CLINICAL APPROACH TO COMA

M6 unit

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Introduction
Certain terms
Normal Sleep Confusion Delerium Drowsiness Stupor
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consciousness
Akinetic

Mutism Catatonia Persistent Vegetative State Locked-in Syndrome

Coma

CLINICAL APPROACH TO A COMATOSE PATIENT

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 Coma is always a symptomatic expression of an

underlying disease

A methodical approach that leaves none of the

common and treatable causes of coma unexplored

History taking , examination , and management go hand

in hand.

Best thing is one person should take history and other

person examine simultaneously along with taking care of immediate management

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When a comatose patient is 1st seen.

ABC Maintain airway.oropharyngeal endotracheal. Breathing shallow.?........ Aspiration? If trauma check for bleeding If hypotension iv fluids, pressors, volume expanders or blood preferably monitoring central venous pressure O2 inhalation

Cervical Fracture ? Injection Thiamine followed by glucose

(After taking blood for basic investigations)
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History
Onset Fever Headache Vomiting.types.. Trauma Recent altered behaviour..? h/o diabetes? Hypertension? controlled? www.similima.com Poison..? Prior suicidal attempts?

History
Drugs?
Insulin,

OHA Antipsychotics Sedatives Steroids Anti coagulants Diuretics

Acute or Chronic alcohol intake Seizure disorder Prior episode of coma Elderly nothing predictable www.similima.com

General Examination..
Odor
Alcohol

DKA Uriniferous Uremia Musty fetor of Hepatic coma Burnt almond odor of Cyanide Organophospherous
Fruity
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Skin
Colour
Pallor
Severe

internal hemorrhage, Hypothyroidism , Hypopituitarism , CKD

Cyanosis

of lips and nails Cherry red CO Facial plethora alcoholism Maculo hemorrhagic rash

Meningococcemia , Typhus, RMSF, Staph endocarditis

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General Examination..
Diffuse petechiae TTP, DIC, Fat embolism Echymotic patches.. Drug induced CLD DIC Trauma Nasal bleed, CSF leak Aural bleed
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Large blisters
If

the patient has been motionless for a time Acute barbiturate, alcohol, or opiate intoxication

Facial puffiness
CKD Myxedema,

Hypopituitarism

Central obesity, striae Nail

Splinter

hemorrhage White nail Half and half nail Clubbing

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 Jaundice Features of chronic liver disease Fever Pneumonia, sepsis, meningitis, sepsis Hyperthermia
Drugs

with anticholinergic activity Heat stroke

Hypothermia
Alcoholic Drowning Exposure

or barbiturate intoxication

to cold Peripheral circulatory failure

Myxedema
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Bradycardia
Heart

Hypotension
DKA Alcohol,

block due to drugs Myxedema Raised ICT

Marked hypertension
IC

bleed Raised ICT Hypertensive encephalopathy

Barbiturate Internal hemorrhage Myocardial infarction Dissecting aortic aneurysm Septicemia Addison disease Massive brain trauma
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Respiration
Slow

Opiate or barbiturate hypothyroidism

Kussmaul Pneumonia, DKA, Uremia, Pulmonary edema, or Intracranial disease Cheyne-Stokes Raised ICT
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Neurologic Examination

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Most important even though limitted Simple observing of the patient may give valuable

clues Abnormal posturing of body Abnormal movement of one side The state of responsiveness
Vocalization Grimacing and deft avoidance movements of the

stimulated parts are preserved in light coma The Glasgow Coma Scale www.similima.com

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The Glasgow Coma Scale

Motor Response

6 - Obeys commands fully 5 - Localizes to noxious stimuli 4 - Withdraws from noxious stimuli 3 - Abnormal flexion, i.e. decorticate posturing 2 - Extensor response, i.e. decerebrate posturing 1 - No response

Total 15 Poor - 3 or 4

Verbal Response

5 - Alert and Oriented 4 - Confused, yet coherent, speech 3 - Inappropriate words, and jarbled phrases consisting of words 2 - Incomprehensible sounds 1 - No sounds

Eye Opening
4 - Spontaneous eye opening 3 - Eyes open to speech 2 - Eyes open to pain www.similima.com 1 - No eye opening

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Signs of meningeal irritation

Meningitis Subarachnoid

hemorrhage (after 12-24 hrs in some) In the infant, bulging of the anterior fontanel better sign

Confused with meningeal irritation

Phenothiazine

poisoning Temporal lobe or cerebellar herniation

Decerebrate

rigidity

Cervical

spondylosis
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Hemiplegia
Lack

of movement on noxious stimuli leg lies in a position of external rotation ( // fracture femur)

Hemiplegic

Thigh

may appear wider and flatter than the nonhemiplegic one expiration, the cheek and lips puff out on the paralyzed side
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In

Hemispherical lesions

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 Eyes are often turned away from the paralyzed side Opposite may occur with brainstem lesions Hemiplegia and an accompanying Babinski sign are

indicative of a contralateral hemispheral lesion ( beware of Kernohan-Woltman sign )

A moan or grimace may be provoked by painful stimuli

on one side but not on the other, reflecting the presence of a hemianesthesia
During grimacing, facial weakness may be noted www.similima.com
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Brain stem lesions

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Of the various indicators of brainstem function,

the most useful are pupillary size and reactivity, ocular movements, oculovestibular reflexes, and, to a lesser extent, the pattern of breathing.
These functions, like consciousness itself, are to

a large extent dependent on the integrity of structures in the midbrain and rostral pons
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Pupil

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 Unilaterally enlarged pupil (>5.5 mm diameter) ipsilateral

3rd nerve compression

With continued compressioncorectopia (oval or pear ) The light-unreactive pupil continues to enlarge to a size of 6

to 9 mm diameter, associated with slight outward deviation of the globe

In unusual instances, the pupil contralateral to the mass may

enlarge first
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 As midbrain displacement continues, both pupils dilate

and become unreactive to light

The last step in the evolution of brainstem compression

tends to be a slight reduction in pupillary size, to 5 to 7 mm

Normal pupillary size, shape, and light reflexes indicate

integrity of midbrain structures and a cause of coma other than a mass lesion
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 Pontine tegmental lesions cause extremely miotic pupils

(<1 mm in diameter) with only a slight reaction to strong light

Ciliospinal reflex lost A Horner syndrome homolateral to a lesion of the

brainstem or hypothalamus or as a sign of dissection of the internal carotid artery

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 Pupil is spared in metaboic conditions and intoxications Exceptions

Morphine

extremely pin point Barbiturate pin point 1cm or more Atropine Dilated, non reacting even to physostigmine Tricyclics Hippus metabolic encephalopathy

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NORMAL

B/L PIN POINT

U/L CONSTRICTED

U/L 3RD N

HORNERS
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THALAMIC HGE

BRAIN DEATH

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Movements of Eyes and Eyelids and Corneal Responses

In light coma of metabolic origin, the eyes rove

conjugately from side to side in random fashion, sometimes resting briefly in an eccentric position
These movements disappear as coma deepens and the

eyes then remain motionless in slightly exotropic positions

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 A lateral and slight downward deviation of one eye

suggests the presence of a third nerve palsy

Medial deviation sixth nerve palsy Away from the side of the paralysis large cerebral

lesion

Toward the side of the paralysis with a unilateral

pontine lesion

Wrong-way conjugate deviation thalamic and

upper brainstem lesions

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 During a one-sided seizure, the eyes turn or jerk toward

the convulsing side

The eyes may be turned down and inward (looking at

the nose) with hematomas or ischemic lesions of the thalamus and upper midbrain

Retraction and convergence nystagmus lesions in the

tegmentum of the midbrain

Ocular bobbing Pons Ocular dipping Anoxia and Drug intoxications

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The coma-producing structural lesions of the brainstem abolish most conjugate ocular movements, whereas metabolic disorders generally do not. (except for rare instances of hepatic coma and anticonvulsant drug overdose)
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Oculocephalic reflex

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Elicitation of these reflexes in a comatose

patient provides two pieces of information

Evidence

of unimpeded function of the oculomotor nerves and of the midbrain and pontine tegmental structures that integrate ocular movements of the cortical inhibition that normally holds these movements in check
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Loss

 Sedative or anticonvulsant intoxication serious enough

to cause coma may obliterate the brainstem mechanisms for oculocephalic reactions Asymmetry in elicited eye movements remains a dependable sign of focal brainstem disease

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Caloric response

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 10 mL of cold water In comatose patients, the fast corrective phase of

nystagmus is lost and the eyes are tonically deflected to the side irrigated with cold water or away from the side irrigated with warm water; this position may be held for 2 to 3 min
With brainstem lesions, these vestibulo-ocular reflexes

are lost or disrupted

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Corneal reflex
Progressive deterioration in response to corneal touch

are among the most dependable signs of deepening coma.

A marked asymmetry in corneal responses indicates

either an acute lesion of the opposite hemisphere or, less often, an ipsilateral lesion in the brainstem.

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 Restless movements of both arms and both legs and

grasping and picking movements intact corticospinal tracts

The occurrence of focal motor epilepsy usually indicates

that the corresponding corticospinal pathway is intact

Massive destruction of a cerebral hemisphere focal

seizures are seldom seen on the paralyzed side

Definite choreic, athetotic, or hemiballistic movements

indicate a disorder of the basal ganglionic and subthalamic structures, just as they do in the alert patient
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Abnormal postures

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The decerebrate State

Brainstem In

at the intercollicular level

a variety of conditions

Midbrain

compression due to a hemispheral mass with cerebellar or other posterior fossa lesions Anoxia and hypoglycemia; Rarely with hepatic coma and profound intoxication

Ipsilateral

to a one-sided lesion, hence not due to involvement of the corticospinal tracts

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Decorticate rigidity
Lesions at a higher levelin the cerebral white matter

or internal capsule and thalamus

Bilateral decorticate rigidity is essentially a bilateral

spastic hemiplegia

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 Diagonal postures, e.g., flexion of one arm and

extension of the opposite arm and leg, usually indicate a supratentorial lesion
Forceful extensor postures of the arms and weak flexor

responses of the legs are probably due to lesions at about the level of the vestibular nuclei
Lesions below this level lead to flaccidity and abolition

of all postures and movements. The coma is then usually profound and often progresses to brain death
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 Only in the most advanced forms of intoxication and

metabolic coma, as might occur with anoxic necrosis of neurons throughout the entire brain, are coughing, swallowing, hiccoughing, and spontaneous respiration all abolished

Tendon reflexes are usually preserved until the late

stages of coma due to metabolic disturbances and intoxications

Plantar flexor responses, succeeding extensor

responses, signify ether a return to normalcy or, in the context of deepening coma, a transition to brain death
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Motor response

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Motor response

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Breathing patterns
Cheyne-Stokes Massive supratentorial lesion Bilateral deep-seated cerebral lesions
disturbances Presence of CSR signifies bilateral dysfunction of cerebral structures, usually those deep in the hemispheres or diencephalon, and is seen with states of drowsiness or stupor
Coma with CSR is usually due to intoxication or a severe metabolic
Metabolic

derangement and occasionally to bilateral lesions, such as subdural hematomas

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Central neurogenic hyperventilation

Lesions

of the lower midbrainupper pontine tegmentum, either primary or secondary to a tentorial herniation of the medulla, lower pons, and midbrain

Tumors Primary

brain lymphoma without brainstem involvement

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 Apneustic breathing Low pontine lesions, usually

due to basilar artery occlusion

Biot breathing (chaotic) lesions of the dorsomedial

part of the medulla

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Signs of Increased Intracranial Pressure

Headache before the onset of coma Recurrent vomiting Severe hypertension beyond the patient's static level Subhyaloid retinal hemorrhages Papilledema develops within 12 to 24 h in cases of

brain trauma and hemorrhage, but if it is pronounced, it usually signifies brain tumor or abscessi.e., a lesion of longer duration
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Case 1
15 yr old girl, recent weight loss and polydipsia

presenting with a comatose state. She is dehydrated and in shock. Examination showed tachypnea and sweet odour

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Case 2
A middle aged man brought in a comatose state by

some passengers who got him from the pavement. There was smell of alcohol in his breath, and had dilated right pupil and left extensor plantar.

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Case 3
A 10 yr old boy with h/o Fallots tetrology was brought

by his parents with h/o headache and fever for 2 weeks, severe vomiting and progression into coma. He had left hemiplegia and lateral rectus palsy and b/l papilledema

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Case 4
35 yr old lady who was on insulin for diabetic ketotic

coma. Her sugar values and blood acetone improved, but she persisted in the comatose state. She had 3 episodes of GTCS. On examination she had b/l extensor plantar response and b/l papilledema.

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Case 5
60 yr old lady presented with comatose state to the

casualty. She had developed sudden onset of left sided weakness along with headache and vomiting. She had left hemiplegia, and bilateral papilledema. Her BP was normal. She had mild numbness in the left upper and lower limbs for last 1 month.

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Case 6
21 yr old primi in 9th month of gestation presented with

severe vomiting, headache and GTCS. She had mild fever also.She didnt have any hypertension or edema during pregnancy. Examination showed normal BP and bilteral papilledema. There was no meningeal signs.

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Case 7
56 yr old chronic alcoholic presented in comatose state

to the gastroenterology department. He had mild abdominal pain for last 5 days. Examination showed b/ l extensor plantar response.

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Case 8
65 yr old lady was admitted in a comatose state. She

had received an injection for chest pain from a local hospital. Her skin was dry, she had low temperature. She had excessive day time somnolence for last 1 month

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Thank you.

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