Coma

Peilin LuNeurology Department SRRSH

A 32 year-old woman is found on the floor at work, unconscious, but spontaneously breathing. In the ER, BP is 146/75, pulse 80, afebrile. Her left pupil is 5 mm and sluggishly reacts to light; the right pupil is 2 mm and briskly reacts to light. She does not grimace or move to painful stimuli, nor attempt to speak.

What is the problem?

What can I do to make diagnosis?

How to check and treat?

Definition• Coma

• appears to be asleep • and incapable of being aroused by

external stimuli or inner need• serious disturbance of consciousness.

Arousal disorders • Disturbance of consciousness

• waking disorder (Arousal disorder), Drowsiness, Lethargy Coma

Light coma Moderate coma Deep coma

• conscious content disturbance

Drowsiness Drowsiness is the lightest kind of

disturbance of consciousness, continuous pathological sleep state, patients can be woke up by mild

stimulation and correctly answer questions or make various responses,

but go back to sleep soon after stimulation stopping.

Lethargy• disturbance of conscious status whose

awakening level is more severe than drowsiness ，

• may show a short awakening after strong or repetitive stimulation,

• having no response or incorrect response to language,

• falling into lethargy very soon once the stimulation is stopped.

Coma• a kind of severe disturbance of consciousness• appears to be asleep • incapable of being aroused by external stimuli or

inner need• patients can not recognize themselves or the

surrounding environment, • no eyes open movement and spontaneous language

movement, • rare spontaneous limb movement• physiological reflex

• normal, reduced or lost, • vital signs can be stable or unstable.

Light coma Moderate coma Deep coma pain stimulation

simple response no response no response

reflexes

Many reflexes are normal, such as corneal reflex, cough reflex, swallowing reflex and tendon reflex,

could exist but were obviously weakened ， Tendon hyperreflexiapathologic reflexes are positive

No reflexes ， no tendon reflex no pathological reflex ， Tetraplegia,

vital signs stable could be normal unstable

others completely tetraplegia,

eyeball fixation, mydriasis,

Brain death over-coma. irreversible brain damage loss of whole brain function, The termination of the cerebral

circulation The dysfunctional nervous system

which can not maintain the stability of the body environment

Disturbance of conscious content• Confusion

• mainly characterized by serious thought disorder, may be accompanied with disorientation, hallucinations, paranoia, anxiety, and so on.

Delirium state• Also known as acute mental disorder

state, • Appears as poor performance of

arousal level, disorientation, lax attention, and serious disorders of many aspects such as perception, intelligence, emotion, and so on.

Persistent vegetative state A serious disturbance of

consciousness complete loss of perception, thought,

emotion, memory, will and language activities,

No response to external stimulation and no limb spontaneous activities

Altered states of consciousness:

• Stupor • severely impaired arousal with some

responsiveness to vigorous stimuli

Spirit inhibiting status • Common in hysteria or after severe mental

trauma, • Patients lose their response to external

stimulation suddenly, • May accompanied with fast breathing or

breath holding, • Their eyes are closed or blinking rapidly, • Pupil light reflex are more sensitive, • Limbs are straight, buckling, • Neurological examination has no positive sign.

Locked-in syndrome the losing of all other movement functions

except eyes open, eyes close and eyes vertical movements, but the conscious is not affected.

BEHAVIORAL STATE

DEFINITION LESION COMMENTS

Locked-in syndrome

Patient alert and aware, quadriplegic with lower cranial nerve palsy

Bilateral ventral pontine

Similar state may be seen with severe polyneuropathies, myasthenia gravis, neuromuscular blocking agents

Persistent vegetative state

Absent cognitive function but retained “vegetative” components

Extensive cortical gray or subcortical white matter with relative preservation of brainstem

Synonyms include apallic syndrome, coma vigil, cerebral cortical death

Abulia Severe apathy: patient neither speaks nor moves spontaneously

Bilateral frontal medial

Severe cases resemble akinetic mutism, but patient is alert and aware

Catatonia

Mute, with marked decrease in motor activity

Usually psychiatric May be mimicked by frontal lobe dysfunction or drugs

Elements of clinical diagnosis of coma

Anatomic basis of coma.

• Consciousness is maintained • by the normal functioning of

• brainstem reticular activating system above the mid pons

• and its bilateral projections to the thalamus and cerebral hemispheres.

• Coma results from lesions that affect • either the reticular activating system • or both hemispheres.

• The content of consciousness resides in the cerebral hemispheres;

Causes of coma 1· Supratentorial mass lesions 2· Infratentorial mass lesions 3· Metabolic

History Severe traumatic brain injury, Poison taking, Medication, Happened in active state, The suddenly happen of coma after a

meal

Environment factors Common CO poisoning, CO2 poisoning, Chloride poisoning Mostly caused by poor ventilation of

living or working places of patients.

The changing process of symptoms Coma after : Fever Severe headache Precordial angina and profuse

perspiration

Concomitant symptoms• Coma accompanied with: • Hyperspasmia• Vomiting• Hemiplegic paralysis• Incontinence of urine and feces• Right upper abdominal pain, • Eyelid edema • Asthma and cyanosis • Extremely thin

Past history Injury happened in or longer than a

week before coma, Headaches, blurred vision and

paroxysmal dementia, Paroxysmal limbs convulsions,

abnormal sensation or numbness

Past history Hypertension Liver disease Diabetes mellitus, Kidney disease,

Past history Heart disease, Lungs Original infection Original endocrine disease history Tumor or cancer,

Personal history Endemic areas living history Toxic substances contacting history Radioactive materials exposure history Clues to the diagnosis of local and

occupational diseases Family history Congenital or genetic disease.

Signs Basic vital signs General physical checkup The neurologic examination

Basic vital signs Breathing, Body temperature, Heart rate Blood pressure.

Breathing Respiratory rate

Normal : 14-20 times/min, Bradypnea: <9 times/min

intracranial hypertension, respiratory failure, Slow and sighing like breath is mostly

caused by morphine poisoning; Tachypnea: >30 times/min,

acute infections

Breathing manner • Bilateral hemispheric or diencephalic damage:

Cheyne-Stokes respirations (CSR) are a patter of periodic breathing in which phases of hyperpnea regularly alternate with apnea.

• Of all the respiratory patterns listed, this has the least

• specificity.   

Hypothalamic-Midbrain damage Central neurogenic

hyperventilation is a sustained, rapid, and fairly deep hyperpnea that often occurs in patients with dysfunction involving the rostral brainstem tegmentum.

Pons damage• Apneustic breathing • prolonged inspiratory cramp

• (a pause at full inspiration). • uncommon but localizes accurately

to a lesion in the mid- or caudal-pontine level.       

Medullary damage• Ataxic breathing • (Biot’s respirations) • completely irregular and chaotic breathing

pattern • deep and shallow breaths occur randomly. • The lesion involves the respiratory centers

in the reticular formation of the medulla that control the normal to-and-fro pattern of breathing.

Respiratory depth Shallow and regular breathing

low blood sugar; Snoring breathing accompanied by one side of facioplegia

cerebral hemorrhage; Inspiratory phase > expiratory phase (stridulous

breathing) intra tracheal foreign body and severe laryngitis;

Inspiratory phase < expiratory phase chronic obstructive pulmonary disease;

Fast, deep and regular breathing diabetic ketone poisoning, uremia, sepsis, and poisoning by

methanol, paraldehyde, vinylethyl alcohol and salicylates, often leading to respiratory alkalosis.

Breath odor Ammonia smell breath - Fruity breath - Bitter almond smell

breath - The garlic smell breath

- Liver odor - Alcoholic smell plus

vomiting -

uremia, Diabetes hydrocyanic acid

poisoning organophosphate

poisoninghepatic coma

excessive drinking

Fever Infection Absorption of necrosis, Intracranial infection, Brain hemorrhage. Fever accompanied with neck soft

cerebral malaria; Fever accompanied with neck rigidity

meningitis, encephalitis subarachnoid hemorrhage.

Hypothermia shock, hypoglycemia, poisoning and

endocrine dysfunction. Negative urine sugar accompanied

with watery stool cholera,

Positive urine sugar diabetic coma.

Heart rate Accelerated heart rate

belladonna poisoning, Fine and speed pulse

meningitis, Slow and loud pulse

cerebral hemorrhage and alcoholism, Slow and weak pulse

morphine poisoning..

Blood pressure Low blood pressure is likely seen in

myocardial infarction, pulmonary infarction, aneurysm rupture, post-traumatic entorrhagia and the late phase of severe intracranial hypertension,

High blood pressure is likely seen in hypertensive cerebral hemorrhage.

General physical checkup

General inspection: Dry and burning heat skin -thermoplegia; Moist skin -hypoglycemia, morphine poisoning,

myocardial infarction and heatstroke; Pallor -hypoglycemia and uremia; Flushing -cerebral hemorrhage, alcoholism and

belladonna poisoning; Jaundice -hepatic coma; Bleeding spots -epidemic cerebrospinal

meningitis; Roseola -typhoid fever.

Cherry red lips carbon monoxide poisoning,

Cyanosis hypoxic diseases such as heart

insufficiency and pulmonary insufficiency, Herpes

lobar pneumonia, meningococcal meningitis and viral infection which is accompanied with vivax malaria.

Panda eye signs such as bilateral periorbital blue ， nose bleeding or bloodstain, occipital or postmastoid ecchymosis,

basal skull fracture.

Chest, abdomen, spine and limbs inspection Hemorrhagic shock

pneumohemothorax and abdominal internal haemorrhage,

Fat embolism long bone fracture.

The neurologic examination   Mental Status Examination

language function If no respond to verbal questioning, use

painful stimulation (deep nailbed pressure, sternal rub, or a cotton swab inserted into the nasopharynx, etc)

GCSvoice-listening eyes open 3

answer reply, not to the point

4can locate the sting site and raise hand to the pain site 5

eyes open after prickling

2answer the

question not asked

3limbs can retract when sting 4

can not open eyes 1

only make voice, no

language 2

both upper limbs are hyperflexionwhen sting 3

can not make voice 1

all limbs are hyperextension when sting

2

body relaxation and no action when sting 1

Pupils• Pupillary size depend on the balance

between• parasympathetic nervous system

• (causing constriction via cranial nerve III)• the sympathetic nervous system

• (causing dilation via the complicated sympathetic innervation of the pupil)

Pupillary abnormalities ·Small pupils: Bilateral small and fixed pupils

pressure transmitted to the pons , A hemorrhage within the pons, for example,

Only one pupil is small and associated with ptosis (Horner’s syndrome),

Large pupils•  Bilateral large pupils:

– adrenergic stimulation – the stress of illness – in association with delirious states – drug withdrawals– epinephrine, atropine, and stimulant

drugs (cocaine and PCP)– Central herniation through the tentorial

notch results in bilateral third nerve palsies.

• Ipsilateral large pupils:– ipsilateral 3rd nerve palsy

– if a mass lesion with herniation causes the ipsilateral uncus to push the 3rd cranial nerve against the tentorium,.

– A 3rd nerve palsy that came on suddenly in association with a headache would imply a posterior communicating aneurysm

Eye movements The oculocephalic (Doll's eyes) and

oculovestibular (calorid testing) Doll's eyes phenomenon

when neck flexion, two eyelids are pulled up, two eyes open widely and two eyeballs turn to the upper side

Fundus examination Papilledema is seen in intracranial

space-occupying lesions; Retinal exudation is seen in uremia; Fundus hemorrhage is seen in

subarachnoid hemorrhage or cerebral hemorrhage, and so on.

Sensory Coma patient in light extent may

have hypoalgesia and other superficial sense drops, and will show frown or defensive reflex such as avoidance to the pain stimuli;

For the coma patients in deep extent, all senses disappear completely.

Movement Movement inspection

muscle strength muscle tone involuntary movements

Muscle strength Nervus supraorbitalis compression

can be used to observe the corners of mouth and limbs movement,

Limbs dropping test can be used to confirm paralysis.

Involuntary movements Flapping tremor

hepatic coma or pulmonary encephalopathy; Paroxysmal hyperspasmia

CO2, atropine or organic chlorine poisoning; Tonic convulsion

CO, organic phosphorus, cyanide or strychnine poisoning;

Epileptic seizure hematencephalon, craniocerebral injury;

Choreiform movements rheumatic encephalopathy.

Reflex Positive pathological reflexes

coma may caused by primary or secondary brain lesions,

Positive meningeal irritatation sign intracranial infection, subarachnoid hemorrhage, intracranial hypertension.

Motor response• Decortical posturing (flexed arms and

extended legs) • a lesion at the level of the diencephalon

or above. • Decerebrate posturing (extension of

arms and legs due to overactivation of the lateral vestibulospinal tract) • rostral brain stem lesions.

Localization diagnosis The key organ that affecting the

consciousness is brain, The important organs that affecting

the brain function are heart, lungs, liver, kidneys, pancreas, adrenal and blood system,

Cardiogenic Pulmonary Hepatic Coma and cardiac arrest occur simultaneously Arterial pulse disappears, heart sounds disappear Lips cyanosis, respiratory arrest Mydriasis and no light reflex

Chronic lung disease history with acute infection Chest tightness, cyanosis, cough, tachypnea, frothy sputum and other symptoms Concentration disperses, indifferent, bluntness, distracted and other psychological symptoms, and then transferred into drowsiness, coma Blood gas analysis shows hypoxemia and hypercapnia

Chronic liver disease history, symptoms and signs, such as liver palms, ascites, spider angioma, etc. Paroxysmal or persistent psychiatric symptoms (especially flapping tremor), then gradually transferred into coma Hepatic odor with the performance of multiple organ failure when coma happened Serious damage of liver function, the ratio of albumin and globulin upside down, blood ammonia increasesEEG shows bilateral symmetrical high amplitude θ or δ waves

Nephrogenic Pancreatic Blood system Late chronic kidney disease history with multiple organ failure Former psychiatric symptoms such as apathy, lack of concentration, delirium, etc. Miosis, light reflex and oculovestibular reflex exist Uremic symptoms, such as positive urinary protein, increased blood urea nitrogen and creatinine,etc.

Pancreatitis history, symptoms and signsDelirium and insanity happened 3-5d after incidence of disease, then transferred into coma gradually Performance of severe pancreatitis, such as elevated serum amylase, decreased serum calcium concentration, etc

Anemia and exsanguine blood disease historyFactors that can lead to lack of cerebral blood flow and nutrient substances such as severe anemiaAdvanced leukemia, systemic failure Disseminated intravascular coagulation secondary other diseases

Assistant examination Low hemoglobin concentration of blood (HCB)

anemia, hemorrhagic shock;

Increased leukocyte severe infection, cerebral hemorrhage, post-traumatic stress;

Decrease leukocyte viral encephalitis, viral meningitis, typhoid.

Positive urine glucose Positive urine glucose with positive

ketones diabetic ketoacidosis coma;

Positive urine glucose with negative ketones diabetic lactic acidosis coma, diabetic hyperosmotic nonketonic coma, cerebral hemorrhage

Urine test Positive urinary protein

uremia, eclampsia accompanied with renal damage, hypertensive encephalopathy, cerebral hemorrhage

Positive urinary bilirubin and urobilin hepatic coma, acute infection accompanied with liver

damage.

Blood sugar Increased blood sugar

stress reaction diabetic coma ,ketone bodies should be

further test in order to confirm the cause of the diabetic coma;

Low blood sugar is common in severe liver damage, insulin shock or islet cell tumor, and so on.

Elevated blood ammonia Hepatic coma (hepatic encephalopathy)

elevated blood ammonia accompanied with normal liver function, Hashimoto encephalopa should be rule

Lumbar puncture Bloody cerebrospinal fluid

all types of intracranial hemorrhage, Increased neutrophil

intracranial bacterial purulent infection, Increased lymphocytes

viral infection, High content of sugar

diabetic, lower content of sugar

intracranial infection and low blood sugar.

ECG and EEG ECG

myocardial infarction, arrhythmia and so on,

EEG Most EEG pattern of coma patients is

continuous δ wave; Epilepsy

CT or MRI

TREATMENT OF COMA

Coma: emergent care “A-B-Cs”

rule out primary cardiopulmonary cause Immediately rule out hypoglycemia,

or give 50% dextrose IV Urgent brain CT

(rule out blood or edema) if head trauma or focal neuro deficit

Correct any hypothermia Check metabolic panel, drug screens

Coma: emergent care---headache, fever, stiff neck

Urgent LP to rule out bacterial meningitis If focal signs or papilledema, get brain CT

first to verify abscess or other mass lesion Empirical IV ceftriaxone & vancomycin (&

ampicillin in older or debilitated adults)

If viral encephalitis suspected, get brain MRI, EEG, CSF PCR for Herpes simplex

"Coma Cocktail" The treatment of coma depends on the

cause, General treatment rules (if the cause is

unknown):"coma cocktail" thiamin (a vitamin that can help in alcoholic or

nutritionally starved patients), glucose (a sugar that can help diabetics who

have developed a coma due to low sugar level), naloxene (a substance that reverses the action

of many narcotics and is used to treat overdoses).

Correcting for Electrolyte Imbalance or Toxic Substances

Decreasing Intracranial Pressure hyperventilation, Diuretics surgery

Thank you