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Nikhilesh Jain
Director and Chief Intensivist
Dept. Of Critical Care Medicine
CHL Hospitals, Indore
Today's goals

To develop an understanding of a comatose

patient assessment on a first contact basis
Understand the finer nuances of managing
Looking for differentials in a comatose patient
Initial management of the above subsets
Neural basis

State of awareness of self and surrounding and

cannot be readily defined in terms of anything
The use of terms other than coma and stupor to
indicate the degree of impairment of
consciousness is beset with difficulties and more
important is the use of coma scales (Glasgow
Coma Scale and FOUR score)
Coma is characterized by total absence of arousal
and awareness lasting for at least one hour
Definitions of levels of arousal

Alert (Conscious) - Appearance of wakefulness,

awareness of the self and environment
Lethargy - mild reduction in alertness
Obtundation - moderate reduction in alertness.
Increased response time to stimuli.
Stupor - Deep sleep, patient can be aroused only by
vigorous and repetitive stimulation. Returns to deep
sleep when not continually stimulated.
Coma (Unconscious) - Sleep like appearance and
behaviorally unresponsive to all external stimuli (Un
arousable unresponsiveness, eyes closed)
Disorders of consciousness
Clinical pearls

General examination:
On arrival to ER immediate attention to:
1. Airway
2. Circulation
3. establishing IV access
4. Blood should be withdrawn: estimation of glucose
# other biochemical parameters # drug
Subsequent Assessment

Attention is directed towards

- Assessment of pt.
- Severity of coma
- Diagnostic evaluation
All possible info
- Relatives, paramedics and people who have
witnessed the episode esp. regarding mode of
Prior medical history- DM/Drug history/Epilepsy
Examination- remote trauma, needle marks, log
Points of interest

In case of TBI neck stabilization takes

GCS for initial management especially in TBI
Brainstem and motor function
Clues in general examination

- Bradycardia Brain tumours, myxoedema, opiates
- Tachycardia- Hyperthyroidism, Uremia
- High- Hypertensive encephalopathy
- Low- Addisonian crisis, Alcohol, Barbiturate
- Low- Hypopituitarism, hypothyroidism, CPZ,
environmental exposure, elderly, cold water
- High- Infection, Metabolic, vascular,
Some more clues

Skin- Injuries, bruises, dry, moist, cherry red ,

needle marks and rash
Pupils- Size, equality and reaction to light
- Most metabolic encephalopathies give small pupil
with preserved light reflex
- Structural lesions are more commonly associated
with pupillary asymmetry and loss of light reflex
Mucosal examination

Petechiae &ecchymosis TTP,ITP,DIC,meningococcemia,

Hypermelanosis Addisons, chemotherapy,
porphyria, melanoma
Cherry red skin CO poisoning
Gray blue cyanosis Methemoglobinemia

Telangiectasia Chronic alcoholism, vascular

Ecthyma gangrenosum Pseudomonas sepsis
Anemia, sepsis ,leukemia,
Splinter hemorrhages' endocarditis
Pigmented macules
Tuberous sclerosis , neuro-
Daily assessments
Pupils Binstem reflexes
4-pupil & corneal reflex present
3-open pupil wide & fixed Eye response
2-pupil/corneal reflexes absent 4-eyelid open or opened, tracking or
1-pupil & corneal reflex absent blinking to command
0-absent pupil, corneal & cough 3-eyelids open, not tracking
reflexes 2-eyelids closed, open to loud voice, not
1-eyelids closed, open to pain, not
Respiration tracking.
4-not intubated, regular breathing 0-eyelids remain closed with pain
pattern Motor response
3-not intubated, cheyne-stokes 4-thumbs up, fist, or peace sign to
breathing pattern command
2-not intubated, irregular 3-localizing to pain
breathing pattern 2-flexion response to pain
1-breathes above ventilator rate 1-extensor posturing
0-breathes at ventilator rate 0-no response to pain or generalized
How to interpret Pupils
Herniation signs
What about breathing patterns?
Abnormal breathing patterns in coma

Cheynes - Stokes

Central Neurogenic



What about motor system?
Asymmetry of tone/movt
Asymmetry of plantar
Tendon reflexes are not
so important
Motor response to DPS
(supraorbital/nail bed)
Flexion of upper limb with
extension of lower limb
(decorticate response)
Extension of upper and
lower limb (decerebrate
Signs of lateralization

Unequal pupils
Deviation of eyes/turning of head to one side
Facial /deep reflexes asymmetry
Unilateral Hyper/hypotonia ,extensor
plantars/focal or jacksonian fits
Epidemiology in a non neurological

Metabolic encephalopathy-28.6%
Hypoxic ischemic encephalopathy-23.5%
Sepsis is major cause of neurological
A major break up

Acute stroke- 1-4%

Post reversible leucoencephalopathy
Associations of hypertensive crisis/
Seizures -0.8-4%
Dys electrolytemias and pH disturbances
Renal/hepatic dysfunction
Hypoxic ischemic encephalopathy
Sepsis (70% in a medical ICU)
Epidemiology in a surgical ICU

Cholesterol embolization
Fat embolus
Multifocal ischemic stroke
Transplants-organ related/procedure
related/therapy related
Supratentorial v/s infratentorial

Starts with focal Affect RAS in pontine

cerebral dysfunction region
Rostral to caudal Involvement of brain
progression stem nuclei/tract with
Signs usually localise a focal findings
single area Sudden onset of coma
(Diencephalon / mid Brainstem signs
brain/brain stem precede/accompany
Asymmetrical motor onset of coma
signs Cranial nerve palsies
are usual
Bizarre resp patterns
at onset

Cerebral hemisphere
Decorticate posture
Diencephalon supra
Diagonal posture
Upper brain stem
Decerebrate posture
Abnormal ext arm
Weak flexion leg
Common patterns
A word about EEG

Fast activity is commonly seen with drug overdose

whereas slow wave abnormalities are more
commonly associated with metabolic and anoxic
An iso electric EEG is more common with drug
induced comas though otherwise it indicates
severe cerebral damage
To summarise.
Primary ABC
Blood for sugar, electrolytes, ABG and osmolality
Sample storage for subsequent screens
Distinguish between metabolic and structural
cause of coma and plan imaging accordingly
LP may be needed
CXR,ECG and EEG (fast activity/slow wave
abnormalities/anoxic coma)
Treatment of cause
Nursing care
Maintain normal physiology
Care of skin and prognostication
How do I identify stroke?

Cincinnati scale LAPPS

What to do next?

Support ABCs with SOS oxygen

Do a pre hospital stroke assessment
Establish time of onset
Transport to a stroke unit with prior relevant info
Neurologic screening assessment
Activation of stroke team
12 lead ECG
Emergent CT scan Brain
What if my CT is fine?
Rule out stroke mimics
Inclusions of fibrinolytic therapy
What if his BP is high?
Supportive things?

Admission to a stroke unit

Monitoring to maintain normothermia, euglycemia
and euvolemia
Treatment of acute seizures
Induced hypothermia
Treatment of UTI/Pneumonia
Swallow assessments
DVT prophylaxis
Treatment of concomitant systemic diseases
Decompressive craniotomy has a mortality benefit
Extending the time windows for
thrombolysis? (3-4.5 hrs)

Inclusions remain the same

Exclusions include age>80 years, INR< 1.7,NHS
Even with thrombolysis NHS>20 are known to
have poor outcomes

Defined as bleeding within the cranial vault

What is my work up gonna be?
Traumatic ICH

Spinal clearance from a neurosurgeon

Racoon eyes/battle sign
ENT consult for skull base fractures
Neurosurgical inputs with mass effect, on going
herniation/obstructive hydrocephalous
Specifics of ICH diagnosis
Initial management
What are my BP targets?
What drugs do I use?

Wait during the initial 24 hrs

Use short acting agents such as esmolol,
hydralazine, enalaprilat, nicardipine or labetalol
Caution with holding beta blockers and clonidine
What about anticonvulsants?
Other Supportive measures

Treating ICP with mannitol/HTS (periodic

monitoring of sodium and osmolality) and MV sos
Stress ulcer prophylaxis
Control of temperature, fever and shivering
What if my patient was on an anti
thrombotic agent?
When do I think about neurosurgery?
Summing up

ICH is a neurologic emergency which may require

Non contrast CT helps
Definitive indications of surgery
Optimizing medical and critical care interventions
goes a long way in improving outcomes
Thank you