Assessment of coma

JP Byass, 4th year, HYMS

Introduction

• Consciousness is a state of awareness of self and the environment. This state is determined by 2 separate & independent functions:

Awareness (content of consciousness)

Arousal (level of consciousness)

• Coma – caused by disordered arousal

• Due to: Failed ascending reticular activating system and connections to diencephalic structures.

Diffuse, bilateral hemisphere damage

• “A state of profound unconsciousness caused by disease, injury, or poison. The patient is unresponsive and cannot be roused.”

Introduction• Important to remember that arousal is not all or nothing

• i.e. a reduced conscious level need not be a comatose state

• It could be an intermediate state: Stupor - similar to coma in that responsiveness is greatly diminished. However,

the person can still be partially roused by some stimuli, such as by pain.

Obtundation - reduced awareness to surroundings. Again the patient can respond to some stimuli, eg pain.

Drowsiness - this is similar to obtundation and probably represents a lesser loss of consciousness.

• Rapid initial assessment could be asking patient to ‘put tongue out’, ‘wiggle your toes’ or ‘squeeze my fingers’

• More accurate and a quantitative measure is Glasgow Coma Scale (GCS)

Glasgow Coma Scale

EYES

BEST MOTOR RESPONSE

Interpreting GCS

• The GCS is of no diagnostic value, but is a reliable way of elucidating the clinical course without understanding a cause.

• 3 = lowest score i.e. deep coma or death

• <8 = severe reduction in consciousness and patient unlikely to maintain airway spontaneously i.e. intubate and ventilate

• 15 = highest score i.e. fully conscious

Reticular activating system• First discovered by Moruzzi

and Magoun (1949) in studies looking at sleep-wake cycles in cats

• Reticular formation found in brainstem core (known as tegmentum)

• Structures regulating consciousness run into higher cerebral areas via the thalamus.

Processes affecting RAS

• Diffuse encephalopathy – generalised disturbance of brain function affecting whole brain, including RAS

• Supratentorial lesions – massive lesions, or those associated with distortion of brainstem e.g. ‘coning’

• Infratentorial lesions – direct damage to brainstem

CAUSES

ISCHEMIA Cerebral hypoperfusion, eg impaired cardiac output, Cerebrovascular accident, Intracerebral bleed, Hypertensive encephalopathy

TOXIC Ethanol, Drug overdose (opiates, benzodiazepines, neuroleptics), Sedatives, Recreational drugs (gamma-hydroxybutyrate, ecstasy, cocaine), Poisons (carbon monoxide, solvent)

METABOLIC Hypoglycaemia or hyperglycaemia, Hyponatraemia or hypernatraemia, Hypercalcaemia, Hypopituitarism, Hypercapnia, Hypoxia/anoxia, Hypothyroidism, Acid base disturbances, Liver failure, Renal failure

NEUROLOGICAL Epilepsy and status epilepticus, Raised intracranial pressure (cerebral oedema), Obstructive hydrocephalus

TRAUMA Subdural haematoma, Depressed cranial fracture, Intracerebral haemorrhage, Subarachnoid haemorrhage

INFECTIVE Meningitis, Encephalitis, Septicaemia, Abscess, Malaria, Toxoplasmosis

AUTOIMMUNE Vasculitis

STRUCTURALLESIONS

Space occupying lesion with raised ICP

Assessment of coma

• Resuscitate and stabilise patient first• Emergency management should include ABCD• At D (disability), exclude alcohol, drugs, hypoglycemia and

assume trauma to CNS unless proven otherwise• NG tube, urinary catheter, maintain BP• Metabolic control esp. glucose and thiamine• Control seizures and body temperature• Specific treatments e.g. naloxone for opiate overdose, thiamine

for alcohol, flumazenil for benzo overdose, steroids for Addisonian crisis.

• Abx and LP if suspected infection/risk of aspiration• Mannitol if raised ICP • Once stable, try to obtain collateral history from family, friends,

ambulance crew

History

• Has patient sustained a head injury?

• Did patient collapse suddenly?

• Did limb twitching occur?

• Have symptoms occurred in preceding weeks?

• Has patient suffered a previous illness i.e. is this pre-existing e.g. cardiac arrhythmia, systemic sepsis?

• PMH – history of seizures or neurological signs?

• Medication?

• Recent travel?

• Immunosuppressed?

General examination• Signs of head injury e.g. Battle’s sign or

panda eyes

• Neck stiffness

• Skin - needle marks on arms, hyperpigmentation, cherry-red discoloration (carbon monoxide poisoning), anaemia, jaundice, purpura (sepsis), myxoedema

• Evidence of tongue biting

• Smell breath – ketones, alcohol, solvents

• Baseline obs – BP, PR, RR, temperature, blood glucose, oxygen sats

• Then do respiratory, abdominal (for abdominal bleed), cardiovascular and neuroexaminations

Neuro examination in coma

• Keep doing GCS to assess consciousness and prognosis i.e. eyes, motor response, verbal response

• Careful examination can localise lesion

• Remember in coma, it’s likely to be in brainstem (RAS) or cerebral hemispheres

• Pupillary response, spontaneous eye movements, gag reflex, oculocephalic (doll’s eye) response, oculovestibuar response (caloric testing) and corneal reflex all test brainstem function

• Also fundoscopy for papilloedema

Occulocephalic (doll’s eye) response

• Rotation/flexion of head in a comatose patient produces transient eye movements in the opposite direction

• i.e. eyes roll like a doll • Note whether eyes

move conjugate(parallel) or dysconjugate (not parallel)

Oculovestibular response (caloric testing)

• Water at 30 degrees irrigated into external auditory meatus

• Nystagmus usually develops after 20s and lasts for a few minutes

• Test is repeated after 5 mins at 45 degrees

• Cold water produces eye drift towards irrigated ear and nystagmus to opposite ear