Approach to

Unconsciousness (Coma)

Kepaniteraan Klinik Ilmu Penyakit Dalam

FKUPH-SHLV/RSUS
Topic Discussion

Alrein P. Wajong (07120100103)

Pembimbing: dr. Theo Audiyanto, SpPD
CONSCIOUSNESS is a state of awareness
of self and the environment.

Determined by two separated function:

Arousal ( level of consciousness)
Awareness (content of consciousness)

Coma - a deep sleeplike state from which the patient cannot

be aroused
Consciousness depends on two component

an intact ascending reticular activating

substance (ARAS) in the brainstem as the
alerting or awakening element of
consciousness level of consciousness or
arousal

a functioning cerebral cortex of both

hemisphere which determines the content of
that consciousness or awareness

Content depends on arousal

but normal arousal does not guarantee normal
content
Brain Stem : Midbrain, Pons &
Medulla
Many cranial nerves exit
Midbrain
eye movement control (vertical
gaze center)
Pons
Eye movement (horizonral gaze
center)
breathing, signal relay

Medulla involuntary functions

Examples: Blood pressure,
vomiting
Reticular formation:
Network in brain stem
Arousal, sleep, pain
THE ARAS
Extending from the medulla through the pons to the midbrain
which is continous caudally with the reticular intermediate grey
lamina of the spinal cord and rostrally with the subthalamus, the
hypothalamus and the thalamus
Receives input from numerous somatic afferents
Projects to midline thalamic nuclei (which are in a circuit with
cortical structures) and the limbic system
Function of ARAS-Thalamic-Cortical
system depends on:
Anatomic integrity of structures
Metabolic integrity (circulatory integrity)
Communicative integrity
(neurotransmitter function)
cholineric system
monoaminergic system
GABA (-aminobutyric acid) system
COMA

A state in which the patient makes no

purposeful response to the environment
and from which subject cannot be
aroused
COMA implies dysfunction of :
ARAS or
Both hemi-cortices

Anatomically, this means

Central brainstem structures (bilaterally)
from caudal medulla to rostral midbrain
Both hemisphere
 Carbonminoxide)
Miscellaneous
(hyperthermia,
severe systemic
infection)
Coma Due to Metabolic
Disorders
Systemic metabolic abnormalities cause
coma
interrupt delivery of energy substrates
(hypoxia, ischemia, hypoglycemia)
alter neuronal excitability (drug and
alcohol intoxication, anesthesia, and
epilepsy)
Approach to Coma
Acute respiratory and cardiovascular
problems FIRST prior to neurologic
assessment.
 HISTORY
In many cases, the cause is immediately evident
(e.g., trauma, cardiac arrest, or known drug ingestion).
the circumstances and rapidity with which neurologic
symptoms developed;
the preceding symptoms (confusion, weakness, headache,
fever, seizures, dizziness, double vision, or vomiting);
the use of medications, illicit drugs, or alcohol; and
chronic liver, kidney, lung,heart, or other medical disease.

Direct history taking of family and observers on the scene, in

person or by telephone, is an important part of the initial
evaluation.
GENERAL PHYSICAL EXAMINATION

VITAL SIGNS
Fever systemic infection, bacterial meningitis, or
encephalitis; central fever a brain lesion that has
disturbed hypothalamic temperature-regulating centers RARE
Hyperthermia, 4244C, associated with dry skin
suspicion of heat stroke or anticholinergic drug intoxication.
Hypothermia observed with alcoholic, barbiturate, sedative, or
phenothiazine intoxication; hypoglycemia; peripheral
circulatory failure; or hypothyroidism.
Hypothermia itself causes coma only at <31C. .
GENERAL PHYSICAL EXAMINATION

Tachypnea systemic acidosis or pneumonia

Shallow, slow, but regular breathing
metabolic or drug depression.
Cheyne-Stokes respiration CYCLIC: progressively deeper
and faster breathing gradual decrease temporary
apnea. The pattern repeats, with each cycle usually taking
30 seconds to 2 minutes.ending with a brief apneic period
bihemispheral damage or metabolic suppression and
commonlyaccompanies light coma.
Rapid, deep (Kussmaul) breathing
implies metabolic acidosis but may also occur with
pontomesencephalic lesions.
Agonal gasps lower brainstem (medullary) damage and
are well known as the terminal respiratory pattern of severe
brain damage.
 GENERAL PHYSICAL EXAMINATION

Hypertension either indicates hypertensive

encephalopathy or rapid rise in intracranial pressure
(ICP; the Cushing response) most often after
cerebral hemorrhage or head injury.
Hypotension is of coma from alcohol or barbiturate
intoxication, internal hemorrhage, myocardial
infarction, sepsis,profound hypothyroidism, or
Addisonian crisis.
 GENERAL PHYSICAL EXAMINATION

Funduscopic examination
Detects subarachnoid hemorrhage (subhyaloid hemorrhages),
hypertensive encephalopathy (exudates, hemorrhages, vessel-
crossing changes, papilledema), and increased ICP
(papilledema).
NEUROLOGICAL ASSESMENT OF
COMA

Eye opening
Motor Respon
Level of cosciousness: GCS
Verbal Response

Brainstem function
Cranial nerve examination Pupillary reactions
Corneal responses
Spontaneous eye movement
Respiratory pattern Oculocephalic response
Oculovestibular respon
Gag Reflex
Motor function Motor response
Muscle tone
Tendon reflexes
Seizures
response
possible
Level focal
of consciousness
lesion
BRAINSTEM FUNCTION

The brainstem reflexes are particularly

important in helping to identify those lesions
that may affect the ARAS, explain the
reason of coma
BRAINSTEM FUNCTION

Assessment of brainstem function via reflexes

Pupillaryreaction (CN 2,3)

Corneal reflex ( CN 5,7)
Oculocephalic/caloric (CN 3.4.6.8)
Gag Reflex (CN 9,10)
PUPILLARY REACTION
 PUPILLARY REACTION

Abnormal response:
Lesions on afferent OR
efferent pathways
Midbrain integrity/tectum

Brainstem areas controlling

consciousness are anatomically
adjacent to those controlling the
pupils,
pupillary changes presence and
location of b rainstem diseases
causing com a
HOW TO LOOK PUPILLARY
REFLEX
Have the patient look at a distant object
Look at size, shape and symmetry of pupils.
Shine a light into each eye and observe
constriction of pupil.
Flash a light on one pupil and watch it
contract briskly.
Flash the light again and watch the opposite
pupil constrict (consensual reflex).
Repeat this procedure on the opposite eye
Gb pupillary reflex
CONCLUSION

Pupillary reflex is pupillary respon to light

stimulus with CN2 as afferent and CN3
as efferent
Abnormal pupil response can represent
impairment of afferent or efferent
pathway and midbrain integrity
 from a
supratentorial
mass
PUPILLARY REACTION
PUPILLARY REACTION
Pinpoint pupils (1-1,5 mm in diameter)
Focal damaged at pontine level
Opioid overdose
Organophospate poisoning
Miotic eye drops
Asymetric pupils (anisocoria) with
difference 1 mm
Structural lession affecting the mid
brain or oculomotor nerve
CORNEAL REFLEX

Afferent : trigeminal nerve

(N. V)
Efferent :
Facial nerve (eye closure)
N. VII
To test pontine integrity
 Oculovestibular reflex = caloric
test
Stimulus cold/warm water
REFLEX irrigation
EYEagaintsMOVEMENT
the
tympanic membrane
vestibulo-ocular reflex

Lateral gaze centers : in the

paramedian pontine reticular
formation (PPRF)
OCULOCEPHALIC
RESPONSE
Move head passively and observe motion of the
eyes. The eyes should move conjugately in the
direction opposite to the movement. An abnormal
response (absent or assymmetric) implies
brainstem disease. Do not perform when neck
instability is suspected
OCULOCEPHALIC RESPONSE

Rotate the patients head from side to side and

observing the eyes.
coma with intact brainstem: eyes will move
conjugately and in a direction opposite to the
head movement

Sudden rotation of the head to the left results in

movement of endolymph within the
semisircular canals whose project to the
vestibular nuclei, the signal sent to right-sided
lateral gaze center and triggers eye movement
to the right, stabilizing the image on the retina.
meatus.

A dysconjugate response or no
response indicates braistem
damage
CALORIC TEST
Caloric response: if dolls eye movement are absent proceed to
calorics. Ice cold water applied to the tympanic membrane normally
elicits a slow conjugate deviation to the irrigated side. Absence
indicates brainstem disease. Caloric testing is more sensitive than
the oculocephalic response. Check if tympanic membrane is intact
before testing
Ataxic irreguler,
medullary
damage,
preterminal
RESPIRATION

Low pontine
damage
MOTOR
RESPONSE
Localize the stimulus

TO arm
PAIN
A decorticate response to pain (flexion of the
at the elbow, adduction at the shoulder,
extension of the leg and ankle)
A decerebrate response to pain (extension at
the elbow, internal rotation at the shoulder &
forearm, leg extension)
Asymmetric posturing
Facial weakness
Limb weakness
MOTOR
RESPONSE
TO PAIN
MOTOR
RESPONSE
TO PAIN
MOTOR
RESPONSE
Tone & reflex

TO PAIN
Plantar response : Babinski
Neurological sign in coma
with downward transtentorial herniation
WORK UP
LABORATORY
Chemical-toxicologic analysis of blood
presence of exogenous drugs or toxins, eg. alcohol, does not exclude the
possibility that other factors, particularly head trauma, are also
contributing to the clinical state.
ABG analysis: helpful in patients with lung disease and acid-
base disorders.
Common metabolic derangement: electrolytes, glucose,
calcium, osmolarity, and renal (blood urea nitrogen) and
hepatic (NH3) function.
Lumbar puncture less common today in coma diagnosis
because neuroimaging
Perform if meningitis suspected clinically
 WORK UP
IMAGING & Others
ECG
CT Cranial: normal CT scan DO NOT excludes anatomic
lesions
EG: Bilateral hemisphere infarction, acute brainstem infarction,
encephalitis, meningitis, difuse axonal injury,, and subdural hematomas
that are isodense to adjacent brain, etc
MRI
EEG
Differential Diagnosis
No focal or lateralizing neurologic signs, usually with
normal brainstem functions; Normal CT scan and CSF
content
a. Intoxications: alcohol, sedative drugs, opiates, etc.
b. Metabolic disturbances: anoxia, hyponatremia, hypernatremia,
hypercalcemia, diabetic acidosis, nonketotic hyperosmolar
hyperglycemia,
hypoglycemia, uremia, hepatic coma, hypercarbia, addisonian crisis,
hypo- and hyperthyroid states, profound nutritional deficiency
c. Severe systemic infections: pneumonia, septicemia, typhoid
fever,
malaria, Waterhouse-Friderichsen syndrome
d. Shock from any cause
e. Postseizure states, status epilepticus, subclinical epilepsy
f. Hypertensive encephalopathy, eclampsia
g. Severe hyperthermia, hypothermia
h. Concussion
Meningeal irritation with/without fever, with excess of
WBCs or RBCs in the CSF, without focal or lateralizing
cerebral or brainstem signs; CT or MRI shows no mass
lesion

a. Subarachnoid hemorrhage from ruptured aneurysm,

arteriovenous
malformation, trauma
b. Acute bacterial meningitis
c. Viral encephalitis
d. Miscellaneous: Fat embolism, cholesterol embolism,
carcinomatous
Diseases that cause focal brainstem or lateralizing
cerebral signs, with or
without changes in the CSF; Abnormal CT and MRI
a. Hemispheral hemorrhage (basal ganglionic, thalamic) or
infarction (largmiddle cerebral artery territory) with secondary
brainstem compression
b. Brainstem infarction due to basilar artery thrombosis or embolism
c. Brain abscess, subdural empyema
d. Epidural and subdural hemorrhage, brain contusion
e. Brain tumor with surrounding edema
f. Cerebellar and pontine hemorrhage and infarction
g. Widespread traumatic brain injury
h. Metabolic coma with preexisting focal damage
i. Miscellaneous: cortical vein thrombosis, herpes simplex
encephalitis, multiple cerebral emboli due to bacterial endocarditis,
acute hemorrhagic leukoencephalitis, acute disseminated
(postinfectious) encephlomyelitis, thrombotic thrombocytopenic
purpura, cerebral vasculitis,
References

Murray et al. Oxford Handbook of Clinical Medicine 8th ed.

Oxford University Press, UK
Fauci et al. Harrisons Principle of Internal Medicine 18th Ed.
McGrawHill New York USA
Fauci et al. Harrisons Manual of Medicine 18th ed. McGrawHill
New York USA
Thank You