Koma Dan Penurunan Kesadaran

 Sebagai tanda emergensi Neurologi

 Jika koma menetap kondisi bisa bertambah buruk
dan berakibat fatal
 Bisa mengakibatkan kerusakan yang irraparably
baik fungsi mental maupun fisik
 Mekanisme Penurunan Kesadaran

Pusat Kesadaran :
1.ARAS
2.Kortek serebri bilateral
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.
 DIFFERENT DEGREES OF COMA

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.
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.
MECHANISMS CAN BE IMPAIRED

The following are the mechanisms by which the

reticular activation of the cerebral cortex can be
impaired :
1. A generalized seizure.
2. Cerebral concussion.
3. Drugs.
4. Metabolic derangements.
5. Destructive lesions.
6. Massive lesion of one cerebral hemisphere.
7. 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 Specific disorder

I. Coma with focal or Brain tumor

lateralizing signs of Slowly progressive papilledema
brain diseases. 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 Meningitis

- Fever, subacute onset
lateralizing signs, with change in CSF.
signs of meningeal Subarachnoid haemorrhage
- Sudden onset severe
irritation. headache.
- Bloody or xanthochromic
CSF
Alcohol intoxication
- Alcohol breath
- History of alcohol intake
III. Coma without focal - High blood alcohol
neurologic signs or Barbiturate intoxication
meningeal irritation; CT Hypothermia
Hypotension
scan and CSF normal.
Opiate intoxication
-Slow respiration, cyanosis,
constricted pupils.
General group Specific disorder

IV. Coma without Carbon monoxide intoxication.

- Cherry red skin
focal neurologic - Lab. Finding : carboxy
signs or meningeal haemoglobin.
irritation; CT scan Anoxia.
normal 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 Symptoms and signs

A. Uncal Laterally Ipsilateral dilated

herniation located pupil oculomotor
(herniation supratentorial nerve palsy stupor-
of uncus mass lesion coma ipsilateral
through the hemiplegia
tentoril (Kernohan’s notch)
hiatus bilateral Babinski
sign decerebrate
rigidity.
Type Causes Symptoms and signs
B. Central Medially located Change in alertness
herniation supratentorial or behavior
mass lesion drowsiness-coma
(herniation yawn.
of dience-
Cheyne-Stokes
phalon respiration small
reactive pupils
ipsilateral paratonia
bilateral Babinski
sign decorticate
rigidity.
Type Causes Symptoms and signs
C. Tonsillar Posterior fossa Arching of the neck
herniation mass lesion or stiff neck
(herniation progression of respiratory arrest.
of cerebral central
herniation
tonsils
through the
foramen
magnum.
Type Causes Symptoms and signs
D. Upward Posterior fossa Upward gaze palsy
tentorial mass lession. stupor-coma signs
herniation similar to uncal
(herniation of herniation.
cerebellum
and midbrain
upward
through the
tentorial
hiatus).
Type Causes Symptoms and signs
E. Subvalcial Frontal lobe Midline shift is seen
herniation mass lession with CT scan
usually no
(herniation of symptoms anterior
cingulate gyrus cerebral artery
toward the may be compressed
opposite side
under the falx)
II. Symptoms and signs of raised intracranial pressure
Symptoms Signs

Headache Papilledema

Nausea and vomiting Abducens nerve palsy

Hypertensia
Diplopia
Bradycardia
Decreased level of
consciousness Macrocrania (infant, child)

Amblyopic attack Bulging fontanel (infant)

Separated sutures (infant)

III. Common causes of raised intracranial pressure.

 IV. Reversed and irreversible stages

Reversible stage Irreversible stage

A. Uncal herniation
Pupils Ipsilateral large fixed Bilateral midposition
pupil fixed pupil
Caloric test Ipsilateral oculomotor No response
nerve palsy

Respiration Normal-central Central neurogenic

neurogenic
Hyperventilation Hyperventilation

Motor response Decerebrate or Decerebrate rigidity

decorticate rigidity
B. Central hernation
Pupils Bilateral small reactive Bilateral
pupils midposition fixed
pupils

Caloric test Full conjugate No response

movement
Respiration Yawns Central
neurogenic
Cheyne-Stokes
respiration Hyperventilation
Motor response Decorticate rigidity Decerebrate
rigidity
Ipsilateral paratonia
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. Vital signs and emergency management.
II. 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 Hypotension, hypertension
Pulse Slow, irregular, rapid.
Respiration Hyperventilation,
hypoventilation, Kussmaul’s
respiration, rapid slow
respiration, Cheyne-Stokes
respiration, central
neurogenic respiration,
ataxic respiration.

Temperature fever, hypothermia.

Evidence of head Battle’s sign, raccoon’s eyes,

trauma 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 Arrhythmia, heart murmur.

Lungs 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,
drugs.
IV. Neurological examination
Level of consciousness
Visual field
Optic fundi
Pupils and light reflex
Eye position and extraocular
movement
Posture, muscle tone,
weakness, movements
Reflexes
Stiff neck and Kernig’s sign
Deep coma, semicoma, stupor,
somnolence.
Blinking response to visual threat
Papilledema
Pinpoint pupils, anisocoria, dilated
pupils.
Gaze preference, skew deviation
Hemiplegia, decorticate rigidity,
decerebrate rigidity.
Muscle stretch reflexes, Babinski
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.
Chest, skull, cervical spine if
X rays
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 Wernicke’s encephalopathy

Naloxone 0.4 – 0.8 mg IV for opiate overdossage
Immersion in an ice–water 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 Indications

External decompression 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 Suction, intubation or
failure tracheostomy
Gastrointestinal Ice water lavages, volume
bleeding 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 patient’s 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. Electro- Differentiate ventricular fibrillation
cardiogram from asystole.
 Cardiopulmonary resuscitation 2

F. Fibrillation External defibrillation D. C. 100-400

treatment 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 1
To pain 2
To verbal stimuli 3
Spontaneously 4
Best verbal response
No response 1
Incomprehensible 2
Inappropriate words 3
Disoriented and converses 4
Oriented and converses 5
 Best motor response
No response 1
Extension (decerebrate rigidity) 2
Flexion Abnormal (decorticate rigidity) 3
Flexion withdrawal 4
Localizes pain 5
Obeys 6
3-15

Circle the appropriate number and compute the total

KESIMPULAN
1. Koma sebagai tanda emergensi neurologi dimana
etiologinya cukup banyak.
2. Manajemen pasien koma berupa penegakan
diagnosis dan terapi dilakukan secara serentak.
3. Perlu perawatan intesif meliputi :
a. 5-B
b. Terapi etiologik
c. Alat bantu diagnostik
d. Perawatan (ICU)
- Nutrisi parental total
- Ventilator/respirator
e. Brain activator
 Kesimpulan

4. Prognosis :
 Hati-hati
 Dubia ad malam
 Penjelasan yang tepat kepada keluarga
pasien.
 Dokter dalam posisi “transaksi upaya” (inspaning
verbentenis).

Wassalam