CLINICAL APPROACH TO COMA

M6 unit

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Introduction Certain terms…

Normal consciousnessSleep ConfusionDelerium DrowsinessStupor

Akinetic Mutism Catatonia Persistent Vegetative State Locked-in Syndrome

Coma 2www.similima.com

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…OnsetFeverHeadache Vomiting….types..TraumaRecent altered behaviour..?h/o diabetes…?Hypertension? controlled…?Poison..? Prior suicidal attempts…? 6www.similima.com

History…Drugs…?

Insulin, OHA Antipsychotics Sedatives Steroids Anti coagulants Diuretics

Acute or Chronic alcohol intakeSeizure disorder…Prior episode of comaElderly… nothing predictable… 7www.similima.com

General Examination..

OdorAlcoholFruity DKAUriniferous Uremia Musty fetor of Hepatic comaBurnt almond odor of CyanideOrganophospherous

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Skin

Colour Pallor

Severe internal hemorrhage, Hypothyroidism , Hypopituitarism , CKD

Cyanosis of lips and nailsCherry red COFacial plethora alcoholismMaculo hemorrhagic rash

Meningococcemia , Typhus, RMSF, Staph endocarditis

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General Examination..Diffuse petechiae

TTP, DIC, Fat embolismEchymotic patches..

Drug inducedCLDDICTrauma

Nasal bleed, CSF leakAural 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, striaeNail

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 or barbiturate intoxication Drowning Exposure to cold Peripheral circulatory failure Myxedema

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BradycardiaHeart block due to drugsMyxedemaRaised ICT

Marked hypertensionIC bleedRaised ICTHypertensive

encephalopathy

HypotensionDKAAlcohol, BarbiturateInternal hemorrhageMyocardial infarctionDissecting aortic

aneurysmSepticemiaAddison diseaseMassive brain trauma

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Respiration Slow

Opiate or barbiturate hypothyroidism

Kussmaul Pneumonia, DKA, Uremia, Pulmonary

edema, or Intracranial diseaseCheyne-Stokes

Raised ICT14www.similima.com

Neurologic Examination

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Most important even though limittedSimple observing of the patient may give valuable

cluesAbnormal posturing of bodyAbnormal movement of one sideThe state of responsivenessVocalization Grimacing and deft avoidance movements of the

stimulated parts are preserved in light coma The Glasgow Coma Scale 16www.similima.com

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

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 1 - No eye opening

Total – 15Poor - 3 or 4

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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

Hemiplegic leg lies in a position of external rotation ( // fracture femur)

Thigh may appear wider and flatter than the nonhemiplegic one

In expiration, the cheek and lips puff out on the paralyzed side

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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 21www.similima.com

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 intoxicationsExceptions

Morphine extremely pin pointBarbiturate pin point 1cm or moreAtropineTricyclicsHippus metabolic encephalopathy

Dilated, non reacting even to physostigmine

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NORMAL

B/L PIN POINT

U/L CONSTRICTED

HORNER’S

U/L 3RD N

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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 (horizontal eye movements are preserved ) 33www.similima.com

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

Loss of the cortical inhibition that normally holds these movements in check

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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 reflexProgressive 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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Brainstem at the intercollicular level

In a variety of conditionsMidbrain compression due to a hemispheral masswith cerebellar or other posterior fossa lesionsAnoxia and hypoglycemia;Rarely with hepatic coma and profound intoxication

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

The decerebrate ‘State’

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Decorticate rigidity

Lesions at a higher level—in 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 patternsCheyne-Stokes

Massive supratentorial lesion Bilateral deep-seated cerebral lesions Metabolic 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 derangement and occasionally to bilateral lesions, such as subdural hematomas

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Central neurogenic hyperventilation

Lesions of the lower midbrain–upper pontine tegmentum, either primary or secondary to a tentorial herniation

Tumors of the medulla, lower pons, and midbrain

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 levelSubhyaloid 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 abscess—i.e., a lesion of longer duration

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Case 115 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 2A 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 3A 10 yr old boy with h/o Fallot’s 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 435 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 560 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 621 yr old primi in 9th month of gestation presented with

severe vomiting, headache and GTCS. She had mild fever also.She didn’t have any hypertension or edema during pregnancy. Examination showed normal BP and bilteral papilledema. There was no meningeal signs.

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Case 756 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 865 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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