Presentation PKB SH Edy Bismillah.. 12

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HAEMORRHAGE STROKE By: Edy Irwanto Moderator : dr. Y ovita Andhitar a, Msi.Med, Sp. S, FINS WARD CASE PRESENTATI ON 

Transcript of Presentation PKB SH Edy Bismillah.. 12

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HAEMORRHAGE STROKE

By:

Edy Irwanto

Moderator :

dr. Yovita Andhitara, Msi.Med, Sp.S, FINS

WARD CASE PRESENTATION 

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Definition of stroke•

WHO : a clinicalsyndrome consisting ofrapidly developing clinicalsigns of focal (or global in

case of coma) disturbanceof cerebral functionlasting more than 24hours or leading to deathwith no apparent cause

other than a vascularorigin.

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According to AHA/ASA 2013

Definition of ischemic stroke: An episode of neurological

dysfunction caused by focal cerebral, spinal, or retinal infarction.

Definition of stroke caused by intracerebral hemorrhage:

Rapidly developing clinical signs of neurological dysfunction

attributable to a focal collection of blood within the brain parenchyma or 

ventricular system that is not caused by trauma.

Definition of stroke caused by subarachnoid hemorrhage: Rapidlydeveloping signs of neurological dysfunction and/or headache because of 

bleeding into the subarachnoid space (the space between the arachnoid

membrane and the pia mater of the brain or spinal cord), which is not

caused by trauma

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Epidemiology

USA Cause of

death in the 3rd

ranks after heart

disease and

cancer.

Riskesdas

20078,3/1000

 population

201312,1/1000

 population

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Blood Vessels Anatomy of The Brain

•The main supply of bloodto the brain by two internal

carotid arteries and two

vertebral arteries. These

four artery located inside

subarachnoid space and

the branches anastomoses

on the inferior surface of

the brain to form the circle

of Willis

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Classification of Stroke

• Based on the anatomical pathology and its causes

Ischemic Stroke

Transient ischemic attack

Cerebral Thrombosis

Cerebral EmbolismHaemorrhage Stroke

Intracerebral haemorrhage

Subarachnoid haemorrhage

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Classification of Stroke

• Based on the stage / time considerations

TIA

Stroke-in-evolution 

Completed stroke 

•Based on the vascular system

Carotid system

Vertebrobasilar system

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Rupture of blood vessels of the brainICH

SAH ICH

PrimarySecondary

•Pathogenesis

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Chronic HypertensionC aused by chronic

hypertension which causes

cerebral vasculopathyleading to rupture of blood

vessels in the brain

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ICH usually occur due to rupture of microaneurysms (Berryaneurysm) as a result of malignant hypertension. It mostoften occurs in subcortical regions, cerebellum, pons and

 brainstem.

In this type of bleeding, artery that serves the vascularitationin to the brain ruptures, so will cause leakage of blood to thebrain and sometimes cause brain depressed due to theaddition of fluid volume

Chronic hypertension causes arterioles vessel with 100-400micrometers in diameter changes in to pathological conditionin blood vessel walls in the form of hipohialinosis, fibrinoidnecrosis and the occurrence of Bouchard aneurysms

ICH

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secondary hemorrhage

•C ongenital vascular

anomalies, coagulopathy,brain tumors, non-

hypertensivevasculopathy (cerebralamyloid), vasculitis,moya-moya, post

ischemic stroke,anticoagulant medication(fibrinolytic orsympathomimetic)

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S

Subarachnoid hemorrhage (SAH) is the extravasation of

blood into the subarachnoid space between the arachnoid

membrane and the piamater

SAH ½ of spontaneous intracranial hemorrhage

Etiology ruptured aneurysm, vascular malformations

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severe headacheand vomiting.

•Can be accompanied by astiff neck .

• Residif during the first 24-

72 hours

severecerebral vasospasm+ brain infarction

• Symptoms   Suddenly

Subarachnoid hemorrhage 

SAH

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Risk Factors& Etiology

Hypertension(modifiable)

Aneurysms

 Arteriovenous

malformation

(AVM)

Anticoagulationtherapy

Leukemia andThrombocytopenia

Gangguan FaktorPembekuan

Darah

Amyloidangiopathy

Antiplatelettherapy

Hemorrhagictransformation

Excessive

Alcohol

Consumption

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Clinical Manifestations

• Headache

• Focal Neurologic Deficits

• Weakness or paresis to one side

of extremities

Disturbances of sensibility inone or more extremity

(hemihipestesi)

• A sudden change in mental

status (somnolence, delirium,

lethargy, stupor or coma)

• Facial weakness

F.A.S.T

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Clinical Manifestations

• Monocular and binocularblindness

• Blurred vision or visual field

defects

• Dysarthria or comprehensiondisorders

• Vertigo or ataxia

• Aphasia

• Seizure

F.A.S.T

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Pemerikasaan Penunjang

• aboratory

Routine blood testBlood chemistry test

Random blood sugar: in acute stroke can occur reactive

hyperglycemia, blood sugar can reach 250 mg in the

serum and then gradually then gradually decrease

Urea, creatinine, uric acid, liver function (SGOT / SGPT /

CPK) and lipid profile (total cholesterol, triglycerides,

LDL, HDL)

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Pemerikasaan Penunjang

Examination of hemostasisProthrombin time

APTT

Fibrinogen levelsD-dimer

INR

Plasma viscosity

Additional examination depend on indicationsProtein S

Protein C

ACA

Hemosistein

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Pemeriksaan Penunjang

• CT ScanNon contrast computedtomography (CT) is a

standard imaging modalityfor the initial evaluation ofpatients with acute strokesymptoms. The mainadvantage of the diagnostic

CT in hyperacute phase (0-6hours) that can showbleeding

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• In ICH bleeding volume was estimated by calculating

validated method that can give you a prognosis at the time of

initial clinical evaluation. The formulas used are as below

(A x B x C) / 2

A = length of lesions

B = width of lesion

C = high of lesions

(the number of

pieces contained

CT picture of

bleeding)

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Prevalent findings on CT scan in patients ICH

based on the onset of events

Onset 7-10 first day

Onset 11 days – 2 month

Onset > 2 monthIsodens area with a decrease in the

intensity enhancement

In the lesions area become the low-

density with ring enhancement in the

vicinity (hemosiderin deposition).

homolateral ventricular enlargement(in small hematoma in hipodens area

can be a isodens area)

Clearly defined, homogeneous lesions,

hiperdens, oval or irregularly shaped

frequently accompanied by edema in

the surrounding areas with hipodens

picture with narrow limits.

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MRIExamination of magnetic resonance imaging

(MRI) including diffusion-weighted imaging

(DWI) has an excellent ability to display the

appearance, size, location and extent of

ischemia

C b l i h

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Cerebral angiography

Angiography is strengthened by processing

of digital images accurately showedstenosis and occlusion of blood vessels andthe extracranial and intracranialaneurysms, vascular malformations andother vascular disorders such as arteritis

and vasospasm

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T  ranscranial Doppler (TCD)•u ntuk meneliti kelainan

neurovaskular termasuk USG

doppler, yang dapat

menunjukkan plak ateroma dan

stenosis pembuluh darah besarterutama di karotis dan juga

arteri vertebrobasiler

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General Management

• Fast imaging examinations with CT or MRI

• CT angiography and CT with contrast

• Patients deficiency of coagulation factor replacement

therapy or severe thrombocytopenia or platelet

coagulation factors

• In ICH Patients and ↑ INR related to oral anticoagulant

drug ≠ warfarin, therapy to replace with vitamin K-dependent factor + Correcting INR + intravenous

vitamin K 

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General Management

• Correction of coagulation disorders Vitamin K 10mg intravenously, FFP 2-6 units of correcting adeficiency of blood clotting factors

• Preventing venous thromboembolism with intermittent pneumatic compression

• Heparin effect can be overcome by administration of protamine sulfate 10-50 mg IV within 1-3 minutes

• Systole BP (SBP)> 200 mmHg or mean arterial pressure (MAP) > 150 mmHg, derived usingcontinuous intravenous antihypertensive drugs with

 blood pressure monitoring every 5 minutes.

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General Management

• If the SBP > 180 mmHg or MAP > 130 mmHgaccompanied by symptoms and signs of increasedintracranial pressure (ICP) ICP have to monitored.

• ↓ BP withintravenous antihypertensive drugs

continuously or intermittent and monitoring ofcerebral perfusion pressure ≥ 60 mmHg.

• If the SBP > 180 mmHg or MAP > 130 mmHg absenceof symptoms and signs of increased ICT, ↓ BP carefullyusing continuous intravenous antihypertensive

medication or intermittent monitoring of bloodpressure every 15 minutes until the MAP 110 mmHg orBP 160/90 mmHg , SBP up to 140 mmHg are stillallowed

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General Management

• In ICH patients with SBP 150-220 mmHg, decreased

SBP rapidly to 140 mmHg quite safe. After

craniotomy the target of MAP is 110 mmHg

• Pain management is important in reducing BP in patients with intracerebral hemorrhage stroke

• Management of seizure with anti-epileptic drugs.

Continuous ECG monitoring.

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Best surgery is in

patients with initial

GCS < 14 and

hematoma volume

> 40 ml• ur ry

• Meanwhile patients with higher GCS andsmaller lesions tend to have good results withconservative measures or non-surgical

management.• Ventricular drainage as the treatment of

hydrocephalus can be considered in patientswith a decreased level of consciousness.

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pRognoSis• Depending on the severity

of stroke as well as the

location and extent of

 bleeding

• GCS ↓ associated with

 poor prognosis and ↑

mortality.• ↑ bleeding volume is also

associated with poor

 prognosis.

• ↑ bleeding volume poor

functional outcome and

mortality ↑

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Score intracerebral hemorrhage is often used to predict outcome in

hemorrhagic stroke. The score is calculated as below

GCS score 3 – 4 : 2 points

GCS score 5 – 12 : 1 point

GCS score 13 – 15 : 0 point

Age ≥ 80 years : Yes 1 point, No 0 point

Infratentorial origin : Yes 1 point, No 0 point

Intracerebral hemorrhage volume ≥ 30 cm3 : 1 point

Intracerebral hemorrhage volume < 30 cm3 : 0 point

Intraventicular hemorrhage : Yes 1 point, No 0 point

Hemphill et.al study, all patients with intracerebral hemorrhage score = 0 can survive

and all patients with a score of 5 died.

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WARD CASE REPORT

Haemorrhage Stroke

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I. Patient’s Identity

•  Name : Mrs. S

• Age : 46 yo

• Sex : Woman• Marriage status : Married

• Last education : Senior High School

• Occupation : Private employees

• Address : Boyolali, Central Java

• Hospital admission : February 09th, 2015

• MR Number : A552909

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III. Subjective Data

Autoanamnesis on Februari 09th, 2015

1. Chief complaint : weakness of left extremity

2. Recent history :

- Location : left extremity

- Onset : ± 1 day before hospital admission (suddenly)

- Quality : left extremity can only hold light to middle resistance

- Quantity : ADL helped by family

- Cronology :

+ 1 day before hospital admission while wake up in the morning andgoing to prayers, patient suddenly fell down because weakness and got

heavy of the left extremity. Left extremity can only hold light to middle

resistance. Patient can work as usual. Numbness in the left extremity (+)

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III. Subjective Data

Slurred speech (-), shifting of the mouth (-), headache (+), vomiting (-),

swallowing impairment (-), seizures (-), fever (-), loss of consciousness (-),

bowel and bladder (+) normal. In the late afternoon patient feel the left

extremity more weakened so patient more difficult to doing an activity,

slurred speech (+) and mouth shifting to the right and headache was not

reduced, vomiting (-), seizures (-), loss of consciousness (-) then patient

brought into the ER Dr. Kariadi. Hospital

- Aggravating Factors : (-)

- Relieving Factors : (-)

- Concomitant Symptoms : headache, slurred speech, the mouth shiftingto the right

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3. Past Medical History:o History of Hypertension (+) since 14 y ago, routine consumption

captopril.

o DM (+) routine consumption metformin 500 mg and glimepirid,

o Heart disease (+) since 1 y ago with pain in the left chest and has

done a treadmill stress test with the results is positive of stress tests

of ischemia, patient regularly take amlodipine 10 mg and 2.5 mg

bisoprolol

o History of stroke before was denial

o History of trauma was denial

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4. Family Medical History:

o History of stroke before was denial

o History of HT was denial

o History of DM was denial

o History of Heart disease was denial

5. Social-economy :

Patients works as a cashier at the tofu factory, her husband works as a

construction worker with 2 sons dependent, medical expenses covered by

National Insurance (BPJS).

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IV. Objective Data

1. Present States

General state : Looked moderately ill

Vital sign : BP : 150/80 mmHg

HR : 94 times / minute, regular

RR : 20 times / minute

T : 36,7 C

VAS : 3

2. Internal state

Head : symmetrical, mesochepal

Eyes : Anemia of conjunctiva -/-, icteric of scleral -/-

Neck : Nuchal rigidity (-), lymph node enlargement (-), struma (-)

Chest

Cor : Normal heart sound, murmur (-),gallop (-)

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Lungs : normal breathing, Rhonchi -/-, Wheezing -/-

Abdomen :normal peristaltic sound, unpalpable liver and spleen

Extremity : Edema (-/-), turgor normally, cyanosis -/-

Nutrition Status

Height : 158 cm

Weight : 70 KgBMI : BB = 70 Kg = 29,1 Kg/m2 (overweight)

TB2 (1.58m)2

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3. Psychological Status

Way of thinking : realistic

Mood : normothymic

Behavior : normoactive

Memory : adequate

Cognitive : adequate

4. Neurologic status

Level of Consiousness : GCS: E4M6V5=15

Eyes : pupil round isocor, Ф 2,5 mm/2,5 mm, light reflex +/+

Leher : nuchal rigidity (-)Cranial nerves : The mouth shift to the right and the tongue shift to the left

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Motoric : Superior Inferior

Movement + / ↓ + / ↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex ++/++ ++/++

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Within normal

Coordination, Gait & Balance Test

Gait : Not perfomedRomberg Test : Not perfomed

Dysdiadochokinesis : (-)

Ataxia : (-)

Rebound phenomen: (-)

Dysmetria : (-)

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Abnormal movement

Tremor : (-)Athetose : (-)

Myoclonic : (-)

Chorea : (-)

ECG result (21/3/2013):

Impression : Normo sinus rythme, LAD,LVH

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Thorax Foto AP (09-02-2015)

Impression : Cor dan Pulmo within normal

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CT Scan Non Contras (09-02-2015)

Impression:

Intracerebral

hemorrhage on

lentiformis nucleus and

right external capsule

(± 5.78 cc volume)

which causes anarrowing of the right

lateral ventricle and

corticalis sulcus and

fissures sylvii at lession

area. No sign ofincreased ICP

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Laboratory Result Unit Normal Value

HEMATOLOGI

Hemoglobin 14.3 g/dL 12.00 – 15.00

Hematocryte 40.8 % 35 – 47

Erythrocyte 4.8 10^6/uL 4.4 – 5.9MCH 29.8 pg 27.00 – 32.00

MCV 84.9 fL 76 – 96

MCHC 35.1 g/dL 29.00 – 36.00

Leucosite 8.4 10^3/uL 3.6 – 11

Thrombocyte 277.1 10^3/uL 150 – 400

RDW 13.1 % 11.60 – 14.80

MPV 7.7 fL 4.00 – 11.00

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Clinical Chemistry

Random GlucoseLevel

117 mg/dL 80 – 160

Ureum 17 mg/dL 15 – 39

Creatinin 0.80 mg/dL 0.60 – 1.30

ELECTROLYTE

Sodium 144 mmol/L 136 - 145

Potassium 3.2 mmol/L 3.5 – 5.1

Chlorida 106 mmol/L 98 – 107

Impression: hypocalemiaOsmolarity: 2(144 + 3.2) + 117/18 + 17/6 = 303.7

Fluid defisit: (303.7 – 295)/295 x 0.6 x 56 = 0.9 liter

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V. Summary

Subjective :

A woman 46 y.o coming to the RSDK ER with hemiparese sinsitra (UMN

Type), 1 day onset accompanied with parese N.VII and XII of the left (UMN

Type), chepalgia and hemihipestesi sinistra.

Objective :

Praesens Status : BP: 150/80 mmHg, HR: 94 times / minute,

RR: 20 times / minute, T: 36,7 C, VAS: 3

Internal Status : Within normal

Neurologic StatusGCS : E4M6V5 = 15

Eyes : pupil round isocor, Ф 2,5 mm/2,5 mm, light reflex +/+

Neck : nuchal rigidity (-)

Cranial Nerves : Parese of N.VII and XII sinistra (UMN Type)

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Motoric : hemiparese sinsitra (UMN Type)

Sensibility : hemihipestesi sinistraVegetative : Within normal

ECG : Normo Sinus Rhythm, LAD, LVH

Thorax Foto : cor and lungs within normal

CT Scan : Intracerebral hemorrhage on lentiformis nucleus and rightexternal capsule (± 5.78 cc volume) which causes a narrowing

of the right lateral ventricle and corticalis sulcus and fissures

sylvii at lession area. No sign of increased ICP

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VI. DIAGNOSIS :

Clinical Diagnosis : Hemiparese sinistra (UMN Type)Parese N.VII and XII sinistra (UMN Type)

Hemihipestesi sinistra

Chepalgia

Topical Diagnosis : lentiform nucleus and right external capsula

Etiological Diagnosis : Haemorrhage Stroke (ICH)

Hypertension stage I

Hypocalemia

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V. Initial Plan

Haemorrhage Stroke

IpDx : Lab: GD I/II, HbA1c, profil lipid, urid acid, PPT, PTTK

- Consult cardiologist (history of heart disease)

- Consult to clinical nutrition

- Consult to opthalmologist (funduscopy)- Consult to physic rehabilitation

IpTx : Infus RL 20 gpm

O2 3 liter/min

Inj. Citicolin 500 mg intravena

Inj Tranexamic Acid 1 gr/6 hr intravena

Inf. Manitol 125 mg/6 hr intravena

Inj Ranitidin 50 mg intravena

Paracetamol 500 mg/8 hr p.o

IpMx : General state of conciousness, neurological deficit, VS

IpEx : Explaining about the disease, the management plan.

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Hypertension

IpDx : Consult to opthalmologist (funduscopy)IpTx : Amlodipin 10 mg/24 hr p.o

IpMx : General state of conciousness, neurological deficit, VS

IpEx : Explaining about the disease, examination plan

Hipokalemia

IpDx : -IpTx : KCL tab / 8 hr p.o

IpMx : General state of conciousness, neurological deficit, VS

IpEx : Explaining about the disease, management plan

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VIII. DAILY PROGRESS REPORT

ay - -

S H d h W k f h l f i

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S Headache, Weakness of the left extremity

O

GCS : E4M6V5 = 15

VS : BP:150/80 mmHg , HR:84x/minute, RR:20x/minute, T : 36,80C VAS=3

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke Hipertension Hypocalemia

P

Head elevation 30⁰ Inf. RL 20 tpm,

Inj. Citicoline 500 mg/8 hr, Inj.AsamTraneksamat 1 gr/6 hr, Inj. Ranitidin

50 mg/12 hr, Paracetamol 500

mg/8 hr p.o

Amlodipin 10

mg/24 hr p.o

KCL tab/8 hr

MX : KU, GCS, vital sign, neurologic defisit

Ex : Tetap

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Result of consult to opthalmology:

ODS: Grade III hipertension retinopathy, grade II arteriolosclerosis, non

proliperative DM retinopathy, non CSME mild.SuggestionManaging of risk factor of DM and HT

Result of consult to clinical nutrition dept:

Nutrition status: obesity

metabolic Status : hypermetabolicgastrointestinal status : functional

Energy demand: 1600 kcal/day

Protein demand : 60 gr/day

carbohydrate demand : 195 gr/day

Fatty demand: 31 gr/day

Dietary Plan:Diit given from 80% of the target and increased gradually with low salt, DM

1300 kcal

ay - -

S H d h W k f th l ft t it

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S Headache, Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 2

VS : BP:140/80 mmHg , HR:88x/minute, RR:22x/minute, T : 36,40C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia,

Hypertriglyserid

Ischemic heart

disease

P

Head elevation 30⁰

Inf. RL 20 tpm,Inj. Citicoline 500 mg/8 hr, Inj.Asam

Traneksamat 1 gr/6 hr, Inj. Ranitidin

50 mg/12 hr, Paracetamol 500

mg/8 hr p.o

Amlodipin 10mg/24 hr p.o

-KCL tab/8 hr-Fenofibrate 300

mg/24 hr

-Simvastatin10 mg/24 hr

MX : KU, GCS, vital sign, neurologic defisit

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Result of Consult to Physic Rehabilitation Dept:

Breathing exercise, Gentle AAROM exercise, Mobilitation, backrestsitting in bed

Result of Consult to Cardiology Dept

A: Ischemic heart disease

P: If no contra indication

Valsartan 160 mg/24 hr (if the BP target has not been reached)Amlodipin keep on

Simvastatin 10 mg/24 hr (@night)

Echo if possible

Lab Result (11-02-2015)

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Laboratory Result Unit Normal Value

HEMATOLOGY

HbA1c 5.4 % 6.0 – 8.0PPT 10.3 detik 10 -15PTTK  30,7 detik 23.4-36.8

CLINICAL CHEMISTRY

Fasting Glucose Level 97 mg/dL

80 – 109: Good;

110 – 125: Average;

> 126: Bad.

Reduction I -

2 Hours Post Prandial 104 mg/dL80 – 140: Good; 145 – 170:

Average; > 180: Bad.

Reduction II -

Total Cholesterol 152 mg/dL < 200

Triglycerides 180 mg/dL < 150

HDL Cholesterol 29 mg/dL 40 – 60

LDL direct 84 mg/dL 0 – 100

Ureum 30 mg/dL 15 – 39

Creatinin 0.81 mg/dL 0.60 – 1.30

Urid Acid 4.4 mg/dL 2.6 – 6.0

Impression: Hipertriglyserides

ay - -

S Headache Weakness of the left extremity Can’t defecate for 5 days

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S Headache, Weakness of the left extremity, Can’t defecate for 5 days

O

GCS : E4M6V5 = 15 VAS = 2

VS : BP:140/70 mmHg , HR:85x/minute, RR:24x/minute, T : 36,70C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HypertensionHypocalemia

Hypertriglyserid

Ischemic heart

disease

P

Head elevation 30⁰

Inf. RL 20 tpm,Inj. Citicoline 500 mg/8 hr, Inj.Asam

Traneksamat 1 gr/6 hr, Inj. Ranitidin

50 mg/12 hr, Paracetamol 500

mg/8 hr p.o, dulcolax supp I extra

Amlodipin 10

mg/24 hr p.o

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Headache Weakness of the left extremity defecate (+)

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S Headache, Weakness of the left extremity, defecate (+)

O

GCS : E4M6V5 = 15 VAS = 3

VS : BP:140/100 mmHg , HR:90x/minute, RR:20x/minute, T : 36,30C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰ Inf. RL 20 tpm,Inj. Citicoline 500 mg/8 hr, Inj.Asam

Traneksamat 1 gr/6 hr, Inj. Ranitidin

50 mg/12 hr, Paracetamol 500

mg/8 hr p.o

Amlodipin 10

mg/24 hr p.o

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Headache Weakness of the left extremity

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S Headache, Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 3

VS : BP:150/100 mmHg , HR:90x/minute, RR:20x/minute, T : 36,30C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰ Inf. RL 20 tpm,Inj. Citicoline 500 mg/8 hr, Inj.Asam

Traneksamat 1 gr/6 hr, Inj. Ranitidin

50 mg/12 hr, Paracetamol 500

mg/8 hr p.o

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

Simvastatin 10

mg/24 hr

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Headache Weakness of the left extremity

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S Headache, Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 3

VS : BP:140/90 mmHg , HR:80x/minute, RR:20x/minute, T : 36,70C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰ Inf. RL 20 tpmAff, Citicoline 500 mg/12 hr po,

Asam Traneksamat 500 mg/8 hr po,

Ranitidin 150 mg/12 hr po,

Paracetamol 500 mg/8 hr p.o

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Weakness of the left extremity

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S Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 1

VS : BP:150/70 mmHg , HR:82x/minute, RR:20x/minute, T : 36,70C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰, Citicoline 500mg/12 hr po, Asam Traneksamat 500

mg/8 hr po, Ranitidin 150 mg/12 hr

po, Paracetamol 500 mg/8 hr p.o

Program TCD (on Friday, 20/02/2015)

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Headache Weakness of the left extremity

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S Headache, Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 3

VS : BP:140/80 mmHg , HR:86x/minute, RR:20x/minute, T : 36,70C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰, Citicoline 500mg/12 hr po, Asam Traneksamat 500

mg/8 hr po, Ranitidin 150 mg/12 hr

po, Paracetamol 500 mg/8 hr p.o

Program TCD (on Friday, 20/02/2015)

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

Program Echo

(on Monday

23/02/2015)

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Weakness of the left extremity

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S Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 1

VS : BP:120/70 mmHg , HR:84x/minute, RR:22x/minute, T : 36,30C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰, Citicoline 500mg/12 hr po, Asam Traneksamat 500

mg/8 hr po, Ranitidin 150 mg/12 hr

po, Paracetamol 500 mg/8 hr p.o

Program TCD today

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

Program Echo

(on Monday

23/02/2015)

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Weakness of the left extremity

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S Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 1

VS : BP:120/80 mmHg , HR:90x/minute, RR:24x/minute, T : 36,70C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰, Citicoline 500

mg/12 hr po, Asam Traneksamat 500

mg/8 hr po, Ranitidin 150 mg/12 hr

po, Paracetamol 500 mg/8 hr p.o

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

Program Echo

(on Monday

23/02/2015)

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

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Result of TCD:

An increase in resistance to blood flow in the internal carotid artery right / left.

The speed and resistance to blood flow in the right middle cerebral artery,

posterior cerebral artery right and left, right and left vertebral artery and basilar

artery is still within normal limits.

Left middle cerebral artery can not be accepted by the wave doppler

(hyperostosis?)

Impression: suspicious of atherosclerosis in the carotid artery right & left

ay - -

S Weakness of the left extremity

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S Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 1

VS : BP:100/70 mmHg , HR:80x/minute, RR:20x/minute, T : 36,30C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

Head elevation 30⁰, Citicoline 500

mg/12 hr po, Asam Traneksamat 500

mg/8 hr po, Ranitidin 150 mg/12 hr

po, Paracetamol 500 mg/8 hr p.o

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

Program Echo

today

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

ay - -

S Weakness of the left extremity

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S Weakness of the left extremity

O

GCS : E4M6V5 = 15 VAS = 1

VS : BP:100/70 mmHg , HR:80x/minute, RR:20x/minute, T : 36,30C

Nn Cranialis : Parese N.VII and XII sinistra (UMN Type)

Motoric : Superior InferiorMovement +/↓ +/↓

Strength 5-5-5/4-4-4 5-5-5/4-4-4

Tonus N/N N/N

Trophy E/E E/E

Physiologic reflex +/+ +/+

Pathologic reflex -/- - / -

Clonus - / -Sensibility : Numbness in the left extremity

Vegetative : Defecate and urinate normally

A Haemorrhage Stroke HipertensionHypocalemia

Hypertriglyserid

Ischemic Heart

Disease

P

DischargeHead elevation 30⁰, Citicoline 500

mg/12 hr po, Asam Traneksamat 500

mg/8 hr po, Ranitidin 150 mg/12 hr

po, Paracetamol 500 mg/8 hr p.o

Amlodipin 10

mg/24 hr p.o

Valsartan 80

mg/24 hr po

KCL tab/8 hr

Fenofibrate 300

mg/24 hr

-Simvastatin

10 mg/24 hr

MX : KU, GCS, vital sign, neurologic defisitEx : Teta

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Result of Echocardiography:

LVH(+) consentric,

Fungsional sistolic LV global is good, LVEF : >70%

diastolic Disfuncsion LV gr 1, E/A: 0,68

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10 – 2 – 2015(Day-0)

S: A woman 46 y.o coming to the RSDK ER with hemiparese sinsitra spastic, 1 day

onset accompanied with parese N.VII and XII of the left central, chepalgia and

hemihipestesi sinistra

O:

Status praesen : BP: 150/80mmHg, HR: 94 times / minute,

RR: 20 times/ minute,T: 36,7 

C,VAS: 3Statusinternus : Withinnormal

Status neurologi

Motoric : Weakness of left extremity

Sensbil ity : Numbness in the left extremity

CT Scan : Intracerebral hemorrhage on lentiformis nucleus and right external

capsule. No sign of increased ICP.

Lab : Potassium 3.2

ECG : Normo Sinus Rhythm, LVH, LAD

Thorax Foto : cor dan lung within normal

A : Haemorrhage Stroke (ICH),Hypertension st I, Hypocalemia

P : lab GD I/II, HbA1c, Profil lip id, urid acid, PPT, PTTK 

Consult : Cardiologist, Clinical nutrition,opthalmologist, physic rehabilitation

Tx: Infus RL 20 tpm, O2 3 liters/mnt, Inj. Citicolin 500 mg/8 hr i.v, Inj Tranexamic

Acid 1 gr/6 hr i.v, Inj Ranitidin 50 mg i.v, Paracetamol 500 mg/8 hr p.o

12-2-2015 ( Day - 3)

S : Headache, Weakness of the left

extremity, Can’t defecate for 5 days

O :

PE : GCS: E4M6V5 = 15BP : 140/70 mmHg, N : 85x/mnt, RR :

24x/mnt, t : 36,7oC VAS:2

A : Haemorrhage Stroke (ICH),

Hypertension st I, Hypocalemia,

Hypertriglycerid

P : tx : Dulcolax supp I, Fenofibrate

300 mg/24 hr 

10-2-2015 (Day 1) :

S : Headache, Weakness of the left extremity

O : GCS: E4M6V5= 15

BP: 150/80mmHg,N : 84x/mnt,RR : 20x/mnt,t : 36,8oCStatus internus : tetap

Status neurologis: tetap

Result of consult to opthalmology (+)

Result of consult to clinicalnutritiondept (+)

A : Haemorrhage Stroke (ICH),Hypertension st I, Hypocalemia

P : Waitingfor lab result

Tx : Infus RL 20 tpm, O2 3 liter/menit, Inj. Citicolin 500 mg/8 jam i.v,

Inj Asam traneksamat 1 gr/6 jam i.v, Inf. Manitol 125 mg/6 jam i.v, Inj

Ranitidin 50 mg i.v, Paracetamol 500 mg/8 jam p.o, amlodipin 10

mg/24 jam p.o, KCL tab/8 jam p.o

14-2-2015 (Day-5) :S : Headache, Weakness of the left extremity

O : GCS: E4M6V5 = 15

BP:150/100 mmHg, HR:90x/mnt, RR:20x/mnt,

t : 36,3oC, VAS:3

A : tetap

P: Tx: valsartan80 mg/24hr p.o

11-2-2015 (Day-2) :

S : Headache, Weakness of the left extremityO : GCS: E4M6V5= 15

BP : 140/80 mmHg, HR :88x/mnt,RR : 22x/mnt,

t : 36,4oC, VAS:2

Result of Consult to Cardiology Dept (+)

Result of Consult to Physic Rehabilitation(+)

A: Haemorrhage Stroke (ICH), Hyper tens ion st I,

Hypocalemia, Hypertriglycerid, Ischemic heart disease

P: Echoif possible

Tx: Fenofibrate 300 mg/24 hr,Simvastatin 10 mg/24 hr 

 p.o (night)

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23-2-2015 (Day-14) :

S : Weakness of the left extremity

O : GCS: E4M6V5= 15

BP:120/70 mmHg,HR : 86x/mnt,

RR : 22x/mnt, t : 36,6oC

Hasil TCD (+)

A: Haemorrhage Stroke (ICH),

Hypertension st I, Hypocalemia,

Hypertriglycerid, Ischemic heart

disease

P: Waiting schedule for echo

Tx: : Head elevation 30⁰, Citicoline

500 mg/12 hr po, Asam Traneksamat

500 mg/8 hr po, Ranitidin 150 mg/12 hr

 po, Paracetamol 500 mg/8 hr p.o

Tanggal 18-2-2015 (Day-9) :

S : nyeri kepala, lemah anggota gerak kiri

O : GCS: E4M6V5= 15

TD : 150/70 mmHg, N : 82x/mnt, RR :20x/mnt, t : 36,7oC

A : Haemorrhage Stroke (ICH), Hypertension

st I, Hypocalemia, Hypertriglycerid, Ischemic

heart disease

P : Program TCD  Friday (20/02/2015)

Tx : Head elevation 30⁰, Citicoline 500 mg/12

hr po, Asam Traneksamat 500 mg/8 hr po,

Ranitidin 150 mg/12 hr po, Paracetamol 500

mg/8 hr p.o

24-2-2015 (Day-15) :

S : Weakness of the left extremity

O : GCS: E4M6V5 = 15

BP : 140/90 mmHg, HR : 90x/mnt, RR : 20x/mnt, t :

36,3oC

Result of Echo (+)

A:Haemorrhage Stroke (ICH), Hypertension st I,

Hypocalemia, Hypertriglycerid, Ischemic heart disease

P: Discharge after echocardiography

Tx: Head elevation 30⁰, Citicoline 500 mg/12 hr

 po, Asam Traneksamat 500 mg/8 hr po, Ranitidin

150 mg/12 hr po, Paracetamol 500 mg/8 hr p.o

20-2-2015 (Day-11) :

S : Weakness of the left extremity

O : GCS: E4M6V5 = 15

TD : 120/70 mmHg, N : 86x/mnt, RR :22x/mnt, t : 36,3oC

A: Haemorrhage Stroke (ICH), Hypertension

st I, Hypocalemia, Hypertriglycerid, Ischemic

heart disease

P: Program for TCD today

Tx: : Head elevation 30⁰, Citicoline 500

mg/12 hr po, Asam Traneksamat 500 mg/8 hr

 po, Ranitidin 150 mg/12 hr po, Paracetamol

500 mg/8 hr p.o

19-2-2015 ( Day- 10)

S : Weakness of the left extremity

O :

PF : GCS: E4M6V5 = 15

TD : 140/80 mmHg, N : 86x/mnt,RR : 20x/mnt, t : 36,5oC VAS:2

A : Haemorrhage Stroke (ICH),

Hypertension st I, Hypocalemia,

Hypertriglycerid, Ischemic heart disease

P : Registering Echo schedule

24/02/2015

tx : : Head elevation 30⁰, Citicoline

500 mg/12 hr po, Asam Traneksamat

500 mg/8 hr po, Ranitidin 150 mg/12

hr po, Paracetamol 500 mg/8 hr p.o

16-2-2015 ( Day- 7)

S : Headache, Weakness of the left

O :

PF : GCS: E4M6V5 = 15

BP : 140/90 mmHg, HR : 80x/mnt,RR : 20x/mnt, t : 36,7oC VAS:3

A : Haemorrhage Stroke (ICH),

Hypertension st I, Hypocalemia,

Hypertriglycerid, Ischemic heart disease

P : tx : Head elevation 30⁰ Inf. RL 20

tpm Aff, Inj. Citicoline 500 mg/12 hr

 po, Inj.Asam Traneksamat 500 mg/8 hr

 po, Inj. Ranitidin 150 mg/12 hr po,

Paracetamol 500 mg/8 hr p.o

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VI Li f P bl

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VI. List of Problems

No Active Problem Tgl No Pasive Problem Tgl

1.

2.3.

4.

5.

6.

7.8.

Hemparesis sinistra (UMN)  6

Chepalgia 6Paresis of N.VII sinistra (UMN) 6

Paresis N.XII sinistra (UMN) 6

Hemihipestesi sinistra 6

Haemorrhage Stroke

Stage I HypertensionHypocalemia

09-02-2015

09-02-201509-02-2015

09-02-2015

09-02-2015

09-02-2015

09-02-201509-02-2015

.

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 Thanx You...