Loss of conciousness e.

c CVD
Non Hemorrhage
Aulia Alvianti Akbar, S.Ked
Cahaya Intan, S.Ked

Pembimbing:
dr. H. A. R. Toyo, Sp.S (K)
Neurolgy Deparment
RUMAH SAKIT MOHAMMAD HOESIN PALEMBANG
FAKULTAS KEDOKTERAN UNIVERSITAS SRIWIJAYA
 Introduction
• Cerebrovascular disease refers to a group of conditions that can lead to a
cerebrovascular event, such as a stroke. These events affect the blood supply
to the brain.

• If damage leads to a cerebrovascular attack, there will be little or no blood

supply to parts of the brain. No blood means no oxygen, and, without oxygen,
the brain cells will start to die.

• Some common forms of cerebrovascular disease are stroke, transient ischemic

attack (TIA) and subarachnoid hemorrhage.

• According to Depkes (2011), stroke is the highest cause of death with the
proportion of incidence rate is 15,4% and Approximately 2.85% of people with
stroke in Indonesia died due to stroke
CASE REPORT

Identification

Name : Mr. HB Religion : Islam

Sex : Female Status : Married

Age : 58 y.o Address : Ogan II, Palembang

Education : Senior High Admitted : 9 November

School 2017

Nation : Indonesia
Medical History

1st Paragraph 2nd Paragraph

2 days before entered RSMH
• Patient was
• Patient cames suddenly with decreasing
admitted to consciousness. Patient also didn’t have

Neurologic headache, vomitting, nausea, and seizure.

Patient have experienced weakness on her
Deartement of
right arm and right limb. Bicara pelo can not be
Mohammad Hoesin assessed, mulut mengot can not be assessed.

General Hospital Sensibilities disorders such as sense

numbness, pain and tingling can not be
because of
assessed. Everyday the patient works using the
suddenly right hand. The ability of patient to reveal her

decreasing mind verbally, writings, and cues can not be

assessed. The ability of patient to understand
consciusness
thee thoughts of others expressed verbally,
Medical History

3rd Paragraph 4th Paragraph

• When the attack the patient have

experience heart palpitations and

The patient have
shortness of breath. History of high
experienced this illness
blood preassure since ± 3 years ago, second time. The first
did not take medication & control time since ± 2 years
regularly. History of stroke since ± 2 ago, that was said

years ago. History of diabetes stroke type not

mellitus since ± 2 months ago did

explained, residual
symptoms do not exist.
not take medication & control

regularly. There is no trauma.

Case Report

Physical Examination

Internal State Internal State

Consciousness : E3M5V2 Heart : No abnormality
Blood Pressure : 160/70 mmHg Lungs : No abnormality
Pulse Rate : 61 beats/min, Liver : No abnormality
reguler Spleen : No abnormality
Respiratory Rate : 18 times/min, Extremities : see neurological
reguler state
Temp. : 36,1ºC Genital : No abnormality
Weight : 60 kg
Height : 160 cm
BMI : 23,04 (overweight)
Case Report

Physical Examination

Phychiatric State Neurological State

Attitude : can not be Head

assessed Shape : normocephaly
Attention : can not be Size : normal
assessed Symetric : yes
Facial Expression : no Hematome : no
Phych. contact : no Tumor : no
Case Report
Physical Examination

Neurological State Neurological State

Head Neck
Deformity : no Position : Normal
Fracture : no Torticolis : No
Fr. Pain : no Nuchal rigidity : No
Vessel : no widening Deformity : No
Pulsation : no Tumor : No
Vessels : No widening (-)
Physical Examination

N.I: Olfactory Right Left

Nerves
Smelling Not yet Not yet
N.II: Optical Nerves
Visual acuity Not yet Not yet
Visual field VOD VOS
Anopsia Not yet Not yet
Hemianopsia No No
Oculi fundus
Papil edema No abnormalities No abnormalities
Papil atrophy No abnormalities No abnormalities
Retinal bleeding No abnormalities No abnormalities
Physical Examination
Right Lef
N.III: Occulomotorius
N.IV: Trochlearis
N.VI: Abducens
Diplopia Not yet Not yet
Eyes gap No No
Ptosis No No
Eyes position
-Strabismus Not yet Not yet
-Exophtalmus No No
-Enophtalmus No No
-Deviation conjugae No No

Eyes movement Not yet Not yet

Pupil
-Shape Round Round
-Size d=3 mm d=3 mm
-Isochor/anisochor Isochor Isochor
-Midriasis/miosis - -
Physical Examination

N.III: Occulomotorius Right Lef

N.IV: Trochlearis
N.VI: Abducens

Light reflex
-Direct Positive Positive
-Consensuil Positive Positive
-Accomodation Positive Positive

N.V: Trigeminus nerve

Motoric:
-Biting Not yet Not yet
-Trismus Not yet Not yet
-Corneal reflex Not yet Not yet

Sensory:
-Forehead Not yet Not yet
-Cheek Not yet Not yet
-Chin Not yet Not yet
Physical Examination

N.VII: Facialis nerve Right Lef

Frowning Not yet Not yet
Eyes closing Not yet Not yet
Giggling Normal Mouth angel lef
behind
Nasolabial fold flat lef
Facial shape
-Rest Symmetrical Symmetrical
-Speaking/whistling Not yet Not yet

Sensory
- 2/3 anterior tongue Not yet Not yet

Autonomy
-Salivation Not yet Not yet
-Lacrimation Not yet Not yet
-Chovstek’s sign No No
Physical Examination

N.VIII: Statoacusticus Right Lef

nerve
Cochlearis nerve
Whispering Not yet Not yet
Hour ticking Not yet Not yet
Weber test Not yet Not yet
Rinne test Not yet Not yet
Vestibularis nerve
Nystagmus Not yet Not yet
Vertigo Not yet Not yet
N. IX: Glossopharingeus
N.X: Vagus nerve
Pharyngeal arch No abnormalities No abnormalities
Uvula No abnormalities No abnormalities
Swallowing disorder Not yet Not yet
Physical
N. IX:
Examination
Right Lef
Glossopharingeus
N.X: Vagus nerve
Hoaring/nasalising Not yet Not yet
Heart beat No abnormalities No abnormalities
Reflex
-Vomiting No abnormalities No abnormalities
-Coughing No abnormalities No abnormalities
-Occulocardiac No abnormalities No abnormalities
-Caroticus sinus No abnormalities No abnormalities
Sensory
- 1/3 posterior Not yet Not yet
tongue
N.XI: Accessorius
nerve
Shoulder raising Not yet Not yet
Head twisting Not yet Not yet
Physical Examination
N.XII: Hypoglossus nerve Right Lef
Tongue showing Not yet Not yet
Fasciculation Not yet Not yet
Papil atrophy Not yet Not yet
Dysarthria Not yet Not yet
MOTORIC
Arms
Motion Right lateralization
Power
Tones Increased Normal
Physiological Reflex
-Biceps Increased Normal
-Triceps Increased Normal
-Radius Increased Normal
-Ulna Increased Normal
Physical Examination
MOTORIC Right Lef
Pathological Reflex
Hoffman Tromner No No
Leri No No
Meyer No No
Legs
Motion Right lateralization
Power
Tones Increased Normal
Clonus
-Thigh Negative Negative
-Foot Negative Negative

Physiological Reflex
-KPR Increased Normal
-APR Increased Normal
Physical Examination
MOTORIC Right Lef
Pathological Reflex
- Babinsky Positive Positive
- Chaddock Negative Negative
-Oppenheim Negative Negative
- Gordon Negative Negative
-Schaeffer Negative Negative
-Rossolimo Negative Negative
- Mendel Bechterew Negative Negative
Abnormal skin reflex
-Upper No abnormalities No abnormalities
-Middle No abnormalities No abnormalities
-Lower No abnormalities No abnormalities
-Tropik No abnormalities No abnormalities

SENSORY
Not yet
Physical Examination
VEGETATIVE Right Lef
FUNCTION

Micturition Catheter
Defecation Not yet
VERTEBRAL
COLUMN
- Kyphosis No
-Lordosis No
-Gibbus No
-Deformity No
-Tumor No
-Meningocele No
-Hematome No
-Tenderness No
Physical Examination

MENINGEAL REFLEX Right Lef

Nuchal rigidity No No
Kerniq No No
Laseque No No
Brudzinsky
-Neck No No
-Cheek No No
-Symphisis No No
- Leg I No No
- Leg II No No
Physical Examination

Gait Balance and Coordination

Ataxia : Not yet Romberg : Not yet

Hemiplegic : Not yet Dysmetri : Not yet

Scissor : Not yet finger – finger : Not yet

Propulsion : Not yet finger nose : Not yet

Histeric : Not yet heel - heel : Not yet
Limping : Not yet Rebound phenomenon : Not yet

Steppage : Not yet Dysdiadochokinesis : Not yet

Astasia-Abasia : Not yet Trunk Ataxia : Not yet

Limb Ataxia : Not yet

Physical Examination
ABNORMAL MOVEMENTS LIMBIC FUNCTION

Tremor : No Motoric aphasia : No yet

Chorea : No Sensoric aphasia : No yet
Athetosis : No Apraksia : No yet
Ballismus : No Agraphia : No yet
Dystoni : No Alexia : No yet
Myoclonus : No Nominal aphasia : No yet
Laboratory Finding (20th July 2017)

Haematology Electrolite Kidney Function

• Ureum 133 mg/dL

• Hb 6.1 mg/dL
• Ca 10,2 mEq/L • Creatinin 1.43 mg/dL
• RBC 2.00x106 jt/mm3
• Na 154 mEq/L
• WBC 6.6x103/mm3
• K 4.5 mEq/L
• Ht 18 vol%
• Cl 116 mmol/L
• PLT 13x10 /m3
3

• DC 0/0/44/52/4 %

Haemostasis Carb. Metabolism

• PT, aPTT, INR normal Blood Sugar 444 mg/dL

 Chest X-Ray (25th August CT-Scan ( July 2017)
2017)

Cardiomegaly

Intracebral hematom size 4x2 cm

in lobus frontali dextra
Midline pushed to the left 1 cm
Oedem Cerebri
Intraventricular hematom in
ventricel lateral dextra et sinistra,
Diagnosis

• Unconsciousness + hemiparese sinistra

Clinical flaksid type + parese N. VII sinistra central

Diagnosis type + Monitor General tonic clonic
convulsion

Topical • Frontal dextra, ventricel lateral dextra et

Diagnosis sinistra, III, IV

Etiological • CVD Hemmoraghic

Diagnosis
Case Report

Non-pharmacology Management Pharmacology

• IVFD NS 0,9% gtt xx/menit

• Head elevation 30 o
(makro)
• Bed rest • Inj. Neurobion 1x1 (IV)
• Inj. Citicoline 2x500 (IV)
• O2 NRM 8-10 L/min • Inj. Ranitidin 2x50 (IV)
• Diet : 1600 kkal • Inj. Aspilet 1x80 (IV)
• Inj. Candesartan 1x8 (IV)
• Vital sign and GCS Obs.
Case Report

PROGNOSIS

Quo ad Vitam : Dubia ad malam

Quo ad Functionam : Dubia ad malam
Quo ad sanationam : Dubia ad malam
Loss of Consciousness
Consciousness is a state in which a person is fully aware of his/herself
and his/her surroundings.

The content of consciousness describes the whole of the cortex

cerebri 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 looks confused

A decrease in consciousness becomes an indication of malfunction of

brain integrity and as a "final common pathway" of organ failure such
as heart failure, breathing and circulation will lead to brain failure that
could make people died.
 Loss of consciousness can be assessed
qualitatively and quantitatively
Qualitative Quantitative

 compos mentis Glasgos Coma Scale (GCS)

 somnolen
 stupor or sopor
 light coma and coma
 delirium
Etiology
• Etiology of consciousness is divided into two
groups : metabolic / functional disorders and
structural disorders.

• Metabolic disorders include hypoglycemic /

hyperglycemic states, impaired liver function,
impaired renal function, electrolyte balance
disorder, drug intoxication, food intoxication as
well as chemicals and central nervous system
infections.

• Structural disorders can be subdivided into

supratentorial lesions and infratentorial lesions
Pathophysiology
Loss of consciousness is a form of brain dysfunction
involving left or right hemispheres or other structures
from within the brain or both. Loss of consciousness
caused by cortical disorders in general in metabolic
disorders, and can also be caused by brain-induced
ARAS disorders, to reticular formation in the thalamus,
hypothalamus and mesencephalon.

This system includes areas in the middle of the brain

stem, extending from the midbrain to the hypothalamus
and thalamus, and these structures send the
transmission of diffuse physiological effects to the cortex,
either directly or indirectly, in its role to consciousness.
Diagnosis loss of consciousness

Anamnesis
Physical examination
Neurologic physical examination
Additional examination
Anamnesis
Ask the patient for the course of his/her illness
(Autoanamnesis / Alloanamnesis)

a. Time, surroundings.
Patient age is an important part of anamnesis. 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.
b. 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 encephalitis, vision changes, difficulty in swallowing,
hearing loss, step or balance disorders, tremor.
c. Use of drugs or alcohol.
d. History of heart disease, lung, liver, kidney, or anything else
Physical examination

A. 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
B. Skin examination
need to be observed signs of trauma, stigmata liver disorders and
other stigmata including crepitations and injection injection.
C. Head and neck
In patients with head trauma, the neck examination should be
performed with extreme caution or should not be done if a cervical
fracture is suspected
D. Toraks/abdomen dan ekstremitas.
Check the presence or absence of fracture.
Neurologic physical examination
1). General
• Open the eyelid to determine the comma
• Head deviation and glance indicate ipsilateral hemisphere lesions
• Watch for myoclonus (metabolic process), twitching rhythmic muscle (seizure activity)
or tetani (spontaneous, old muscle spasmus).

2). Awareness level

• Qualitative (apathetic, somnolen, delirium, stupor and coma)
• Quantitative (using GCS)

3). Pupil
• Checked: size, light reactivity
• Symmetrical / normal light reactivity, a hint that the mesensefalon integrity is good.
• Funduscopy
Oculovestibular / oculocephalic reflex (dolls eye maneuver)

4). Examination of meningeal stimuli

5). Examination of motor function
Additional Examination

• Immediate laboratory examinations generally include blood glucose

examination, leukocyte count, hemoglobin level, hematocrit, and
blood gas analysis.
• ECG
• CT SCAN
Management of loss of
consciousness

 Airway
 Breathing
 Circulation
STROKE
Definition

A serious medical condition where one part of the brain is damaged by a lack of blood supply or
bleeding into the brain from a burst blood vessel

Non hemorrhagic stroke is most commonly caused by extracranial embolism or intracranial

thrombosis. In addition, non hemorrhagic stroke can also be caused by a decrease in cerebral flow.
At the cellular level, any process that interferes with blood flow to the brain causes an ischemic
cascade that results in the death of neurons and cerebral infarction.
STROKE
Etiology
1. Emboli

The source of embolization may be located in the carotid or vertebral

artery but may also be at the heart and systemic vascular system.
a) Cardiogenic embolization may occur in:
• Heart disease with a "shunt" connecting the right with the left atrial
or ventricle;
• Acute or chronic rheumatoid heart disease that leaves the disorder
of the mitral valve;
• atrial fibrillation;
• Acute cordial infarction;
• Embolus derived from the pulmonary vein
• Occasionally in cardiomyopathy, endrocardial fibrosis, systemic
myxicosis of the heart;
b) Embolization due to systemic disturbance may occur as:
• Septic embolia, eg from lung abscess or bronchiectasis.
• Metastasis of neoplasms that have arrived in the lungs.
• Embolization of fat and air or N gas (such as "caisson" disease).
2. Thrombosis

The thrombotic stroke can be divided into strokes in large blood

vessels (including the carotid artery system) and small blood vessels
(including the circle of Willis and the posterior circle). The most
frequent site of thrombosis is a branching point of the cerebral artery
primarily in the distribution area of the internal carotid artery. The
presence of arterial stenosis can lead to blood flow turbulence (thereby
increasing the risk of thrombus formation of atherosclerosis (plaque
ulceration), and platelet adhesions.
 STROKE
Classification
An ischemic stroke occurs when a blood
vessel that supplies blood to the brain is
blocked by a blood clot or plaque. A clot, or
thrombus, may form in an artery that is
already narrow. A stroke happens when the
lack of blood supply results in the death of
brain cells.

A hemorrhagic stroke occurs when a blood vessel in part of the brain becomes weak and
bursts open, causing blood to leak into the brain. This puts pressure on the brain tissue, causing
tissue damage. The hemorrhage can also cause a loss of blood supply to other parts of the
brain

An aneurysm or a subarachnoid hemorrhage can result from defects in the blood

vessels of the brain. If a blood vessel ruptures, the flow of blood that follows can
damage brain cells.

An embolism happens when a clot breaks off from elsewhere in the body and travels
up to the brain to block a smaller artery. This may cause an embolic stroke. This is
more common in people who have arrhythmias, such as atrial fibrillation.
STROKE
Clinical Manifestation

1. Stroke in the carotid system or hemispheric stroke

Symptoms that occur suddenly in the form of hemiparesis, pelo
talk, and others.
2. Diagnostic abnormalities of the vertebral-bacillary system
A severe loss of consciousness, a combination of disturbed brain
nerves with vertigo, diplopia, and bulbar disorders, a combination
of various brain neurological disorders accompanied by long-tract
sign disorders such as vertigo with the fourth paresis of limb
members (distal ends).
Patofisiology
STROKE
DIAGNOSIS

Anamnesa

In the anamnesa will be found paralysis of limbs, mouth

mengot or talk pelo that occur suddenly while on the move. In
addition, the anamnesa also needs to be asked for prior
diseases such as diabetes mellitus or heart abnormalities.

Drugs consumed, family history of the disease also need to be

asked in anamnesa.
DIAGNOSIS

Bamford (1992), proposed a clinical classification that could be used only

(Bamford, J. 1992)

1) Total Anterior Circulation Infarct (TACI)

In TACI, the sufferer may have a noble dysfunction such as aphasia, there is a
visual deficit, and there is impaired motor and / or sensory function.

2) Partial Anterior Circulation Infarct (PACI)

The symptoms are more limited to the smaller regions of the cerebral circulation
in the carotid system. Patients may experience 2 of these three disorders of
noble dysfunction such as aphasia, there is visual diffusion, and there is impaired
motor and / or sensory function.
3) Lacunar Infarct (LACI)
Caused by a more sensitive small infarct in the brain artery seen with MRI than a
brain CT scan. Patients may experience 1 of these three disorders of noble
dysfunction such as aphasia, there is visual deficit, and there is impaired motor
and / or sensory function.

4) Posterior Circulation Infarct (POCI)

Occlusion occurs in the brainstem and / or occipital lobe. The cause is very
heterogeneous compared to the previous 3 types.
Clinical symptoms:
i. Brain dysfunction of the brain, one or more ipsilateral side and motor
disturbance / sensory contralateral.
ii. Motor disturbance / bilateral sensory.
iii. Impaired eye conjugate movement (horizontal or vertical)
iv. Cerebellar dysfunction without ipsilateral long-tract disorders.
v. Isolated hemianopia or cortical blindness.
STROKE
DIAGNOSIS

How to calculate:
SSS = (2.5 x consciousness) + (2 x vomiting) + (2 x
headache) + (0.1 x diastolic pressure) - (3 x atheroma) -
12
- Nilai SSS Diagnosa
- >1 Perdarahan otak
- < -1 Infark otak
- -1 < SSS < 1 Diagnosa meragukan (Gunakan kurva atau CT Scan)
STROKE
Diagnosis

Physical Examination

In stroke patients need to do physical examination of neurology such as

level of consciousness - GCS
movement agility
 muscle strength
 tendon reflex
 pathological reflex
cranial nerve function.

Additional Examination
 CT Scan
 MRI
 Angiography
 USG
 Lumbal Puncture

Examination to determine risk factors such as routine blood, blood chemistry components (urea,
creatinine, uric acid, lipid profile, blood sugar, hepatic function), blood electrolytes, Photo
Thorax, EKG, Echocardiography.
STROKE
Management of stroke non hemorraghe

a. Fluid
Give an isotonic fluid such as 0.9% saline with the goal
of maintaining euvolemia. Giving hypotonic or glucose-
containing fluids should be avoided except in the state of
hypoglycemia

b. Nutrition
The lateral enteral nutrition should be given within 48
hours, oral nutrition should only be given after the
swallow function test results are good. If there is a
swallowing disorder or decreased awareness of food is
given through NGT
STROKE
Management of stroke non hemorraghe

c. Prevention and overcoming complications

Early mobilization and assessment to prevent subacute complications
(aspiration, malnutrition, pneumonia, DVT, pulmonary embolism, decubitus,
orthopedic complications and contractures need to be done.

d. Management of Blood Pressure

Ca Channel Penyekat kanal 5mg/jam IV, Awitan cepat (1-5 Takikardi atau
Blocker Kalsium 2,5 mg/jam menit) , tidak terjadi bradikardi hipotensi, durasi
Nikardipin Dilitiazem tiap 15 menit, rebound yang bermakna lama (4-6 jam)
sampai 15mg/jam jika dihentikan. Eliminasi
tidak dipengaruhi oleh
fungsi hepar dan renal.
Potensi interaksi obat
rendah.
Vasodilator Langsung NO terkait 2,5-10 mg IV Serum sickness, drug
Hidralasin dengan bolus (sampai 40 induced lupus, durasi
mobilisasi mg) lama 3-4 jam, awitan
kalsium dalam lambat (15-30 menit)
ototpolos
Nitrogliserin Nitrovasodilator 5-100 Awitan 1-2 menit, Produksi methemoglobin,
mcg/kgbb/men it durasi 3-5 menit takikardia
IV
CASE ANALYSIS
 Anamnesis

• Suddenly decreased conciousness

• Weakness of lef arm and lef limb
CVD non
• Cephalgia (+)
• Vommiting and nausea (+)
hemorrhage
• Seizures (+)
• History of Hipertension
uncontrolled
Clinical Diagnostic

Internal state Neurological exam N. Cranialis exam

• Somnolen • Lateralization to • Angel of mouth

• E3M4V2 the lef arm and lef behind
• BP: 180/100 limb • Flatted of plica
mmHg • Tonus decreased nasolabialis
• Klonus (-) • Frowning & eye
• Reflex Physiologi closing not yet
decreased assessed
• Reflex Babinsky
(+) on lef foot

Unconsciousne hemiparese dextra spastic parese N. VII dextra

ss type central type
 Etiological Diagnosis

Siriraj Stroke Score

= (2,5 x concioussness) + (2 x vomitting) + (2 x cephalgia) +
(0,1 x diastole preassure) – (3 x ateroma) – 12
= (2,5 X 1) + (2 X 0) + (2 X 0) + (0.1 X 70) – (3X1) – 12
= 0,5

Stroke Non Hemmorhagic

Bamford Criteria

Partial Anterior Circulation Infarct (PACI)

Aphasia
and
there is impaired motor and / or sensory function.
Topical diagnosis

• CT
Ssan

• Frontal dextra, ventricel lateral dextra

et sinistra, III, IV
 Treatment

Citicolin • Neuroprotector

• Decreased of drug side

Omeprazole effect to GI tract

Tranexamat • Antifibrinolitic
acid