Management of comatose
patient
DR.H.N.SARKER
MBBS,FCPS,MRCP(UK),
FRCP(Edin)
Associate Professor
Medicine
Introduction


Consciousness means wakefulness
with awareness of self and
surroundings.
The state of consciousness is the
product of complex interactions
between parts of the reticular
activating system in brainstem and
medial part of thalamus , cortex,
and all sensory stimuli.
Introduction


For a person, in order to maintain
consciousness, the two important
neurological components must function
perfectly.
The first is the cerebral cortex which is the
gray matter covering the outer layer of
the brain, and the other is a structure
located in the brainstem, called reticular
activating system (RAS or ARAS).
Introduction

Injury to either, or both of these
components is sufficient to cause a
patient to experience altered
consciousness.
Introduction
Introduction

Altered / Disturbed consciousness:
definitions of some terms■ Clouding of consciousness –
means reduced wakefulness and/or selfawareness, sometimes with confusion.
■ Confusion means that the subject is
bewildered and misinterprets his/her
surroundings.
■ Delirium is a state of confusion,
sometimes with visual hallucination, and
often high arousal (e.g. delirium
tremens, ).
Introduction
■ Sleep is normal mental and physical
inactivity: the subject can be roused.
■ Stupor is abnormal; a sleepy state from
which the subject can be aroused by
vigorous or repeated stimuli.
The term is also used for psychiatric
states, e.g. catatonic and depressive
stupor.
■ Coma means unrousable
unresponsiveness. Coma is a state of
unconsciousness whereby a patient cannot
react with the surrounding environment.
Mechanisms of coma

Altered consciousness is produced by
three mechanisms affecting
brainstem, reticular formation and
cortex.
■ Diffuse brain dysfunction.
Generalized severe metabolic or toxic
disorders (e.g. alcohol, sedatives,
uraemia, septicaemia) depress
overall brain function.
Mechanisms of coma
■ Direct effect within the
brainstem. A brainstem lesion
inhibits the reticular formation.
■ Pressure effect on the
brainstem. A mass lesion within the
brain compresses the brainstem,
inhibiting the reticular formation.
Mechanisms of coma

A single focal hemisphere (or
cerebellar) lesion does not produce
coma unless it compresses or
damages the brainstem.
Causes of coma

Principal causes of coma
Diffuse brain dysfunction
Drug overdose, alcohol abuse
 CO poisoning, anaesthetic gases
 Hypoglycaemia, hyperglycaemia
 Hypoxic/ischaemic brain injury
 Hypertensive encephalopathy

Causes of coma
Diffuse brain dysfunction





Severe uraemia
Hepatocellular failure
Respiratory failure with CO2 retention
Hypercalcaemia, hypocalcaemia
Hypoadrenalism, hypopituitarism and
hypothyroidism
Causes of coma
Diffuse brain dysfunction
 Hyponatraemia, hypernatraemia
 Metabolic acidosis
 Hypothermia, hyperpyrexia
 Trauma to brain
 Epilepsy
Causes of coma
Diffuse brain dysfunction
 Encephalitis, cerebral malaria,
septicaemia
 Subarachnoid haemorrhage
 Metabolic rarities, e.g. porphyria
 Cerebral oedema from chronic
hypoxia
Causes of coma
Direct effect within brainstem
• Brainstem haemorrhage or infarction
• Brainstem neoplasm, e.g. glioma
• Brainstem demyelination
• Wernicke–Korsakoff syndrome
• Trauma
Causes of coma
Pressure effect on brainstem
• Hemisphere tumour, infarction,
haematoma, abscess,
• encephalitis or trauma
• Cerebellar mass
Causes of coma

Common causes of coma
(remember by MnomonicAEIOU,DAMM )
• A-Alcohol, Abscess
• E- Epilepsy, Encephalitis, Endocrine and
Electrolyte disturbance
• I- Head injury, Brainstem Infarction or
haemorrhage
Causes of coma
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

O-Opium,drug Overdose
U- Uraemia
D- Diabetes(Hypoglycaemia, diabetic
ketoacidosis, nonketotic
hyperosmolar hyperglycemia)
Causes of coma


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A-Apoplexy, Epidural and subdural
hemorrhage, Subarachnoid
hemorrhage
M- Meningitis,cerebral Malaria
M-Metabolic(hepatic failure)
Causes of coma



A-Apoplexy, Epidural and subdural
hemorrhage, Subarachnoid
hemorrhage
M- Meningitis, cerebral Malaria
M-Metabolic (hepatic failure)
Approach to the Patient: Coma
Immediate assessment
Actions that take seconds save lives.

• Assess airway, breathing, circulationresuscitate.
• Give 100% O2, monitor pulse oximetry
and obtain venous access.
• Withdraw blood for glucose, other
biochemical parameters and drug
screening
Immediate assessment




Record the GCS and check the pupil
size and reaction.
Check the bedside glucose and the
temperature.
Consider the differential diagnosis.
Look for a Medic alert bracelet or
necklace.
Immediate therapy



If hypoglycaemia, give 50 ml 50%
glucose i.v.
If hypothermia, start rewarming.
If pupils are small, R rate is low or
signs of drug abuse are present, give
400µg of naloxane i.v stat and
repeat.
Subsequent management

After initial therapy, subsequent
assessment is done by taking history
and physical examination including
General and neurological
examination
History

All possible information from
Relatives
Paramedics
Ambulance crew
Bystanders
History



Particularly about the mood of onset
and circumstances
Previous medical historyepilepsy, DM, drug history
Clues obtained from pt’s clothing and
handbag
Examination



A thorough examination of all
systems is essential but concentrate
on the following.
1.Trauma requires complete
exposure and roll to examine back
2. Neddle mark
Examination


3. Severity of coma-assessed by
Glasgow Coma Scale
Eye opening (E)
• Spontaneous
• To speech
• To pain
• No response
4
3
2
1
Examination

Motor response (M)
• Obeys
• Localizes
• Withdraws
• Flexion
• Extension
• No response
6
5
4
3
2
1
Examination

Verbal response (V)
• Orientated
• Confused conversation
• Inappropriate words
• Incomprehensible sounds
• No response
5
4
3
2
1
Examination
Glasgow Coma Scale = E + M + V
(GCS minimum = 3: maximum = 15)

Examination
Examination
Examination
4. Pupil size and reaction-
Examination
5.Spontaneous eye movementAbnormal conjugate deviation
suggests intracerebral damage.
Dysconjugate deviation implies
damage to 3,4 or 6th nerve palsy
Examination
6.Respiratory rate and pattern-
Examination
7. Signs of Lateralisation suggest focal
neurological damage
Examination
Investigations


Often, the cause is evident (e.g.
head injury, cerebral haemorrhage,
self-poisoning);
if no cause is evident, further
investigations are essential.
Investigations

Blood and urine
■ Drugs screen (e.g. salicylates,
diazepam, narcotics, amfetamines).
■ Routine biochemistry (urea, electrolytes,
glucose, calcium, liver biochemistry).
■ Metabolic and endocrine studies (TSH,
cortisol).
■ Blood and urine cultures.
■ Other, e.g. cerebral malaria (request
thick blood film).
Investigations


Imaging
CT or MR brain imaging may indicate
an unsuspected mass lesion or intracranial
haemorrhage.
CSF examination
Lumbar puncture should be performed
in coma only after careful risk
assessment. It is contraindicated when an
intracranial mass lesion is a possibility:
Investigations
CT is essential to exclude this. CSF
examination is likely to alter therapy
only if undiagnosed
meningoencephalitis or other
infection is present.
 Electroencephalography
EEG is of some value in the diagnosis
of metabolic coma and encephalitis.
Management

Comatose and stuporose patients –
at home or outside, on a trolley, in a
ward or ITU – need immediate
careful nursing,
• meticulous attention to the airway
(protected airway) , and
• frequent monitoring of vital functions
and high flow O2.
Management

Longer-term essentials are:
■ skin care – turning (to avoid pressure
sores and pressure palsies), removal
of jewellery,
a suitable pressure-relieving
mattress.
■ oral hygiene – mouthwashes, suction
■ eye care – prevention of corneal
damage (lid taping, irrigation)
Management
■ fluids – intragastric or i.v.
■ calories – liquid diet through a fine
intragastric tube, 3000 kcal daily
■ sphincters – catheterization when
essential ; rectal evacuation.
Management


Broad spectrum antibiotics and/or
antivirals should be given empirically
if there is any suggestion of bacterial
infection or encephalitis .
Half-hourly neuro-observations.
Management

Specific treatmentTreatment of specific causes of
coma.