Coma and lesser degrees of impaired
consciousness are :
Arresting and alarming neurologic emergencies.
If persistent, the conditions that cause them often
end fatally or, even worse.
Patient irreparably damaged, mentally and
physically.
Coma : is the equivalent to loss of
consciousness, in practical terms
means a loss of awareness of and an
inability to respond to external stimuli
or inner needs.
PROFOUND COMA :
Different degrees of coma are distinguishable.
In profound coma, all stimuli, even the most
severely painful ones, have no effect.
SEMICOMA :
A somewhat lighter state of coma (semicoma) is
manifested by groaming, stirring, quickening of
respiration, or a brief opening of the eyes when
the patient is pinched or shaken.
STUPOR :
A stuporous patient will open his eyes and make
some simple response to loud voice or manipulation
of his body but does not speak.
CONFUSED :
A confused patient reveals in conversation an
inability to respond and think with customary speed
and clarity.
LOCKED IN SYNDROME :
Notable is the fact that the foregoing states of
impaired consciousness include both a reduced
receptivity to stimulation and a reduced
responsivity. When only the later defect exists,
the patient being paralyzed but alert and aware of
his surroundings, the condition is referred to as
the locked-in syndrome (also as de-efferented
state or pseudocoma).
LOCKED IN SYNDROME
CLINICAL FEATURE No movement except for
eye blinking and vertical
eye movement.
Mute, conscious.
Can communicate using
eye blink.
SITE OF LESION
Ventral part of pons
PERSISTENT VEGETATIVE STATE
A persistent vegetative state is observed in patients
who have barely emerged from coma or have
progressed into a state of profound dementia.
The patient is awake, blinks to threat, and is
capable of a few primitive postural and reflex
movements but is otherwise without awareness and
responsiveness.
PERSISTENT VEGETATIVE STATE
CF
: No discrete localizing motor responses.
Lack of cognitive function.
Sleep-Wake cycle (+).
Intact brainstem reflexes
Open eyes in response to verbal stimuli.
Does not follow verbal commands.
S of L : Scattered lesions in the CNS.
AKINETIC MUTISM :
CF
: Mental activity and motor activity are
almost entirely absent.
The patients follow object with their eyes
but do not recognize.
Mute, intact-sleep-wake cycle (+).
Relative paucity of signs.
S of L : Ventral diencephalon.
PROFOUNDCOMA
Profound coma, with total unreceptivity of all
forms of stimulation and total unresponsivity, is
often accompanied by loss of all brainstem and
spinal reflexes. The pupils are fixed and dilated.
Spontaneous breathing and blink, vestibuloocular, and oropharyngeal reflexes are abolished.
In the absence of hypothermia or the severe
effects of depressant medication and the
presence of an isoelectric EEG, the condition
conforms to brain death.
MECHANISMS WHEREBY CONSCIOUSNESS IS
DISTURBED BY DISEASES
NORMAL FUNCTION
Consciousness depends on the normal functioning
of the reticular formations of the midbrain and
thalamus and their connections with all parts of
the cerebral cortex, to which they send and from
which they receive fibers.
LESION PRODUCING COMA
1. Lesion damaging, ARAS which is located
from the upper medulla to the
hypothalamus.
2. Diffuse or bilateral lesions in the cerebral
cortex.
SMALLEST LESIONS
From this it follows that a diffusely decorticate
person is comatose. But the smallest lesions that
produce coma are always to be found in the upper
brainstem reticular formation; they deactivate the
cerebral cortex. Lesser degrees of impairment of
these structures cause drowsiness, inattentiveness,
and an inability to sustain mental activity.
MECHANISMS CAN BE IMPAIRED
The following are the mechanisms by which the
reticular activation of the cerebral cortex can be
impaired :
1.
2.
3.
4.
5.
6.
7.
A generalized seizure.
Cerebral concussion.
Drugs.
Metabolic derangements.
Destructive lesions.
Massive lesion of one cerebral hemisphere.
Critical decline in blood pressure.
CAUSES OF COMA :
Most Frequent Causes of Coma In the Series of Plum
Posner, from the New York Hospital, approximately
one-third of the patients admitted in coma proved
to be suffering from drug poisoning, one-third from
metabolic disease, anf one third from
cerebrovascular disease.
IMPORTANT POINTS IN THE DIFFERENTIAL DIAGNOSIS
OF THE COMMON CAUSES OF COMA
General group
I.
Coma with focal or
lateralizing signs of
brain diseases.
Specific disorder
Brain tumor
Slowly progressive papilledema
Cerebral haemorrhage
Cerebral thrombosis
Cerebral embolism
- Sudden onset of
hemiplegia/bilateral
- SSS
Fracture or concussion
- Head trauma
- Skull fracture
Subdural hematoma
-History of head trauma
Brain abscess
- Headache, papilledema
- Chronic ear, sinus or
pulmonary infection.
General group
Specific disorder
II. Coma without focal or
lateralizing signs, with
signs of meningeal
irritation.
Meningitis
- Fever, subacute onset
change in CSF.
Subarachnoid haemorrhage
- Sudden onset severe
headache.
- Bloody or xanthochromic
CSF
Alcohol intoxication
- Alcohol breath
- History of alcohol intake
- High blood alcohol
Barbiturate intoxication
Hypothermia
Hypotension
Opiate intoxication
-Slow respiration, cyanosis,
constricted pupils.
III. Coma without focal
neurologic signs or
meningeal irritation; CT
scan and CSF normal.
General group
IV. Coma without
focal neurologic
signs or meningeal
irritation; CT scan
normal
Specific disorder
Carbon monoxide intoxication.
- Cherry red skin
- Lab. Finding : carboxy
haemoglobin.
Anoxia.
Hypoglycemia.
Diabetic coma.
Uremia.
Hepatic coma.
Hypercapnia.
Severe infections (septic
Shock); heat stroke.
Idiopathic epilepsy.
HERNIATION OF THE BRAIN
I. Types of brain herniation
Type
Causes
A. Uncal
herniation
(herniation
of uncus
through the
tentoril
hiatus
Laterally
located
supratentorial
mass lesion
Symptoms and signs
Ipsilateral dilated
pupil oculomotor
nerve palsy stuporcoma ipsilateral
hemiplegia
(Kernohans notch)
bilateral Babinski
sign decerebrate
rigidity.
Type
Causes
Symptoms and signs
B. Central
herniation
(herniation
of diencephalon
Medially located
supratentorial
mass lesion
Change in alertness
or behavior
drowsiness-coma
yawn.
Cheyne-Stokes
respiration small
reactive pupils
ipsilateral paratonia
bilateral Babinski
sign decorticate
rigidity.
Type
C. Tonsillar
herniation
(herniation
of cerebral
tonsils
through the
foramen
magnum.
Causes
Posterior fossa
mass lesion or
progression of
central
herniation
Symptoms and signs
Arching of the neck
stiff neck
respiratory arrest.
Type
Causes
Symptoms and signs
D. Upward
tentorial
herniation
(herniation of
cerebellum
and midbrain
upward
through the
tentorial
hiatus).
Posterior fossa
mass lession.
Upward gaze palsy
stupor-coma signs
similar to uncal
herniation.
Type
E. Subvalcial
herniation
(herniation of
cingulate gyrus
toward the
opposite side
under the falx)
Causes
Frontal lobe
mass lession
Symptoms and signs
Midline shift is seen
with CT scan
usually no
symptoms anterior
cerebral artery
may be compressed
II. Symptoms and signs of raised intracranial pressure
Symptoms
Signs
Headache
Papilledema
Nausea and vomiting
Abducens nerve palsy
Diplopia
Decreased level of
consciousness
Amblyopic attack
Hypertensia
Bradycardia
Macrocrania (infant, child)
Bulging fontanel (infant)
Separated sutures (infant)
III. Common causes of raised intracranial pressure.
IV. Reversed and irreversible stages
Reversible stage
Irreversible stage
Pupils
Ipsilateral large fixed
pupil
Bilateral midposition
fixed pupil
Caloric test
Ipsilateral oculomotor
nerve palsy
No response
Respiration
Normal-central
neurogenic
Central neurogenic
Hyperventilation
Hyperventilation
Decerebrate or
decorticate rigidity
Decerebrate rigidity
A. Uncal herniation
Motor response
B. Central hernation
Pupils
Bilateral small reactive
pupils
Bilateral
midposition fixed
pupils
Caloric test
Full conjugate
movement
No response
Respiration
Yawns
Central
neurogenic
Cheyne-Stokes
respiration
Motor response
Decorticate rigidity
Ipsilateral paratonia
Hyperventilation
Decerebrate
rigidity
V. Criteria for brain death
A. Coma or unresponsiveness
B. Apnea
C. Absence of brainstem reflexes
D. Electrocerebral silence
E. Absence of drug intoxication
F. Persistence of conditions for 6-24 hours
G. Absence of short-latency auditory evoked potentials
except for wave I
H. No intracerebral filling in angiography (option)
EXAMINATION OF COMATOSE PATIENTS
I.
II.
Vital signs and emergency management.
History from relatives or friends
Trauma
Lucid interval
Drugs and chemicals
Narcotics, drugs, alcohol, toxic
substances
Time course
Onset and progression
Proceeding symptoms
Seizure, headache, depression,
hemiplegia, fever, vertigo,
vomiting
Previous illness
Previous attack, hypertension,
diabetes mellitus, epilepsy,
lung disease, heart disease, uremia,
hepatic cirrhosis, cancer, allergy,
infectious disease, endocrine
disease, TIA, psychiatric disease.
III. Physical examination
Blood pressure
Pulse
Respiration
Temperature
Evidence of head
trauma
Hypotension, hypertension
Slow, irregular, rapid.
Hyperventilation,
hypoventilation, Kussmauls
respiration, rapid slow
respiration, Cheyne-Stokes
respiration, central
neurogenic respiration,
ataxic respiration.
fever, hypothermia.
Battles sign, raccoons eyes,
Scalp laceration or swelling,
blood or CSF in nares or an ear,
Localized tenderness.
PHYSICAL EXAMINATION 2
Breath odor
Alcohol, acetone, fetor hepaticus,
uriniferous smell.
Heart
Lungs
Arrhythmia, heart murmur.
Consolidation, fluid, pulmonary
congestion
Abdomen
Distention, mass, ascites, enlarged liver,
defense musculaire.
Skin
Laceration, ptechiae, cyanosis, cherry
red skin, sweating, pallor, jaundice,
needle mark.
Clothes
Blood, vomitus, alcohol, urine, feces,
IV. Neurological examination
Level of consciousness
Visual field
Optic fundi
Pupils and light reflex
Deep coma, semicoma, stupor,
somnolence.
Blinking response to visual threat
Papilledema
Pinpoint pupils, anisocoria, dilated
pupils.
Eye position and extraocular
movement
Gaze preference, skew deviation
Posture, muscle tone,
weakness, movements
Hemiplegia, decorticate rigidity,
decerebrate rigidity.
Reflexes
Muscle stretch reflexes, Babinski
sign
Stiff neck and Kernigs sign
V. Laboratory examination.
Blood
CBC, differential count, BUN,
glucose, ammonia, electrolytes,
calcium, magnesium, arterial blood
gas, alcohol.
If necessary, perform screening tests
for drugs and toxic substances, liver
function studies, viral titers, thyroid
studies, adrenal studies, coagulation
studies and blood culture.
Urine
Screening tests for drugs and toxic
substances, protein, glucose,
acetone
Laboratory examination 2
Electrocardiogram
Myocardial infarction, atrial
fibrillation complete AV block.
X rays
Chest, skull, cervical spine if
necessary.
Head CT scan or MRI
Mass lesion.
Lumbar puncture
Pressure, color, cell counts, protein,
glucose, culture, Gram stain.
EEG
Seizure activity, triphasic waves
Cerebral angiography
It is performed when brain tumor or
subarachnoid hemorrhage is
suspected.
Gastric aspirate or lavage
It is performed when drug ingestion
is suspected.
MANAGEMENT OF COMATOSE PATIENTS
I.
Emergency management.
Maintain respiration
Airway, suctioning, oxygen
inhalation, intubation and
artificial ventilation may be
necessary.
Maintain circulation
Treatment of shock if
present.
Insert IV catheter, draw blood and give 50%
glucose 50ml IV.
Treatment of seizure if present.
II. Specific treatment.
Thiamine 100 mg IV for Wernickes encephalopathy
Naloxone 0.4 0.8 mg IV for opiate overdossage
Immersion in an icewater bath for heat stroke
III. Medical treatment of raised intracranial pressure if
present.
Hyperventilation
By using a respirator, the Pco2
should be lowered to 25-30 mmHg
Mannitol
250-500ml of 20% solution infused
over 30 minutes (used with caution
in patients with heart failure).
Glycerol
May be used instead of mannitol.
Dexamethasone
10mg IV immediately, then 4mg IV
or IM every 6 hours (used with
caution in patients with bleeding
peptic ulcer).
IV. Surgical treatment of raised intracranial pressure
If indicated.
Techniques
External decompression
Indications
Diffuse swelling (failure on
medical therapy).
Internal decompression
Large space-occupying lesion
(focal mass effect).
Ventricular drainage
Obstruction of CSF pathway.
V. Symptomatic treatment.
Urinary retention
Indwelling catheter
Severe ventilatory
failure
Suction, intubation or
tracheostomy
Gastrointestinal
bleeding
Ice water lavages, volume
replacement
Heart failure
Digoxin 0.25-0.5mg IV, followed by
0.25mg at 4-hour intervals if
needed to a total dose of 1 mg
(average digitalizing dose is 1-2mg)
Fever
Ice bag, antibiotics if indicated
Vomiting
Prochlorperazine (used with
caution in patients with severe CNS
depression
Agitation
Diazepam 10mg IM
VI. Nursing care
Nutrition
IV solutions initially, later tube
feeding.
Frequent suction Suction the nasopharynx and mouth
Skin
Turn the patient every 1-2 hours to
prevent decubitus ulcer.
Cornea (eyes)
Tape the patients eyelids shut and
use methylcellulose eyedrops.
VII. Cardiopulmonary resuscitation
A. Airway
Tilt the head back, manual clearing
of the mouth, suction, tracheal
intubation.
B. Breathing
Mouth-to-mouth breathing, O2
inhalation with Ambu bag, respirator
C. Circulation
External cardiac massage
D. Drugs
Epinephrine, IV (every 5-15 minutes
if necessary)
E. Electrocardiogram
Differentiate ventricular fibrillation
from asystole.
Cardiopulmonary resuscitation 2
F. Fibrillation
treatment
External defibrillation D. C. 100-400
watt-seconds (repeat shock as
necessary).
Lidocaine HCl 50-100mg IV (in 1-2
minutes), followed by 1-3mg/min drip
infusion (50ml of 1% lidocaine HCl in
500ml of 5% dextrose in water.
Table : Glassgow Coma Scale
Eyes open
Never
To pain
To verbal stimuli
Spontaneously
Best verbal response
1
2
3
4
No response
Incomprehensible
Inappropriate words
Disoriented and converses
Oriented and converses
Best motor response
No response
Extension (decerebrate rigidity)
Flexion Abnormal (decorticate rigidity)
Flexion withdrawal
Localizes pain
Obeys
6
3-15
Circle the appropriate number and compute the total
KESIMPULAN
1. Koma sebagai tanda emerjensi neurologi dimana
etiologinya cukup banyak dan rumit.
2. Manajemen pasien koma berupa penegakan
diagnosis dan terapi dilakukan secara serentak.
3. Perlu perawatan canggih meliputi :
a. 5-B
b. Terapi etiologik
c. Alat bantu diagnostik canggih
d. Perawatan canggih (ICU)
- Nutrisi parental total
- Ventilator/respirator
e. Brain activator
Kesimpulan
4. Prognosis :
Hati-hati
Dubia ad malam
Penjelasan yang canggih kepada keluarga
pasien.
Dokter dalam posisi transaksi upaya (inspaning
verbentenis).
Wassalam
