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APPROACH TO THE COMATOSE PATIENT

CHAIRPERSON: DR.ARDAMAN SINGHSPEAKER: DR.MANISH VINAYAK

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In hospital emergency, the clinical analysis of unresponsive and comatose patient is always an urgency.

Physician must therefore be prepared to implement a rapid, systematic investigation and need for prompt therapeutic action.

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NEURAL BASIS OF CONSCIOUSNESSMaintenance of consciousness depends on

interaction between ascending reticular activating system (ARAS) and the cerebral hemispheres.

ARAS extends from the lower border of pons to the ventromedial thalamus and then project to whole of the cerebral cortex.

It receives collaterals from the spinothalamic and trigeminal thalamic pathways.

Disorders that distort normal anatomical relationships of the midbrain, thalamus, and cortex appear to impair arousal.

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TERMINOLOGYCOUNSCIOUSCONFUSIONDROWSINESSSTUPORCOMA

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CONSCIOUSNESSIt means the state of patient`s awareness of

self and environment and his responsiveness to external stimulation and inner need.

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CONFUSIONTraditionally referred as “CLOUDING OF

SENSORIUM”.It denotes inability to think with customary

speed, clarity and coherence, accompanied by some degree of inattentiveness and disorientation.

Confusion results most often from process that influences the brain globally, such as toxic or metabolic disturbance or a dementia.

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DROWSINESSIt is inability to sustain a wakeful state

without application of external stimuli.The patient shift positions in bed or chair.Slow arousal is elicited by speaking to the

patient or applying a tactile stimulus.

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STUPORStupor describes a state in which the patient

can be aroused only by vigorous and repeated stimuli.

Response to spoken commands is either absent or slow and inadequate.

Restless or stereotyped motor activity is common in stuporous patients and there is a reduction in the natural shifting of positions.

When left unstimulated, these patients quickly drift back into a sleep-like state.

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COMAComa is a deep sleep like stage from which

patient cannot be aroused to respond appropriately to stimuli even with vigorous stimulation. The patient may grimace in response to painful stimuli and limbs may demonstrate stereotyped withdrawal responses, but the patient does not make localized responses or discrete defensive movements.

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INITIAL MANAGEMENT OF COMATOSE PATIENT ON ARRIVALAirwayBreathingCirculationEvaluate for intracranial hypertension and

imminent herniation and treat.

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AIRWAYEvaluate- Is airway patent??? Is there trauma or

foreign body obstructing airway???Patient with head injury may also have suffered a

fracture of cervical vertebrae, in which case caution must be exercised in moving the head and neck.

If breathing is adequate- oropharyngeal airway is sufficient.

If respirations are shallow or labored or if there is emesis with threat of aspiration, tracheal intubation and mechanical ventilation are instituted.

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BREATHINGEvaluate - is patient moving adequate air, is

respiratory rate appropriate, is gas exchange adequate, are breath sounds adequate and symmetrical.

Must assure oxygenation and ventilation.Identify and immediately treat problems -

pneumothorax, airway obstruction, etc..

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CIRCULATIONIs patient in shock?

Check pulses, heart rate, blood pressure. Remember hypotension is late sign of shock

Start treatment for shock Do not restrict fluids in comatose patient with inadequate

intravascular volume.

Use isotonic solutions and blood, as indicated.Do not use hypotonic solutions to treat shock,

particularly patients with coma or possible cerebral edema

Identify life threatening hemorrhage and control it.

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HISTORYInquire about-i. History of diabetesii. Hypertensioniii. Head injuryiv. Convulsionsv. Alcohol or drug usevi. Circumstances in which patient was foundvii. Medications in hospitalized patient like

anesthetics, sedatives, antiepileptic, opiates, antidepressants, antipsychotics.

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REMEMBER CHRONIC ADMINISTRATION OF NITROPRUSSIDE FOR HYPERTENSION CAN INDUCE STUPOR FROM CYANIDE TOXICITY.

Onset of coma-i. Sudden onset- vascular origin especially

brainstem stoke or SAH.ii. Rapid progression from hemispheric signs to

coma- intracerebral haemorrhage.iii. Protracted course- tumor, abscess, chronic SDH.iv. Coma preceded by confusional or agitated state

& without lateralizing signs- metabolic cause.

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GENERAL EXAMINATION1. 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) SAH6. FUNDUS- a) Raised ICP (Pappiloedema) b) SAH ( Subhyaloid haemorrhages) c) Hypertensive encephalopathy7. SKIN INSPECTION- a) Rash suggests

menigococcemia, staphylocoocal endocarditis, typhus, RMSF

b) Excessive sweating suggest hypoglycemia or shock c) Diffuse petechiae suggest TTP, DIC, fat embolism

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NEUROLOGICAL ASSESMENTObservation 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 physician to track neurological changes over time.

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GLASGOW COMA SCALEThree components. Score derived by adding

the score for each component.

Eye opening (4 points)Verbal response (5 points)Best motor response (6 points)

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GLASGOW COMA SCALEEye 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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POSTURE IN COMATOSE PATIENTDecerebrate 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.

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BRAINSTEM REFLEXESPupillary size and reactivityOcular movementsCorneal responsesOcular-vestibular reflexesPattern 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 barbtiturate overdose 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.Conjugate deviation of eyes towards hemispheric

lesion and away from unilateral pontine lesion.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 and 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 REFLEXAlso 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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OCULOVESTIBULAR OR CALORIC TESTPerformed by irrigating external auditory canal

with cold water.Normally it causes slow conjugate deviation of eyes

towards irrigated ear followed in few seconds by compensatory nystagmus (i.e fast component away from irrigated ear)

Loss of conjugate ocular movements indicate brainstem damage.

In metabolic or B/L hemispheral damage, fast corrective nystagmus is lost and eyes are tonically deflected to side irrigated with cold water & this position may be held for 2-3 mins.

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RESPIRATORY PATTERNSSlow, 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 and 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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a) Cheynes stokes respiration

b)Central neurogenic hyperventilation

c)Apneustic breathing

d)Cluster breathing

e)Ataxic / Biot’s breathing

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PATHOLOGICAL ANATOMY OF COMAOnly 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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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.

APPEARANCE OF A BABINSKI SIGN ON THE NONHEMIPARETIC SIDE HAS BEEN A DEPENDABLE SIGN OF SECONDARY BRAIN TISSUE SHIFT.

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HERNIATION SYNDROMESTRANSFALCINE: Across the falx cerebri.TRANSTENTORIAL: Through the tentorial

cerebelli aperture.

Transtentorial herniation is divided into two groups:

a) CENTRAL HERNIATION SYNDROME: Downward displacement and midline compression of brainstem

b) UNCAL SYNDROME: Unilateral insinuation of the medial temporal lobe into the tentorial opening.

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CENTRAL HERNIATION SYNDROMERostral to caudal progression of respiratory, pupillary and

motor findings. May not have other focal findings.Neurological signs at any given time point to one

anatomic area- thalamus, midbrain or brainstem.There is first confusion, drowsiness and often periodic

cheyne-stokes respiration; following this pupils become small and very little reactive. B/L babinski and decorticate posture appear.

These signs give way to brainstem signs: medium sized fixed pupils, loss of oculocephalic reflex, B/L decerebrate posture

Lastly, irregular breathing pattern that implicate medullary destruction; and then death.

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ROSTRAL-CAUDAL PROGRESSION

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ROSTRAL-CAUDAL PROGRESSION

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UNCAL SYNDROMEResult of herniation of medial temporal lobe

into the tentorial opening.In it drowsiness in early stages is

accompanied by unilateral pupillary dilatation.

Sometimes due to lateral mass effect, opposite cerebral peduncle is crushed against the tentorium: this causes babinski sign and weakness of arm and leg ipsilateral to the lesion (KERNOHAN WOLTMAN SIGN)

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TRANSTENTORIAL HERNIATION

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LABORATORY STUDIES AND IMAGINGComplete blood countRandom blood sugarRFT, LFTSerum electrolytesUrine examination for specific gravity, glucose, acetone

& protein content.ABG analysisChest X-Ray ECGCT or MRI ScanLumbar PunctureEEG

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CLASSIFICATION OF COMAThe approach to clinical evaluation is used to

categorise coma into:i. Coma without focal signs or signs of

meningism.ii. Coma with meningism and without any

focal signs.iii. Coma with focal or lateralizing signs.

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COMA WITHOUT FOCAL SIGNS OR MENINGISMCauses are:i. Exogenous intoxicants: alcohol, barbiturate, opiatesii. Endogenous metabolic disturbances: anoxia, hypoglycemia,

DKA, HONK, uraemia, hepatic failure, hypo or hypernatremia, addisonian crisis, carbon monoxide poisoning, myxedema.

iii. Severe systemic infections: septicemia, typhoid fever, cerberal malaria, pneumonia, peritonitis, waterhouse friedrichsen syndrome.

iv. Circulatory collapse (shock) from any causev. Post seizure statesvi. Hypertensive encephalopathyvii. Hyper and hypothermiaviii. Concussionix. Acute hydrocephalus

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COMA WITH MENINGISMCauses are:i. SAHii. Acute bacterial meningitisiii. Viral meningoencephalitisiv. Neoplastic meningitisv. Parasitic meningitisvi. Pituitary apoplexy

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COMA WITH FOCAL SIGNSCauses are:i. Hemispheral haemorrhage or massive cerebral

infarctionii. Brainstem infarctioniii. Brain abscess, subdural empyema, herpes

encephalitisiv. Epidural and subdural haemorrhage, brain

contusionv. Brain tumourvi. Miscellaneous: TTP, fat embolism, ADEM, cortical

vein thrombosis, focal infarction caused by bacterial endocarditis.

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TAKE HOME MESSAGERemember 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