case bersama - is 2

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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case bersama - is 2

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