Evaluation &

management of comaDR ABDUL RUB

2ND YEAR PG MEM

COMA

Coma is prolonged Unconsciousness Or Unarousable Unresponsiveness

DISORDERS OF CONSCIOUNESS

Really Simple Neuroanatomy

Arousal: where is it localized?

Ascending Reticular Activating System (ARAS) ‘core of the brainstem’

receives input from numerous somatic afferents

projects to midline thalamic nuclei (which are in a circuit with cortical structures)

and the limbic system

GLASGOW COMA SCALE

Eye opening Best Motor Response

4 – spontaneous 6 – obeys

3 - to speech 5 - localizes

2 - to pain 4 - withdraws

1 – none 3 – abnormal flexion

Verbal Response 2 – abnormal extension

5 – oriented 1 - none

4 - confused conversation

3 - inappropriate words

2 - incomprehensible sounds

1 - none

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The sum obtained in this scale is used to the assess Coma and Impaired consciousness

Mild is 13 through 15 points Moderate is 9 to 12 points Severe 3 through 8 points

Patients with score less than 8 are in Coma

Coma - Aetiology

Metabolic:-

Ischemic hypoxic

Hypoglycaemic

Organ failure

Electrolyte disturbance

Toxic

Structural:-

Supratentorial bilateral

Unilateral large lesion with transtentorial

herniation

Infratentorial

Supratentorial Lesions

Epidural or Subdural Hematoma

Intraparenchymalhaemorrhage

Large Ischemic Infarction

Tumour

Trauma

Abscess

Supra tentorial mass lesion

differential characteristics

Initiating signs usually of focal cerebral

dysfunction

Signs of dysfunction progress rostral to caudal

Neurologic signs at any given time point to

one anatomic area - diencephalon, midbrain,

brainstem

Motor signs are often asymmetrical

Infratentorial Lesions

Basilar artery thrombosis

Pontine or Cerebellar

Hematoma

Ischemic Cerebellar

Infarction

Tumour

Abscess

Infratentorial Mass Lesions

Differential Characteristics

History of preceding brainstem dysfunction or sudden onset of

coma

Localizing brainstem signs precede or accompany onset of

coma and always include oculovestibular abnormality

Cranial nerve palsies usually present

“Bizarre” respiratory patterns common, usually present at onset of

coma

Plum and Posner, 1982

Why coma management?

Common medical emergency 3-5%

Large proportion of comatose patient recover

Untreated coma may lead to further brain damage

Emergency treatment

Maintain ventilation oxygenation

Maintain circulation

Control seizure

Reduce icp

Maintain temperature

Control hypoglycemia

Maintain ventilation

Insert oral airway

Clean oropharyngeal secretion

Insert cuffed endotracheal tube if apnea, hypoventilation or liable to

aspirate

Mechanical ventilation if apnea or raised intracranial pressure

Maintain circulation

If hypotenstion ( <90mmHg systolic)

Replace fluid:

Saline if hyperglycemia or suspected stroke, diabetes

Dextrose saline or isolyte if undiagnosed

Vasopressor if low systolic pressure inspite of fluid

Hypertension: Betablocker, Nitroglycerine or Nitropruside

Reduce intracranial pressure

Inj Mannitol 20% 1gm/kg IV fast

Hyperventilatin to bring pCO2 25-30mmHg

Control Seizure

Inj Lorazepam 4mg or Midazolam 5mg IV slowly

Inj Diazepam 10-20mg iv slowly

Inj Phenytoin 15-20mg/Kg 50mg/min IV

Inj Phenobarb 15-20mg/Kg 50mg/min IV

Inj Sodium valproate 200-400mg IV

Maintain Temperature

Hperthermia: tapid sponging, paracetamol

Hypothermia: heating blanket

HISTORY

Inquire about-

i. History of diabetes

ii. Hypertension

iii. Head injury

iv. Convulsions

v. Alcohol or drug use

vi. Circumstances in which patient was found

vii. Medications in hospitalized patient like anesthetics, sedatives, antiepileptic, opiates, antidepressants, antipsychotics.

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GENERAL EXAMINATION

1. SIGNS OF TRAUMA- a) Racoon eyes

b) Battle`s sign

c) CSF rhinorrhea or otorrhea

2. BLOOD PRESSURE- Hypertension suggests-

a) Hypertensive encephalopathy

b) Intracerebral haemorrhage

Hypotension suggests-a) Myocardial infarction

b) Septicemia

c) Addison disease

d) Alcohol or barbiturate intoxication

e) Internal haemorrhage.

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3. PULSE- Bradycardia with periodic breathing and hypertension (CUSHING REFLEX) suggests raised ICP.

4. TEMPERATURE- Hypothermia suggests-

a) Alcohol or barbiturate intoxication

b) Myxedema

c) Advanced tubercular meningitis

d) Peripheral circulatory failure

Hyperthemia suggests- a) Systemic infection

b) Meningoencephalitis

c) Heat stroke

d) Anticholinergic drugs abuse

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5. SIGNS OF MENINGEAL IRRITATION-

a) Meningitis

b) SAH

6. FUNDUS- a) Raised ICP (Papilledema)

b) SAH ( retinal haemorrhages,disc swelling)

c) Hypertensive encephalopathy

7. SKIN INSPECTION- a) Rash suggests menigococcemia, staphylocoocalendocarditis, typhus, RMSF

b) Excessive sweating suggest hypoglycemia or shock

c) Diffuse petechiae suggest TTP, DIC, fat embolism

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NEUROLOGICAL ASSESMENT

Observation first without examiner intervention.

Simply watch posture of limbs and body, position of head and eyes, presence or absence of spontaneous movements on one side, rate and depth of respiration.

Yawning and spontaneous shifting of body position indicates minimal degree of unresponsiveness.

Multifocal myoclonus almost always indicate metabolic disorder.

Assess responsiveness by noting patient`s reaction to calling his name, or to noxious stimuli such as supraorbital or sternal pressure.

Glasgow coma scale allows rapid assessment and allows to track neurological changes over time.

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POSTURE IN COMATOSE PATIENT

Decerebrate rigidity: consists of opisthotonus, clenching of jaws, stiff

extension of limbs with internal rotation of arms & plantar flexion of feet.

Precise correlation between extensor posturing & level of lesion is rarely

possible because extensor posturing arises in variety of settings: midbrain

compression, cerebellar lesions, metabolic, drug intoxication etc.

Decorticate rigidity: arms in flexion and adduction and legs extended signify lesion rostral to midbrain.

Extensor posture of arms with weak flexor responses of legs is seen with

lesions at level of vestibular nuclei (medulla)

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REFLEXES

BRAINSTEM REFLEXES

Pupillary size and reactivity

Ocular movements

Corneal responses

Ocular-vestibular reflexes

Pattern of breathing

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AS A RULE, WHEN THESE BRAINSTEM ACTIVITIES ARE PRESERVED,

PARTICULARLY THE PUPIL REACTIONS AND EYE MOVEMENTS, COMA MUST BE

ASCRIBED TO BILATERAL HEMISPHERAL DISEASE. THE CONVERSE, HOWEVER,

IS NOT ALWAYS TRUE, AS A MASS IN THE HEMISPHERES MAY BE THE

UNDERLYING CAUSE OF COMA BUT NONETHELESS PRODUCE BRAINSTEM

SIGNS BY INDUCING TRANSTENTORIAL HERNIATION.

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PUPILLARY REACTIONS

Symmetrically reactive round pupils: Exclude midbrain damage.

Enlarged and unreactive pupil (>5 mm): Intrinsic midbrain lesion (ipsilateral) or by ipsilateral mass.

Oval and slightly eccentric pupils: Early midbrain or third nerve compression.

Bilateral dilated and unreactive pupils: Severe midbrain damage by transtentorial herniation or anticholinergic drugs toxicity (atropine, TCA).

Reactive bilaterally small but not pin point (1-2.5 mm): Metabolic encephalopathies or thalamic haemorrhages.

Very small but reactive pupil (less than 1 mm) : Opioid or barbtiturateoverdose or bilateral pontine haemorrhage.

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EYE MOVEMENTS

In light coma of metabolic origin, eyes rove conjugately from side to side in

random fashion. These movements disappear as coma deepens.

Adducted eye at rest: 6th nerve palsy. If it is bilateral it is due to raised ICT.

Abducted eye at rest: 3rd nerve palsy.

Downward and inward deviation of eyes: Lesions of thalamus and upper

midbrain.

Eyes turn toward convulsing side in focal seizures.

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OCULAR BOBBING: Brisk downward and slow upward movements of the

eyes associated with loss of horizontal eye movements is diagnostic of

lesions in midbrain and pons.

OCULAR DIPPING: Slow downward followed by faster upward movement

in patients with normal horizontal gaze and it indicates diffuse cortical

anoxic damage and drug intoxication.

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OCULO-CEPHALIC REFLEX

Also called Doll`s-eye movement.

Elicited by briskly turning or tilting the head.

Response in coma of metabolic origin or that due to bihemispheral structural lesions consist of conjugate movements of eyes in the opposite direction.

Positive response indicates-

i. Oculomotor, abducent, midbrain and pons are intact.

ii. There is loss of cortical inhibition on brainstem that normally holds these movements in check.

Absent reflex indicates damage within brainstem but also can be due to

profound overdose of sedatives or anticonvulsants.

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RESPIRATORY PATTERNS

Slow, shallow, regular breathing: metabolic or drug depression.

Cheyne-Stokes respiration: Massive supratentorial lesions, B/L

cerebral lesions & mild metabolic disturbance.

Central neurogenic hyperventilation: Lesions of lower midbrain &

upper pons either primary or secondary to transtentorial herniation.

Apneustic breathing: Lower pontine lesions.

Biot`s or ataxic breathing: Lesions of dorsomedial part of medulla.

Agonal gasps: B/L lower brainstem damage & terminal respiratory

pattern.

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PATHOLOGICAL ANATOMY OF COMA

Only if cerebral lesions are bilateral and extensive, then consciousness will

be impaired.

Unilateral mass lesions like infarct or hemorrhage if are causing coma, it

means compression of midbrain and subthalamic region of RAS has

occurred.

Either lateral displacement or herniation of temporal lobe can cause their

compression.

Even small lesions in upper brainstem and thalamus are sufficient to cause

coma.

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Onset of coma-

i. Sudden onset- vascular origin especially brainstem stoke or SAH.

ii. Rapid progression from hemispheric signs to coma- intracerebralhaemorrhage.

iii. Protracted course- tumor, abscess, chronic SDH.

iv. Coma preceded by confusional or agitated state & without lateralizing signs-metabolic cause.

v. REMEMBER FRONTAL AND OCCIPITAL HEMORRHAGES ARE LESS LIKELY TO DISPLACE DEEP STRUCTURES AND TO CAUSE COMA THAN ARE CLOTS OF EQUIVALENT SIZE IN THE PARIETAL OR TEMPORAL LOBES

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LABORATORY STUDIES AND IMAGING

Complete blood count

Random blood sugar

RFT, LFT

Serum electrolytes

Urine examination for specific gravity, glucose, acetone & protein content.

ABG analysis

Chest X-Ray

ECG

CT or MRI Scan

Lumbar Puncture

EEG

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TAKE HOME MESSAGE

Remember clinical analysis of comatose patient is urgency.

Evaluate for airway, breathing & circulation.

History & systematic general and neurological assessment will help a lot.

Presence or absence of brainstem reflexes helps to localize the lesion.

Evaluate for imminent herniation.

Implement rapid & systematic investigation and take prompt therapeutic

action.

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THANKS 36