon eyes – periorbital eccymoses(bassilar skull
fracture)
 Blood behind the tympanic membrane
(haemotypanum)
 Battle’s sign – discoloured swelling over the mastoid
bone behind the ear(fracture base of the skull)
 CSF Rhinorrhoea/Otorrho

8. Vital Signs
- BP
o HT may indicate intracerebral haemorrhage or stroke
o May also give clue to the cause of the coma (SAH?)
- Temp
o Hypothermia – ETOH, sedatives, hypoglycaemia
o Hyperthermia – heat stroke, infection, hypothalamic lesions
- Respiration
o Cheyne- Stokes (periodic respiration with hyperpnoea & apnoea due
to delay in medullary chemoreceptor response – LVF, brain damage,
altitude)
o Kussmaul (acidotic) – deep sighing hyperventilation due to
stimulation of inspiratory centres – DKA, uraemia, metabolic acidosis
o Ataxic – shallow, halting irregular respiration in response to
medullary respiratory centre damage

9. Pupils
Normal
- 3-4mm in diameter, equal bilaterally
- Constrict briskly+ symmetrically to light
- Metabolic acidosis & CNS depressant drugs (not opiates)
Pin-point
- 1-1.5mm in diameter
- Opioid overdose
- Pontine lesions, organophosphate poisoning

10. Pupils
Fixed Dilated
- 7mm or more and fixed (not reactive to light
- Results from compression of CN III
- Common in herniation of the medial temporal lobe
- Fixed Mid-size
- 5mm in diameter & fixed
- Commonly from brainstem lesion at midbrain level
Anisocoria (Assymetrical)
- Less than 1mm difference in normal people (20% cases)
- Pupil that has reduced constriction – lesion affecting midbrain or
CNIII

11. Optic Fundi
- Papilloedema/retinal haemorrhages – HT or raised ICP
- Subhyaloid (superficial retinal) haemorrhages – SAH
Ocular Movements
- Ocular Axes
o Usually slightly divergent in coma
o Slow, roving, side to side eye movements in light coma
- Doll’s Eye Reflex (Vestibulo-ocular reflex)
o Passive head turning produces ocular deviation away from the direction of
head rotation
o Lost in very deep coma and brainstem lesions
- Calorics Testings
o Ice water is irrigated into the tympanic membrane
o Slow tonic ocular deviation towards irrigated ear (intact brainstem)
o Commonly used to Dx brainstem death

12.  History
-Circumstances +Rapidity of devt of symptoms
-antencedent symptoms(confusion,weakness,
headache, fever, seizures, dizziness, double
vision, or vomiting
-Illicit drug use
-Chronic dz:liver,renal,lung,hiv,DM

13.  Physical Examination
-Evidence of trauma
-Fever:meningitis,malignant hyperthermia,heat
stroke,cerebral malaria
-Hypothermia:alcohol,sedatives,hypoglycaemia,
-tachypnoea:systemic acidosis,pneumonia

14. -HTN:hypertensive encephalopathy,cushing
response
-Hypotension: alcohol intoxication,internal
haemorrhage,sepsis
-Fundoscopy:icp,hypertensive encephalopathy
- Pattern of breathing:Cheyne-
Stokes,Kussmaul,Central Pontine Respiration

15.  Assess level of consciousness (Glasgow Coma
Scale)
 Signs of head injury
 local bruising, fractures and wounds
 bleeding from nose or ears
 Splint the neck: head injury may be
associated with fracture of the cervical spine
 If no evidence of injury (history and
examination) check for neck stiffness

16.  Check resting pupillary size, and pupillary
responses to light
 Ocular movements: spontaneous, following
and to 'doll's head' (if no voluntary response)
 Limbs: posture, tone and movement
 Reflexes and plantar responses
 Fundi

17.  RBS(always confirm hypoglycaemia by laboratory
measurement)
 Hb, Hct, WBC count, clotting
 Electrolytes and liver function tests
 Blood gases and pH
 CT head scan
 Chest X-ray
 X-ray of suspected fractures/bruised limbs
 Blood for cross-matching
 Drug screen ,Urinalysis
 LP

18.  Locked-in syndrome
 Psychogenic unresponsiveness
 Akinetic mutism

19.  prevention of further NS damage
So rapidly correct
hypoglycaemia,hypercapnia,hypotension,hyperthermia
,hypercalcaemia, and hypoxia
 Wernickes:IV Thiamine(400mg bd x 5days +glucose)
 Narcotic overdose:Naloxone
 Anti-cholinergic overdose: Physostigmine
 Hypoglycaemia:20-50g of 50% glucose

20.  This is a state of cessation of cerebral
function with preservation of cardiac activity
and maintenance of somatic function by
artificial means