220 likes | 521 Views
Coma & Brain Death. Brain Death. Defined by documentation of irreversible coma and irreversible loss of brainstem reflex responses and f(x) of respiratory centre OR by the demonstration of the cessation of intracranial flow. Brain Death.
E N D
Brain Death • Defined by documentation of irreversible coma and irreversible loss of brainstem reflex responses and f(x) of respiratory centre • OR by the demonstration of the cessation of intracranial flow
Brain Death • 2 Clinical examinations must be performed by 2 medical practitioners 6 hours apart; • Response to painful stimulation within cranial nerve distribution • Pupillary responses to light • Corneal reflexes • Gag reflex • Cough reflex • Vestibulo-ocular reflexes • Respiratory function • Apnoea test – Preoxygenation with 100% O2 followed by cessation of ventilation • While mechanical ventilation is stopped O2 is supplied through tracheal catheter • AT the end of the period w/o O2 apnoea must persist in the presence of adequate stimulus to spontaneous ventilation PCO2 > 60mmHg and arterial pH < 7.30
Brain Death • If this assessment is not possible then radiocontract angiography can be used to look at intracranial blood flow • Flow should be absent in the supratentorial & vertebro-basilar circulation to show brain death • NB: All reversible causes should be ruled out
Coma • A state of unconsciousness where patient cannot be wakened or aroused by external stimuli • Occurs from damage to brain regions that control consciousness; • Brainstem reticular activating system above midpons & Both cerebral hemispheres • Defined a; • Not opening eyes • Not obeying commands • Not understanding words
Persistent Vegetative State • Coma has progressed to wakefulness without detectable awareness • Usually just need feeds, no ventilation • May open eyes and have sleep cycles
Causes of Coma • Diffuse Brain Dysfunction (generalised metabolic toxic injury/widespread inflammation) • Hyperglycaemia (DKA)/Hypoglycaemia • ETOH • Drug intoxication • Hypoxic/IBI • Electrolyte imbalances • Acidosis (resp or metabolic) • SAH • Encephalitis • Cerebral Malaria • Endocrine (hypothroidism/hypoadrenalism)
Causes of Coma • Direct Effect within Brain Stem • Trauma • Brainstem haemorrhage/infarction • Neoplasm • Pressure effect of the Brain Stem • Hemisphere tumour or abscess • Cerebellar mass lesion • Trauma (SDH/EDH) • Encephalitis
Assessment • Signs of Trauma • Swelling of soft tissues • Racoon eyes – periorbital eccymoses • Blood behind the tympanic membrane (haemotypanum) • Battle’s sign – discoloured swelling over the mastoid bone behind the ear • CSF Rhinorrhoea/Otorrho
Assessment Vital Signs • BP • HT may indicate intracerebral haemorrhage or stroke • May also give clue to the cause of the coma (SAH?) • Temp • Hypothermia – ETOH, sedatives, hypoglycaemia • Hyperthermia – heat stroke, infection, hypothalamic lesions • Respiration • Cheyne- Stokes (periodic respiration with hyperpnoea & apnoea due to delay in medullary chemoreceptor response – LVF, brain damage, altitude) • Kussmaul (acidotic) – deep sighing hyperventilation due to stimulation of inspiratory centres – DKA, uraemia, metabolic acidosis • Ataxic – shallow, halting irregular respiration in response to medullary respiratory centre damage
Assessment 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
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
Assessment Optic Fundi • Papilloedema/retinal haemorrhages – HT or raised ICP • Subhyaloid (superficial retinal) haemorrhages – SAH Ocular Movements • Ocular Axes • Usually slightly divergent in coma • Slow, roving, side to side eye movements in light coma • Doll’s Eye Reflex (Vestibulo-ocular reflex) • Passive head turning produces ocular deviation away from the direction of head rotation • Lost in very deep coma and brainstem lesions • Calorics Testings • Ice water is irrigated into the tympanic membrane • Slow tonic ocular deviation towards irrigated ear (intact brainstem) • Commonly used to Dx brainstem death
CGS • 8 is the critical score • 90% less than 8 – coma • After 6 hours at 8 50% death rate
Investigations • FBE • Biochemistry – U&E’s, Glucose, Ca, LFt’s • Drugs screen – salicylates, benzodiazepines, narcotics, amphetamines • TFT’s • Blood cultures • CT or MRI – mass leson or intracranial haemorrhage • CSF • EEG – metabolic coma, encephalitis, brain death
Management (ED) • DRABC • IV catheter and Bloods • IV infusion (routine) • Thiamine 100mg + dextrose 25g • Thiamine always precedes dextrose as dextrose along can worsen Wernicke’s encephalophaty • Naloxone 0.4-1.2mg (routine)
Management (LT) • Fluids & Feeding (NGT or paraenteral) • Skin Care (Pressure sores) • Oral Hygiene (mouth washes + suction) • Eye care – tape eye lids • Physiotherapy – muscles + joints • TED stockingss/heparin – DVT risk • Sphincter Control – Catherisation, rectal evacuation • Family Wishes References: Acknowledgment J Koh & D Cheng