Differential diagnosis of coma

Pathophysiology of coma
Insufficient oxygen supply
Insufficient energy supply (glucose)
Change in CSF and brain pH
Increase in ICP
Inadequate CPP (CPP = MAP-ICP)
Toxic/metabolic injury
 Understanding Coma
Coma (from the Greek koma, meaning
deep sleep) is a prolonged period of
unconsciousness.
Unconsciousness is the lack of
appreciation of (or reaction to) a stimulus.
Coma differs from sleep in that one cannot
be aroused from a coma.
 Disturbed consciousness:
definitions
Sleep is the state of normal mental and physical inactivity from which the
subject can be roused.
Confusion is the state of altered consciousness in which the subject
misinterprets his or her surroundings.
Somnolent easily aroused and aware
Stupor aroused with difficulty, impaired awareness (i.e. an abnormal,
sleepy state from which the subject can be aroused by stimuli.
Comatous unarousable and unaware
Persistent vegetative state produced by diffuse cerebral injury, the
patient is awake (eyes open) but is unresponsive to verbal or noxious
stimuli. Patients in a vegetative state may appear somewhat normal and
may occasionally grimace, cry, or laugh.
Locked-in syndrome - is a state of unresponsiveness due to massive
brainstem damage, the patient is awake and aware, but cannot move or
communicate except by vertical eye movement (has a functioning cerebral
cortex).
Delirium is a state of high arousal (seen typically in delirium tremens), in
which there is confusion and often visual hallucination.
 Traps

Coma is not the same as brain death, which is the

irreversible cessation of all brain activity.
One can be in a coma but still exhibit
spontaneous respiration;
One who is brain-dead, by definition, cannot do
Basic anatomy of altered
consciousness
 Etiology and pathogenesis
A)
intracranial
extracranial
exogenous
endogenous

B)
Structural changes
Vessel injury (clot, rupture)
Infection
Herniation as a consequence of expansive i.c. processes

Metabolic causes
incl. intoxication
 Differential diagnosis according to a
neurological assessment
I. Coma and focal signs
Tumours, stroke (hemorrhage, embolism, thrombosis), subdural or
epiddural hemorrhage, SAH, abscess, hypertensive encephalopathy

II. Coma and meningismus

Meningitis, SAH, leptomeningeal carcinoma or lymphoma.

III. Coma without focal signs and meningismus

Intoxication (alcohol, drugs (barbiturates, bezodiazepines, hypnotics),
opiates, SSRI, CO
Metabolic: hypoxic encephalopathy,hypoglycemia, diabetic coma,
uremia, liver failure, hyperkapnia (pCO2 > 10kPa), nonconvulsive
status epilepticus, hypothyroidism, sepsis, shock,
hypothermia/hyperthermia, Wernickes encephalopathy
In critically ill patients: acute toxo-metabolic encephalopathy (TME)
 The unconscious patient:
an approach and management

Usually, coma and other altered states of

unconsciousness are considered
neurological emergencies, and actions
need to be taken quickly to avoid
permanent damage.
Vital signs assessment (ABC, VIP)
i.v. line!
 Glasgow Coma Scale
The Glasgow Coma Scale is a standardized system used to assess
the degree of brain impairment and to identify the seriousness of
injury in relation to outcome.
The Glasgow Coma Scale involves three determinants:
eye opening,
verbal responses
and motor response (movement)

These determinants are evaluated separately according to a

numerical value that indicates the level of consciousness and the
degree of dysfunction.
Scores run from a high of 15 to a low of 3. Persons are considered
to have experienced a "mild" brain injury when their score is 13 to
15. A score of 9 to 12 is considered to indicate a "moderate" brain
injury and a score of 8 or less reflects a "severe" brain injury.

CAVE: "mild", "moderate" and "severe" are used as relative terms to

describe the severity of the brain injury and are not meant to
trivialize the seriousness of any brain injury.
GCS 8 = deep coma, OTI!
 The unconscious patient:
an approach and management

Medical history (DM, kidney, liver, epilepsy), changes acute,

subacute, chronic?
Physical Exam including blood pressure, temperature, skin,
breath [ketones, alcohol, hepatic and uraemic fetor], respiration
pattern
Neurological examination in coma
 Neurological examination in coma
1. Evaluate brainstem reflexes (presence or absence)
a) Pupils - Record size and reaction to light. The following patterns are seen:
Dilatation of one pupil - indicates herniation of the uncus of the
temporal lobe (coning) which compresses the third nerve. This is a
neurosurgical emergency (possibly subdural/extradural haematoma).
Bilateral mid-point reactive pupils (i.e. normal pupils) are characteristic
in metabolic comas and following most CNS-depressant drugs except
opiates.
Bilateral light-fixed, dilated pupils are a cardinal sign of brainstem
death. They also occur in deep coma of any cause, but particularly in
coma due to barbiturate intoxication or hypothermia.
Bilateral pinpoint, light-fixed pupils occur with pontine lesions (e.g. a
pontine haemorrhage) that interrupt sympathetic pathways, and with
opiate drugs.
Mydriatic drugs administered in coma can confuse diagnosis. Previous
pupillary surgery can also sometimes cause diagnostic difficulty.
b) Corneal reflex (evaluates cranial nerves V and VII)
2. Evaluate level of responsiveness (see GCS)
a) Purposeful movement
b) Withdrawal response to noxious stimuli
c) Decorticate posturing
d) Decerebrate posturing

3. Others
a) Nuchal rigidity (meningitis, SAH)
b) Battles sign (basilar skull fraction, subdural
or epidural hemorrhage)
a) Persistent nystagmus (may be seen in status
epilepticus)
 Key findings
Pupillary response
Corneal reflex
Spontaneous respiration
Motor response
 Key tests
Complete blood count
Biochemical profile (incl.glycemia, electrolytes, liver and renal
tests)

Arterial blood gases

Toxicology screen (ethanol, opiates, benzodiazepines, illicit drugs,
and others)
Brain computed tomography (infarction, hemorrhage,
edema, SAH, SH, skull fracture)

Electroencephalography
CSF examination