ASUHAN

KEPERAWATAN PADA
KLIEN STROKE

OLEH : Achlish Abdillah, S.ST

17/03/05 By Achlis 1
Definisi

Gangguan fungsi otak, fokal atau global

yang timbul mendadak, berlangsung >
24 jam (kecuali bila mengalami
pembedahan atau meninggal sebelum
24 jam, disebabkan oleh karena
kelainan peredaran otak ) ( WHO,
MONICA PROJECT,1995 )
Stroke merupakan penyakit saraf yang :

Sering dijumpai
Paling banyak dirawat
Menimbulkan kecacatan
Dan kematian
KLASIFIKASI
1. STROKE PERDARAHAN
• INTRA SEREBRAL (ICH)
• SUBARAKHNOID (SAH)
2. ISKEMIK/INFARK
• TROMBOTIK
• EMBOLITIK
Anatomi
Darah ke otak melalui

2 arteri karotis interna ke otak besar (cerebrum)

2 Arteri Vertebralis ke otak kecil (cerebellum) dan
Batang otak Hemisfer otak bagian belakang dan
bawah

Kedua arteri tsb membentuk SIRKULUS WILLISI

STROKE INFARK

PEMBAGIAN KLINIS
1. TIA (SOS) Semua gejala neurologis sembuh dalam 24 jam
TRANSIENT ISCHEMIC ATTAC
2. RIND Gejala neurologis sembuh dalam waktu >24 jam
sampai < 2 mg
REVERSIBLE ISCHEMIC NEUROLOGIC DEFICIT
3. PROGRESSIVE STROKE YI Gejala stroke makin lama
makin berat
atau STROKE IN EVOLOTION
4. COMPLETED STROKE YI Gejala stroke yang datang sudah
total
FAKTOR RESIKO TDK DAPAT
DIKENDALIKAN

1. GENETIK
2. RAS
3. UMUR
4. SEX

FAKTOR RESIKO YG DAPAT DIKENDALIKAN

1. DM * HIPERHOMOSISTEINEMIA
2. HT * ROKOK
3. HIPERURISEMIA * PIL KB
4. DISLIPIDEMIA * PENYAKIT KOLLAGEN
5. HIPERFIBRINOGENEMIA * PJK
6. POLISITEMIAVERA * ALKOHOL
* OBESITAS
GEJALA
PERDARAHAN INFARK
1 PERMULAAN SANGAT AKUT SUB AKUT

2 WKT SERANG AKTIF BANGUN PAGI

3 TIA - +

4 NYERI KEPALA ++ -

5 MUNTAH ++ -

6 KEJANG ++ -

7 KESADARAN ++ +/-

8 BRADIKARDI HARI I HARI 4

9 KAKU KUDUK ++ -

10 PTOSIS ++ -

11 PAPILEDEM + -

12 PERDARAHAN RETINA ++ -

13 LOKASI SUB KORTICAL KORTICAL/SUBCORTICAL

14 Ct SACN AREA HIPERDENS SGR AREA HIPODENS STH HR KE

3

15 SIRRAJ SKOR <1 >1

ICH SAH
NYERI KEPALA ++ +++
KAKU KUDUK + +++
GG. N III,IV + +++
KELUMPUHAN HEMIPLEGI HEMIPARESIS

HT ++ 
DIAGNOSIS
STROKE INFARK
CT SCAN
PENGOBATAN
PERHATIKAN GOLDEN PERIOD DALAM 6 JAM
HARUS DIOBATI

PENGOBATAN FAKTOR RESIKO

• REHABILITASI AKTIF SEDINI MUNGKIN
• PENGENDALIAN 6 B (Breath, Blood, Brain, Bowel,
Bladder, Bone and Body Skin’s}
MANIFESTASI KLINIK
. PENURUNAN FGS MOTORIK
Hemiplegi-hemiparese
Flacid Paralyse, /kehilangan reflek
kedalaman tendon
PENURUNAN FGS KOMUNIKASI (AFASIA)
GANGGUAN PERSEPSI ( HEMIANOPSIA, VISUS,
HILANGNYA SENSORI
PERUBAHAN MENTAL DAN PSIKOLOGIS
- Lobus frontal   belajar, memori, intelektual,
motivasi
- depresi  emosi labil, frustasi, tdk kooperatif
• BLEDDER/BOWEL  INC. URI, RETENSI URIN,
INC. BOWEL
PENATALAKSANAAN FASE AKUT

BIASANYA 48- 72 JAM

PERTAHANKAN JALAN NAFAS,
VENTILASI ADEKUAT
POSISI KEPALA ELEVASI td
ENDOTRACHEAL INTUBASI
OBS. KOMPLIKASI PARU (ASPIRASI,
ATELEKTASIS, PNEUMONI)
EVALUASI JANTUNG
PENGKAJIAN

PERUBAHAN TK. KEKAKUAN LEHER

RESPON PASIEN BUKA MATA
OBS. GERAKAN REFLEK PUPIL
VOLUNTER/INVOL TANDA VITAL
UNTER KEMAMPUAN
EXTREMITAS BICARA
OBS. INTAKE, OUT ORIENTASI
PUT
FASE PASCA AKUT
STATUS MENTAL PERGERAKAN
MEMORI, EXTREMITAS
PERHATIAN, ATAS, BWH, FGS
ORIENTASI, BLEDDER
BICARA PERUBAHAN
FUNGSI FUNGSI PASIEN
SENSORIS/PERSE DALAM ADL
PSI (PERSEPSI
NYERI, SUHU)
DX KEPERAWATAN UTAMA

PERUBAHAN MOBILISASI FISIK BD

HEMIPARESIS, INKOORDINASI, SPASME,
TRAUMA KEPALA
SELF CARE DEFISIT (ph, Pindah posisi,
makan) BD GEJALA SISA STROKE
INCONTINENSIA BD FLACID BLEDDER,
TDK STABIL OTOT DESTRUSOR, Gg
KOMUNIKASI
PERUBAHAN PROSES FIKIR BD
DAMPAK GANGGUAN OTAK, TDK
MAMPU MENGIKUTI INSTRUKSI
PERUBAHAN KOMUNIKASI VERBAL
BD GANGGUAN OTAK
PERUBAHAN PROSES KELUARGA
BD ADANYA ANGGOTA KLG SAKIT
MASALAH KOLABORATIF

PENURUNAN CBF
TDK ADEKUAT OKSIGENASI OTAK
FASE REHABILITATIF

TUJUAN UTAMA INTERVENSI

KEPERAWATAN
1. PASIEN MULAI MELATIH GERAKAN
2. TERHINDAR NYERI BAHU
3. TERCAPAI PERAWATAN DIRI
4. TERCAPAI CONTROL BLEDDER]
5. TERCAPAI BENTUK KOMUNIKASI
6. KEUTUHAN INTEGRITAS KULIT BAIK
7. PEMULIHAN DG MELIBATKAN KLG
8. TDK ADA KOMPLIKASI
MONITOR & PENCEGAHAN POT.
KOMPLIKASI

KAJI TANDA VITAL DAN STATUS

OKSIGENASI
CEGAH GANGGUAN PERTUKARAN
GAS  02, SUCTION, FISIOTERAPI
DADA
PERTAHANKAN KARDIO OUT PUT
SCR ADEKUAT  OBAT, CAIRAN
MOBILITAS DAN MENCEGAH
DEFORMITAS
LAKUKAN POSISI UTK MENCEGAH
KONTRAKTUR, CEGAH TEKANAN
JAGA POSISI FLAT KETIKA MELAKUKAN
ADL
CEGAH KAKI DAN TUNGKAI DROP 
MEMBERI PAPAN PADA KAKI
 CEGAH ADDUKSI BAHU DG KETIAK
 ELEVASI LENGAN UTK MENCEGAH
EDEMA
POSISIKAN JARI FLEKSI DAN
TEMPATKAN TANGAN PADA POSISI
SUPINASI
RUBAH POSISI TIAP 2 JAM
ETREMITAS

LATIH ROM 4-5 KALI DALAM SEHARI

MENCEGAH KONTRAKTUR
OBS TANDA GANGGUAN NAFAS SELAMA
LATIHAN
AMBULASI
MULAI DAN PROGRAM REHABILITASI BILA
KESADARAN TERCAPAI
LATIH KESEIMBANGAN DUDUK SEBELUM
LATIHAN BERDIRI
PERTAHANKAN PERIODE LATIHAN
AMBULASI
SELF CARE

DORONG PASIEN MELAKUKAN PH

ARAHKAN TUJUAN AKTIVITAS YG
REALISTIS
TINGKATKAN MORAL PASIEN
BANTU PASIEN DLM AKTIVTS
BERPAKAIAN
BERI SUPPORT MENTAL
CONTROL BLEDDER
- OBSERVASI POLA
BAK DAN JADWAL PROSES BERFIKIR
BERKEMIH
- LATIH PASIEN
MENGGUNAKAN
PERSEPSI
KOGNITIF, VISUAL,
ORIENTASI
REALISTIS
- BERI PUJIA PSIEN
KOMUNIKASI

PROGRAM KOMUNIKASI SCR

KONSISTEN
ORIENTASIKAN PASIEN DG OBYEK
DISEKITAR PASIEN
PERTAHANKAN PERHATIAN PASIEN,
BICARA SCR PELAN DAN DAMPINGI
PASIEN SELAMA LATIHAN
Diagram of a cerebral hemisphere in coronal
section showing the territories of the major
cerebral vessels.
 Figure 361-1. Diagram of the brainstem, cerebellum, inferior right frontal lobe, and transected temporal lobe. Principal
branches of the vertebral basilar arterial system are pictured. The stem of the middle cerebral artery with its small, deep
penetrating lenticulostriate arteries and the circle of Willis with its small, deep penetrating branches are shown. Roman
numerals I, II, III, and IV represent some of the possible variations of the circle of Willis due to atresia of one or more of its
arterial components. A, B, C, and D arrows indicate the four levels of the brainstem diagrammed below (D, Fig. 361-6; A, Fig.
361-7; B, Fig. 361-8; C, Fig. 361-9). Although typical vascular syndromes of the pons and medulla have been designated by the
shaded areas in Figs. 361-6, 361-7, 361-8, and 361-9, the shading is approximate only. Great variability in infarct size and
location occurs when the basilar or vertebral arteries or one of their penetrating branches becomes occluded. This variability is
because of variation in arterial anatomic location and available collateral circulation. Thus the stroke syndromes produced are
often atypical, incomplete, or merge with one another.
(Courtesy of CM Fisher, MD.)
Copyright© 2001 McGraw-Hill. All rights reserved.
Diagram of a cerebral hemisphere, lateral aspect, showing the
branches and distribution of the middle cerebral artery and the
principal regions of cerebral localization. Note the bifurcation of
the middle cerebral artery into a superior and inferior division.
(Courtesy of CM Fisher, MD.)

Copyright© 2001 McGraw-Hill. All rights reserved.

Diagram of a cerebral hemisphere, medial
aspect, showing the branches and distribution
of the anterior cerebral artery and the principal
regions of cerebral localization.
 Inferior aspect of the brain with the branches and
distribution of the posterior cerebral artery and the
principal anatomic structures shown.
(Courtesy of CM Fisher, MD.)
 (Courtesy of CM Fisher, MD.)Signs and Symptoms: Structures involved
1. Medial medullary syndrome (occlusion of vertebral artery or of branch of vertebral or lower basilar artery)
On side of lesion
Paralysis with atrophy of half the tongue: Ipsilateral twelfth nerve
On side opposite lesion
Paralysis of arm and leg sparing face; impaired tactile and proprioceptive sense over half the body: Contralateral
pyramidal tract and medial lemniscus
2. Lateral medullary syndrome (occlusion of any of five vessels may be responsible¾vertebral, posterior inferior
cerebellar, superior, middle, or inferior lateral medullary arteries)
On side of lesion
Pain, numbness, impaired sensation over half the face: Descending tract and nucleus fifth nerve
Ataxia of limbs, falling to side of lesion: Uncertain¾restiform body, cerebellar hemisphere, cerebellar fibers,
spinocerebellar tract (?)
Nystagmus, diplopia, oscillopsia, vertigo, nausea, vomiting: Vestibular nucleus
Horner's syndrome (miosis, ptosis, decreased sweating): Descending sympathetic tract
Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord, diminished gag reflex: Issuing fibers ninth and
tenth nerves
Loss of taste: Nucleus and tractus solitarius
Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei
On side opposite lesion
Impaired pain and thermal sense over half the body, sometimes face: Spinothalamic tract
3. Total unilateral medullary syndrome (occlusion of vertebral artery): Combination of medial and lateral syndromes
4. Lateral pontomedullary syndrome (occlusion of vertebral artery): Combination of lateral medullary and lateral inferior
pontine syndromes
5. Basilar artery syndrome (the syndrome of the lone vertebral artery is equivalent): A combination of the various
brainstem syndromes plus those arising in the posterior cerebral artery distribution
Bilateral long tract signs (sensory and motor; cerebellar and peripheral cranial nerve abnormalities): Bilateral long tract;
cerebellar and peripheral cranial nerves
Paralysis or weakness of all extremities, plus all bulbar musculature: Corticobulbar and corticospinal tracts bilaterally;

Copyright© 2001 McGraw-Hill. All rights reserved.

(Courtesy of CM Fisher, MD.)Signs and Symptoms: Structures involved
1. Medial midpontine syndrome (paramedian branch of midbasilar artery)
On side of lesion
Ataxia of limbs and gait (more prominent in bilateral involvement): Pontine
nuclei
On side opposite lesion
Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract
Variable impaired touch and proprioception when lesion extends
posteriorly: Medial lemniscus
2. Lateral midpontine syndrome (short circumferential artery)
On side of lesion
Ataxia of limbs: Middle cerebellar peduncle
Paralysis of muscles of mastication: Motor fibers or nucleus of fifth nerve
Impaired sensation over side of face: Sensory fibers or nucleus of fifth
nerve
On side opposite lesion
Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract

Copyright© 2001 McGraw-Hill. All rights reserved.

(Courtesy of CM Fisher, MD.)Signs and symptoms: Structures involved
1. Medial inferior pontine syndrome (occlusion of paramedian branch of basilar artery)
On side of lesion
Paralysis of conjugate gaze to side of lesion (preservation of convergence): "Center" for
conjugate lateral gaze
Nystagmus: Vestibular nucleus
Ataxia of limbs and gait: Middle cerebellar peduncle (?)
Diplopia on lateral gaze: Abducens nerve;
On side opposite lesion
Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract in lower pons
Impaired tactile and proprioceptive sense over half of the body: Medial lemniscus
2. Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery)
On side of lesion
Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopia: Vestibular nerve or
nucleus
Facial paralysis: Seventh nerve
Paralysis of conjugate gaze to side of lesion: "Center" for conjugate lateral gaze
Deafness, tinnitus: Auditory nerve or cochlear nucleus
Ataxia: Middle cerebellar peduncle and cerebellar hemisphere
Impaired sensation over face: Descending tract and nucleus fifth nerve
On side opposite lesion
Impaired pain and thermal sense over half the body (may include face): Spinothalamic tract

Copyright© 2001 McGraw-Hill. All rights reserved.