ASUHAN KEPERAWATAN

PADA KLIEN CVD SI/SH

HELTTY, MKep., Sp.KMB

Brain Anatomy
Some stroke facts
Stroke is the 3rd leading cause of death
in the UK.
Leading cause of disability.
Kills twice as many women as breast
cancer.
130,000 people suffer a stroke in the UK
each year (a stroke is happening every 5
minutes to some-one)
Approx 20-30% of people who have a
stroke will die within the first month.
1000 children suffer strokes per year
 Some stroke facts
People aged between 65 and over increased
by 4 million between 1952-2002, the
projected % of older people in England is
expected to rise from 16% in 2003- 23% in
2031- this will increase the numbers of people
with stroke

7 billion is spent on stroke by the NHS and

wider economy each year

A huge issue and likely to get bigger with the

rise in the ageing population- this is why
stroke is currently in the spot-light
Some stroke facts
Approx 12,000 under the age of 55-
of all strokes are in the under
65s.
Approx 900,000 people are living
with stroke in England and around
50% of those are dependant on
others for help with everyday
activities
Approx 1 in 4 people who live until
the age of 85 can expect to have a
stroke
 Definisi Stroke
sindrom klinis dengan gejala berupa gangguan
fungsi otak secara fokal maupun global, yang
dapat menimbulkan kematian atau kecacatan
yang menetap lebih dari 24 jam, tanpa penyebab
lain kecuali gangguan vaskuler.
Menurut Penyebab dibagi menjadi:
Jenis Iskemik disebabkan emboli atau Trombus
Jenis perdarahan disebabkan pecahnya pembuluh
darah otak dapat karena berry aneuris akibat
hipertensi tak terkontrol yang mengubah
morfologi arteriol otak atau pecahnya pembuluh
darah otak karena kelainan kongenital pada
pembuluh darah otak tersebut.
 Stroke Haemorhagic

Stroke yang terjadi karena pembuluh

darah di otak pecah sehingga timbul
iskhemik dan hipoksia di hilir. Penyebab
stroke hemoragi antara lain: hipertensi,
pecahnya aneurisma, malformasi arteri
venosa. Biasanya kejadiannya saat
melakukan aktivitas atau saat aktif,
namun bisa juga terjadi saat istirahat.
Kesadaran pasien umumnya menurun
Stroke non Haemorhagic

Dapat berupa iskemia atau emboli

dan thrombosis serebral, biasanya
terjadi saat setelah lama beristirahat,
baru bangun tidur atau di pagi hari.
Tidak terjadi perdarahan namun
terjadi iskemia yang menimbulkan
hipoksia dan selanjutnya dapat
timbul edema sekunder . Kesadaran
umummnya baik.
Menurut Black (2005) Stroke dibagi :
Transient Icchemic Attack/TIA atau serangan otak
sepintas.Transient Icchemic Attack/TIA adalah terjadinya
defisit neurologik dalam waktu 30 menit dan berlangsung
kurang dari 24 jam tanpa meninggalkan gejala sisa.Selama
terjadi serangan neurologik tidak terdapat defisit neurologik
permanent.TIA dapat diakibatkan karena mikroemboli dari
plak atherosklerotik pembuluh darah ekstrakranial dan
untuk sementara menginterupsi oksigenasi otak.
Reversible Ischemic Neurologic Deficit (RIND) atau
serangan otak iskemik yang reversibel. Istilah serangan
otak iskemik yang reversibel kadang-kadang digunakan jika
gejala sisa defisit neurologik masih terjadi setelah 24 jam
serangan tetapi tidak mengakibatkan gejala sisa setelah
beberapa hari atau beberapa minggu.
 Sroke in Evolution. atau stroke progressif
terjadi dalam beberapa jam sampai
beberapa hari. Stroke progresif ini terjadi
akibat pembesaran thrombus di
dalampembuluh darah arteri. Perburukan
neurologik dapat ditemukan sampai 72
jam setelah jaringan otak mengalami
infark.
Completed Stroke /Completed Stroke
terjadi defisit neurologik tidak mengalami
perbaikan dalam waktu 2 3 hari.
Stroke dapat juga diartikan sebagai
gangguan fungsional otak yang
bersifat
fokal dan atau global
akut
berlangsung antara 24 jam atau
lebih
disebabkan gangguan aliran darah
otak
tidak disebabkan karena
tumor/infeksi
Faktor Risiko
1). Hipertensi, yang merupakan faktor
risiko utama terjadinya strok iskemik dan
strok hemoragik.
2). Penyakit kardiovaskular dan atrial
fibrilasi.
3). Diabetes Melitus dapat meningkatkan
risiko strok.
4). Faktor risiko lainnya : hiperlipidemia,
merokok cigarette, konsumsi alkohol
berlebihan, penggunaan kokain dan
obesitas
 Non- modifiable Risk Factors

Frequency of Stroke Men

Women
related to age &
gender

Race: (e.g Afro-Americans increased risk)

Family history of stroke (inheritance ?)
History of stroke or myocardial infarction (Early
recurrence is observed after embolic stroke:
cardioembolism & stroke from extracranial
atherosclerosis)

NHANES: 1999-2002 CDC/NCHS and NHLBI

 Modifiable risk factors

Major Other

Obesity
Insulin resistance
Hypertension Decreased physical activity
Increased alcohol
Diabetes consumption
Heart disease (CHD, CHF)
Dyslipidaemia Vasculitis
(infectious or collagen
Smoking diseases)
Migraine
Risk for embolic events Hypothyroidism
in heart or carotid disease Sleep apnoea syndrome
Hematological disorders
(Hypercoagulation or emboli)
Predisposition for thrombotic
events
(Hyperhomocysteinemia,
female hormones)
 What Is the Cause of Ischemic Stroke?

Atherothrombosis
Embolus:
Material: Red (fibrin rich) or White (platelet
rich)
Source: Cardiac? Aortic? Carotid Artery?
Small artery disease
Hypoperfusion: Hemodynamic
Others: arterial dissection, arteritis, etc.
PATOFISIOLOGI
Oklusi
Penurunan perfusi jaringan serebral
Iskemia
Metabolisme anaerob
Asam laktat meningkat
Edema serebral
Aktivitas elektrolit terganggu
Pompa na dan Kalium gagal
Edema cerebral
Perfusi otak menurun
Nekrosis jaringan otak
Gangguan neurologis
Trombosis (penyakit trombo - oklusif) merupakan
penyebab stroke yang paling sering.
Arteriosclerosis selebral dan perlambatan sirkulasi
selebral adalah penyebab utama trombosis
selebral, yang adalah penyebab umum dari stroke.
Tanda-tanda trombosis selebral bervariasi. Sakit
kepala adalah awitan yang tidak umum. Beberapa
pasien mengalami pusing, perubahan kognitif atau
kejang dan beberapa awitan umum lainnya.
Secara umum trombosis selebral tidak terjadi
secara tiba-tiba, dan kehilangan bicara sementara,
hemiplegia atau parestesia pada setengah tubuh
dapat mendahului awitan paralysis berat pada
beberapa jam atau hari.
Trombosis terjadi biasanya ada kaitannya
dengan kerusakan local dinding pembuluh
darah akibat aterosklerosis. Proses
aterosklerosis ditandai oleh plak berlemak pada
pada lapisan intima arteria besar. Bagian intima
arteria sereberi menjadi tipis dan berserabut,
sedangkan sel sel ototnya menghilang.
Lamina elastika interna robek dan berjumbai,
sehingga lumen pembuluh sebagian terisi oleh
materi sklerotik tersebut. Plak cenderung
terbentuk pada percabangan atau tempat
tempat yang melengkung. Trombi juga dikaitkan
dengan tempat tempat khusus tersebut.
Pembuluh pembuluh darah yang mempunyai
resiko dalam urutan yang makin jarang adalah
sebagai berikut : arteria karotis interna, vertebralis
bagian atas dan basilaris bawah. Hilangnya intima
akan membuat jaringan ikat terpapar. Trombosit
menempel pada permukaan yang terbuka
sehingga permukaan dinding pembuluh darah
menjadi kasar.
Trombosit akan melepasakan enzim, adenosin
difosfat yang mengawali mekanisme koagulasi.
Sumbat fibrinotrombosit dapat terlepas dan
membentuk emboli, atau dapat tetap tinggal di
tempat dan akhirnya seluruh arteria itu akan
tersumbat dengan sempurna.
 Atherosclerosis
From risk factors to endothelial injury & CVD

LDL-C BP Risk factors Diabetes Smoking Cardiac failure

Oxidative stress

Endothelial dysfunction

NO Local mediators Tissue ACE-Ang II

Endothelium Collagen growth Proteinolysis

PAI-1 VCAM,ICAM,
factors
cytokines

Vascular injury &

Thrombosis Inflammation Vasocontraction Plaque rupture
remodeling

Adhesion molecules
VCAM: vascular cell adhesion molecule, CV Clinical events
ICAM: intercellular adhesion molecule
PAI-1: plasminogen activator inhibitor 1
Gibbons GH. N Engl J Med 1994
Normal Arterial Wall
(intima, Media, Adventitia)

Intima:
Endothelium
Internal elastic laminae

Media:
Smooth muscle cell
Lumen
Collagen proteins

External elastic laminae

Endothelial dysfunction in atherosclerosis
(Early changes)

up-regulation of endothelial
adhesion molecules

Leucocyte migration into the

arterial wall

Penetration of lipoproteins

greater permeability of
the endothelium

Leucocyte adhesion
Lipid core formation (fatty streak) in atherosclerosis

Platelets adhesion and

coagulation

Migration of smooth
muscle cells

Foam cells formation

T cells activation

Adhesion and penetration

of leucocytes
Formation of atherosclerotic plaque
(death & rupture of foam cells in fatty streak)

Formation of necrotic core

Accumulation of macrophages

Formation of fibrous cap

Rupture of plaque and thrombus formation (supsequent
luminal occlusion)

Intravascular thrombus

Lipid layer

Thrombus inside the plaque

 Progression of atherosclerosis
Threshold

Decades Years-Months Months-Days

Healthy Subclinical Symptomatic

Intima
Lumen
Media

Plaque

Threshold

Thrombus
Intima
Lumen
Media

Plaque

PRIMARY SECONDARY
SECONDARY
HEALTH PRIMARY
HEALTH POLICY
POLICY PREVENTION
PREVENTION
PREVENTION
PREVENTION
Diet
Diet and
and lifestyle
lifestyle changes
changes Aggressive
Aggressive drug
drug
Drug
Drug treatment
treatment
Embolisme
Embolisme sereberi termasuk urutan kedua dari
berbagai penyebab utama stroke. Penderita
embolisme biasanya lebih muda dibanding dengan
penderita trombosis. Kebanyakan emboli sereberi
berasal dari suatu trombus dalam jantung, sehingga
masalah yang dihadapi sebenarnya adalah
perwujudan dari penyakit jantung. Meskipun lebih
jarang terjadi, embolus juga mungkin berasal dari
plak ateromatosa sinus karotikus atau arteria karotis
interna. Setiap bagian otak dapat mengalami
embolisme, tetapi embolus biasanya akan
menyumbat bagian bagian yang sempit.. tempat
yang paling sering terserang embolus sereberi
adalah arteria sereberi media, terutama bagian atas.
perdarahan serebri termasuk urutan ketiga dari
semua penyebab utama kasus GPDO (Gangguan
Pembuluh Darah Otak) dan merupakan
sepersepuluh dari semua kasus penyakit ini.
Perdarahan intrakranial biasanya disebabkan oleh
ruptura arteri serebri.
Ekstravasasi darah terjadi di daerah otak dan /atau
subaraknoid, sehingga jaringan yang terletakdi
dekatnya akan tergeser dan tertekan. Darah ini
sangat mengiritasi jaringan otak, sehingga
mengakibatkan vasospasme pada arteria di sekitar
perdarahan. Spasme ini dapat menyebar ke
seluruh hemisper otak dan sirkulus wilisi
Bekuan darah yang semula lunak menyerupai selai
merah akhirnya akan larut dan mengecil. Dipandang
dari sudut histologis otak yang terletak di sekitar
tempat bekuan dapat membengkak dan mengalami
nekrosis. Karena kerja enzim enzim akan terjadi
proses pencairan, sehingga terbentuk suatu rongga.
Sesudah beberapa bulan semua jaringan nekrotik akan
terganti oleh astrosit dan kapiler kapiler baru
sehingga terbentuk jalinan di sekitar rongga tadi.
Akhirnya rongga terisi oleh serabut serabut astroglia
yang mengalami proliferasi.
Perdarahan subaraknoid sering dikaitkan dengan
pecahnya suatu aneurisme. Kebanyakan aneurisme
mengenai sirkulus wilisi. Hipertensi atau gangguan
perdarahan mempermudah kemungkinan ruptur. Sering
terdapat lebih dari satu aneurisme.
PRINSIP-PRINSIP PATOFISIOLOGI
Jika aliran darah ke setiap bagian otak
terhambat karena trombus atau embolus
mulai terjadi kekurangan oksigen ke jaringan
otak
Kekurangan selama satu menit dapat
mengarah pada gejala-gejala yg dapat pulih
seperti kehilangan kesadaran
Kekurangan oksigen dalam waktu yang lebih
lama menyebabkan nekrosis mikroskopik
neuron
Area nekrotik disebut infark
 Kekurangan oksigen pada awalnya mungkin akibat
iskemik umum (karena henti jantung, hipotensi,
hipoksia, proses anemia, atau kesukaran bernapas)
Jika neuron hanya mengalami iskemik, dan belum
terjadi nekrosis ada peluang untuk
menyelamatkannya
Stroke karena embolus dapat merupakan akibat
dari bekuan darah, plak ateromatosa fragmen,
lemak atau udara
Emboli pada otak kebanyakan berasal dari
jantung, sekunder terhadap infark miokard atau
fibrilasi atrium
 Jika etiologi stroke adalah hemoragi: maka faktor
pencetus: biasanya hipertensi abnormalitas
vaskular seperti anuerisma serebral lebih rentan
terhadap ruptur dan menyebabkan hemoragi pada
keadaan hipertensi
Sindrom neurovaskular yg lebih sering terjadi pada

stroke trombotik atau embolik karena

keterlibatan arteri serebral mediana: arteri ini
mensuplai bagian lateral hemisfer serebri
Infark pada bagian tersebut menyebabkan defisit

kolateral motorik dan sensorik

Jika infrak hemisfer adalah dominan terjadi

masalah bicara dan disfasia

 Stroke trombotik atau embolik besarnya otak
yg mengalami iskemik dan infark sulit
ditentukan peluang stroke akan meluas
setelah serangan pertama dapat terjadi
edema serebral masif dan peningkatan TIK
pada titik herniasi dan kematian setelah
trombotik terjadi pada area yg lebih luas
Prognosisnya tergantung pada daerah otak yg
terkena dan luasnya saat serangan
Karena stroke trombotik sering karena
ateroskelerosis maka resiko terjadi stroke
berulang dimasa datang
 Stroke embolik pasien mengalami kans terjadi
stroke berulang jika penyebabnya tidak ditangani
Jika luas jaringan otak yg rusak akibat stroke
hemoragik tidak besar dan bukan pada tempat
yg vital maka pasien dapat pulih dengan
defisit minimal
Jika hemoragi luas atau terjadi pada daerah yg
vital pasien mungkin tidak pulih
Sekitar 30% hemoragi intraserebral terjadi tidak
masif sehingga survival masih mungkin
terjadi
 Thromboembolic

ISCHEMIC Brain
infarct

HEMORRHAGIC

Brain vessel
thrombosis

Willis Emboli from

cycle
extracranial
thrombosis
Arterio-venous
TIA
Dysplasia

Intracerebral
hemorrhage
 Pathophysiology of ischemic infarct -
Penumbra
The occlusion of a cerebral vessel is Infarct Penumbra
followed by formation of a central
irreversible tissue necrotic lesion,
where the brain blood flow is
reduced < 15% (<20 ml/100gr/min),
with a peripheral zone, the Penumbra
(20 - 30 ml/100gr/min), where tissue
is viable and functional disturbance is
reversible due to partial preservation
of blood supply via emissary vessels,
if ischemia reverses on time
Depending on the grade of blood
flow reduction and its duration, after
an ischemic interval, Penumbra
becomes necrotic
Experimental studies report that the
infarct s formed 3-12 h after
initiation of ischemia and continues to
develop even after 24h, although in a
much slower rate (24-72h <30%
increase)
 Tanda dan Gejala
Penurunan Kesadaran
Kehilangan Fungsi Motorik
Gangguan Sensori
Gangguan Komunikasi
Gangguan Perilaku dan Emosional
Disfungsi Kandung Kemih
Gangguan Koordinasi dan Gait
Stroke hemisfer kiri
Hemiparesis atau hemiplegia sisi
kanan
Perilaku lambat dan sangat hati-hati
Kelainan bidang pandang kanan
Ekspresif, reseptif, atau disfagia
global
Mudah frustrasi
Stroke hemisfer kanan
Hemiparesis atau hemiplegia sisi kiri
Defisit spasial perseptual
Penilaian buruk
Memperlihatkan ketidaksadaran
defisit pada bagian yg sakit oleh
karenanya mempunyai kerentanan
untuk jatuh atau cedera lainnya
Kelainan bidang visual kiri
 Gejala sisa:
Kelumpuhan pada salah satu sisi tubuh (hemiparese
atau hemiplegia)
Lumpuh pada salah satu sisi wajah Bells Palsy
Tonus otot lemah atau kaku
Menurun atau hilangnya rasa
Gangguan lapang pandang Homonimus Hemianopsia
Gangguan bahasa (Disatria: kesulitan dalam
membentuk kata; afhasia atau disfasia: bicara
defeksif/kehilangan bicara)
Gangguan persepsi
Gangguan status mental
 Pemeriksaan
CT Scan. Pemeriksaan awal untuk nenentukan
apakah pasien termasuk strok hemoragik atau non
hemoragik. Pemeriksaan ini dapat melihat adanya
edema, hematoma, iskemia dan infark.
Angiografi Serebral. Membantu menentukan
penyebab strok secara spesifik, seperti perdarahan
atau obstruksi arteri, ada tidaknya oklusi atau
rupture.
Pungsi Lumbal. Menunjukkan adanya tekanan
normal dan biasanya ada trombosisi, emboli
serebral, TIA.
MRI. Menunjukkan daerah yang mengalami infakr,
hemoragik, kelainan bentuk arteri-vena.
EEG. Mengidentifikasi masalah didasarkan pada
gelombang otak dan mungkin
Brain CT : Perdarahan intraserebral di lobus
frontotemporal dekstra volume kira-kira
30 cc + midline shift (+)
 Penatalaksanaan
Penatalaksanaan strok dapat dibagi
menjadi dua fase yaitu fase akut dan
fase paska akut. Selama fase akut
tindakan keperawatan ditujukan
untuk mempertahankan fungsi vital
pasien (life saving) dan memfasilitasi
perbaikan neuron.
Stroke Strategy

Prevention and Public Awareness

Emergency Care

TIA and Minor Stroke

Hospital Care

Post-Hospital Care

Workforce
 Key stroke strategy
themes Better
The stroke pathway: outcomes
Prevention and early
Shorter intensive acute &
diagnosis: managing rehabilitative hospital stay, followed by
specialist care closer to home
risk factors, raising
awareness of
Direct to CT scan, CT scan < 24 hrs
symptoms, and thrombolysis Stroke unit care
tackling TIAs

Time = brain
Stroke Local
Taking people direct to
centre hospital
specialist services
Improving Paramedic
triage
rehabilitation and
community based care; 999 call
longer term support to Informed
regain independence public
Time is brain

Person Experiences Stroke Like Symptoms

Active symptoms Recent resolvedOlder

symptoms
resolved symptom

999 call; ambulance GP refers to GP refers to

confirms likely stroke TIA clinic (low risk), or direct to TIA service
and pre-notifies hospital Hospital (high risk), advises no
driving and prescribes aspirin
(unless strong suspicion of
haemorrhage/contraindications)
Direct to stroke serviceOne-stop specialist service; investigated,
treated in 24 hours
Time is brain- Stroke
Pathway
Management of Stroke
Minority Majority High risk TIA
Acute Stroke Unit
Stroke Unit Specialised clinical assessment
Specialised Urgent brain imaging
assessment and care for those who need it (next CT slot or
Swallowing test within 1hr out of hours)/ MRI
Brain scan within Thrombolysis if appropriate
24hrs Swallowing test
Intensive (hyper-acute) stroke unit care
End-of-life care for 24/48 hours
Specialist rehabilitation/inpatient and ESD
Specialist review at 6 weeks and 6 months Carotid intervention
Long-term community stroke and
support services
 National Recommendations for a Stroke
Pathway
All stroke patients should spend at least 90% of
their hospital stay in a specialist stroke unit.

Pathway should be made up of distinct phases of

care;

1. Initial urgent specialist assessment- direct

transfer to dedicated stroke unit (within 4
hours)
2. Hyper-acute- up to 48 hours (monitored
beds/intensive nursing)
3. Acute- up to 7 days
4. Sub-acute- 7-12 days
5. Intensive inpatient rehabilitation-up to 21 days
6. Specialist Community rehabilitation- from 3-6
months
7. Medium/Long-term- 6 month review- life long
 Specialist validated immediate
assessment- Recognition Of Stroke
In the Emergency Room (ROSIER)
Validated scoring
system.
For use by health
professionals.
ROSIER
Symptom onset: Date & Time.
Assessment: Date & Time.
BP GCS Eyes Motor Verbal
Has there been loss of consciousness or Syncope Y (-
1) N (0)
Has there been any seizure activity Y (-1) N (0)
Is there New acute onset (or awakening from sleep)
of:-
1. Asymmetrical facial weakness Y (+1) N (0)
2. Asymmetrical arm weakness Y (+1) N (0)
3. Asymmetrical leg weakness Y (+1) N (0)
4. Speech disturbance Y (+1) N (0)
5. Visual field defect Y (+1) N (0)
. Total score: (Stroke is unlikely but not completely
excluded if total score is < or = to 0)
HASU- Hyper Acute Stroke Units
Aim of hyper acute care
Stroke is associated with significant
physiological disturbance in vascular
and neuronal function
Aim to;
Optimise physiological variables
Maintain brain perfusion
Maintain homeostasis- to try to restore
normal state once it has been disturbed.
Early detection and intervention
Prevent secondary events
Safe administration of thrombolysis
Hyper acute nursing care
Hypoxia- O2 sats<92%
Hyper/ hypoglycaemia
Hypertension- closely monitored- no clear
consensus on optimal management- should
be treated post stroke (usually after 7 days)
Intracranial pressure- drowsiness/gaze
palsy/breathing problems
Pyrexia- worsens infarct- needs to be
lowered if over 37.5
Dehydration- maintain hydration
Aspiration
DVT / PE
Seizures
 Time is Brain
Impact of thrombolysis
Number making full recovery per 100 treated

3
0 Benefit

2
0
Harm
1
0 0 2 4 6
Time (hours)

0 Saver, Stroke 2006

The changing face of stroke- not just an inevitability of old
age
But can happen to anyone at any age
What used to happen
What happens now
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2: Components of acute inpatient care

Risk for venous thromboembolism,
temperature, mobilization, continence,
nutrition and oral care should be addressed
in all hospitalized stroke patients
Appropriate management strategies should be implemented for
areas of concern identified during screening
Discharge planning should be included as part of the initial
assessment and ongoing care of acute stroke patients

REVIEW
4.2a Venous Thromboembolism Prophylaxis
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2a Venous thromboembolism prophylaxis

All stroke patients should be assessed for their
risk of developing venous thromboembolism
High risk patients include patients with inability to move one or both
lower limbs and those patients unable to mobilize independently
Patients who are identified as high risk for
venous thromboembolism should be considered
for prophylaxis provided there are no
contraindications
Early mobilization and adequate hydration should be encouraged with
all acute stroke patients to help prevent venous thromboembolism

REVIEW
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2a Venous thromboembolism prophylaxis

In addition to secondary stroke prevention,
antiplatelet therapy should be used for
people with ischemic stroke to prevent VTE;
The following interventions may be used with
caution for selected people with acute
ischemic stroke at high risk of VTE:
Heparin in prophylactic doses (5000 units BID) or low molecular
weight heparin (with appropriate prophylactic doses per agent)
External compression stockings

REVIEW
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2b Temperature Management

Acute Inpatient Stroke Care
Best Practices Recommendations

4.2b Temperature Management

Should be monitored as part of routine vital
sign assessments (every 4 hours for first 48
hours and then as per ward routine or based
on clinical judgment)
For temperature more than 37.5C, increase frequency of
monitoring and initiate temperature reducing measures
For temperature more than 38C, iidentify and treat source (site
and etiology) of fever in order to start tailored antibiotic treatment
and antipyretics

REVIEW
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2c Mobilization
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2c: Mobilization
Acute stroke patients should be mobilized as
early and as frequently as possible preferably
within 24 hours of stroke
Mobilization
symptom onset, unless contraindicated
Assessment of patients ability in activities of daily
is defined
living should be completed and reassessed as the act
regularly of getting a
Within the first 3 days after stroke, blood pressure, patient to
oxygen saturation and heart rate should be move in the
monitored before each mobilization
Acute stroke patients should be assessed by
bed, sit up,
rehabilitation professionals as soon as possible stand, and
after admission preferably within the first 24 to 48 eventually
hours walk.

REVIEW
Acute Inpatient Stroke Care
Mobilization: Physiological Monitoring
AVERT Trial
Within the first 3 days after stroke, blood pressure, oxygen saturation, and
heart rate should be monitored before each mobilization
If during mobilization, there is a drop in blood pressure of greater than 30
mmHg this mobilization attempt should cease. If a drop of greater than 30
mmHg occurs on 3 consecutive attempts, further medical assessment is
required.

Julie Bernhardt PhD*; Helen Dewey PhD; Amanda Thrift PhD; Janice Collier PhD; and Geoffrey Donnan MD. (2008). A Very Early
Rehabilitation Trial for Stroke (AVERT) Phase II Safety and Feasibility. Stroke. Published online before print January 3,
2008, doi: 10.1161/STROKEAHA.107.492363

REVIEW 4/13/17
74
Acute Inpatient Stroke Care
*Contraindications to Mobilization
Deterioration in the persons condition in the first
hour of admission that:
resulting in direct admission to ICU,
a documented clinical decision for palliative treatment
(e.g. those with devastating stroke)
immediate surgery.
Unstable coronary or other medical condition.
A suspected or confirmed lower limb fracture at the
time of stroke preventing mobilization
Systolic blood pressure less than 110, or greater
than 220mmHg.
*AVERT Trial recommendations

REVIEW 4/13/17
75
Acute Inpatient Stroke Care
*Contraindications to Mobilization
Oxygen saturation of less than 92% with
supplementation.
Resting heart rate of less than 40 or greater than
110 beats per minute.
Temperature of greater than 38.5C.
Persons who have received rt-PA can be mobilized
if the attending physician permits.

*AVERT Trial recommendations

REVIEW 4/13/17
76
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2d Continence
All stroke patients should be screened for
urinary incontinence and retention (with or
without overflow), fecal incontinence and
constipation
Stroke patients with urinary incontinence should be assessed by
trained personnel using a structured functional assessment
A bladder training program should be implemented in patients who
are incontinent of urine
A bowel management program should be implemented in stroke
patients with persistent constipation or bowel incontinence

REVIEW
Acute Inpatient Stroke Care
Incontinence
40-60% of stroke patients have urinary
incontinence
25% of incontinent patients will have
urinary incontinence at discharge
15% will have incontinence at 1 year post
stroke
Urinary incontinence within 24 hours of a
stroke is a predictor of functional disability

REVIEW 4/13/17
78
Acute Inpatient Stroke Care
Bladder Incontinence
All stroke patients should be screened for urinary
incontinence and retention (with or without
overflow)
Urinary incontinence should be assessed by
trained personnel using a structured functional
assessment
The use of indwelling catheters should be
avoided. If used, indwelling catheters should be
assessed daily and removed as soon as possible

REVIEW 4/13/17
79
Acute Inpatient Stroke Care
Bladder Incontinence
The use of a portable ultrasound (bladder
scanner) is recommended as the
preferred non-invasive painless method
for assessing post void residual and
eliminates the risk of introducing urinary
infection or causing urethral trauma by
catheterization

REVIEW 4/13/17
80
Assessment of Incontinence

Incontinence history Post residual volume

Fluidintake Urine culture
Medical history Vaginal examination
Medications Rectal examination
Functional ability

Acute Inpatient Stroke Care

81
4/13/17
Acute Inpatient Stroke Care
Strategies for Urinary Incontinence
Ensure adequate fluid intake (1500-2000
mls)
Assess post void residuals (normal is 50-
100 mls)
Review medications (?diuretics)
Introduce a regular toileting routine

REVIEW 4/13/17
82
Acute Inpatient Stroke Care
Strategies for Urinary Incontinence
Encourage bladder retraining (urge
incontinence)
Pelvic muscle exercises Kegals
Double voiding, Crede maneuver and
intermittent catheterization (overflow
incontinence)
Limit use of dietary bladder irritants
( caffeine, etoh, spicy foods)

REVIEW 4/13/17
83
Acute Inpatient Stroke Care
Bowel Incontinence
Bowel incontinence occurs in 30% of
stroke patients and 97% regain control
within one year.
Incontinence may result due to the
following:
Altered consciousness
Cognitive deficits
Impaired communication
Neurogenic bowel without sensation
or control

REVIEW 4/13/17
84
Acute Inpatient Stroke Care
Bowel Incontinence
Bowel function risk factor assessment
should include:
mobility, inactivity, adequate fluid and food intake, polypharmacy, etc.

All stroke patients should be screened for

fecal incontinence
A bowel management program should be
implemented in stroke patients with
persistent constipation or bowel
incontinence
REVIEW 4/13/17
85
Acute Inpatient Stroke Care
Establishing a Bowel Program
Encourage appropriate fluids, diet, and
activity.
Choose an appropriate rectal stimulant.
Provide rectal stimulation initially to trigger
defecation daily.
Select optimal scheduling and positioning.
Select appropriate assistive techniques.
Evaluate medications that promote or inhibit
bowel function
Source: www.guideline.gov/

REVIEW 4/13/17
86
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2e Nutrition
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2e Nutrition
The nutritional and hydration status of
stroke patients should be screened within
the first 48 hours of admission using a valid
screening tool
Results from the screening process should guide appropriate
referral to a dietitian for further assessment and the need for
ongoing management of nutritional and hydration status

REVIEW
Acute Inpatient Stroke Care
Nursing Interventions for Dysphagia/Nutrition
Maintain all patients with stroke NPO
(including oral medications) until a
swallowing screen has been administered
and interpreted, within 24 hours of patient
being awake and alert
Screening results should guide appropriate
referral to a Dietician for further assessment
and the need for ongoing management of
nutritional and hydration status
REVIEW 4/13/17
89
Acute Inpatient Stroke Care
Dysphagia/Nutrition
Consideration of enteral nutrition support
within 7 days of admission for patients
who are unable to meet their nutrient and
fluid requirements orally
This decision should be made
collaboratively with the multidisciplinary
team, patient and their caregivers/family

REVIEW 4/13/17
90
Acute Inpatient Stroke Care
Nursing Interventions for Dysphagia
Assess for signs & symptoms of
dysphagia
Choking on food
Stifled, suppressed or overt coughing during meals
Nasal regurgitation
Moist, wet voice
Complaints of food sticking in the throat
Drooling or loss of food &/or fluid from the mouth
Pocketing of food in cheeks
Slow, effortful eating
Delay in initiating swallow (i.e. > 5 seconds)

REVIEW 4/13/17
91
Acute Inpatient Stroke Care
Dysphagia
All stroke
Points topatients
Remembershould have a nutritional
screen within 48 hours of admission
Many dysphagic patients aspirate without
any external sign that food or liquid is
entering the airway instead silent
aspiration
Although many stroke patients will recover
from dysphagia spontaneously, all stroke
patients should have a SLP/RD
assessment
The presence of a gag reflex does not exclude
REVIEW the possibility of dysphagia 92
4/13/17
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2f Oral Care

Acute Inpatient Stroke Care
Best Practices Recommendations

4.2f Oral care

All stroke patients should have an oral/dental
assessment, which includes screening for obvious
signs of dental disease, level of oral care and
appliances, upon or soon after admission
For patients wearing a full or partial denture it must be determined if they have the
neuromotor skills to safely wear and use the appliance(s)
An oral care protocol should be established and
include:
Frequency
Types of oral care products
Strategies for patients with dysphagia
Consultation with dentistry

REVIEW
Acute Inpatient Stroke Care
Oral Care
Consider consulting dentistry,
occupational therapy, speech language
pathologists, and/or a dental hygienist to
develop an oral care protocol
A referral to dentistry for consultation and
management of oral health and/or
appliances should be made as soon as
possible

REVIEW 4/13/17
95
Acute Inpatient Stroke Care
Best Practices Recommendations

4.2g Discharge planning

Discharge planning should be initiated as soon
as possible after patient admission to hospital
(emergency department or inpatient care)
A process should be established to ensure involvement of patients
and caregivers in the development of the care plan, management and
discharge planning
Discharge planning discussions should be ongoing throughout
hospitalization to support a smooth transition from acute care
Information about discharge issues and possible needs of patients
following discharge should be provided to patients and caregivers
soon after admission

REVIEW
PENGKAJIAN
Change in the level of consciousness or responsiveness as
evidenced by movement, resistance to changes of position,and
response to stimulation; orientation to time, place, and person
Presence or absence of voluntary or involuntary movements of the
extremities; muscle tone; body posture; and position of the head
Stiffness or flaccidity of the neck
Eye opening, comparative size of pupils and pupillary reactions to
light, and ocular position
Color of the face and extremities; temperature and moisture of the
skin
Quality and rates of pulse and respiration; arterial blood gas
values as indicated, body temperature, and arterial pressure
Ability to speak
Volume of fluids ingested or administered; volume of urine
excreted each 24 hours
Presence of bleeding
Bloodd [ressure changing
PENGKAJIAN
Perubahan pada tingkat kesadaran atau responivitas yang dibuktikan
dengan gerakan, menolak terhadap perubahan posisi dan respon
terhadap stimulasi, berorientasi terhadap waktu, tempat dan orang
Ada atau tidaknya gerakan volunteer atau involunter ekstremitas,
tonus otot, postur tubuh, dan posisi kepala.
Kekakuan atau flaksiditas leher.

Pembukaan mata, ukuran pupil komparatif, dan reaksi pupil terhadap

cahaya dan posisi okular.
Warna wajah dan ekstremitas, suhu dan kelembaban kulit.

Kualitas dan frekuensi nadi, pernapasan, gas darah arteri sesuai

indikasi, suhu tubuh dan tekanan arteri.
Kemampuan untuk bicara

Volume cairan yang diminum dan volume urin yang dikeluarkan setiap
24 jam.
Riwayat hipertensi, kebiasaan merokok, kebiasaan makanan dan
umur.
DIAGNOSA KEPERAWATAN
Ketidakefektifan perfusi jaringan serebral bd gangguan aliran aretri/vena,
penurunan suplai O2
Hambatan mobilitas fisik berhubungan dengan hemiparesis, kehilangan
keseimbangan, spastis dan trauma otak
Nyeri bahu berhubungan dengan hemiplegia and Disuse
Perawatan Diri (hygiene, toileting, grooming, and feeding); kesiapan untuk
meningkatkan berhubungan dengan gejala sisa
Gangguan persepsi sensori berhubungan dengan perubahan resepsi sensori,
integrasi dan nterpretasi.
Gangguan menelan berhubungan kelemahan otot menelan
Inkontinensia . (fungsional? Refleks?) berhubungan dengan kelemahan bladder,
instabil detrusor, atau kerusakan komunikasil
Gangguan proses pikir berhubungan dengan kerusakan otak, kebingungan, atau
ketidakmampuan mengikuti perintah
Hambatan komunikasi verbal berhubungan dengan kerusakan otak
Risiko kerusakan integritas kulit berhubungan dengan hemiparesis/hemiplegia,
atau penurunanmobility
Gangguan (?) proses keluarga berhubungan dengan beban caregiving
Ketidakefektifan pola seksualitas berhubungan dengan gangguan neurologi, takut
gagal
1. Perfusi jaringan tidak efektif : cerebral : penurunan
sulpai oksigen sebagai akibat dari kegagalan mensuplai
jaringan sampai (NANDA, hal 191)
Faktor yang berhubungan :
. Kerusakan transport oksigen melalui alveolar dan atau

membran kapiler
. Masalah pertukaran

. Penurunan aliran darah vena atau arteri

Karakteristik :
. Perubahan bicara

. Perubahan reaksi pupil

. Kelemahan ekstremitas atau paralysis

. Gangguan status mental

. Kesulitan menelan

. Perubahan respon motorik

. Perubahan perilaku
Tujuan (NOC):
Perfusi Jaringan : Perifer :rentang dimana aliran darah melalui pembuluh darah kecil

dari ekstremitas dan mempertahankan fungsi jaringan.

Status neurologi : rentang dimanan sistem saraf pusat dan perifer menerima,

memproses dan merspon stimulus internal dan eksternal.

Status Sirkulasi : rentang dimana aliran darah tidak terhambat, satu arah dan pada

tekanan yang sesuai melalui pembuluh darah besar dari sirkulasi pulmuner dan
sitemik.
Kemampuan Kognitif : kemempuan untuk menjalankan proses mental secara komplek

Kriteria Evaluasi :
Mendemonstrasikan status sirkulasi yang ditandai dengan :

- Tekanan darah sistole dan diastole dalam rentang yang diharapkan

- Tidak ada ortostatik hipotensi

- Tidak ada bruit pembuluh darah besar

- Tidak ada tanda-tanda PTIK ( tidak lebih dari 15 mmHg )

Mendemonstrasikan kemempuan kognitif yang ditandai dengan :

- Berkomunikasi dengan jelas dan sesuai dengan kemampuan

- Menunjukkan perhatian, konsentrasi dan orientasi

- Memproses informasi

- Membuat keputusan dengan benar

Menunjukan fungsi sensori motori cranial yang utuh

- Tingkat kesadaran mambaik

- Tidak ada gerakan-gerakan involunter

NIC: MANAGEMENT SENSASI
PERIFER
Monitor adanya parastesi mati rasa dan tengling
Monitor sataus cairan termasuk intake dan output

Monitor fungsi bicara

Upayakan suhu dalam batas normal

Monitor GCS secara teratur

Catat perubahan dalam penglihatan

Monitor Tekanan Intra Kranial (TIK )

Monitor TIK pasien dan neurologi, bandingkan dengan keadaan

normal
Monitor tekanan perfusi serebral

Posisikan kepala agak tinggi dan dalam posisi anatomis

Pertahankan keadaaan tirah baring

Pantau tanda-tanda vital

Kolaborasi pemberian oksigen, obat antikoagulasi, obat antifibrolitik,

antihipertensi, vasodilatasi perifer, pelunak feses sesuai indikasi.

 Askep selanjutnya: tugas Individu!!!!!!!!
Increased Intracranial Pressure
Nursing Care: Assessment

Change in level of consciousness

Changes in vital signs (Cushing triad)
Widening pulse pressure
Tachy/Bradycardia
Increased systolic BP
Irregular respirations
Increased Intracranial Pressure
Nursing Care: Assessment

Ocular signs

Decrease in motor strength and

function
Assess movement
Assess response to stimuli
Assess:
Decerebrate posturing (extensor)

Indicates more serious damage
Decorticate posturing (flexor)

Decorticate and Decerebrate
Posturing

Fig. 55-6
107
Increased Intracranial Pressure
Nursing Care: Assessment

Headache
Often continuous and worse
in the morning
Vomiting
Not preceded by nausea
Projectile
Increased Intracranial Pressure
Collaborative Care

Hyperventilation therapy: suctioning

hyperventilate with 100% oxygen

Adequate oxygenation
PaO22 maintenance at 100 mm Hg or
greater
ABG analysis guides the oxygen therapy
May require mechanical ventilator
Increased Intracranial Pressure
Collaborative Care

Drug therapy
Mannitol
Loop diuretics
Corticosteroids
Barbiturates
Antiseizure drugs
Increased Intracranial Pressure
Collaborative Care

Nutritional therapy
Patient is in hypermetabolic and
hypercatabolic state
Need for glucose
Keep patient normovolemic
IV 0.45% or 0.9% sodium
chloride
Increased Intracranial Pressure
Nursing Management

Overall goals:

ICP WNL
Maintain patent airway
Normal fluid and electrolyte balance
No complications secondary to
immobility
Respiratory function
Fluid and electrolyte balance
Increased Intracranial Pressure
Nursing Management

Overall goals (contd)

Body position maintained in

head-up position: elevate HOB
30
Protection from injury: positioning/turning
Pain control
Psychologic considerations
 Nursing diagnoses:
Ineffective airway clearance related to diminished protective
reflexes (cough, gag)
Ineffective breathing patterns related to neurologic
dysfunction (brain stem compression, structural
displacement)
Ineffective cerebral tissue perfusion related to the effects of
increased ICP

114
 Planning and goals
Maintenance of a patent airway
Normalization of respiration
Adequate cerebral tissue perfusion through reduction in ICP

115
 Nursing Interventions:
Maintaining patent airway.
Assess the patency of the airway.
Suction with care the secretions obstructing the airway, because transient

elevations of ICP occur with suctioning.

The patient is hyperoxygenated before and after suctioning to maintain

adequate oxygenation.
Discourage coughing because it increases ICP.

Auscultate the lung fields at least every 8 hours to determine the presence of

abnormal breath sounds.

Elevate the head of the bed may aid in clearing secretions as well as

improving venous drainage of the brain.

Continued.

116
 Achieving an adequate breathing pattern
Monitor the patient constantly for respiratory irregularities. This includes
Cheyne-Stokes respirations (alternating periods of hyperpnea and apnea)
(See picture below) and hyperventilation (increased rate and depth of
breathing) (Next slide).
Continued on Slide 23

117
Hyperventilation

118
 Monitor PaCO2 (normal range 35 to 45 mm Hg) if hyperventilation therapy
has been decided to reduce ICP (by causing cerebral vasoconstriction and a
decrease in cerebral blood volume).
Maintain a neurologic observation record. Repeated assessments of the patient

are made frequently to immediately note improvement or deterioration.

Prepare for surgical intervention in case of deterioration.

119
 Optimising cerebral tissue perfusion
Maintain head alignment and elevate head of bed 30 degrees. The rationale is
that hyperextension, rotation, or hyperflexion of the neck causes decreased
venous return.
Avoid extreme hip flexion as this increases intra-abdominal and intrathoracic

pressures, leading to rise in ICP.

Avoid the Valsalva maneuver (straining at stool) as it raises ICP. Administer

stool softeners as prescribed. If appropriate, provide high fiber diet.

Note abdominal distention. Avoid enemas and cathartics (sorbitol, magnesium

citrate, sodium sulfate).

Continued

120
 When moving or being turned in bed, instruct the patient to exhale to avoid the
Valsalva maneuver.
If the patient is on mechanical ventilation, preoxygenate and hyperventilate

him, before suction, using 100% oxygen on the ventilator. Suctioning should
not last longer than 15 seconds.
Avoid activities that raise ICP if possible. Space nursing interventions; this

may prevent transient increases in ICP.

During nursing interventions, the ICP should not rise above 25 mm Hg and

should return to baseline levels within 5 minutes. Patients with

Patients with the potential for a significant increase in ICP should receive

sedation or paralyzation before initiation of many nursing activities.

121
 Avoid emotional stress, frequent arousal from sleep, and environmental stimuli
(noise, conversation).
Isometric muscle contractions (Pushing against an immovable wall) are also

contraindicated because they raise the systemic blood pressure and hence the
ICP.

122
15 min

LETS TAKE A BREAK

 Kasus
Pemicu :Kasus IV
Keluhan utama pasien masuk RS adalah kelemahan
anggota gerak sebelah kiri secara tiba-tiba saat pasien
akan tidur, mual tudak ada, rasa pusing berputar
(+),muntah (-), bicara pelo(+), tersedak (+), meracau (+),
riwayat DM (-), hipertensi sejak 5 tahun yang lalu dan
pasien jarang memeriksakan diri, riwayat strok (-). Tekanan
darah 180/100 mmHg, Hasil EKG VES, LVH dan RVH. Pasien
masuh ruang rawat pada tanggal 8 maret 2009 dan penulis
melakukan pengkajian pada tanggal 9 Maret 2009.
Setelah dirawat dikajiDiit 1600 kalori cair, bising usus
13x/menit, perkusi timpani, palpasi supel, Disfagia derajat
II (disfonia, ngiler, dan batuk), muntah (-), pasien
mengeluh perut terasa kembung dan ingin muntah. Hasil
laboratorium : albumin 3 mg/dl, kolesterol 150 mg/dl
trigliserida 78 (50 150 mg/dl), HDL 45 mg/dl (N 45 60
mg/dl), LDL 86 mg/dl (50 130). Tinggi badan adalah 160
cm, LILA 33 cm, perkiraan BB berdasar tinggi badan dan
LILA adalah 70 kg,
 Perdarahan lambung 200 cc, warna coklat
kehitaman, turgor elastis, edema tidak
ditemukan, bibir dan mukosa lembab.
masukan cairan per NGT 2000 cc. IVFD
1000 cc. 2000 cc. Hasil laboratorium: Na
155 meq/L (N 132-147 meq/L), K 3.4
meq/L (N 3.3 -5.4 meq/L), Cl 111 meq/L
(94 111 meq/L), Cr darah 0.4 mg/dl (0.5-
1.3 mg/dl, ureum darah 25 mg/dl ( 10 50
mg/dl), asam urat darah 2.5 mg/dl (2.6 6
mg/dl)., Ht 3.4 mg/dl
 Pertanyaan:
1. Susunlah diagnosa keperawtan
pada Ny TS
2. Susunlah rencana keperawatan
pada Ny TS