Approach to a patient in COMA

Content
• Definition
• Anatomy and physiology
• Etiology
• Approach to diagnosis
• Differential diagnosis
• Management
• CONSCIOUSNESS :is a state of normal cerebral
function in which the patient is aware of
himself and his environment and is able to
respond to changes both with in himself and
his environment.
 COMA
(Unarousable, unresponsiveness)

• Deep sleep, (Greek)

• It is profound state of unconsciousness from
which the person is
– Unawakable
– Unresponsive to external stimuli
– Absent sleep/wake cycles, with
– No voluntary action
 Level of Consciousness
• Alert

• Drowsy

• stupor

• Coma
 Anatomy & Physiology
• The state of alertness is maintained by the
reticular activating system (RAS)
• RAS - a network of nerve pathways and nuclei
throughout the brainstem, connecting motor
nerves and sensory nerve to and from the spinal
cord, the cerebellum, and the cerebrum
• Principle causes of Coma
– Damage to RAS or its projections
– Damage to large portions of both cerebral
hemispheres
– Suppression of RAS by drugs, toxins or metabolic
derangements (e.g.. Hypoglycemia, anoxia, uremia,
hepatic failure….)
 Etiology
1) With NO focal neurologic deficit or lateralizing
neurologic signs
– Metabolic disturbances- DKA, uremia, hypoglycemia,
electrolyte abnormalities………
– Intoxications: alcohol, opiates, sedative drugs
– shock
– Severe systemic or CNS infections
– Post seizure state
– Hypertensive encephalopathy, eclampsia
– Severe hypo-/hyper-thermia
– Head trauma (concussion)
2) With focal neurologic deficit
A)supratentorial (hemispheric) lesions
• Epidural or subdural hematoma
• Intraparenchymal hemorrhage
• Large ischemic infarction
• Tumor, abscess
B) Infratentorial lesions
• Pontine or cerebellar lesions
• Basilar artery thrombosis
• Ischemic cerebellar infarction
• Tumor, abscess
 Approach to a comatose patient
A) Assessment and maintenance of vital functions
- ABCs of life
- ALWAYS r/o cervical injury
B) Establish cause of coma
1) History
- immediately evident causes(e.g.. Trauma, cardiac
arrest, drug ingestions……)
- points to remember
- circumstance & rapidity of SSx
- antecedent SSx (headache, fever…)
- medication or drug use
- known medical illness(cardiac, liver, renal….)
2) Physical examinations
A) V/S
# BP
– High - HTN encephalopathy, raised ICP
- Low – alcohol or barbiturate intoxication, Internal h’ge, MI, Sepsis,
Profound hypothyroidism, addisonian crisis

# Temp.
- Fever – systemic infection, pyogenic Meningitis, Brain
lesions(central fever)
- Hypothermia – alcoholic, barbiturate, sedative intoxication,
hypoglycemia, hypothyroidism

# Respiratory rate
- Tachypnea – systemic acidosis or pneumonia
- Aberrant patterns – brainstem disorders

# Pulse Rate
- slow…..irregular
General Physical Examination
HEENT – trauma (battle sign, raccoons eye….)
- breath odor (alcohol, acetone…..)
Heart – arrhythmia, murmur
Chest – consolidation, congestions
Abdomen –mass, ascites, hepatomegaly….
Skin – petechiae (Meningococcemia, bleeding
diathesis…..)
- Jaundice (hepatic encephalopathy…)
Fundoscopic exam
- HTN (exudates, h’ge, vessel crossing,
papilledema)
- Increased ICP (papilledema)
B) Brain stem reflexes
- Helps establish localization. Includes

1) Pupillary light reflex

2) Ocular movements
3) Corneal reflex
4) Respiration
A) Pupillary light response
- Normally reactive and round pupils of mid
size (2.5 to 5mm) essentially exclude
midbrain damage
- One enlarged( > 6mm) & unreactive =
compression or stretching of third nerve,
temporal herniation (mass effect)
• Bilaterally dilated and unreactive = severe
midbrain damage (anoxia)
• Reactive in drugs
Bilaterally small and reactive (not pinpoint) = metabolic
or bilateral hemispheric lesions ( e.g.. Hydrocephalus,
thalamic haemorrhage
Very small and reactive ( pinpoint) = narcotic or
barbiturate overdose, pontine haemorrhage
-Mid position and fixed = midbrain
damage(structural)
B) Ocular movements
Elevate the lids and note resting position
Resistance to opening to opening the eye lids –
hysteric conversion
Easy eyelid opening with slow closure-sever coma
Dysconjugate gaze(abduction adduction )-CN
abnormalities
Spontaneous eye movement –damage at d/t site
Eyes look towards hemispheric lesion and away
from a brainstem lesion
Occulocephalic reflex
Elicited by moving head from side to side or
vertically with eyes held open
Eyeball move to the opposite direction of the head
movement-intact brainstem function (“doll`s
eyes” movement is positive)
Eyeballs move to the same direction-brainstem
dysfunction
Caloric test ( occulovestibular)
Irrigating the ear with ice (cold) to stimulate
vestibular apparatus
Eyes move to irrigating ear-intact brain stem
Corneal reflex
• Lost if connection between fifth and seventh
cranial nerves is severed ( pontine damage)
Respiration
• Shallow slow but regular metabolic or drug
suppression
• Cheyne stokes = bihemispherical damage
metabolic suppression
• Kussmaul’s = acidosis
• Agonal gasps = severe brain damage near
death situation
C) Motor function/response
- Quadriparesis & flaccidity – pontine and
medullary damage
• Decorticate posturing – severe bilateral or
unilateral hemispheric (damage above the mid
brain)
 - Decerebrate Posturing – damage to the
brainstem

• If the patient is yawning, swallowing, coughing or

moaning the coma is not deep
• Abnormal body movement-status epileptics ,
uremia…
 Differential Diagnosis
• Locked-in syndrome
• Akinetic Mutism
• Hysteric Coma
• Catatonia
• Persistent vegetative state
• Conditions mistaken for coma
• Some conditions can be mistaken for coma, despite the preservation of
some degree of arousal and awareness, because the pt is unable to

respond voluntarily .
• Complete paralysis
• Locked-in syndrome injury to the base of the
pons, usually by embolic occlusion of the
basilar artery
• Consciousness is preserved;
• however, the patient cannot move muscles in
the limbs, trunk, or face, except that voluntary
blinking and vertical eye movements remain
intact
• Other causes of severe motor paralysis (eg,
Guillain Barre syndrome, botulism) may also
lead to a similar condition.
• Psychiatric unresponsiveness
• often resist passive eye opening
• turn the eyes towards the floor regardless
of which side they are lying on, or
demonstrate non epileptic seizures
• Catatonia is distinguished from coma by
the patient's preserved ability to
maintain posture
• Akinetic mutism — A lack of motor response
in an awake individual might arise from injury to
the prefrontal or premotor (including supplementary
motor) areas responsible for initiating movements
• patient is able to form impressions and think,
• but remains virtually immobile and mute.
• The patient's tone, reflexes, and postural
reflexes usually remain intact
 Investigations
- Blood - CBC, RBS, Electrolyte, RFT, LFT
- U/A
- Imaging – Skull, cervical and chest x-ray,
- Echocardiography……
- CT scan, MRI
- EEG
- Cerebral angiography
- CSF analysis
- Toxicology analysis
- Gastric aspirate or lavage……
 Management
1) ABC
2) Initial therapy
1) -Thiamine (IV) – 100 mg
2) - 40% dextrose
3) - Naloxone – 0.4 mg…….opiate intoxication
4) - ? Flumazenil…….benzodiazepine or hepatic
coma
• Raised ICP
– Elevate head 30-40 degree
– Hyperventilation
– Mannitol
– Dexamethasone (ICSOL with inflammatory edema)
• Surgical management of Increased ICP
– Decompression,
– Ventricular drainage
Symptomatic treatment
• Urinary retention – indwelling catheter
• Severe respiratory failure – suction, intubation
or tracheostomy
• GI bleeding – ice water lavage, volume
replacement
• CHF – treat accordingly
• Fever – ice bags
• Agitation – diazepam......
Watch out for nosocomial infections
• Monitor vital sign
• Nutrition
– iv solution initially, later tube feeding
• Frequent suctioning
• Skin – turn patient every 1-2 hours....bed sore
• Cornea – tape patient’s eyelids
- eye drops
• Care for IV line and indwelling catheter
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