Coma

COMAOmaido Blair Andrew

CONTENT Definition Epedimiology Aetiology Approach to a comatose patient Brain death

DEFINITIONComa 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)

PRINCIPAL CAUSES1. 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.

Outline of causes of coma BodyA. 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

FocalSupratentorial 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

ASSESSMENT 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

GCS

ASSESSMENTVital Signs- BPo HT may indicate intracerebral haemorrhage or strokeo May also give clue to the cause of the coma (SAH?)- Tempo Hypothermia – ETOH, sedatives, hypoglycaemiao Hyperthermia – heat stroke, infection, hypothalamic lesions- Respirationo 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

ASSESSMENTPupilsNormal- 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

PupilsFixed 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

ASSESSMENTOptic Fundi- Papilloedema/retinal haemorrhages – HT or raised ICP- Subhyaloid (superficial retinal) haemorrhages – SAH

Ocular Movements- Ocular Axes

o Usually slightly divergent in comao 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 rotationo Lost in very deep coma and brainstem lesions

- Calorics Testingso Ice water is irrigated into the tympanic membraneo Slow tonic ocular deviation towards irrigated ear (intact brainstem)o Commonly used to Dx brainstem death

APPROACH TO A PT IN COMA 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

APPROACH… Physical Examination-Evidence of trauma-Fever:meningitis,malignant

hyperthermia,heat stroke,cerebral malaria

-Hypothermia:alcohol,sedatives,hypoglycaemia,

-tachypnoea:systemic acidosis,pneumonia

PE…-HTN:hypertensive

encephalopathy,cushing response-Hypotension: alcohol intoxication,internal

haemorrhage,sepsis-Fundoscopy:icp,hypertensive

encephalopathy- Pattern of breathing:Cheyne-

Stokes,Kussmaul,Central Pontine Respiration

CNS EXAM 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

CNS… 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

INVESTIGATIONS 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

DIFFERENTIALS Locked-in syndrome Psychogenic unresponsiveness Akinetic mutism

MANAGEMENT prevention of further NS damageSo 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

BRAIN DEATH This is a state of cessation of cerebral

function with preservation of cardiac activity and maintenance of somatic function by artificial means