APPROACH TO

COMA
Presenter :- Dr. Wondwosen M. (R1)
Moderator:- Dr. Desalegn Y. (Assistant Professor & Consultant Neuologist)

Arsi University
Dep’t Of Internal Medicine
1st August, 2023
 OUT LINE
 Introduction
 Anatomy of Consciousness
 Coma Mimics
 Causes of Unconsciousness
 Approaches to Unconscious Patients
 Investigations
 Management
 Prognosis
 References
 Introduction
• Coma is among the most common neurologic emergencies encountered in
general medicine and requires an organized approach
• Consciousness: a state of awareness of self and Environment

Has two domains:

 Arousal ( Level of consciousness)
• sustained by deep brainstem and medial thalamic structures.
 Cognition (Content of consciousness)
• through integrity of the cerebral cortex and its subcortical structures
• A full function of consciousness (arousal) requires the stimulation of the caudal
brainstem reticular activating system (RAS) to the cerebral cortices
 Introduction

• Levels of consciousness are classified into four levels, these being alert,
drowsy, stupor, and coma
• Drowsiness simulates light sleep and is characterized by easy arousal and
the continuation of alertness for a brief period
• Stupor refers to a state of near unresponsiveness that needs strenuous or
repeated stimulus to elicit a response
• Coma is a deep sleep like state with eyes closed, from which the patient
cannot be aroused, failure in responding to external stimuli,incapability in
responding to inner needs, and incompetence of interaction with the
environment
 Anatomy of Consciousness

• Arousal requires the interplay of both: ARAS and The cerebral hemispheres

• The RAS consists of multiple neuronal

networks, including the locus
coeruleus, raphe nuclei, posterior
tuberomammillary hypothalamus, and
pedunculopontine tegmentum, linking
the brain stem to the cortex
 Coma Mimics

• There are also Several conditions that render patients unresponsive and
simulate coma :-
– Persistent vegetative state

– Minimal conscious state

– Locked in syndrome
 Persistent Vegetative State

Unresponsiveness wakefulness syndrome

 Patients have lost cognitive neurological function but retain vegetative
 Patients are awake but unaware
 They display no speech, comprehension, or purposeful movement
 Yawning, sneezing, bruxism, and occasional meaningless smiles may occur
 Display no interactive behavior and no ability to express emotion
 The pathology invariably entails massive bilateral hemispheric damage with a
spared and intact brainstem
 Minimal Conscious State

• Criteria for a diagnosis of MCS include:

 following simple commands

 responding with verbal or gestural yes/no answers

 Understandable verbalization, and purposeful behavior

• Patients recovering at better rates than those in PVS

• Intermittent, behavioral evidence of awareness of self or environment

 Locked in syndrome

 Ventral brainstem destruction sparing the RAS renders the patient mute and
quadriplegic but not comatose
 Patient is awake but speechless and motionless, with little response to stimuli
 Lesion usually involves the mid pons and results in paralysis of facial movement and
horizontal gaze
 There is preservation of vertical eye movements and the patient may be able to
blink
 Sensory pathways, hearing and vision are largely spared
 The principal cause of locked-in syndrome is brainstem stroke (86%), but it may
also occur after trauma (14%)
Table: Behaioral state confused with Coma

Abulia severe aphaty, patient neither speaks no moves Bilateral frontal medial
spontaneously
Pseudocoma Feigned coma
 Brain Death
• Brain death is a condition in which systemic circulation is preserved but complete
and irreversible loss of cerebral and brainstem function
• Common causes : cerebral anoxia, ICH, aneurysmal SAH and TBI
• The diagnosis of brain death should ideally be after
– Identified underlying Cuase
– Exclusion of Confounding Medical conditions
– Neurologic examination must demonstrate
• Coma
• No brain-generated response to external stimuli
• Absent brainstem reflexes
• An apnea test
 The Apnea Test

Prerequisites
Steps
• Disconnect the patient from the ventilator
• PaCO2 b/n 35 mmHg and 45 mmHg • Deliver O2 at 6 L/min through a catheter
• SBP ≥100mmHg with/out vasopressors advanced through the tracheal tube until
close to the carina
• Administer 100% oxygen for at least 10 • Look carefully for any respiratory mov’ts

minutes (ideal PaO2 >200 mmHg with while monitoring pulse oximetry and BP
• If no respiratory movements after ≈(8-10)’ ,
PEEP ≤ 5 cmH2O) obtain arterial blood gases
• Absence of clinical signs of • Apnea is established if PaCO2 ≥ 60 mmHg

hypovolemia (or 20 mmHg greater than baseline)

 Causes of Unconsciousness
• Brain lesions causing comatous conditions:-
 Widespread dysfunction in both cerebral cortices from ischemia, trauma or
inflammation/infection, etc
 Extrinsic agents suppressing cortical function toxins, hypoxia or internal
metabolic derangements such as hypoglycemia, azotemia, hepatic failure, or
hypercalcemia
 Any brainstem lesions that cause impairment to the RAS from either primary
upper brainstem lesions or secondary lesions from hemispheres

• Bilateral hemispheric dysfunction and impairment of RAS lead to alteration of

consciousness
The leading causes of coma
 Herniation syndromes

• Due to shifting of brain structures caused by increased intracranial pressure

• They are evidence of severe disease, and are life-threatening

• The more common and important one are central transtentorial, lateral

transtentorial (uncal), and tonsillar (foramen magnum) herniation

• Signs of herniation tend to progress generally in a rostrocaudal manner

Drug Overdose
 Causes Of Coma

• Traumatic brain injury (TBI) is the most common cause of coma in children

• Hypoxic-ischemic encephalopathy (HIE) and stroke are the most common cause

of nontraumatic coma in adults

 Approaches To Unconscious Patients

Initial assesssment
• Three requirements for rescue treatments remain a priority for the initial assessment
of unconscious patients

 Airway

 Breathing

 Circulation
– establishing IV access

– Blood should be withdrawn: estimation of glucose , other biochemical parameters , drug screening
 History
The history will often be limited, sources may be relatives, friends,or witnesses if available

• The details of the present illness should include:-

– onset of unconsciousness (sudden or gradual)

– recent complaints (headaches, depression, focal weakness, or vertigo)

– recent injuries

– underlying medical illnesses(diabetes, uremia, or heart disease)

– possible exposure to drugs (sedatives or psychotropic drugs)

• Informative history-taking is crucial for the management of unconscious patients

 Physical Examination

• Careful PE uncovers clues leading to the diagnosis of the cause of unconsciousness

• Evidence of trauma leads to suspicions of traumatic brain injury

• Signs of an acute or chronic systemic illness may be related to metabolic coma

• Evidence of needle marks or alcoholic breath, points to drug intoxication

• Examinations for nuchal rigidity should not be performed unless neck damage has

been excluded
 Physical Examination

Vital Signs
• Blood Pressure
– High: hypertensive encephalopathy, elevated ICP, or a massive intracranial hemorrhage

– Low: Addisonian crisis, alcohol, barbiturate, MI, sepsis

• Pulse
– Bradycardia: brain tumors, opiates, ICT, myxedema

– Tachycardia: sepsis, hyperthyroidism, uremia

 Physical Examination

• Respiratory rate

– Tachypnea in acidosis or pneumonia

– Aberrant respiratory patterns in brainstem disorders

• Temperature

– Fever in sepsis, meningitis, encephalitis, heat stroke, anticholinergic drug intoxication

– Hypothermia in alcohol, barbiturate, sedative intoxication; hypoglycemia, peripheral

circulatory failure
 Physical Examination

• Skin

– Injuries, Bruises: traumatic causes

– Dry Skin: DKA, Atropine

– Moist skin: Hypoglycemic coma

– Cherry-red: CO poisoning

– Needle marks: drug addiction

– Rashes: meningitis, endocarditis

 Physical Examination

• Odour Of Breath

– Acetone: DKA

– Fetor Hepaticus: in hepatic coma

– Urineferous odour: in uremic coma

– Alcohol odour: in alcohol intoxication

 Neurological examination

• The initial goal of the neurological examination is to determine whether it is from a

structural cause or a metabolic abnormality, or possibly from both

• Two findings that strongly indicate a structural lesion include

 persistent asymmetrical signs between right and left sides and

 Abnormal reflexes that indicate specific areas with in the brainstem

 Level of arousal

• The Glasgow Coma Scale (GCS)

– The GCS is generally helpful in evaluating consciousness levels in patients with
altering degrees of consciousness

• The FOUR (Full Outline of Unresponsiveness) score

– Has four components (eye, motor, brainstem, and respiration)

– Each component has a maximal score of four

– It may address some shortcomings of the GCS, especially in ventilated patients

– It can detect locked-in syndrome and is superior to the GCS due to the evaluation of brainstem

reflexes, breathing patterns, and the ability to recognize different stages of herniation
Four Score
 Brainstem Reflexes

• The brainstem reflexes that are examined are:-

– Pupillary reflex

– Ocular movements

– Corneal reflex

– Respiratory pattern

• As a rule, coma due to bilateral hemispheral disease preserves these brainstem activities
 Pupillary Reflex

• Pupillary examination is beneficial to determine the localization of the lesions

• The pupils become small symmetrical & intact light reflex in Metabolic Uncsc

• Unilateral fixed dilated pupil suggests an ipsilateral oculomotor nerve compression

• Mid-position and non-reacting pupils suggest a Midbrain lesion

• Pinpoint pupils with poor reaction to light suggest a pontine tegmental lesion

• Opiates intoxication leads to pinpoint pupils

• Atropine intoxication leads to widely dilated and fixed pupils

Pupillary Reflex in comatous patient
 Ocular Motility

 The position of the eyes at rest

 Presence of spontaneous eye movement

 The reflex responses to oculocephalic and oculovestibular maneuvers

 The eyes look toward a hemispheral lesion and away from a brainstem lesion
 Oculocephalic Reflexes (Doll's eye movement)

• The intact reaction of oculocephalic reflexes (Doll’s eye movement) consists of the

deviation of both ocular globes towards the opposite direction of cephalic turning

• Once an unconscious patient does not express these symptoms, then a lesion must be

located at either the afferent or efferent arm of the reflex loop

• If the connective pathways b/n the afferent and efferent arms in the pons & medulla

become interrupted in unconscious patients, the doll’s eyes reflex will also be absent
 Oculovestibular Reflex

• Irrigating ear with cold water/saline introduces ipsilateral deviation of both eyes

with contralateral fast phase nystagmus lasting for one to two minutes

• The absence of any or abnormal responses indicates brainstem dysfunction

• Metabolic diseases & Structural diseases of the brainstem often give rise to

abnormal responses

• The presence of oculo-cephalic and vestibulo-ocular reflexes in unconscious

patients implies an intact connection between the pons and the midbrain
Oculovestibular reflex
 Corneal reflex

• The corneal reflex indicates the degree of intactness of the pathway from the
ophthalmic branch of 5th CN through the pons to the 7th & facial muscles
• Gently touching the cornea with a thin wisp of sterile cotton will lead to
– involuntary closure of the ipsilateral eye
– closing of the contralateral eye (consensual response)
• Bilateral loss of the corneal reflex with light unconsciousness indicates the influence
of drugs or local anesthetics in both eyes
• The unilateral loss of the corneal reflex indicates a focal neurological disease
• The existence of the corneal reflex in unconscious patients indicates that the lesion is
likely located outside the pons
 Respiratory patterns

• Hyperventilation indicates midbrain or upper pons lesions and commonly occurs

in Metabolic disorders

• Hypoventilation indicates a Medullary or Upper cervical spinal lesion

• Normal respiration depends on:

 A brainstem mechanism, located between the midpons and cervical medullary

junction, that regulates metabolic needs; and

 Forebrain influences that subserve behavioral needs such as speech production

 The Motor System

• Resting posture

 Head and eye deviation to one side, with contralateral hemiparesis, suggests a

supratentorial lesion where as Ipsilateral paralysis indicates a brainstem lesion

 External rotation of the lower limb is a sign of hemiplegia or hip fracture

 The motor system

• Motor response for painful stimuli should be assessed carefully

– Particular attention should be directed towarad assymertry of tone and movement

• Asymmetric responses indicate structural lesions, either in the cerebral hemisphere

or brainstem

• Symmetric responses indicate more diffuse lesions (metabolic encephalopathy)

• Asymmetric motor response in unconscious patients indicates a focal lesion

 The motor system

 Adventitious movements
• Helps to differentiate metabolic from structural
 Myoclonic jerk
 Rhythmic myoclonus
 Cerebellar fits
 More subtle twitches, random or sustained
• Sensory examination
 Look for asymmetry for painful stimuli
• Meningeal sign
 Sign of lateralization

• Unequal pupils
• Deviation of the eye to one side
• Facial asymmetry
• Turning of the head to one side
• Unilateral hypotonic/hypertonia
• Asymmetric deep tendon reflex
• Unilateral extensor plantar response
• Unilateral focal or jacksonian fits
 Posturing

Decorticate rigidity
 Flexion of the elbows and wrists and
supination of the arm
 Bilateral damage rostral to midbrain

Decerebrate rigidity
 Extension of the elbows and wrists
with pronation
 Damage to motor tracts in the
midbrain or caudal diencephalon
 Investigation

• Laboratory studies remain primary for patients with potential diffuse lesions
– cerebrospinal fluids (CSF)
– serum glucose
– complete blood count (CBC)
– calcium, sodium, potassium, magnesium
– arterial blood gases and pH,
– liver and renal functions
– drug levels, and blood for metabolic panels and
– blood culture
 Investigation

• In the case of potential focal lesions, Neuroimagings are the recommended

investigations include :-
– skull radiographs
– computer tomography (CT)/magnetic resonance imaging (MRI) of the brain
– ventriculography
– electroecephalography (EEG)
– electrocardiography (ECG)
– cardiac monitoring and
– carotid/vertebral angiography
 Management

General Mgm’t
• The ABCDE (A for airway, B for breathing, C for circulation, D for disability, and E
for exposure) approach to resuscitation must be applied
• The establishment of a clean airway includes
– maintaining an initial lateral position
– suction to remove secretions
– endotracheal intubation
– mechanical ventilation if patients cannot protect against aspiration, hypoxia, or
hypoventilation
 Management

• Adequate respiration needs to be ensured throughout the course of management.

• Pulmonary embolism is a preventable cause of death in unconscious patients

• Feeding should not be delayed in unconscious patients

• The patients’ bowels, bladder, hygiene & skin care should not be ignored
 Monitoring and Management of ICP

• The treatment for ICP depends on the cause

• Regardless of the cause, ICP is a medical emergency, and treatment should be
undertaken as expeditiously as possible.
• If a diagnosis of elevated ICP is suspected and an immediately treatable proximate
cause is not present, then ICP monitoring should be instituted
• The goal of ICP monitoring and treatment should be to keep ICP < 20 mmHg
• Interventions should be utilized only when ICP is elevated above 20 mmHg for >5
to 10 minutes
 Monitoring and Management of ICP

ICP Monitors

• We Consider ICP Monitoring

When
• GCS < 8
• Significant IVH or Hydrocphalus
• Clinical evidene of Herniation
 Monitoring and Management of ICP

General Care
 Monitoring and Management of ICP

• First-line therapies
Emergency
Neurological Life Support • Noninvasive maneuvers-
(ENLS) repositioning, ventilator changes,
ICP treatment algorithm
sedation, analgesia

• Second-line therapies
• Osmotic agents
• Hyperventilation
• CSF diversion

• Third-line therapies
• Metabolic suppression with
anesthetic agents
• Induced hypothermia
• Surgical decompression
 Prognosis

• Targeted temperature management is an essential, acute treatment that may

improve outcomes in conscious-impairment patients after cardiac arrest

• In general, for patients who remain comatose for more than four weeks, the chance

of meaningful recovery is low

• A coma patient may still progress toward unresponsive wakefulness syndrome,

minimally conscious state or functional recovery

 Prognosis

• In general, coma carries a serious prognosis

• This is dependent to a large extent on the underlying cause
• Coma due to depressant drugs carries an excellent prognosis provided that
resuscitative and supportive measures are available and no anoxia has been sustained
• Metabolic causes, apart from anoxia, carry a better prognosis than structural lesions
and head injury
• Length of coma and increasing age are of poor prognostic significance
• Brainstem reflexes early in the coma are an important predictor of outcome
 References

• Harrison’s principles of Internal Medicine 21st edition

• Dejong’s The Neurologic Examination; 8th ed,
• Bradley and Daroff neurology in clinical practice 8th ed.
• Uptodate online
• Plum and Posner’s Diagnosis and Treatment of Stupor and Coma. 5th ed
• Winchana Srivilaithon, Sombat Muengtaweepongsa. Clinical approach to coma
patients: tips and tricks. Signa Vitae. 2022; 18(2): 8-18. doi:10.22514/sv.2021.230
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