Coma & Brain Stem Death

8/7/2019 Coma & Brain Stem Death

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Coma & Brain stem death

Rifdy Mohideen


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What is coma?

Coma is a state ofunarousable unresponsiveness

No evidence of arousal

no spontaneous eye opening no comprehensible speech

no voluntary limb movement

No response to external stimuli & surrounding environment

There may be abnormal postures adopted

eyes may open, or grunts may be elicited in response to pain

involuntary movements, e.g. seizures or myoclonic jerks, mayoccur.


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Coma differs from

Sleep (arousable)

Syncope (brief)

Stupor (aroused with repeated stimuli)

C

oma should be differentiated from Locked-in syndrome: actually conscious but unable to speak or move,

may move eyes (massive brainstem damage)

Vegetative state: patients appear to be awake but show no sign of

awareness of themselves or their environment (brainstem intact butwidespread cortical damage); may breath spontaneously


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What is consciousness?

Consciousness is a state of awareness ofselfand the

environment

This state is determined by two separate functions:

awareness (contentof consciousness)

arousal (levelof consciousness )


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Coma is caused by disordered arousal rather than

impairment of the content of consciousness

Arousal is dependent on an intact reticular

activating system located in the brainstem and its

ascending connections


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Is there a way of objectively measuring

consciousness?

GCS is a useful way ofassessing and monitoring level

of consciousness

This analyses three markers of consciousness

eye opening

motor

verbal responses


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Eye Opening Score

Spontaneous 4

To voice 3

To painful stimuli 2

None 1

Motor

Obeys commands 6

Localises pain 5

Withdraws to painful stimuli 4

Flexion to painful stimuli 3

Extension to painful stimuli 2

Makes no movement 1

Verbal

Oriented 5

Confused 4

Inappropriate words 3

Unintelligible sounds 2

Makes no sound 1

Brain injury classification

3 coma or death

== 13 minor

Individual responses and total

scores important

Reported as E3 M3 V4

Tracheal intubation and severe

eye/facial injury may invalidate

verbal response

Glasgow Coma Scale


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Mechanisms of coma

diffuse or extensive processes affecting the

whole brain (toxins, metabolic, ischaemic,

infections)

supratentorial mass lesions causing tentorial

herniation with brain stem compression

infratentorial mass lesions and vascular

lesions


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Management of coma

detect and treat any immediately life-threatening

condition

determine the site and cause of the lesion

history (eyewitness, family, friends)

examination (general and neurological; motor

responses to stimuli, respiratory patterns, pupils, and

eye movements)

investigations (focused)


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Brain death

vital functions can now be maintained artificially for

a long period of time after the brain has ceased to

function but is futile

need to diagnose brain death with utmost accuracy

and urgency

brain dead is legally and clinically dead

ethical reasons retrieval of organs


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Brain death - definition

an irreversible loss of all functions of the brain,

including the brainstem

three essential findings

coma

absence of brainstem reflexes

apnoea (no spontaneous respiration)


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Brain death - pathology

swelling of brain and brainstem

tentorial and foraminal herniation

absence of blood flow

10% of brain and 60% of spinal cord may appear

normal


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Diagnosis of brain death

The diagnosis of brain death is primarily clinical

No other tests are required if the full clinical

examination, including each of two assessments of

brain stem reflexes and a single apnoea test, are

conclusively performed


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Determination of brain death

history or physical examination findings

exclusion of conditions that might confound the subsequent examinationof cortical or brain stem function

performance of a complete neurological examination including the

standard apnea test and 10 minute apnea test assessment of brainstem reflexes

clinical observations compatible with the diagnosis of brain death

responsibilities of physicians

notify next of kin

interval observation period

repeat clinical assessment of brain stem reflexes

confirmatory testing as indicated

certification and brain death documentation


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History & physical examination of brain

dysfunction

identification of the proximate cause and irreversibility of coma

severe head injury

massive intracerebral bleed

aneurysmal subarachnoid hemorrhage, hypoxic-ischemic brain insults

fulminant hepatic failure

Exclude

Shock/ hypotensionHypothermia - temperature < 32C

Drugs known to alter neurologic, neuromuscular function and

electroencephalographic testing

Medical conditions (e.g. brain stem encephalitis)


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Complete neurological examination

Absence ofspontaneous movement, decerebrate or decorticateposturing, seizures, shivering, response to verbal stimuli, and response tonoxious stimuli administered through a cranial nerve path way

Absent pupillary reflex to direct and consensual light

Absent corneal, oculocephalic, cough and gag reflexes

Absent oculovestibular reflex

Failure of the heart rate to increase by more than 5 beats per minute after1- 2 mg. of atropine intravenously

Absent respiratory efforts in the presence of hypercarbia when ventilatoris switched off and PaCo2 rises above 6.7kPa (50mmHg) (apnoea test isperformed after the second examination of brainstem reflexes)


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Assessment of brainstem reflexes

Pupils- no response to bright light (absent light reflex - cranial nerve II andIII)

Ocular movement- cranial nerve VIII, III and VI

No oculocephalic reflex (testing only when no fracture or instability ofthe cervical spine or skull base is apparent)

No deviation of the eyes to irrigation in each ear with 50 ml of coldwater (tympanic membranes intact; allow 1 minute after injection andat least 5 minutes between testing on each side)

Facial sensation and facial motor response

No corneal reflex (cranial nerve V and VII)

No jaw reflex (cranial nerve IX)

No grimacing to deep pressure on nail bed, supraorbital ridge, ortemporo-mandibular joint (afferent V and efferent VII)

Pharyngeal and tracheal reflexes (cranial nerve IX and X)

No response after stimulation of the posterior pharynx

No cough response to tracheobronchial suctioning


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Clinical observations compatible with the

diagnosis of brain death

spontaneous movements of limbs other than pathologicflexion or extension response

respiratory-like movements (shoulder elevation andadduction, back arching, intercostal expansion without

significant tidal volumes) sweating, flushing, tachycardia

normal blood pressure without pharmacologic support orsudden increases in blood pressure

absence of diabetes insipidus deep tendon reflexes; superficial abdominal reflexes; triple

flexion response

absent plantar reflex


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Determination of brain death contd.

notify next of kin

Consent not needed for diagnosis

Consent needed for removal of life support and organ donation

interval observation period 6 hour observation period

repeat clinical assessment of brain stem reflexes

Repeated in full and documented

confirmatory testing as indicated but is not routine

2 physicians required for certification (organ donation)


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Medical Record Documentation

etiology and irreversibility of coma / unresponsiveness

absence of motor response to pain

absence of brainstem reflexes during two separate

examinations separated by at least 6 hours absence of respiration with pCO2 60 mm hg

justification for, and result of, confirmatory tests ifused


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Malaysian guidelines

1993 - Consensus statement on brain death

2003 Review of above statement

(Malaysian Society of Neurosciences)

www.neuro.org.my/index.php?sc=allclinicalpractice

Coma & Brain Stem Death

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