Coma
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Transcript of 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