Acute treatment Strategies of Comatose

Patients and Stages of Coma

Acute treatment Strategies of Comatose

Patients and Stages of Coma

Manisha UttamM.P.T (Neurology)

Consciousness

Consciousness is the state of full awareness of the self and one’s relationship to the environment.

Normal Brain Anatomy

Cerebral Cortex

Brain Stem

Reticular Activating System

Anatomy of Consciousness

Ascending reticular activating system (RAS)is a system of fibers which arises from the reticular formation of the brainstem and projects to the thalamus.

Neurons in the reticular formation receive collaterals from the ascending spinothalamic pathwaysand then projects diffusely to the entire cerebral cortex .

Thus sensory stimuli are involved not only with sensory perception but also play role in the maintenance of consciousness through their connections with the RAS.

Stimulation of RAS produces arousal and destruction of RAS produces coma. Hypothalamus is also important for consciousness, stimulation of posterior hypothalamic region cause arousal.

The degree of alteration in consciousness is roughly proportional to the volume of brain tissue involved in the process.

Consciousness is divided in to two main components Arousal Awareness The physiology of arousal is dependent on the reticular activating system (RAS). The RAS is a poorlylocalized network of cells in the brainstem with projections to the thalamus, hypothalamus and cortex.

Awareness is mediated by the cerebral cortex in widely distributed neuronal networks. Awareness is the product of cortical function that resides within both hemispheres and then projects down to the thalamus and then out, for either motor or sensory functions.

Terms used to describe altered states of consciousness :

Clouding of Consciousness: Mild form of altered mental status. Patient has reduced wakefulness or awareness.Include hyperexcitibility or irritability alternating with drowsiness.

Confusional State:More profound deficit including disorientation and difficulty in following commands due to focal deficit of cognitive function.

Obtundation:Patient has a lessened interest in the environment, slowed responses to stimulation, and tends to sleep more than normal with drowsiness in between sleep states .

Stupor:Only vigorous and repeated stimuli will arouse the individual, and when left undisturbed, the patient will immediately lapse back to the unresponsive state .

Coma:State of unresponsiveness , patient cannot be aroused by stimuli even with vigorous stimulation.

Locked in Syndrome:Ventral brainstem destruction sparing the RAS. Patient is mute and quadriplegic but not comatose, with variable preservation of consciousness. Patient is awake but speechless & motionless with little response to stimuli and Sustained eye opening along with aphonia or hypophonia.

Persistant Vegetative state:Vegetative describes an organic body capable of growth and development but devoid of sensation and thought. Patient have massive bilateral hemisphere damage with intact brainstem. In PVS, patient is awake but unaware of environment.

Minimally Conscious state:Patients shows limited but clear evidence of awareness of themselves or their environment by atleast following simple commands, gestural or verbal yes/no response. Further improvement is more likely than patients in a vegetative state.

Akinetic Mutism: Sub category of minimally conscious state in which patient neither tend to move nor speak, lack motor functions such as speech, facial expression, gestures but demonstrate alertness. They can move their eyes in response to auditory stimulus or move after repeated commands.

Causes of COMA

Structural Non- Structural(Focal) (Diffuse or

metabolic)

Sites and Causes of Coma

Diffuse hemisphere , eg; Trauma, ischaemia, infection

Bilateral thalamiceg: haemorrhagic infarction

Brainstem compressioneg ; supra or infra tentorial lesion

Brainstemeg; ischaemia, haemorrhage

Two major classes of Structural brain injuries cause Coma

Compressive lesions Destructive lesions Indirectly by compressing the directly by destructing or RAS from outside, this process injury to the RAS is due to herniation, whereby a itself. Eg ; brainstem mass lesion or swelling causes stroke or haemorrhage. displacement of cerebral structures ultimately compressing the midbrain and brainstem

Sites and Representative causes of Structural lesions that can cause ComaCompressive Destructive Supratentorial Mass Lesions Ischaemia hematomas Subarachoid haemorrhageStrokes Meningitistumor other mass lesionsabscess  Infratentorial Mass Lesionsbrainstem strokebrainstem hemorrhagebrainstem tumorbrainstem abscess

Non Structural (Diffuse, Metabolic or Multifocal causes of Coma)

A. Deprivation of oxygen, substrate or metabolic cofactors

1. Hypoxia2. Ischaemia3. Hypoglycemia4. Cofactor deficiency (thiamine, niacin, pyridoxine)

B. Toxicity of Endogenous products5. Due to organ failure (hepatic coma, uremic coma)6. Due to hyper or hypofunction of endocrine organs

C. Toxicity of Exogenous poisoning1. Sedative drugs2. Acid poisons/ poisons with acid breakdown3. Psychotropic drugs

D. Abnormalities of ionic or acid base environment of CNS

E. Endocrine disturbances

F. Infections or inflammation of CNS

Mnemonic for Causes of Coma:"SPITE ME NOT”

S – Space occupying lesion M - Metabolic P – Psychiatric E - Epileptic I - infectious/inflammatory T - trauma E - Endocrine

N - Neoplastic O - oxygen T - toxic

Assessment and Examination of Comatose

Examination must be thorough , but brief.

Begin by informally assessing the patient level of consciousness. Examiner addresses the patient verbally If, no response

Examiner speak more loudly & shake the patient If, no response

Formal coma evaluation should begin

Coma Evaluation Scales

Glasgow Coma ScaleGraham and Bryan, Neurosurgery professors developed this scale in 1974 at the University of Glasgow.

15 point scale - Initially used to assess the level of consciousness.

GCS is used to test best motor response (6), best verbal response (5) and best eye response (4).

Score ranges from 3 (deep coma or death) to 15 (fully awake).

According to Glasgow Coma Scale(GCS) (HICKEY 2003)

MILD Head injury or

Admitted to Non ICU observation unit

GCS 13-15

MODERATE Coma

Moderate Head injury

GCS 9-12

SEVERE

HI

GCS less than 9 Deep Coma

Motor Response (total score = 6)

Score 6 – Obeys commands:

o Highest level of motor response

o Accurate response to instruction (twice)

eg: raise eyebrows, stick out tongue.

Score 5 - Localising pain:

o Response to pain stimulus – movement of limb as to

attempt to remove the stimulus. 1. Sternal rub 2.Supra orbital pressure 3. Trapezius squeeze

4. Nail bed pressure

Score 4 - Withdrawal from Pain: o Normal flexion in response to central pain

stimuli, but failing to locate source of pain. o Pulls limb away from painful stimulus.

Score 3 - Flexion to Pain:

o Decorticate posturing: due to a block in motor pathway between cerebral cortex and brain stem

o Slower responseo Flexing upper arm & rotating of wrist & thumb

through fingers and extension of lower limb

Score 2 - Extension to Pain:

o Decerebrate posturing: occurs due to blockage/damage within brainstem.

o Straightening of elbow & internal rotation of shoulder and wrist; leg extension

Score 1- No Motor Response:

oBrain incapable of processing any sensory input & motor activityoRigid to all pain stimuli

Verbal Response (total score = 5)

Score 5 – Oriented

oAwareness of the self and the environment.( Who, Where, When, Why )

Score 4 – Disoriented

oResponses to questions with presence of confusion and disorientation.

Score 3 – Inappropriate words

oSpeech in a random way.

oNo conversational exchange

Score 2- Incomprehensible sounds

oMoaning and Groaning

Score 1- No verbal response

oNo response to any deep or vigorous stimuli

Eye Response (total score = 4)

Score 4 – Spontaneous

oIndicates activity of brainstem arousal mechanisms, but not necessary patient is attentive.

Score 3 – To Speech

Tested by any verbal approach (spoken or shouted), Not necessary the command to open the eyes.

Score 2 – To pain

Tested by a stimulus in the limbs.o (supra- ortibal pressure may cause grimacing)

Score 1 – No Eye response

oNo response to speech or pain

Rapid Assessment Scales for Coma - 2 Scales

AVPU ACDU

Is the patient Is the patientAlert and oriented? Alert and oriented? Responding to voice? Confused? Responding to pain? Drowsy? Unresponsive? Unresponsive?

Grady Coma Scale

Grade State of awareness I Confused, drowsy, lethargic, un co-operative. Does not lapse in to sleep when left undisturbed II Stuporous, un co-operative, disoriented to time, place, person, lapse in to sleep if not disturbed. III Deep Stupor, Requires strong pain to evoke movement. IV Exhibits decorticate or decerebrate posturing to deep pain stimulation. V Does not respond to any stimuli.

Rancho los Amigos Scale (RLA)

It is used as the patient improves or stabilise.There are 8 levels in this scale

Level I - No response to any stimuli - indicates coma

Level II - Generalized response, i.e. patient reacts inconsistently and nonpurposefully to stimuli, Responses are limited such gross body movement - indicates coma

Level III - Localized response, i.e. patient reacts specifically but inconsistently to stimuli, such as turning head toward a sound and following simple commands in an inconsistent, delayed manner - not considered coma, but stimulation techniques appropriate through Levels III.

Level IV - Confused-Agitated, i.e. patient is in a state of severely decreased ability to process information. Does not discriminate among persons or objects. Behavior is often bizarre and un co operative.

Level V - Confused-Inappropriate, Non-Agitated, i.e. patient appears alert and is able to respond to simple commands fairly consistently, but responds to more complex commands in a non-purposeful manner

Level VI - Confused-Appropriate, i.e. the patient shows goal-directed behavior, but is dependent on external input for direction. Responses may be incorrect due to memory problems, but they are appropriate to the situation.

Level VII - Automatic-Appropriate, i.e. the patient appears oriented, goes through daily routines automatically, patient shows minimal to no confusion and shallow recall of activities, and requires at least minimal supervision for learning and safety purposes. Judgment and other higher level cognitive abilities remain compromised.

Level VIII - Purposeful and Appropriate, i.e. the patient is alert and oriented able to recall and integrate past and recent events, is aware of and responsive to the environment, and needs no supervision once learning has occurred.

The FOUR ( Full outline of unresponsiveness) SCALE

New Coma Scale is devised in 2005, due to the shortcomings of GCS such as:

oFailure to assess verbal score in intubated patients.oInability to test brainstem reflexes.

Four componentso(Eye, Motor, Brainstem, Respiration)

Each component has maximum of score of Four.

Wijdicks E, Bamlet WR et al. Validation of New Coma Scale: The Four Scale. Ann Neurol 2005; 58: 585 – 593.

Eye response ( Score – 4)

4 - eyelids open , tracking, or blinking to command3 - eyelids open but not tracking2 - eyelids closed but open to loud voice 1 - eyelids closed but open to pain 0 - eyelids remain closed with pain

Motor response (Score – 4)

4 - thumbs-up, fist, or peace sign 3 - localizing to pain 2 - flexion response to pain 1 - extension response to pain 0 - no response to pain

Brainstem reflexes ( Score – 4)

4 - pupil and corneal reflexes present 3 - one pupil wide and fixed 2 - pupil or corneal reflexes absent 1 - pupil and corneal reflexes both absent 0 - absent pupil, corneal, and cough reflex

Respiration (Score – 4)

4 - not intubated, regular breathing pattern3 - not intubated, Cheyne–Stokes breathing pattern2 - not intubated, irregular breathing1 - breathes above ventilator rate0 - breathes at ventilator rate or apnea

Glasgow Outcome Scale

Examination

History(from relatives, friends, emergency medical personnel)

Onset (abrupt, gradual)

Recent complaints (headache, depression, focal weakness)

Previous medical illness (diabetes, renal failure, heart disease), History of headache of recent onset suggests compressive lesion, depression or psychiatric disease suggests drug intoxication.

General Physical Examination

Vital signs Elevated temperature infection/serious intracranial disease Elevated blood pressure hypertensive encephalopathy/ subarachnoid hemorrhage

ABC (Airway, Breathing, Circulation)

Evidence of trauma (search for signs of head trauma such as bruises, lacerations, fractures & other signs of injury)

Examine the neck, if possibility of trauma, neck should be immobilised.Resistance to Neck flexion suggests meningeal irritation.

Evidence of drug ingestion (needle marks, alcohol on breath)

Neurological Examination

Brainstem reflexes

Respiratory patterns

Motor Response

Sensory status

Deep tendon reflexes

Brain Stem Reflexes

Pupillary Response

Constriction of both pupils

Constriction of pupil only on the ipsilateral eye

Constriction of pupil of opposite eye

Changes in Pupils with lesions at different levels of brain that can cause Coma

Occulo- cephalic response or Doll’s eye maneuver

Turning the head in one direction causes the eye to turn in opposite direction. This response indicates that brainstem is intact & pathways connecting the vestibular nuclei (medulla) to extraocular nuclei (pons and midrain) are functioning. No response or asymmetry indicates brainstem dysfunction.

Cold Caloric testing

If doll’s eye movements are absent proceed to caloric. Ice cold water applied to the tympanic membrane normally elicits a slow conjugate deviation to the irrigated side. Absence indicates brain stem diysfunction. Caloric testing is more sensitive than the oculocephalic response. Check the tympanic membrane is intact before testing.

Examination of Eye movementsHold the eyelids gently in an open position to observe eye position and movements in a comatose patient.

Small flashlight held about 50 cm from the face and shined toward the eyes of the patient & should reflect of the same point in the cornea of each eye if the gaze is conjugate.

Patients with impaired consciousness demonstrate a slight exophoria.

Observe for a few moments for spontaneous eye movements.

Slowly roving eye movements are typical of metabolic encephalopathy.If conjugate, it imply an intact ocular motor system.

Corneal reflex testing

Test is performed by lightly touching the cornea with a cotton swab. The normal response is that the patient should blink both eyes. Testing must be performed bilaterally to evaluate both afferent components of the fifth cranial nerve.

Abnormal Respiratory patterns in coma

Midbrain

Pons

Medulla

ARAS

Cheynes - Stokes

Ataxic

Apneustic

Central Neurogenic

Cheyne – Stokes Respiration

Periods of hyperpnea alternate with periods of hypopnea. Respirations increase in depth and volume up to a peak, then decline until a period of apnea, after which cycle repeats.

Cheyne stokes respiration may be due to bilateral hemisphere lesions, and increased intracranial pressure.

Ataxic breathing

Pattern of breathing is irregular, with erratic shallow and deep respiratory movements. Ataxic breathing occurs with dysfunction of the medullary respiratory centers.

Central Neurogenic hyperventilation

Central neurogenic hyperventilation refers to sustained, rapid, and regular hyperpnea. It is primarily associated with disease affecting the reticular formation in the low midbrain and upper pons, but it may also occur with lesions in other brainstem locations.

Apneustic breathing

Prolonged inspiratory phase, and occurs in pontine lesions justrostral to the trigeminal motor nuclei, or cervicomedullary compression.

Motor Responses

Motor examination in disorders of consciousness requires skilled observation and difficult to recognise the presence of hemiplegia in comatose patient.

If both arms are lifted, affected extremity falls more rapidly and in flail like manner, while normal arm drops slowly and same for lower extremity.

If lower extremities are passively flexed with heels resting on the bed and then released, paretic limb rapidly falls to an extended position with hip in external rotation, while affected extremity gradually returns to its original position.

Other Abnormal Motor Responses

Metabolic Encephalopathy

Patients with forebrain or diencephalic lesions often have a hemiparesis but can generally make purposeful movements with the opposite side.

Upper Midbrain damage

Lesions involving the junction of the diencephalon and the midbrain may show decorticate posturing, including flexion of the upper extremities and extension of the lower extremities.

Upper Pontine damageLesions involving upper pontine may progress to decerebrate posturing, including extension of both upper and lower extremities.

Sensory Examination

Depending on the level of coma, the patient may not perceive even the most painful stimulus, or may respond to painful stimuli by wincing or withdrawing the part of the body stimulated.

Examination must be comparing responses to painful stimulation on the two sides of the body.

Reflex Examination

Extensor plantar response may occur with either structural or metabolic coma.

Frontal release signs (forced grasping, palmomental responses etc) and paratonic rigidity may be present with altered mental status of either structural or metabolic origin.

Stages of Coma

Grade I - Individuals who respond with recognition when their name is called and do not lapse into sleep when left undisturbed.

Grade II - If the alteration in level of consciousnessis more severe, so that the person lapses into sleepwhen undisturbed and is arouse only when a pin istapped gently over the chest wall.

Grade III - Patient who winces in response to deep pain stimulus. Deep pain stimulus may result in abnormal postural reflexes either unilateral or bilateral.

Grade IV – Deep pain stimulus may result in decorticate and decerebrate posturing.

Grade V - The patient who maintains a stateof flaccid unresponsiveness despite deep pain stimulation.

Differential diagnosisConsciousness level

Diagnostic Criteria

Brain deathNo arousal/eye-openingNo behavioral signs of awarenessApneaLoss of brain functions (brainstem reflexes)

Coma

No arousal/eye-openingNo behavioral signs of awarenessImpaired spontaneous breathingImpaired brainstem reflexes

Vegetative State

Arousal/stpontaneous or stimulus-induced eye openingNo behavioral signs of awarenessPreserved spontaneous breathingPreserved brainstem reflexes> 1 month: persistent vegetativegrimaces to pain, localization to soundsvisual fixation, response to threat, inappropriate single words

Consciousness level

Diagnostic Criteria

Minimally Conscious state

Arousal/spontaneous eye-openingFluctuating behavioral signs of awarenessResponse to verbal orderObject localization and manipulationSustained visual fixation Intentional but unreliable communication

Locked in Syndrome

Arousal/spontaneous eye-openingPreserved cognitive functionsCommunication with eye gazeAnarthriaTetraplegia

Acute treatment Strategies

Initial Management of Coma

Even before detailed history & examination, it is important to direct towards emergency measures such as correction of possible deficiencies in glucose, oxygenation and blood pressure.

After determination of vital signs, attention should be towards ensuring an adequate airway, oxygenation and intravenous access.

Immediately after obtaining blood samples, 50 cc of 50% glucose followed by 100 mg of thiamine should be given.

Naloxone and flumazenil are often given in case there has been an opiate or benzodiazepine overdose.

A “Coma cocktail” consisting of dextrose, flumazenil, naloxone and thiamine is sometimes used in the management of the comatose patient.

Preparation of intubation, respiratory support, and use of pressor agents should become necessary.

Always assume a cervical spine injury may be present, and immobilise the neck until a fracture can be ruled out.

Patients in Coma experience sensory deprivation because their ability to respond to internal and external stimuli is altered.

Threshold of activation of Reticular activating system may increase in coma patients.

Practical implication of Sensory deprivation is that controlled stimulation (sufficient frequency, intensity, duration) should be given to meet the higher threshold of reticular neurons and increase cortical activity.

Undamaged axons send out collateral connections that is called collateral spouting which assist in re organizing the brain’s activity.

On the basis of an Animal model, sensory stimulation of sufficient, intensity and duration was given to arouse the brain and improve neuronal organization, increased dendritic branching which in turn stimulate the RAS and increase the level of cognitive function.

Maximum recovery can occur within first few weeks. Delayed intervention may predispose to various complications such as pressure ulcers, muscle wasting.

So, Early Intervention to enhance consciousness recovery is mandatory to minimize these complications

It is hypothesized that frequent sensory stimulation could facilitate dendritic growth, neuronal reorganization, and synaptic re innervation and improve the rate of recovery from coma.

Coma Stimulation / Arousal Therapy

GoalsMay stimulate the RAS and increase arousal and attention to the level necessary to perceive incoming stimuli.

Prevent sensory deprivation, which has been shown to retard recovery and the development of central nervous function and further depress impaired brain functioning.

Allows for frequent monitoring of patient's responsiveness.

May improve the quantity and quality of responses toward purposeful activity.

Principles of Coma Stimulation

Before starting any stimulation, check resting vital signs (heart rate, blood pressure, and respiratory rate).

Avoid or minimize stimulation programs with comatose patients that have a ventriculostomy when increased intracranial pressure (ICP) and/or cerebral perfusion pressure (CPP) are still issues.

The environment should be simple and undisturbed, with a limited number of people around the patient, and with the TV off and the door closed during treatment.

Allow extra time for the patient to respond (because of slow information processing). 1 or 2 minutes between the administration of different stimuli is useful as an initial guide until the length of response delay is established.

Keep sessions relatively brief - patients can usually tolerate up to 15-30 minutes.

Conduct sessions frequently, allowing patients to respond several times daily.

Select meaningful stimuli, such as voice of family and friends, favorite music etc. Stimuli that have emotional significance to the patient are usually more likely to elicit responses.

Avoid overstimulation, indicated by perspiration, agitation, eye closing, sudden decrease in arousal level, increase in muscle tone, and prolonged increase in respiration rate, by alternating periods of stimulation with periods of rest.

Techniques of Coma Arousal TherapyKinesthetic stimulation Each movement was done 2 times, allowing 1 min to respond.

Lying on bed A. Movement of arms – patient's arm was supported at the elbow and hand. And then arm was slowly moved above the head as far as it go. Then it was held for 3 sec then arm was lowered, keeping the elbow as straight as possible.

B. Movement of legs – Patient's leg was supported at the knee and ankle, and was slowly bent toward the chest as far as possible, held for 3 sec and then lowered down, attempting to straighten the knee.

C. Movement of head – Head was turned side to side, stretching as far as it could go.

D. Patient's knees were flexed, placing the feet flat on the bed and then laterally rotated keeping the knees together, held for 3 sec in each position.

 Tactile stimulation 

Stimulus was presented for 5 sec, twice, with a 3 sec break between each stimulus. It was repeated to right and then, left upper extremities; then right and left lower extremities. Materials used were brush, various cloth textures, sandpapers, cotton ball.

Auditory stimulation 

Different stimuli were used in sequence. Each stimulus was presented for 5–10 sec, twice, with a 3 sec break, on right side and then on left side. Materials used are ring bell, familiar voices, and religious chants using ear pieces of ipod.

 Visual stimulation 

Stimulus was presented for 5 sec, twice, with a 3 sec break between each stimulus in front outer, inner upper and lower quadrant/field of vision. Materials used are, brightly colored block, familiar photo, functional object.