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Consciousness is a state in which a person is fully aware of himself and his surroundings.

The judgable
component of a conscious state is the quality of consciousness itself and its content. The content of
consciousness describes the whole of the cerebral cortex function, including cognitive function and
attitude in response to a stimulus. Patients with consciousness disorders usually appear to be fully
conscious, but can not respond well to some stimuli, such as discriminating colors, facial features,
recognizing language or symbols, so it is often said that the patient appears confused4. Decreased
consciousness or coma becomes a hint of malfunctioning brain integrity and as a "final common
pathway" of organ failure such as heart failure, breathing and circulation will lead to brain failure with
death. So, if there is a decrease in awareness of disregulasi and dysfunction of the brain with the
tendency of failure of all body functions. In terms of assessing the decrease in consciousness, there are
known terms used in the clinic of compost mentis, somnolen, stupor or sopor, mild coma and coma.
The terminology is qualitative. Meanwhile, the decline in consciousness can also be quantitatively
assessed, using the Glasgow4 coma scale.

Determining Qualitative Awareness Reduction4.5 a. Compost mentis means normal consciousness,


aware of all intake of the senses (aware or awas) and reacts optimally to all stimuli from the outside or
from the inside (arousal or alert), or in the state of alert and alert. b. Somnolen or drowsiness.
Awareness can be fully recovered when stimulated. Somnolen is also called as: latergi, obtudansi. This
level of consciousness is characterized by the ease with which the patient is awakened, able to give
verbal answers and fend off excitatory pain. c. Sopor or stupor means deep sleep. Patients can still be
awakened with a strong stimulus, but his consciousness soon decreases again. He was still able to
follow a short message, and still looks spontaneous movement. With excitatory pain the patient can not
be built perfectly. The reaction to the command is inconsistent and vague. Can not get verbal answers
from patients. Motion to fend off excitatory pain is still good. d. Lightweight coma (semi-coma). In this
state there is no response to the verbal stimuli. Reflex (cornea, pupils and so forth) is still good.
Movement mainly arises in response to unorganized pain stimuli, a "primitive" answer. Patients can not
be awakened at all. e. Coma (in or complete). There is no spontaneous movement with no response at
all to the excitement of pain which however strong. f. Delirium is an abnormal mental state
characterized by disorientation, fear, irritability, misperception of sensory stimulation, and often
accompanied by visual hallucinations. Such behavior usually puts the sufferer in nature unrelated to his
environment, and sometimes the patient has difficulty recognizing himself. This can also be interrupted
by a lucid interval. Delirium usually causes delusions like a complex, systematic dream world and
continues to have no contact at all with the environment and psychologically. Patients generally
become a lot of talk, talk loud, attacking, suspicious, and agitative. This condition is rapid and rarely
lasts more than 4-7 days but misperceptions and hallucinations can last for weeks, especially in patients
with alcoholics or patients associated with collagen vascular disease. The delogenic state usually
presents in neurological toxic and metabolic disorders such as acute atropine poisoning, drug withdraw
syndrome (alcohol-barbiturate), acute porphyria, uremia, acute liver failure, encephalitis, collagen
vascular disease. The form of epileptic status involving the limbic system often also causes a syndrome
that is difficult to distinguish from this delirium.

Determining Quantitative Decrease of Awareness5 To follow the development of the level of


consciousness can be used Glasgow coma scale that attention to responses (responses) patients to
stimuli and provide value to the response. The response / response of patients to note is: Eye: • E1 does
not open the eyes with excitatory pain • E2 opens the eyes with painful excitement • E3 opens the eyes
with sound excitement E4 opens spontaneous eyes Motoric: • M1 does not perform motor reactions
with excitatory pain • M2 deserebrasi reaction with excitatory pain • M3 decontamination reaction with
excitatory pain • M4 reaction approaches excitatory pain but does not reach the target • M5 reaction
approaches excitatory pain but reaches the target • M6 motor reactions according to command Verbal: •
V1 does not elicit a verbal response with excitatory pain (none) • V2 response moan with excitatory
pain (sounds) • V3 response of words with excitatory pain (words) • V4 talk with sentences but
disoriented time and place (confused) • V5 talk with a sentence with a good orientation If the value of
GCS 14-13 indicates somnolen, 12-9 sopor, and less than 8 indicates a comma.

Two simpler scales ACDU (alert, confused, drowsy, unresponsive), and AVPU (alert, response to
voice, response to pain, unresponsive). The AVPU scale is a quick and easy way to assess the level of
awareness. This examination is ideal as a preliminary and quick assessment, consisting of: 2 • Alert •
Response to sound • Response to pain • Loss of consciousness AVPU is included in some early
warning scoring systems for critical patients, as a simpler way than GCS, but not suitable for long-term
observation2.
a) S: Circulation Includes stroke and heart disease b) E: Encephalitis Keeping in mind the existence of
systemic infection / sepsis that may be underlying or appearing simultaneously. c) M: Metabolic For
example hyperglycemia, hypoglycemia, hypoxia, uremia, hepatic coma d) E: Electrolyte For example,
excessive diarrhea and vomiting. e) N: Neoplasm Both primary and metastatic brain tumors f) I:
Intoxication Intoxication of various drugs and chemicals can cause a decrease in consciousness g) T:
Trauma Especially capitis trauma: komusio, kontusio, epidural bleeding, subdural hemorrhage, can
also trauma abdomen and chest. h) E: Epilepsy Post-attack Grand Mall or on status epilepticus can
cause decreased awareness

Pathophysiology of Decreased Awareness


Decreased consciousness is caused by overall cortical disorders such as metabolic disorders, and may
also be caused by ARAS disorders in the brain stem, to the reticular form in the thalamus,
hypothalamus, or mesencephalon. In the decrease of consciousness, the disorder is divided into two,
namely disturbance of degree (quantity, arousal, wakefulness) awareness and disturbance of content
(quality, awareness, alertness) awareness. The presence of lesions that may interfere with ARAS
interactions with the cerebral cortex, whether supratentorial, subtentorial, infratentorial, and metabolic
lesions will result in decreased awareness. RAS (reticular activating system) is a system that regulates
some important functions such as sleep and waking, attention / focus, one's behavior, breathing and
heart rate. This system resides in the brainstem, divided into ascending (which receives impulses) and
descending (which responds to impulses given). The areas that regulate ARAS (ascending) are
formation of reticularis, mesencephalon, thalamic intralaminar nucleus, dorsal hypothalamus, and
tegmentum. In DRAS (descending), the impulse is passed to the peripheral nerves that end in the end
plate and cerebellum motor. Neurotransmitters that play a role in the RAS pathway are cholinergic and
adrenergic, sometimes GABA also plays a role in the stimulation of pain given to assess a person's
consciousness.

The diagnostic approach is no different from other cases, ie through the order of anamnesis, neurologic
physical examination, and investigation. The difference lies in the demands of the speed of thinking
and acting. Anamnesis (disease history) Decreased Awareness2 Ask the patient or in the introduction
to the surroundings of the onset and the course of the illness. Some important points to ask: - Awitan:
time, surroundings. - Patient age is an important part of history. In previously healthy patients, younger
age, conscious decline occurs abruptly, the possible cause of drug poisoning, subarachnoid
hemorrhage, or head trauma. While in old age, a sudden decrease in consciousness is more likely due
to cerebral bleeding or infarction. - Symptoms that precede in detail (confusion, headache, weakness,
dizziness, vomiting, or seizures), focal symptoms such as difficulty speaking, unable to read, memory
changes, disorientation, numbness or pain, motor weakness, reduced encephal , vision changes,
difficulty in swallowing, hearing loss, step or balance disorders, tremor. - Use of drugs or alcohol. -
History of heart disease, lung, liver, kidney, or anything else

Physical Examination Decreased awareness8


a) Vital signs Examination of vital signs: note the airway, respiratory type and note about the
circulation that includes: blood pressure, pulse and the presence or absence of arrhythmia. b) Breath
and breathing patterns Breath odor may indicate the presence of certain pathologic processes such as
uremia, ketoacidosis, drug intoxication, and even the ongoing death process. Examination of
respiratory pattern such as:
- Cheyne-Stokes (apnea breathing, then gradually increase in amplitude) → upper hemisphere and / or
brainstem disturbance - Kussmaul (fast and deep breathing) → disturbance in tegmentum (between
mesensephalon & pons) - Apneustic (deep inspiration followed expiration cessation for a long time) →
disruption in the punch - Ataxic (shallow, fast, irregular breathing) → disorder in dorsomedial &
medullary fomartioretikularis Oblongata c) Examination of the skin: on skin examination, need to be
observed signs of trauma, stigmata liver disorders and other stigmata including crepitus and injection
injection. In patients with trauma, the head of the neck examination should be performed with extreme
caution or should not be performed if a cervical fracture is suspected. If that possibility does not exist,
then do a stiff examination of the neck and do auscultation karotis to find the presence or absence of
bruit. d) Head: note the presence or absence of hematoma, lacerations and fractures. e) Neck: note
numb stiffness and do not manipulate if suspected cervical fracture (jejas, paralysis of 4 extremities,
trauma in the face). f) Toraks / abdomen and extremities: note the presence or absence of fracture.
Neurological Examination Decreased Awareness8
Neurological physical examination aims to determine the depth of the coma qualitatively and
quantitatively as well as to know the location of the comma process. Neurological examination
includes the degree of awareness and motor examination2. a) General - Open the eyelid determines the
comma - Head and glance deviations show ipsilateral hemisphere lesions - Pay attention to myoclonus
(metabolic process), twitching rhythmic muscle (activity - seizure) or tetani (spontaneous, old muscle
spasmus). b) Awareness level - Qualitative (apathetic, somnolen, delirium, soporo and coma) -
Quantitative (using GCS) c) Pupils - Checked: size, light reactivity - Symmetrical / normal light
reactivity, a hint that the integrity of mesensefalon is good. Normal reaction pupil, corneal reflex and
oculocephalose (-), suspected of a metabolic coma - Midposition (2-5mm), ixixed and irregular, focal
mesenfalon lesions. - Pupil reactive point-point, on the damage of the punch, intoxication of
cholinergic opiate. - Unilateral dilatation and ixixed, herniation occurs. - Bilateral and dilated bilateral
pupils, central herniation, global hypoxic - ischemia, barbituric poisoning. - Funduscopy: At the
funduscopic examination consider the state of papil. whether there is edema, bleeding, and exudation,
and how the state of blood vessels. Increased intracranial pressure may result in paparane edema. d)
Oculovestibular / oculocephalic reflex (dolls eye maneuver) The movement of the eyeball to glance
and focus the view is governed by the oculomotor nerve. The nucleus of the oculomotor nerve gets an
afferent impulse from the cortical, tectal, and tegmental oculomotor systems, as well as direct impulses
from the vestibular system and vestibule cerebellum. The oculovestibular reflex is examined by turning
on the patient's head, but should be cautious in trauma patients who are suspected of fracture or
dislocation of the cervical bone. In addition to allowing the patient's head, it can also test calories.
Normal response of motion that causes impulses in the vestibular to the oculomotor system and makes
the eyes rotate in opposite directions with the motion provided by the examiner. In the conscious
patient, the reflex focuses the view on the reflex, so that the examination of the doll's eye is not
performed on the conscious patient, but in the patient with conscious decline. Oculoauditorik reflex,
when stimulated loud voice of the sufferer will close the eyes then the disruption in the punch. While
on the okulovestibular reflex when the extensus autikus meatus stimulated warm water will arise
nystagmus toward the stimulation of the disruption in the punch.

THERAPY 3B Early therapy


a. Place the patient's head at 30º, head and chest in one area; change the sleeping position every 2
hours; mobilization begins gradually when hemodynamics is stable. Next, free the airway, give oxygen
1-2 liters / minute to obtain the results of blood gas analysis. If necessary, intubation is performed.
Fever is overcome with compress and antipyretics, then look for the cause; if the bladder is full,
emptied (preferably with intermittent catheter).
b. Provision of nutrients with isotonic, crystalloid or colloidal fluids 1500-2000 mL and electrolytes as
needed, avoid fluids containing glucose or isotonic saline. Provision of oral nutrition only if good
swallowing function; if swallowing or decreased awareness is obtained, it is recommended through a
nasogastric tube.
c. Blood sugar> 150 mg% should be corrected to the blood sugar limit at 150 mg% with continuous
intravenous drip insulin for the first 2-3 days. Hypoglycemia (blood sugar <60 mg% or <80 mg% with
symptoms) is treated promptly with 40% dextrose iv until it returns to normal and should be looked for.
d. Headache or nausea and vomiting are treated with symptomatic medication. Blood pressure should
not be reduced immediately unless systolic pressure ≥220 mmHg, diastolic ≥120 mmHg, Mean Arterial
Blood Pressure (MAP) ≥ 130 mmHg (at 2 times measurements by 30 minutes interval), or acquired
acute myocardial infarction, heart failure congestive and kidney failure. Maximum blood pressure
decrease is 20%, and recommended drugs: sodium nitroprusside, alpha-beta receptor blockers, ACE
blockers, or calcium antagonists. In the event of hypotension, ie systolic pressure ≤90 mm Hg, diastolic
≤70 mmHg, given 0.1% NaCl 250 mL for 1 hour, continued 500 ml for 4 hours and 500 mL for 8 hours
or until hypotension can be overcome. If not corrected, ie systolic blood pressure <90 mmHg, can be
given 2-20 μg / kg / min dopamine to systolic blood pressure ≥ 110 mmHg.
e. If seizures, given diazepam 5-20 mg iv slowly for 3 minutes, maximum 100 mg per day; followed by
oral anticonvulsants (phenytoin, carbamazepine). If seizures appear after 2 weeks, long-term oral
anticonvulsants are given.
f. If increased intracranial pressure is increased, intravenous mannitol is given intravenously 0.25 to 1 g
/ kgBW per 30 minutes, and if suspected rebounding phenomenon or general general condition
worsens, 0.25g / kgBW per 30 minutes every 6 hours for 3-5 days. Osmolality (<320 mmol)
monitoring should be performed; Alternatively, a hypertonic solution (NaCl 3%) or a furosemide may
be given.
PATOGENESIS CVD H
Intracerebral haemorrhage occurs in 3 phases, the initial hemorrhage phase, expansion hematoma and
peri-hematoma edema. The initial hemorrhage phase is due to the rupture of the cerebral artery. chronic
hypertension, will lead to pathological changes of the blood vessel wall. Pathological changes of blood
vessel wall can be hypohialinosis, fibrin necrosis and the incidence of Bouchard type aneurysms. A
significant increase in blood pressure and increased heart rate can induce aneurysm rupture, which can
lead to bleeding. This bleeding will be the beginning of the onset of clinical symptoms (phase
hematoma expansion). 1,2,12 In the expansion hematoma phase, clinical symptoms begin to arise such
as increased intracranial pressure. Increased intracranial pressure will interfere with the integrity of
brain tissue and blood brain barrier. Intracerebral haemorrhage over time causes secondary
inflammation and cerebral edema (peri-hematoma edema phase). In this phase the neurological deficit,
which begins to appear in the expansion hematoma phase, will continue to grow. Damage to the
cerebral parenchyma, due to the relatively high volume of bleeding will result in elevation of
intracranial pressure and decrease the pressure of brain perfusion and disruption of brain drainage. The
vasoactive elements of the outbreaking blood and ischemic cascade due to decreased perfusion
pressure cause neurons in the affected area to become more depressed and neurologic deficits will
develop.

a) S: Circulation Includes stroke and heart disease


b) E: Encephalitis Keeping in mind the existence of systemic infection / sepsis that may be underlying
or appearing simultaneously.
c) M: Metabolic For example hyperglycemia, hypoglycemia, hypoxia, uremia, hepatic coma
d) E: Electrolyte For example, excessive diarrhea and vomiting.
e) N: Neoplasm Both primary and metastatic brain tumors
f) I: Intoxication The intoxication of various drugs and chemicals can cause a decrease in
consciousness
g) T: Trauma Especially capitis trauma: komusio, kontusio, epidural bleeding, subdural hemorrhage,
can also trauma abdomen and chest.
h) E: Epilepsy Post-attack Grand Mall or on status epilepticus can cause decreased awareness