PENURUNAN

KESADARAN
Umam Fazlurrahman
 Definisi

 Consciousness can be understood as an individual

experience, which, on the one hand, necessitates the
existence of a “self,” and on the other hand, originates
from the interaction of the self with its inner and outer
world.

 Pragmatically, quantitative and qualitative aspects of

consciousness can be distinguished. Alertness and
attention
 FISIOLOGI

Vigilance/ Kewaspadaan
 Normal activity in the so-called ascending reticular
activation system (ARAS) is necessary for normal
alertness (vigilance; Fig. 32.1).

 This system consists of projections from aminergic and

cholinergic neurons, which are localized in the rostral
(upper) pons, in the tegmental (dorsal) mesencephalon,
and in the posterior hypothalamus
 FISIOLOGI (2)

Lucidity / Sadar
 Currently it is believed that normal lucidity depends on
sufficient tonic activity of the ARAS and cortical regions
as well as “phasic” (i. e., short lasting), synchronized
activation (i. e., binding) of thalamo−corticothalamic
and cortico-cortical networks.

 Synchronized activation of thalamo-prefrontal, as well

as thalamo−temporo−parietal, networks seems to be
the basic requirement for focussed and sustained
attention.
 Disturbances of Consciousness:
Pathophysiology

➤ Diffuse, bilateral, or multifocal cortical diseases (e. g., in

the context of metabolic−toxic encephalopathies)

➤ Focal, supratentorial diseases with space-occupying

effects, transtentorial herniation, and brain stem
compression (e. g., in the context of a cerebral infarct)

➤ Focal, infratentorial diseases (e. g., in the context of a

cerebral infarct).
 Disturbances of Consciousness:
Clinical Features

 Somnolence. is the mildest form of a quantitative

disturbance of consciousness. Simple external
stimulations make the patient who appears slow and
often falls asleep, react adequately.
 Sopor. patient can only be awakened temporarily and
incompletely by very strong and repeated stimulations
(pain, among others).
 Coma. corresponds to a complete state of
unconsciousness with closed eyes and without any
comprehensible reaction to external stimulations,
intelligible verbal expression, or goal-directed motor
resistance (pain reaction).
Disturbances of Consciousness: Clinical
Examination, Signs, and Symptoms
 Disturbances of Consciousness: Clinical
Examination, Signs, and Symptoms (2)

The remaining neurologic examination includes

 the examination of eye movements (spontaneous, during
head rotation [oculo−cephalic reflex] and after ice water
irrigation [so-called vestibulo−ocular reflex]),
 pupillary reflexes,
 corneal reflexes,
 limb movements (spontaneous and on painful
stimulation),
 muscle tone, muscle reflexes,
 Babinski reflex, and meningeal signs
 Additional Diagnostic Procedures.

 laboratory work-up (hemogram, blood glucose,

electrolytes, and kidney and liver parameters), urinalysis,
 ECG
 Chest X-Ray
 blood gas analysis
 thyroid parameters
 Serologies
 Thiamine level should be requested if there is an urgent
suspicion.
 Head CT Scan, EEG
Vigilance, Attention, and Mental
State

 Vigilance
 Attention
If vigilance is normal,
then attention can be
examined -> “forward
digit span”
 Cognitive Function
Physical Examination
 Motor Functions

 Limb movements in flexion or extension, which occur spontaneously

or after painful stimuli, can be seen in a structural, as well as in a
metabolic coma.

 The association of a hemiparesis, possibly with flexion in the arm and

extension in the leg, with a contralateral, upon light exposure
nonreactive, large pupil with ptosis (III-paresis) and an increasing
quantitative disturbance of consciousness, corresponds to a socalled
uncal syndrome and indicates herniation of a supratentorial space-
occupying lesion, which is ipsilateral to the pupillary dysfunction.

 A Babinski reflex can be observed in a coma (as well as during sleep)

and must not be considered at all to be proof of a structural lesion.
 Coma with Primarily Cerebral
Causes

Diffuse (or Multifocal) Diseases/Lesions of the Central Nervous System

➤ A subacute course is most frequent.
➤ Focal neurologic signs are often not present.
➤ Frequently, normal brain stem reflexes are observed.
➤ Neuroimaging (CCT/brain MRI) can be either positive or negative.

Focal Diseases/Lesions of the Central Nervous System

➤ often acute course
➤ focal neurologic signs often predominant
➤ brain stem reflexes primarily normal in supratentorial, primarily
abnormal in infratentorial processes
➤ mostly positive neuroimaging (CCT/brain MRI).
 Psychogenic Coma

 May present as brief syncopelike episodes, as automatism

behaviors (possibly as “fugue”), as catatonic stupor (see
above), and as continuing sopor or coma.
 A passive opening of the eyes, as well as gazing in the
direction of a passive head movement.
 A normal EEG and normal motor-evoked potentials may
be helpful in recognizing a psychogenic coma with
missing motor re-typical nystagmus is observed after
caloric stimulation.
 Patients may also show involuntary eyelid closure after
sponses.
 Coma Due to Metabolic
Disorders

1. Hypoglycemic Coma
 Patients with Diabetes Mellitus
 Being treated with OAD
 Being treated with insulin

 Patients without Diabetes Mellitus

 Reactive Postprandial Hypoglycemia
 Fasting Hypoglycemia
 Other Causes of Hypoglycemia (Growth hormone deficiency,
Insulin (auto-)antibodies, exogenous, i. e., toxic or drug-induced,
hypoglycemia)
 Coma Due to Metabolic
Disorders

2. Diabetic Coma
 Ketoacidotic Coma
 Hyperglycemia ensues with osmotic diuresis, dehydration, and loss
of electrolytes, as well as hyperketonemia with metabolic acidosis.
 Extracellular hyperosmolality causes cerebral dysfunction and in
severe cases, coma
 Hyperglycemic Hyperosmolar Nonketotic Coma
 Coma Due to Metabolic
Disorders

3. Hepatic Coma

Hepatic encephalopathy is a brain dysfunction caused by liver

insufficiency and/or PSS; it manifests as a wide spectrum of neurological or
psychiatric abnormalities ranging from subclinical alterations to coma.
 Coma Due to Metabolic
Disorders
4. Uremic Coma
 Coma Due to Metabolic
Disorders

5. Coma Due to Adrenal Insufficiency

Primary adrenal insufficiency is a rare cause of coma, either in the
setting of a hypoglycemic episode or in an actual addisonian
crisis.

The serum sodium level may remain normal because of

concomitant hemoconcentration. The cortisol deficiency is
reflected by a low plasma glucose concentration and
eosinophilia

low plasma cortisol level despite a simultaneously elevated

concentration of ACTH
 Coma Due to Metabolic
Disorders

6. Coma Due to Pituitary Insufficiency

So-called “lethargia pituitaria” is an extremely rare condition, in

which simultaneous deficiencies of thyroid-stimulating hormone
(TSH) and adrenocorticotropic hormone (ACTH), and therefore
also of thyroxine and cortisol, produce coma
 Coma Due to Metabolic
Disorders
7. Coma Due to Vitamin B1 (Thiamine) Deficiency, i. e.,
Wernicke Encephalopathy
Coma Due to Metabolic
Disorders
8. Septic Enchepalopathy
 Coma Due to Metabolic
Disorders
9. Coma Due to Disturbances of Fluid, Electrolyte, and
Acid−Base Homeostasis
Intoxication-Induced Coma
Intoxication-Induced Coma