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8/13/2019 Case Bersama - Is 2
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A 56 years old male presented with right upperand lower limb weakness since 4 days beforeadmitted to hospital,
Right upper and lower limb
weakness
Chief Complaint
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Right upper and lower limb weakness
since 4 days before admitted to Dr M
Djamil Hospital. Earlier patient werebrought to a general practitioner and
then were admitted to Sijunjung
Hospital for 2 days and then wererefered here from Sijunjung Hospital
Current Illness History
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. Weakness are seen suddenly duringactivity (lifting farming items), and fall.Conscious after attack. The upper and lowerlimb weakness are equal.
Now patient are unable to lift anything andhave to be hold by family to walk. He also
have difficulty in eating and drinking.
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This complain are accompanied with wry
mouth and patient cannot speak. Patientcannot understand conversation and cannotsay any words.
No complain of headache, vomiting,decreased consciousness, and seizures.
No complain in sensing, miction anddefecation
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Known hypertensive since 3 years ago. No regular
checkup to doctor. No previous history of stroke.
No history of diabetes.
Past Illness History
No family history of hypertension, diabetes, heart
disease and stroke.
Family History of Illness
Patient is a farmer, smoke 12 stick of cigarette a
day since 30 years ago.
Socioeconomic Background
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General Appearance: Moderately Ill
Level of Consciousness: compos mentiscooperative
Pulse : 72 x/menit
Respiratory Rate : 20 x/menit
Blood Pressure : 180/120 mmHg
Temperature : 36,7oC
General
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GCS 15 : E4 M6 Aphasia
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Neck stiffness: (-) Brudzinsky II : (-)
Brudzinsky I : (-) Kernig Sign : (-)
Meningeal SIgn
Vomiting (-)
Progressive headache (-)
Intracranial Pressure Examination
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N. I : Difficult to evaluate N. II : Difficult to evaluate
N. III, IV, VI : Light reflex +/+
Doll eye movement N. V : difficult to evaluate
N. VII : Right Nasolabial plica flatter
than the left side, EyelashesReflex +/+
N VIII : difficult to evaluate
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N IX : Vomitting Reflex +, capableto swallow
N X : Pharinx arch symmetric, Uvulaon the midline
N XI : difficult to evaluate N XII difficult to evaluate
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Motor Function Test
Upper Limb Right Left Movement Limited active
Strength 0/0/0 5/5/5
Tonus eutonus eutonus
Trophy eutrophy eutrophy
Fall Test Right side lateralisation
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Lower Limb Right Left Movement Limited active
Strength 0/0/0 5/5/5
Tonus eutonus eutonus
Trophy eutrophy eutrophy
Fall test Right side lateralisation
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Sensibility Test Pain Sensibility +, Tactil Sensibility +.
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Mixturition : neurogenic bladder (-) Defecation : normal
Sweat secretion : normal
Autonomous Nervous System
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Reflex Right LeftBiceps +++ ++
Triceps +++ ++APR +++ ++
KPR +++ ++
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Reflex Right LeftHoffman-Tromer - -
Balbinsky + -Chaddoks - -
Oppenheim - -
Gordon - -
Schaeffer - -
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Hemoglobin : 14.7gr/dl
Leukocyte : 10,500/mm3
Hematocryte : 42%
Thrombocyte : 140 000/mm3
Sodium : 148mmol/L
Potassium : 3.5mmol/L
Chloride : 104mmol/L
Random Blood Glucose: 125gr/dl
Urea : 60mg/dl
Creatinine : 1.4mg/dl
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Blood : PT, APTT, total Cholesterol,uric acid, albumin, globulin,SGOT,SGPT, HDL, LDL, and
Trygliceride.Chest X-RayNon-contrastBrain CT scanEchocardiography
Other Examination
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EKG : Atrial Fibrilation Normoventricular
response
CT Scan : Gambaran infark luasfrontotemporoparietal sinistra.
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Right Hemiparesis+Right NVII and NXII Paresis
central type +Global aphasia
Clinical Diagnosis
Right brain hemisphere, Subcortical
Topic Diagnosis
Cardioemboli
Etiology
Emergency Hypertension, Atrial Fibrillation
Normoventricular Response
Secondary Diagnosis
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Head elevation 30degree
Oxygen 2L/minute
IVFD RL 12hour/kolf
Catheter (fluid balance)Diet Soft Food, Low Sodium II
Supportive
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Piracetam 4x3gr (IV)
Bisoporolol 1x2.5mg (Oral)
Aspilet 2x 80mg
Herbesser Drip 50mg in 50cc Ringer
lactate via syringe pump 50cc/hour
Medicinal Therapy
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Dietary control
Physical Therapy
Family education and prevention on
hypertension and stroke
Medicinal Therapy
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1. History Sudden weakness, conscious after attack, equal
upper and lower limb weakness (hemiparesis), are the
characteristic of subcortical cerebral function
disturbance in that happen in non hemorrhagic
stroke.
It is said subcortical because when a patient haveequal upper and lower limb weakness, it shown that
the disturbance are in brain area where all motor
tract are bundled up together
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The patient also cannot speak or understand
speech. This is called aphasia. Aphasia can occur
in subcortical ischemic stroke if the damage are
extensive enough to cause disturbance in cortical
area. as example this patient have wide
frontotemporoparietal infarc from ct scan.
Wry mouth are caused by paresis of facial nerve
and in this patient are found the central type
paresis.
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Patient also show major stroke risk factor of
smoking and hypertension and minor risk which
is age. Smoking and hypertension contribute to
artherosclerosis build up and could be a major
risk of stroke.
Stroke is characterized by the sudden loss of
blood circulation to an area of the brain,resulting in a corresponding loss of neurologic
function.
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Strokes are classified as either hemorrhagic or
ischemic. Acute ischemic stroke refers to stroke
caused by thrombosis or embolism and is more
common than hemorrhagic stroke.
Ischemic strokes occur as a result of an
obstruction within a blood vessel supplying
blood to the brain. The underlying condition for
this type of obstruction is the development of
fatty deposits lining the vessel walls.
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This condition is called arteroscelrosis these fattydeposits can cause two types of obstruction:
a) Cerebral thrombosis refers to a thrombus(blood clot) that develops at the clogged part ofthe vessel.
b) Cerebral embolismrefers generally to a bloodclot that forms at another location in thecirculatory system, usually the heart and largearteries of the upper chest and neck. A portion ofthe blood clot breaks loose, enters thebloodstream and travels through the brain'sblood vessels until it reaches vessels too small tolet it pass.
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A second important cause of embolism is an
irregular heartbeat, known as atrial
fibrillation. It creates conditions where clots
can form in the heart, dislodge and travel tothe brain.
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2. Physical examination
General physical examination reveals that the
patient are in emergency hypertension state with
blood pressure of 180/120.
Emergency hypertension are blood pressure
elevation with target organ damage.
12x/minute pulsus deficit are also found and this
show cardiac insufficiency and shown as inability
to beat simultaneously with distal pulse. This
happens because of abnormality in cardiac
output.
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Neurological examination reveals this patient
GCS are E4 M6 Aphasia. Aphasia found are global
aphasia.
From reference, Aphasia is a disturbance of the
comprehension and formulation of language,
sensoric aphasia are caused by abnormality in
Wernicke area as the receptive aphasia and
motoric area could be caused by abnormality in
Broca area as the expressive area.
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Global aphasia results from damage to extensive
portions of perisylvian region of the brain. Patients
with global aphasia have difficulty to understand both
spoken or written language and difficult to speak.
This patient have difficulty in naming, repeating,
reading and writing which is the modality to assess
aphasia. These problem usually occurs in left brain
hemisphere. Stroke subcortical can disturb nerveimpuls from and to this language areas.
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Flatter right nasolabial plica are caused byright facial nerve paresis.
In motor function test, limited movementand right upper and lower limb strength are000 interpret as inability to move even the
fingers of hand and feet. In Fall Test, Rightside lateralisation are found and this showsthe weakness in right side limbs.
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Hyper reflex in all right side limbs are caused
by compensation mechanism by the spinal
nerve because of the paresis.
In other hand, positive Babinsky reflex shows
that the lesion or the damage are in upper
motor neuron but the actual pathophysiology
about it remain unknown.
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3. Laboratory and other findings.
No laboratory abnormality are found. But in patients withstroke, complete fat lab test such as total cholesterol, LDL,
HDL, Triglyceride, and also uric acid are also done.
This patients Electrocardiogram shows Atrial fibrillation
Normoventrikular response. Atrial fibrillation are the high
risk cause of stroke. Atrial fibrillation decrease
cerebral blood flow and slows blood flow increaserisk of thrombus formation cause the thrombus to
stuck as emboli at brain end artery.
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Chest X-Ray and Echocardiography are
recommended for this patient because of his
abnormal EKG finding for further heart
investigation.
Echocardiogram could visualize every heart
valve or space and could evaluate heart
contraction abnormality
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Non-contrast Brain CT scan are
recommended to visualize structural braindamage in patient and to confirm diagnosis.
CT-scan are the gold standard to diagnose
ischemic stroke or hemorrhagic stroke.
From the CT scan we could find the location,volume and type of stroke for comfirming the
diagnosis
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For ischemic stroke, the usual findings of
brain CT scan are hypodens lesion with
perifocal oedema and for hemorrhagic stroke
we will found hyperdens lesion with perifocal
oedema, but sometimes we could also foundhypodens lesion in chronic hemorrhagic
stroke.
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4. Therapy
In Supportive therapy, patients head areelevated 30 degree to prevent high pressure
blood flow to further damage the brain.
Oxygen 2L/minute, IVFD RL 12hour/kolf,
Catheter (fluid balance), and Diet Soft Food,
Low Sodium II are given to prevent further
increase of blood pressure.
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For Specific therapy, patients are given
Piracetam 4x3gr (IV), Bisoporolol 1x2.5mg
(Oral), Aspilet 2x 80mg and Herbesser Drip
50mg in 50cc Ringer lactate via syringe pump
50cc/hour.
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The central goal of therapy in acute ischemic
stroke is to preserve the area of oligemia inthe ischemic penumbra.
The area of oligemia can be preserved by
limiting the severity of ischemic injury (ie,
neuronal protection) or by reducing the
duration of ischemia (ie, restoring blood flow
to the compromised area).
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Recanalization strategies, including IV
recombinant tissue-type plasminogen
activator (rt-PA) and intra-arterial
approaches, attempt to establish
revascularization so that cells in the
penumbra can be rescued before irreversibleinjury occurs.
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Restoring blood flow can mitigate the effects
of ischemia only if performed quickly.
Neuroprotective strategies are intended to
preserve the penumbral tissues and to extendthe time window for revascularization
techniques; however, at the present time, no
neuroprotective agents are available andapproved for use in ischemic stroke.
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The ischemic cascade offers many points at
which such interventions could be attempted.Multiple strategies and interventions for
blocking this cascade are currently under
investigation. The timing of the restoration of
cerebral blood flow appears to be a critical
factor.
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Finally, education therapy are also given to
the patient such as physical therapy. Dietary
control and family education are very
recommended and it could be done through
few steps
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4. Therapy
In Supportive therapy, patients head are
elevated 30 degree to prevent high pressure
blood flow to further damage the brain.
Oxygen 2L/minute, IVFD RL 12hour/kolf,
Catheter (fluid balance), and Diet Soft Food,
Low Sodium II are given to prevent further
increase of blood pressure.
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For Specific therapy, patients are givenPiracetam 4x3gr (IV), Bisoporolol 1x2.5mg(Oral), Aspilet 2x 80mg and Herbesser Drip
50mg in 50cc Ringer lactate via syringe pump50cc/hour.
The central goal of therapy in acute ischemic
stroke is to preserve the area of oligemia inthe ischemic penumbra.
The area of oligemia can be preserved by
limiting the severity of ischemic injury (ie,neuronal protection) or by reducing theduration of ischemia (ie, restoring blood flowto the compromised area).
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Recanalization strategies, including IV
recombinant tissue-type plasminogen
activator (rt-PA) and intra-arterial
approaches, attempt to establish
revascularization so that cells in the
penumbra can be rescued before irreversible
injury occurs.
Restoring blood flow can mitigate the effects
of ischemia only if performed quickly.
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Neuroprotective strategies are intended topreserve the penumbral tissues and to extendthe time window for revascularizationtechniques; however, at the present time, no
neuroprotective agents are available andapproved for use in ischemic stroke.
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The ischemic cascade offers many points at
which such interventions could be attempted.
Multiple strategies and interventions for blocking
this cascade are currently under investigation.
The timing of the restoration of cerebral blood
flow appears to be a critical factor.
Finally, education therapy are also given to the
patient such as physical therapy. Dietary control
and family education are very recommended and
it could be done through few steps
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