APPROACH TO COMA
DEMOGRAPHIC PROFILE
■ Name - Mr xyz
■ Age – TT years
■ Gender - Male
■ Resident – Delhi
■ Religion – Hindu
■ Non-consangious marriage
■ History given by Wife
CHIEF COMPLAINTS
■ 1. Fever x 1 week
■ 2. Cough with expectoration x 1 week
■ 3. Increased shortness of breath x 1 week
■ 3. Drowsiness x 1 day
■ 4. Unresponsiveness x 4 hours
HOPI
■ The patient was apparently alright till 1 week back and routine
nebulisations for his COPD when he started complaining of-
■ 1. Fever x 1 week –
Non-documented in nature, Continuous and relieved on taking
medication,No diurnal variation, No chills or rigors
▪ 2. Cough with yellowish expectoration( 2-3 tsps./day, mucoid) without
any blood tinging.
▪ 3. Shortness of breath – Patient already had SOB on climbing one flight
of stairs, worsened to going to washroom since 4 days, at rest since 2
days.
Cont….
■ 2. Drowsiness –
Conveyed by attendants that the patient was completely conscious
till a day before admission when they noticed that the patient had
started sleeping even during the day though was easily arousable.
The drowsiness worsened through the day and the patient started
becoming irritable on getting aroused by the attendants, gradually
leading to a state of deep sleep from which the patient was not getting
aroused.
NEGATIVE HISTORY
■ Headache
■ Nausea/Vomiting
■ Abnormal body movements
■ Cold/ Chest pain
■ Burning micturition
■ Loose stools
■ Abdominal pain
■ Skin, Eye, Ear manifestation
Past history
■ Patient is a reformed bidi smoker, last bidi smoked – 3 months back.
■ K/C/O - COPD on nebulisation since the past 2 years.
■ No H/O – pulmonary kochs or any other comorbidities
MEDICATION HISTORY
■ Patient was currently only on nebulisation ( nebulization with
formeterol and budesonide twice a day) with no medication ingestion
■ Since patient started running fever – medication was taken over the
counter – no documents available
ON GENERAL EXAMINATION
■ General condition – Sick, comatose.
■ Vitals –
Pulse – 121/min – regular weak rapid thready pulse having low volume
Blood Pressure – 70/50 mm of mercury on RT upper arm in supine position –
started on noradrenaline support
Respiratory rate – 45/minute- abdomino - thoracic.
Peripheral Oxygen Saturation – 77% on Room Air
JVP – Not elevated
Pallor+, no icterus, no clubbing, no cyanosis, no lymphadenopathy
Systemic Examination
■ 1. CNS –
GCS – E1,V2,M1
Motor examination – No rigidity
Pupil – B/L 4mm reactive to light
Brainstem reflexes intact
■ 2. Respiratory system – B/L diffuse wheeze, Right infra scapular area
coarse crepts+
■ 3. Per abdomen – Soft, Non-tender, Non-distended
■ 4. CVS – S1S2 +
Impression
■ A TT year male patient, K/C/O COPD presented with fever, cough,
shortness of breath to the Emergency in a comatose state –
HOW DO WE APPROACH THIS PATIENT WHO IS IN COMATOSE STATE.
Coma – What is coma?
“A state of profound unawareness from which the patient
cannot be aroused.”
Crucially, eyes are closed, and a normal sleep–wake cycle is
absent.
What is being Conscious ?
Consciousness is defined as the state of
awareness of the self and environment with
appropriate arousal or wakefulness
(Giacino et
al)
Disorders of Consciousness (DoC): wide
spectrum of correlates of brain’s disruptions
Arousal :
Evidence of eye opening and brain stem reflexes and is defined by a
spectrum of conditions from sleep to complete wakefulness.
Awareness :
Aware - visual pursuit, localization to noxious stimulation, command
following, intelligible verbalization, and object recognition in order to
define the perceiving of the external environment and the voluntary
interaction with it (Laureys et al. 2004).
Mechanism of Coma
■ Consciousness is a function of the ascending reticular activating
system ( ARAS) ans its connections – any injury to the same results in
altered consciousness.
■ The lesion may be in either of the following structures -
1. Upper pons / midbrain
2. Diffuse/ larger bilateral or unilateral cerebral lesion
3. Certain toxins, metabolic or infectious conditions
TME - TOXIC METABOLIC ENCEPHALOPATHY
Interfere with the function of the ARAS and Cx
connection
• Interrupt polysynaptic pathways
• altered excitatory-inhibitory amino acid
balance
Cerebral edema Drug-induced delirium
contributes to acute results from disruption of
fulminant hepatic the normal integration of
encephalopathy and to neurotransmitters,
hypoosmolar including dopamine,
encephalopathies acetylcholine, glutamate,
TME - COMA
gamma-aminobutyric acid
Exogenous toxins, (GABA), and/or serotonin
including carbon
monoxide and
Nutritional disorders
cyanide, cause
Electrolyte disturb cellular energy
impaired oxygen
derangements alter metabolism and may
delivery and
membrane result in neuronal
mitochondrial
excitability death
Classification of the Major Metabolic
Encephalopathies
Due to lack of glucose, oxygen or metabolic
cofactors
• Metabolic encephalopathies
Hypoglycemia
result from alterations of
Ischemia
brain chemistry at both
Hypoxia
neocortical and brainstem
ARAS centers. Hypercapnia
• Respiration may be Vitamin deficiencies
diminished Due to peripheral organ dysfunction
• Pupils appear small but Hepatic encephalopathy
reactive Uremic and dialysis encephalopathies
• Progression - asterixis, also
termed “flapping tremor,”
CLINICAL APPROACH
History – does it provide any
clue?
■ 1. Time and course – Abrupt ( seizure, subarachnoid haemorrhage),
gradual ( intracranial space occupying lesion), fluctuating ( metabolic,
subdural haemorrhage).
■ 2. Associated clinical features - headache and vomiting ( intracranial
hemorrhage, infections), visual symptoms ( Posterior reversible
encephalopathy syndrome).
■ 3. Motor deficits – (structural lesions).
■ 4. Fever – (infection, ICH).
■ 5. History of preceding fall – (SDH).
■ 6. Recent confusion or delirium – (metabolic, toxic cause).
■ 7. Co-morbid illness – (diabetes mellitus, hypertension).
Physical examination – clues.
1. Hyperthermia
■ Infections- cerebral malaria and meningoencephalitis
■ Vascular-pontine haemorrhage
■ Metabolic-thyrotoxicosis
■ Toxic-salicylate and belladonna poisoning
■ Heat stroke
■ Neuroleptic malignant syndrome
Hypothermia: temperature drops
below 95°F (35°C)
■ Toxic-barbiturate and phenothiazine poisoning
■ Metabolic-myxedema coma
■ Circulatory failure
■ Hypothermia per se can cause coma
Respiratory
patterns
■ Cheyne-stokes respiration
– B/L cerebal hemisphere
lesions, B/L thalamic
lesions.
■ Kussmaul breathing -
metabolic or
pontomesencephalic
lesion.
■ Apneustic breathing –
lower pontine lesions.
■ Agonal gasps – Brainstem
lesions – suggestive of a
terminal state
■ Biots - Pons/ medulla -
poor prognosis
Cardiac Evaluation
■ Bradycardia – (Heart block, Raised intracranial pressure, Inferior wall
myocardial infarction, Myxedema coma)
■ Hypertension – (Hypertensive encephalopathy, Intracranial bleed,
Head injury)
■ Hypotension– (Acute coronary syndrome, Myxedema coma, Addisonian
crisis, Sepsis)
Skin Discolouration Odor of Breath
■ Petechiae-bleeding diathesis
associated with: Intracerebral ■ Burnt almond odor - cyanide poisoning,
bleed, Meningococcemia, ■ Musky/fecal odor-hepatic coma,
Staphylococcal endocarditis,
■ Ammoniacal odor-uremia,
Rickettsial infections
■ Acetone breath- diabetic ketoacidosis,
■ Jaundice
■ Alcohol intoxication
■ Reddish discoloration-seen in
carbon monoxide poisoning
■ Cyanosis-seen in circulatory
failure and CO2 narcosis
Meningoccocemia Rash Eschar
Papilloedema
Fundus
examinati
on
■ To look for –
1. Papilloedema
2. Hypertensive changes
3. Retinal hemorrhages
Retinal hemorrhages
Keith-Wagener-Barker Classification of
Hypertensive Retinopathy
Neurological examination
■ The neurological examination of a comatose patient should comprise
of
1. Evaluation of level of consciousness
2. Motor evaluation
3. Brainstem reflexes
Level of consciousness
■ Level of consciousness is assessed by:
■ Glasgow coma scale (GCS): It is a useful index to assess the severity of
coma and for prognosis but is not useful in ascertaining the etiology of
coma and in assessment of mild impairment of consciousness.
■ Full Outline of UnResponsiveness (FOUR): It is more recent scoring
system which has advantages in intubated patients wherein scoring is
done under categories such as eye response, motor response,
brainstem reflexes, and intubation.
GCS -
1974
FOUR Score -
Full Outline of
UnResponsiveness
2009
Iyer VN, Mandrekar JN, Danielson RD, Zubkov AY,
Elmer JL, Wijdicks EF. Validity of the FOUR score
coma scale in the medical intensive care unit. Mayo
Clin Proc. 2009 Aug;84(8):694-701. doi:
10.4065/84.8.694. PMID: 19648386; PMCID:
PMC2719522.
Motor examination-
■ Should be done under 4 headings –
■ 1. Posturing
■ 2. Muscle tone
■ 3. Power
■ 4. Reflexes
Posturing
■ Decorticate posturing: Suggestive of
lesion rostral to midbrain
■ Decerebrate posturing: Suggestive of
lesion below the red nucleus
■ Muscle tone – not affected by metabolic conditions usually though B/L
rigidty can be seen in neuroleptic malignant syndrome, malignant
hyperthermia and hepatic coma.
■ Asterixis or multiufocal myoclonus – Suggestive of metabolic/toxic
encephalopathy.
Evaluation of Pupils
■ Pupillary light reflex is lost in – midbrain involvement/ oculomotor
nerve compression secondary to herniation.
■ Pinpoint pupils – Opioid poisioning or pontine tegmentum
lesions/Hemorrhage
■ Dilated pupils – Anticholinergic and sympathomimetic poisioning.
■ PUPILS ARE USUALLY SPARED IN METABOLIC CONDITIONS.
Oculomotor
Movements
■ Central structures involved in
extraocular movements lie in the
brainstem and are controlled by the
frontal eye fields.
■ According to the dictum "the eyes
look toward a cortical lesion and
away from a brainstem lesion”.
■ Irritative lesions usually results in
deviation of the eye to the opposite
side of the lesion.
■ Downward and medial deviation of
the eyeballs is typical of a thalamic
bleed.
Oculomotor movements
■ Ocular Bobbing
■ Rapid vertical downward movement with slow upward return
■ No horizontal eye movements are seen
■ bilateral brainstem lesion.
■ Ocular Dipping
■ Slow downward movement of eyeballs with fast upward
return
■ Normal horizontal movements
■ Diffuse cortical hypoxic damage.
■ In patients with coma, complete bilateral conjugate roving eye
movements usually indicate an intact brainstem. In their absence,
horizontal eye movements can be tested with vestibulo-ocular reflexes
(VOR).
A. B.
Brainstem reflxes - Oculocephalic Reflexes
(Doll's Eyes)
■ Cervical spine fractures
should be ruled out
■ Head is rotated abruptly from
one side to the other in the
horizontal plane. Present, the
eyes do not turn with the
head but in the opposite
direction as if the patient is
maintaining fixation on a
single point.
■ Absence of doll's eye reflex
indicates brain stem
involvement.
Oculovestibular Reflex (Caloric
Testing)
■ The test is performed by irrigating the external auditory canal with
cold water. After a brief latency, it causes a tonic deviation of both
eyes to the side of cold water irrigation and nystagmus toward the
opposite side.
■ In comatose patients with brainstem lesions, nystagmus may not
occur.
COWS -
Cold opposite ; Warm Same
Corneal reflex
■ Afferent limb – Trigeminal nerve
■ Efferent – Oculomotor nerve
■ Assessment of pontine functions is done using this test.
Laboratory investigations
■ Complete hemogram
■ Metabolic profile – KFT, LFT, Serum ammonia, ABG, thyroid function,
Serum cortisol
■ Microbiological profile – Blood c/s, PSMP, Malaria serology, Urine c/s,
CSF c/s, CSF viral studies, CSF – AFB and GeneXpert.
■ Radiological investigations – NCCT head/ MRI brain
■ Electroencephalogram (EEG) – diagnostic of herpes encephalitis,
Creutzfeldt-Jakob disease
■ Toxicological analysis
EEG in Coma
HIE
Triphasics
PLEDS - ? Encephalitis
Management
■ 1. GCS </= 8 or hypoxemia, vomiting, poor gag/cough reflex –
warrants intubation.
■ Unknown poisoning – 25 gm of dextrose/ Inj. thiamine and dextrose in
malnourished individuals.
■ Suspected toxin ingestion – Gastric lavage.
■ Raised ICT or herniation – Inj. Mannitol 1g/kg I/V.
■ Hyperthermia – Managed with antipyretics and cooling.
■ Suspected meningitis/meningo-encephalitis – Antibiotic/ Anti-viral trial.
