Laporan Kasus Net Str62e He06rag52

Laporan Kasus

penegakan diagnosa stroke hemoragic

seorang Pasien laki-laki usia 60 tahun datang dibawa keluarganya ke UGD RSUD Wonosobo dengan keterangan Pasien mendadak pingsan 3 jam yang lalu, sebelumnya Pasien mengeluh sakit kepala cekot-cekot dan semakin bertambah. Pasien juga mengeluh mual tapi tidak sampai muntah. Selain itu pasien juga mengeluh tangan dan kaki sebelah kiri terasa lemas dan sulit digerakkan. 3 jam sebelum masuk Rumah Sakit pasien ditemukan oleh keluarganya dalam keadaan tergeletak di lantai dan tidak sadarkan diri, oleh keluarga pasien langsung dibawa ke Rumah Sakit. Pasien memiliki riwayat stroke 3 tahun yang lalu, dan Hipertensi sejak 5 tahun yang lalu, Tidak terdapat anggota keluarga yang mengalami sakit serupa dengan pasien.

Pemeriksaan fisik pada pasien ini mendapatkan hasil sebagai berikut:

Keadaan Umum : kesadaran: Koma

Vital Sign : TD = 170/103 mmHg

N = 86x / menit

R = 28x / menit

T = 36,6 0 C

Status Gizi : kesan kurang

Status Neurologik

Kesadaran : koma

Kuantitatif : GCS (E1 V1 M1) =3

Kualitatif : tidak sadar

Orientasi : tidak dapat dinilai

Jalan pikiran : tidak dapat dinilai

Daya ingat : tidak dapat dinilai

Kemampuan bicara : tidak dapat dinilai

Sikap tubuh : tidak dapat dinilai

Cara berjalan : tidak dapat dinilai

Gerakan abnormal : tidak ada

Kepala : bentuk mesocephal, simetris, ukuran DBN, nyeri tekan (-)

Telinga : serumen (+), ganguan pendengaran tidak dapat dinilai

Leher : sikap normal, gerakan bebas terbatas, pulsasi karotis teraba, bentuk vertebra lurus,

Meningeal sign : Kaku kuduk (-)

Brudzinski I (-)

Brudzinski II (-)

Kernig (-)

Nervus Cranialis : Pemeriksaan Nervus cranialis I-XII sulit dinilai karena kesadaran pasien menurun

Ekstremitas :

Gerakan :Tidak bisa dinilai

Kekuatan: :Tidak bisa dinilai

Sensibilitas : Tidak bisa dinilai

Terdapat lateralisasi ke kanan

Refleks fisiologis: Positif

Tonus : Tidak bisa dinilai

Klonus : - / +

Refleks Patologis :

Babinski +

Chaddock +

Tes koordinasi, cara berjalan dan keseimbangan :

Cara berjalan : tidak dapat dinilai

Rebound phenomen : tidak dapat dinilai

Disdiakokinesis : tidak dapat dinilai

Tes Romberg : tidak dapat dinilai

Disimetri : tidak dapat dinilai

Pada pasien ini juga telah dilakukan pemeriksaan penunjang, dengan hasil sebagai berikut:

PEMERIKSAAN PENUNJANG

DARAH RUTIN

WBC 14,85 (5,00 – 10,00)

LYM 4,65 (1,30 – 4,00)

MID 0,60 (0,15 – 0,70)

GRA 9,60 (2,50 – 7,50)

LY% 31,3 (25,0 – 40,0)

MI% 4,0 (3,0 – 7,0)

GR% 64,7 (50,0 – 75,0)

RBC 4,24 (4,00 – 5,00)

HGB 11,1 (12,0 – 16,0)

HCH 35,93 (36,0 – 48,0)

MCHC 30,8 (30,0 – 35,0)

RDWc 15,1 %

PLT 339 (150 – 400)

PCT 0,30 %

Kimia Darah :

GDS 240 Mg% (<150)

Kolesterol total 253

Trigliserit 198

Asam urat 4,40

Urea 28,4

Kreatinin 0,60

SGOT 21

SGPT 9

Dari hasil anamnesa, pemeriksaan fisik dan pemeriksaanpenunjang kami menegakkan diagnosis pada pasien ini adalah : stroke hemoragic

Penatalaksanaan yang diberikan pada pasien ini adalah:

Terapi Umum

- Oksigenasi 3 liter per menit

- Perbaikan jalan nafas

- Awasi KU

Terapi Spesifik

- RL 12 tpm

- Manitol 100cc/ 8jam

- Piracetam 3 X 3 gr

- Lancolin 3 X 250 mg

- Vit K

- Ranitidine 3 X 150 mg

- Pasang NGT

- Pasang DC

- Lab : darah, urin, feses rutin. GDS, SGOT, SGPT, Chol, TG, Ureum, Creatinin

PEMBAHASAN

Penegakan diagnosa stroke hemoragic pada pasien ini berdasarkan dari aloanamnesis, pemeriksaan fisik, dan pemeriksaan penunjang. Adanya riwayat stroke sebelumnya, adanya keluhan nyeri dan lemah pada angota gerak, serta kadaan dimana pasien mendadak hilang kesadaran dan jatuh adalah poin yang mengarahkan diagnosa pada stroke.

Menurut WHO stroke adalah adanya tanda-tanda klinik yang berkembang cepat akibat gangguan fungsi otak fokal (atau global) dengan gejala-gejala yang berlangsung selama 24 jam atau lebih yang menyebabkan kematian tanpa adanya penyebab lain yang jelas selain vaskuler

Etiologi Stroke

Penyebab stroke antara lain:

1. Trombosis ( bekuan cairan di dalam pembuluh darah otak )

2. Embolisme cerebral ( bekuan darah atau material lain )

3. Iskemia ( Penurunan aliran darah ke area otak)

(Smeltzer C. Suzanne, 2002, hal 2131)

Faktor Resiko Stroke

1. Faktor yang tidak dapat dirubah (Non Reversible)

Jenis kelamin : Pria lebih sering ditemukan menderita stroke dibanding wanita. Usia : Makin tinggi usia makin tinggi pula resiko terkena stroke. Keturunan : Adanya riwayat keluarga yang terkena stroke

2. Faktor yang dapat dirubah (Reversible)

Hipertensi Penyakit jantung Kolesterol tinggi

Obesitas Diabetes Melitus Polisetemia Stress Emosional

3. Kebiasaan Hidup

Merokok, Peminum Alkohol, Obat-obatan terlarang. Aktivitas yang tidak sehat: Kurang olahraga, makanan berkolesterol.

Menurut teori gejala stroke dapat dibagi menjadi:

a. Sementara

Timbul hanya sebentar selama beberapa menit sampai beberapa jam dan hilang sendiri dengan atau tanpa pengobatan. Hal ini disebut Transient ischemic attack (TIA). Serangan bisa muncul lagi dalam wujud sama, memperberat atau malah menetap.

b.Sementara, namun lebih dari 24 jam

Gejala timbul lebih dari 24 jam dan ini disebut reversible ischemic neurologic defisit (RIND)

c. Gejala makin lama makin berat (progresif) Hal ini disebabkan gangguan aliran darah makin lama makin berat yang disebut progressing stroke atau stroke inevolution

d. Sudah menetap/permanent

pemeriksaan penunjang yang diperlukan untuk menegakkan diagnosa stroke antara lain:

CT Scan

Memperlihatkan adanya edema , hematoma, iskemia dan adanya infark

Angiografi serebral

Membantu menentukan penyebab stroke secara spesifik seperti perdarahan atau obstruksi arteri

Pungsi Lumbal

- Menunjukan adanya tekanan normal

- Tekanan meningkat dan cairan yang mengandung darah menunjukan adanya perdarahan

MRI : Menunjukan daerah yang mengalami infark, hemoragik.

EEG: Memperlihatkan daerah lesi yang spesifik

Dikarenakan keterbatasan alat yang dimiliki rumah sakit dan keterbatasan biaya dari pihak keluarga pasien, maka pemeriksaan penunjang yang seharusnya dilakukan seperti diebut diatas tidak satu pun yang mampu dilakukan, sehingga pada pasien ini penegakan diagnosa hanya berdasarkan anamnesa, pemeriksaan fisik saja, hal ini sebenarnya bertentangan dengan referensi yang mengatakan bahwa gold standart untuk penegakan diagnosa stroke adalah dengan pemeriksaan penunjang Ct Scan atau MRI.

Alternative lain yang dapat digunakan untuk penegakan diagnosa pada pasien ini adalah dengan menggunakan algoritma stroke gajahmada, dengan variable sebagai berikut:

Penurunan kesadaran

sakit kepala

refleks Babinski.

Daftar pustaka

1. 1. Harsono. 2005. Kapita Selekta Neurologi. Gadjah Mada University Press: Yogyakarta2. Tuti Pahria, dkk, Asuhan Keperawatan pada Pasien dengan Ganguan Sistem

Persyarafan, Jakarta, EGC, 19933. Pusat pendidikan Tenaga Kesehatan Departemen Kesehatan, Asuhan Keperawatan

Klien Dengan Gangguan Sistem Persarafan , Jakarta, Depkes, 1996

Ditulis oleh: Moch. Nizam fahmi

20040310109

RSUD SETJONEGORO WONOSOBO

Bagian syaraf

Stroke, HemorrhagicDenise Nassisi, MD, Assistant Professor, Department of Emergency Medicine, Mount Sinai Medical Center

Updated: Jun 17, 2010

Introduction

Background

The terms intracerebral hemorrhage (ICH) and hemorrhagic stroke are used interchangeably in this discussion and are regarded as separate entities from hemorrhagic transformation of ischemic stroke. Intracerebral hemorrhage accounts for 10-15% of all strokes and is associated with higher mortality rates than cerebral infarctions.[1 ]

Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke. Prior literature indicates that only 8-18% of strokes were hemorrhagic. However, a recent retrospective review from a stroke center found that 40.9% of 757 strokes were hemorrhagic. However, the authors state that the increased percentage of hemorrhagic stroke may be due to improvement of CT scan availability and implementation unmasking a previous underestimation of the actual percentage, or it may be due to an increase in therapeutic use of antiplatelet agents and warfarin causing an increase in the incidence of hemorrhage.[2 ]

Patients with hemorrhagic stroke present with similar focal neurologic deficits but tend to be more ill than patients with ischemic stroke. Patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension; however, none of these findings reliably distinguishes between hemorrhagic stroke and ischemic stroke.[3 ]

An intracerebral hemorrhage is shown in the CT below.

Large intracerebral hemorrhage with midline shift.

Pathophysiology

In intracerebral hemorrhage (ICH), bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. Other mechanisms include bleeding diatheses, iatrogenic anticoagulation, cerebral amyloidosis, and cocaine abuse. Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus, putamen, cerebellum, and brainstem. In addition to the area of the brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the hematoma. A general increase in intracranial pressure may occur.

Frequency

United States

Intracerebral hemorrhage accounts for 10-15% of all strokes.[1 ]Recent reports indicate an incidence exceeding 500,000 new strokes of all types per year.

Mortality/Morbidity

Stroke is a leading killer and disabler. Combining all types of stroke, it is the third leading cause of death and the first leading cause of disability.

Morbidity is more severe and mortality rates are higher for hemorrhagic stroke than for ischemic stroke. Only 20% of patients regain functional independence.[1 ]

The 30-day mortality rate for hemorrhagic stroke is 40-80%. Approximately 50% of all deaths occur within the first 48 hours.[1 ]

o A recent study of 474 ICH patients found that for those younger than 75 years of age, male sex predicted a poor outcome. Within 28 days, 20% of women and 23% of men died (P=0.38); in those 75 years or older, the corresponding figures were 26% and 41%, respectively (P=0.02). Other independent predictors of death were high age, central and brainstem hemorrhage location, intraventricular hemorrhage, increased volume, and decreased level of consciousness.[4 ]

Race

African Americans have a higher incidence of hemorrhagic and ischemic strokes than other races in the United States. The incidence of hemorrhagic stroke in the Japanese population is increased.

Age

The risk of stroke increases with age.

Clinical

History

Patients' symptoms vary depending on the area of the brain affected and the extent of the bleeding.

Hemorrhagic strokes are more likely to exhibit symptoms of increased intracranial pressure than other types of stroke.

o Headache, often severe and sudden onseto Nausea and/or vomiting

Seizures are more common in hemorrhagic stroke than in ischemic stroke. They occur in up to 28% of hemorrhagic strokes and generally occur at the onset of the intracerebral hemorrhage (ICH) or within the first 24 hours.

Physical

Intracerebral hemorrhage (ICH) may be clinically indistinguishable from ischemic stroke.

Hypertension is commonly a prominent finding. An altered level of consciousness or coma is more common with hemorrhagic stroke than

with ischemic stroke. Often, this is due to an increase in intracranial pressure. Meningismus may result from blood in the ventricles. Focal neurologic deficits

o The type of deficit depends upon the area of brain involved.o If the dominant hemisphere (usually left) is involved, a syndrome consisting of

right hemiparesis, right hemisensory loss, left gaze preference, right visual field cut, and aphasia may result.

o If the nondominant (usually right) hemisphere is involved, a syndrome of left hemiparesis, left hemisensory loss, right gaze preference, and left visual field cut may result. Nondominant hemisphere syndrome may also result in neglect when the patient has a left-sided hemi-inattention and ignores the left side.

o If the cerebellum is involved, the patient is at high risk of herniation and brainstem compression. Herniation may cause a rapid decrease in the level of consciousness, apnea, and death.

o Other signs of cerebellar or brainstem involvement include the following: Gait or limb ataxia Vertigo or tinnitus Nausea and vomiting Hemiparesis or quadriparesis Hemisensory loss or sensory loss of all 4 limbs Eye movement abnormalities resulting in diplopia or nystagmus Oropharyngeal weakness or dysphagia Crossed signs (ipsilateral face and contralateral body)

o Many other stroke syndromes are associated with intracerebral hemorrhage (ICH), ranging from mild headache to neurologic devastation. At times, a cerebral hemorrhage may present as a new-onset seizure.

Causes

Hypertension (up to 60% of cases) Advanced age (risk factor) Cerebral amyloidosis (affects people who are elderly and may cause up to 10% of

intracerebral hemorrhages [ICHs]) Coagulopathies (eg, due to underlying systemic disorders such as bleeding diathesis or

liver disease) Anticoagulant therapy Thrombolytic therapy for acute myocardial infarction (MI) and acute ischemic stroke

(can cause iatrogenic hemorrhagic stroke) Abuse of cocaine and other sympathomimetic drugs Arteriovenous malformation Intracranial aneurysm Vasculitis Intracranial neoplasm History of prior stroke (risk factor)

Differential DiagnosesEncephalitis MeningitisHeadache, Migraine Neoplasms, BrainHypernatremia Stroke, IschemicHyperosmolar Hyperglycemic Nonketotic Coma Subarachnoid HemorrhageHypertensive Emergencies Subdural HematomaHypoglycemia Transient Ischemic AttackHyponatremiaLabyrinthitis

Other Problems to Be Considered

Postictal (Todd) paralysisHyperosmolality

Workup

Laboratory Studies

Complete blood count Coagulation profile Electrolyte level Serum glucose level Blood type and screen

Imaging Studies

Brain imaging is a crucial step in a patient's evaluation and must be obtained on an emergent basis. Brain imaging aids in making the diagnosis of hemorrhage. It may identify complications including intraventricular hemorrhage, brain edema, or hydrocephalus. Either noncontrast CT or MRI of the brain is the modality of choice.

o Noncontrast CT of the brain Noncontrast CT differentiates hemorrhagic stroke from ischemic stroke. It is useful in distinguishing stroke from other intracranial pathology. Noncontrast CT can identify virtually all intracerebral hematomas greater

than 1 cm in diameter. CTs of intracerebral hemorrhage are shown below.

CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.

A 59-year-old female with hypertension who presented with left-sided weakness demonstrated a right putaminal hemorrhage on noncontrast CT examination of the head. Tiny hyperdense foci in the basal ganglia and pineal gland represent calcifications.

A 62-year-old female with hypertension who presented with acute-onset ataxia and confusion. Noncontrast CT examination of the head showed a large right cerebellar hemorrhage, which was evacuated to relieve the mass effect on the brainstem and fourth ventricle.

o MRI In the past, noncontrast CT was the criterion standard for diagnosing

hemorrhagic stroke. Recent progress has demonstrated that current MRI techniques are capable of accurately diagnosing hemorrhagic stroke.

MRI, especially newer techniques such as diffusion-weighted imaging, has been shown to identify ischemic stroke earlier and more reliably than CT scanning. MRI is being used with increasing frequency in the evaluation of ischemic stroke.

MRI may identify an underlying vascular malformation or lesion that caused the bleeding.

Intracerebral hemorrhage associated with a right frontal arteriovenous malformation is shown below.

Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.

o Head CT should be obtained in patients with contraindications to MRI. Chest radiography should be obtained to screen for comorbid conditions.

Other Tests

Obtain an electrocardiogram (ECG) and begin cardiac monitoring. Cardiac dysrhythmias and myocardial ischemia have a significant coincidence with stroke.

Treatment

Prehospital Care

Identify and address, as clinically indicated, any compromise of ABCs. Recognize signs and symptoms of stroke. Notify the receiving hospital. Rapid transport to the closest facility capable of providing appropriate stroke care (if

applicable) is indicated. In general, elevations of blood pressure (BP) should not be treated in the field.

Emergency Department Care

Assess the ABCs. Address any compromise in the patient's status as clinically indicated. Establish intravenous (IV) access. Obtain bedside glucose determination.

o Hypoglycemia may mimic stroke.o Hyperglycemia has been associated with poorer outcomes in patients

experiencing stroke. (Also see Metabolic Disease & Stroke: Hyperglycemia/Hypoglycemia.)

Institute cardiac monitoring and obtain an ECG. Intubation should be performed for patients who demonstrate potential loss of airway

protective mechanisms or signs of brainstem dysfunction. If intubation is needed, rapid sequence intubation should be performed with technique and medications aimed at limiting any increase in intracranial pressure.

Seizures:o Early seizure activity occurs in 4-28% of patients with intracerebral hemorrhage,

and these seizures are often nonconvulsive seizures.[5,6 ]

o Seizure activity should be rapidly controlled with a benzodiazepine, such as lorazepam or diazepam, accompanied by either phenytoin or fosphenytoin loading.

o Prophylactic anticonvulsant therapy is recommended in patients with lobar hemorrhages to reduce the risk of early seizures.[5,1 ]However, the use of prophylactic anticonvulsant therapy in all cases of intracerebral hemorrhage is controversial, as no prospective controlled trials have demonstrated a clear benefit.

Careful blood pressure (BP) monitoring is important.o No controlled studies define optimum BP levels.o Greatly elevated BP is thought to lead to rebleeding and hematoma expansion.o Patients who have had a stroke may lose their cerebral autoregulation of cerebral

perfusion pressure.o Rapid or aggressive BP lowering may compromise cerebral perfusion.o Nicardipine, labetalol, esmolol, and hydralazine are agents that may be used when

necessary for BP control. Avoid nitroprusside because it may raise intracranial pressure.

o The American Heart Association guidelines for treating elevated BP are as follows:[1 ]

If systolic BP is >200 mm Hg or mean arterial pressure (MAP) is >150 mm Hg, then consider aggressive reduction of BP with continuous intravenous infusion with frequent BP (every 5 min) checks.

If systolic BP is >180 mm Hg or MAP is >130 mm Hg and there is evidence or suspicion of elevated intracranial pressure (ICP), then consider monitoring of ICP and reducing BP using intermittent or continuous intravenous medications to maintain cerebral perfusion pressure >60-80 mm Hg.

If systolic BP is >180 or MAP is >130 mm Hg and there is NOT evidence or suspicion of elevated ICP, then consider modest reduction of BP (target

MAP of 110 mm Hg or target BP of 160/90 mm Hg) with BP checks every 15 minutes.

Intracranial pressure control:o Elevated intracranial pressure (ICP) may result from the hematoma itself,

surrounding edema, or both. The frequency of increased ICP in patients with intracerebral hemorrhage (ICH) is not known.

o Elevate the head of the bed to 30 degrees. This improves jugular venous outflow and lowers ICP. The head should be midline and not turned to the side.

o Provide analgesia and sedation as needed.o More aggressive therapies such as osmotic therapy (mannitol, hypertonic saline),

barbiturate anesthesia, and neuromuscular blockage generally require concomitant monitoring of ICP and BP with an ICP monitor to maintain adequate cerebral perfusion pressure (CPP) of above 70 mmHg. A randomized controlled study of mannitol in ICH failed to demonstrate any difference in disability or death at 3 months.[7 ]

o Hyperventilation (paCO2 of 25-30-35 mm Hg) is not recommended. Its effect is transient, it decreases cerebral blood flow, and it may result in rebound elevated intracranial pressure.[1 ]

o Glucocorticoids are not effective and result in higher rates of complications with poorer outcomes.

o Ventriculostomy (cerebrospinal fluid drainage by intraventricular catheter drainage) is often used in the setting of obstructive hydrocephalus. Obstructive hydrocephalus is a common complication of thalamic hemorrhage with third ventricle compression and of cerebellar hemorrhage with fourth ventricle compression. Ventriculostomies are associated with high rates of complications including bacterial meningitis.

Hemostatic therapy:o Much interest has been generated to determine if treatment with hemostatic

therapy to stop ongoing hemorrhage or prevent hematoma expansion may be effective.

o Recombinant factor VIIa A preliminary study of treatment with recombinant factor VIIa

demonstrated reduced mortality and improved functional outcomes. However, unfortunately, the results of the larger randomized trial revealed no overall benefit of treatment. Hemostatic therapy with rFVIIa reduced growth of the hematoma but did not improve survival or functional outcome.[8 ]

Diringer et al conducted a study using recombinant activated factor VIIa (rFVIIa) in patients (n=841) presenting less than 3 hours after spontaneous intracerebral hemorrhage.[9 ]Patients considered at higher risk for thromboembolic events (eg, Glasgow Coma Scale score <5, planned early surgery, coagulopathy, recent thromboembolic event) were excluded. Participants were randomized to receive 20 or 80 mcg/kg of rFVIIa, or placebo. Venous events were similar between groups. Arterial events were associated with receiving 80 mcg/kg dose of rFVIIa (P=0.031), cardiac or cerebral ischemia at presentation (P=0.01), advanced age (P=0.0123), or

antiplatelet use (P=0.035). Additional research is needed to measure the benefit of hemorrhage control in patients with cerebral hemorrhage with the risk for arterial thromboembolic events.

o Currently, no effective targeted therapy for hemorrhagic stroke exists. Further studies are necessary to develop other potential treatment options.

Anticoagulation-associated ICH:o Warfarin

Patients on warfarin have an increased incidence of hemorrhagic stroke. Morbidity and mortality for warfarin associated bleeding is high, over half of patients die within 30 days. Most episodes occur with a therapeutic INR but overanticoagulation is further associated with an increased risk of bleeding.

Reversal of warfarin anticoagulation is a true medical emergency and must be accomplished as quickly as possible to prevent further hematoma expansion.

Warfarin reversal options include IV vitamin K, fresh frozen plasma (FFP), prothrombin complex concentrates (PCC), and recombinant factor VIIa.

Because vitamin K requires more than 6 hours to normalize the INR, it should be administered with either FFP or PCC.

FFP needs to be given 15-20 mL/kg and therefore requires a large volume infusion. Prothrombin complex concentrate contains high levels of vitamin K-dependent cofactors with a smaller volume of infusion than FFP, resulting in more rapid administration. If available, PCC is preferable over FFP as a reversal agent.[10,11 ]

Based upon the available medial evidence, the use of factor VIIa is currently not recommended over other agents.

o Heparin Patients on heparin (either unfractionated or low molecular weight

heparin) who develop a hemorrhagic stroke should immediately have anticoagulation reversed with protamine.[1 ]

The dose of protamine is dependent upon the dose of heparin that was given and the time elapsed since that dose.

Reversal of antiplatelet therapy and platelet dysfunction:o Patients on antiplatelet medications including aspirin, aspirin/dipyridamole

(Aggrenox), and clopidogrel should be given desmopressin (DDAVP) and platelet transfusion.

o Patients with renal failure and platelet dysfunction may also benefit from the administration of desmopressin (DDAVP).

Consultations

Emergent neurosurgical or neurological consultation often is indicated; local referral patterns may vary.

o A potential treatment of hemorrhagic stroke is surgical evacuation of the hematoma. The role of surgical treatment for supratentorial intracranial

hemorrhage remains controversial. Outcomes in published studies are conflicting. A published meta-analysis of studies suggested some promise for early surgical intervention. However, one study comparing early surgery versus initial conservative treatment failed to demonstrate a benefit with surgery.[12 ]

o Surgical intervention for cerebellar hematoma has been shown to improve outcome. It can be lifesaving in the prevention of brainstem compression.

o Need for invasive intracranial pressure monitoring should be assessed by the neurosurgeon.

o Need for emergent cerebral angiography should be assessed by the neurosurgeon. Patients with no clear cause of the hemorrhage and who would otherwise be candidates for surgery should be considered for angiographic evaluation.

MedicationThe goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Anticonvulsant

Anticonvulsants prevent seizure recurrence and terminate clinical and electrical seizure activity.

Fosphenytoin (Cerebyx)

Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Following administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.To avoid need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium equivalents (PE). Although can be administered IV and IM, IV route is route of choice and should be used in emergency situations.Concomitant administration of an IV benzodiazepine will usually be necessary to control status epilepticus. The antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, is not immediate.

Dosing

Adult

Loading dose: 15-20 mg PE/kg IV/IM at 100-150 mg PE/minMaintenance dose: 4-6 mg PE/kg/d IV/IM at 150 mg PE/min to minimize risk of hypotension

Pediatric

Loading dose: 15-20 mg PE/kg IV/IMInitial dose: 5 mg PE/kg/d IV/IMMaintenance dose: 4-8 mg PE/kg IV/IM>6 years: May require minimum adult dose (300 mg PE/d) not to exceed 300 mg PE/d

Interactions

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, disulfiram, ethanol (acute ingestion), omeprazole, phenacemide, phenylbutazone, succinimides, fluconazole, isoniazid, metronidazole, miconazole, sulfonamides, trimethoprim, and valproic acid may increase phenytoin toxicityPhenytoin effects may decrease when taken concurrently with barbiturates, carbamazepine, theophylline, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, and sucralfate

Phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, methadone, metyrapone, mexiletine, oral contraceptives, quinidine, theophylline, valproic acid

Contraindications

Documented hypersensitivity; sinoatrial block, second- and third-degree AV block, or Adams-Stokes syndrome

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Blood dyscrasias have occurred and thus should perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter; discontinue use if skin rash appears; if rash is exfoliative, bullous, or purpuric, do not resume use; death from cardiac arrest has occurred after too-rapid IV administration preceded sometimes by marked QRS widening; administer cautiously to patients with acute intermittent porphyria; exercise caution when administering to patients with diabetes; may raise blood sugar levels; discontinue drug if hepatic dysfunction occurs

Phenytoin (Dilantin)

May act in motor cortex where may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited.

Dose to be administered should be individualized. Administer larger dose before retiring if dose cannot be divided equally.

Dosing

Adult

Loading dose: 15-20 mg/kg PO/IV once or divided doses followed by 100-150 mg/dose at 30-min intervalsInitial dose: 100 mg (125-mg susp) IV/PO tidMaintenance dosage: 300-400 mg/d PO/IV divided tid, or qd/bid if using extended release; increase to 600 mg/d (625 mg/d susp) may be necessary; do not exceed 1500 mg/24 hRate of infusion must not exceed 50 mg/min to avoid hypotension and arrhythmias

Pediatric

<6 years: 15-20 mg/kg PO/IV loading dose once or in divided doses; follow by initial 5 mg/kg/d maintenance dose (range, 4-8 mg/kg) PO/IV divided bid/tid>6 years: May require minimum adult dose (300 mg/d); not to exceed 300 mg/d

Interactions

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicityPhenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfatePhenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, valproic acid

Contraindications

Documented hypersensitivity; sinoatrial block, second- and third-degree AV block, sinus bradycardia, or Adams-Stokes syndrome

Precautions

Pregnancy


Precautions

Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a skin rash appears and do

not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugars; discontinue use if hepatic dysfunction occurs

Diazepam (Diastat, Diazemuls, Valium)

Useful in controlling active seizures and should be augmented by longer-acting anticonvulsants, such as phenytoin or phenobarbital.Modulates postsynaptic effects of GABA-A transmission, resulting in an increase in presynaptic inhibition. Appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. Also has been found to be an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders.Rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, serum concentration drops to 20% of Cmax.Individualize dosage and increase cautiously to avoid adverse effects.

Dosing

Adult

5 mg IV q5-10min; total dose not to exceed 20 mg

Pediatric

Not established

Interactions

Phenothiazines, barbiturates, alcohols, and MAO inhibitors increase CNS toxicity when administered concurrently

Contraindications

Documented hypersensitivity; narrow-angle glaucoma; reversal agents (eg, flumazenil) contraindicated when lorazepam used for life-threatening conditions (eg, control of intracranial pressure or status epilepticus)

Precautions

Pregnancy


Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Lorazepam (Ativan)

Short-acting benzodiazepine with moderately long half-life. Has become drug of choice in many centers for treating active seizures.

Dosing

Adult

1-4 mg IV over 2-10 min; may repeat q10-15min

Pediatric

Not established

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAO inhibitors

Contraindications

Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma; reversal agents (eg, flumazenil) contraindicated when lorazepam used for life-threatening conditions (eg, control of intracranial pressure or status epilepticus)

Precautions

Pregnancy


Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Antihypertensive Agent

The treatment of hypertension should be designed to reduce the blood pressure and other risk factors of heart disease. Pharmacologic therapy should be individualized based on a patient's age.

Labetalol (Trandate)

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites decreasing blood pressure.

Dosing

Adult

5-20 mg IV bolus over 2 min, continuous infusion at 2 mg per minute; not to exceed 300 mg/dose

Pediatric

Not established; suggested dose is 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h

Interactions

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia, resulting from nitroglycerin use, without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes

Contraindications

Documented hypersensitivity; cardiogenic shock, pulmonary edema, bradycardia, atrioventricular block, uncompensated congestive heart failure, reactive airway disease, and severe bradycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction; in elderly patients, a lower response rate and higher incidence of toxicity may be observed

Esmolol (Brevibloc)

Ultra–short-acting agent that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. Particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Shown to reduce episodes of chest pain and clinical cardiac events compared to placebo. Can be discontinued abruptly if necessary. Useful in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease, mild-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.

Dosing

Adult

Loading dose: 250 mcg/kg/min IV for 1 min followed by a 4-min maintenance infusion of 25 mcg/kg/minIf adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min (for 4 min); sequence may be repeated up to 4 times if neededAs desired blood pressure is approached, omit loading infusion and reduce incremental dose of maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min or lower; interval between titration steps may be increased from 5-10 min if needed

Pediatric

Not established; suggested dose is 100-500 mcg/kg administered IV over 1 min

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure, bradycardia, cardiogenic shock, and AV conduction abnormalities

Precautions

Pregnancy


Precautions

Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm may worsen when medication is abruptly withdrawn (withdraw drug slowly and monitor patient closely)

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles. Used to treat hypertensive emergencies. The use of a vasodilator will reduce SVR, which, in turn, may allow forward flow, improving cardiac output.

Dosing

Adult

5-20 mg/dose IV push q30 min; continuous infusion of 1.5 to 5 mcg/kg/min

Pediatric

Not established

Interactions

MAO inhibitors and beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin

Contraindications

Documented hypersensitivity; mitral valve rheumatic heart disease

Precautions

Pregnancy


Precautions

Hydralazine has been implicated in myocardial infarction; caution in suspected coronary artery disease

Nicardipine (Cardene, Cardene IV, Cardene SR)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.

Dosing

Adult

5 mg-15 mg/h IV; titrate to desired blood pressure

Pediatric

Not established

Interactions

Fentanyl and alcohol may increase hypotensive effects; calcium channel blocker may increase cyclosporine levels; H2 blockers (cimetidine), erythromycin, nafcillin, and azole antifungals may increase toxicity (avoid combination or monitor closely); carbamazepine may reduce bioavailability (avoid this combination); rifampin may decrease levels (monitor and adjust dose of calcium channel blocker)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy


Precautions

Adjust dose in renal/hepatic impairment; may cause lower extremity edema; allergic hepatitis has occurred but is rare

Diuretic, Osmotic

These agents are used in an attempt to lower pressure in the subarachnoid space. As water diffuses from the subarachnoid space into the intravascular compartment, pressure in the subarachnoid compartment may decrease.

Mannitol (Osmitrol)

Reduces cerebral edema with help of osmotic forces and decreases blood viscosity, resulting in reflex vasoconstriction and lowering of ICP.

Dosing

Adult

0.75-1 g/kg IV, followed by 0.25-0.5 g/kg IV q3-5h to maintain serum hyperosmolarity (approximately 320 mOsm/L)

Pediatric

Not established; dose is dependent on weight, clinical condition, and laboratory results

Interactions

May decrease serum lithium levels

Contraindications

Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure

Precautions

Pregnancy


Precautions

Carefully evaluate cardiovascular status before rapid administration of mannitol since a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

Vitamin, Fat Soluble

Vitamin K is used to promote the formation of clotting factors.

Phytonadione (Mephyton)

Can overcome competitive block produced by warfarin and other related anticoagulants. Vitamin K-3 (menadione) is not effective for this purpose. Clinical effect is delayed several hours while liver synthesis of clotting factors is initiated and plasma levels of clotting factors II, VII, IX, and X are gradually restored.Not to be administered prophylactically. Use only if evidence of anticoagulation exists. Required dose varies with clinical situation, including amount of anticoagulant ingested and whether it is a short-acting or long-acting anticoagulant.

Dosing

Adult

10 mg IV

Pediatric

Not established

Interactions

Effects of warfarin, sodium, and dicumarol are antagonized by phytonadione

Contraindications


Precautions

Pregnancy


Precautions

Ineffective in hereditary hypoprothrombinemia; rapid infusion may result in flushing and a feeling of constriction in chest; relatively nontoxic, even in massive doses

Blood products

These agents are indicated for the correction of abnormal hemostatic parameters.

Fresh Frozen Plasma

Plasma is the fluid compartment of blood containing the soluble clotting factors. For use in patients with blood product deficiencies.

Dosing

Adult

IV as directed by protocol; 15-20 mL/kg IV suggested

Pediatric

Administer as in adults

Interactions

None reported

Contraindications


Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Viral contamination and infection are possible but unlikely due to prescreening; ineffective in patients with factor IX inhibitors; may induce an anamnestic response

Platelets

Platelet activity may be abnormal.

Dosing

Adult

1 random donor U/10 kg when platelet count is <50,000Many institutions use apheresis-derived platelets; 1 apheresis U of platelets is approximately equivalent to 6 random donor platelet U

Pediatric

1 random donor U IV raises platelet count 10,000-12,000/m2 Neonates: 0.1 U/kg IV raises platelet count 30,000

Interactions

Avoid coadministration with antiplatelet agents or drugs that may cause thrombocytopenia; administer in IV line dedicated to blood products to avoid incompatibility with drugs

Contraindications

Documented hypersensitivity; individuals with known IgA deficiency (use caution)

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Product should be CMV safe and leukoreduced; platelets should be irradiated for patients <6 wk and those with primary (ie, inherited) or secondary (ie, HIV, postchemotherapy, bone marrow transplantation) immunodeficiency; multiple transfusions may sensitize patients to platelet antigens

Prothrombin complex concentrate (Bebulin VH, Profilnine SD)

A mixture of vitamin K–dependent clotting factors found in normal plasma. Replaces deficient clotting factors. Provides increase in plasma levels of factor IX and can temporarily correct coagulation defect of patients with factor IX deficiency.

Dosing

Adult

Bebulin VH: Number of Factor IX Int Units Required = Body Weight (kg) X Desired Factor IX Increase (% of normal) X 1.2 Int units/kgProfilnine SD: Number of Factor IX Int Units Required = Body Weight (kg) X Desired Factor

IX Increase (% of normal) X 1 Int units/kgMajor bleeding: Raise factor IX level to 50 to >60% of normal average duration of treatment in 2-3 d or until adequate wound healing

Pediatric

Bebulin VH: Number of Factor IX Int Units Required = Body Weight (kg) X Desired Factor IX Increase (% of normal) X 1.2 Int units/kgProfilnine SD: Number of Factor IX Int Units Required = Body Weight (kg) X Desired Factor IX Increase (% of normal) X 1 Int units/kgMajor bleeding: Raise factor IX level to 50 to >60% of normal average duration of treatment in 2-3 d or until adequate wound healing

Interactions

None reported

Contraindications


Precautions

Pregnancy


Precautions

Viral contamination and infection are remotely possible but unlikely due to prescreening; may induce an anamnestic response

Heparin antidote

This agent is used to neutralize the effects of anticoagulants.

Protamine sulfate

Forms a salt with heparin and neutralizes its effects.

Dosing

Adult

Dose given depends on amount of elapsed time since heparin administrationImmediately: 1-1.5 mg/100 U of heparin IV30-60 min from discontinuation of therapy: 0.5-0.75 mg/100 U of heparin IV>60 min from discontinuation of therapy: 0.25-0.375 mg/100 U of heparin IVIf heparin administered by deep SC injection, give 1-1.5 mg protamine/100 U of heparin IV; not to exceed 50 mg/dose

Pediatric

Not established

Interactions

None reported

Contraindications


Precautions

Pregnancy


Precautions

Upon metabolism, the salt complex may liberate heparin, causing heparin rebound and requiring multiple dosing of protamine; protamine sulfate has its own anticoagulant effect, which may become apparent if given in doses larger than necessary to inactivate heparin

Antihemophilic agents

These agents improve bleeding time and hemostasis.

Desmopressin acetate (DDAVP, Stimate)

Releases von Willebrand protein from endothelial cells. Improves bleeding time and hemostasis in patients with some vWf (mild and moderate von Willebrand disease without abnormal molecular forms of von Willebrand protein). Effective in uremic bleeding. Tachyphylaxis usually develops after 48 h, but the drug can be effective again after several days.

Dosing

Adult

0.3 mcg/kg IV

Pediatric

0.3 mcg/kg IV

Interactions

Coadministration with demeclocycline and lithium decrease effects; fludrocortisone and chlorpropamide increase effects of desmopressin; loperamide increases bioavailability and absorption of desmopressin, thus potentially increasing effect

Contraindications

Documented hypersensitivity; platelet-type von Willebrand disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Avoid overhydration in patients using desmopressin to benefit from its hemostatic effects; may cause severe hyponatremia that can result in seizures and death; caution in patients at risk for water intoxication with hyponatremia (eg, habitual or psychogenic polydipsia, patient taking drugs that cause dry mouth or increased thirst)

Follow-up

Further Inpatient Care

ICU admission is mandatory for patients experiencing hemorrhagic stroke. o Monitor the patient for airway compromise.o Monitor and carefully address the patient's BP.o Reassess the patient’s neurologic status frequently.o Monitor cardiovascular status continuously.o Select patients may require intracranial pressure monitoring.o Select patients may require intraventricular catheterization for hydrocephalus.

Transfer

Patients with intracerebral hemorrhage (ICH) should be considered for transfer to a facility with neurosurgical capabilities.

Complications

Increased intracranial pressure and herniation are the dreaded complications of intracerebral hemorrhage. Worsening cerebral edema is often implicated in neurologic deterioration in the first 24-48 hours.

Early hemorrhage growth is associated with neurologic deterioration. Expansion of the hematoma is the most common cause of neurologic deterioration in the first 3 hours.

In patients who are initially alert, 25% will have a decrease in consciousness within the first 24 hours.

Poststroke seizures may develop. Stroke is the leading cause of permanent disability.

Prognosis

The prognosis varies depending on the severity of stroke and the location and the size of the hemorrhage.

Lower Glasgow Coma Scores are associated with poorer prognosis and higher mortality rate.

A larger volume of blood at presentation is associated with a poorer prognosis. Growth of the hematoma volume is associated with a poorer functional outcome and

increased mortality rate. The presence of blood in the ventricles is associated with a higher mortality rate. In one

study, the presence of intraventricular blood at presentation was associated with more than a 2-fold increase in death.

Patients with oral anticoagulation–associated intracerebral hemorrhage have higher mortality rates and poorer functional outcomes.

Other complicating medical comorbidities also affect the prognosis.

Patient Education

For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

Miscellaneous

Medicolegal Pitfalls

Failure to recognize potential stroke and obtain brain imaging Failure to consult with a neurologist/neurosurgeon Failure to transfer to a facility with neurosurgical capabilities Failure to reverse anticoagulated state

Multimedia

Media file 1: Large intracerebral hemorrhage with midline shift.

Media file 2: CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.

Media file 3: Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.

Media file 4: A 59-year-old female with hypertension who presented with left-sided weakness demonstrated a right putaminal hemorrhage on noncontrast CT examination of the head. Tiny hyperdense foci in the basal ganglia and pineal gland represent calcifications.

Media file 5: A 62-year-old female with hypertension who presented with acute-onset ataxia and confusion. Noncontrast CT examination of the head showed a large right cerebellar hemorrhage, which was evacuated to relieve the mass effect on the brainstem and fourth ventricle.

STROKE

Diagnosis

Stroke akut karakteristik dengan onset mendadak dari defisit neurologis fokal, biasanya

pada pembuluh darah otak. Gambaran klinis terdiri dari hemiparese, kehilangan

hemisensoris, kelemahan wajah, disartria, afasia dan gangguan visual, terjadi sendiri atau

kombinasi.

Stroke diklasifikasikan menjadi :

1. Stroke iskemia (Asia, 70-90%, insiden lebih tinggi pada Kaukasia). Penyebabnya

atherothrombosis arteri besar, cardioembolism dan penyakit pembuluh darah kecil

(lacunar stroke)

2. Stroke perdarahan, yaitu intracerebral haemorrhage ( 10-30%, insiden lebih tinggi pada

group etnis non Kaukasia) dan subarachnoid haemorrhage ( 2%)

Perhatian

Dokter memegang peranan penting dalam edukasi pasien yang beresiko dan keluarganya

untuk mengenali gejala umum stroke, selanjutnya mengetahui gejala dini terjadi stroke.

Selalu cek kadar guka darah kapiler untuk menyingkirkan hipoglikemia.

Bell’s palsy sering rancu dengan stroke. Meskipun bell’s palsy biasanya disertai paralysis

komplit pada wajah tanpa melibatkan otot dahi, membedakan dengan jelas kadang sulit

pada kasus kelemahan wajah parsial, dan dianjurkan merujuk ke neurologis

Pasien dengan TIA beresiko tinggi menjadi stroke iskemia post TIA. Memerlukan

rujukan ke neurolog atau klinik stroke. Antiplatelet dapat diberikan jika tidak ada

kontraindikasi. Pasien dengan TIA berulang atau TIA cressendo harus segera

dikonsulkan ke neurolog

Harus diperhatikan gambaran mirip stroke (table 1). Selalu lakukan pemeriksaan kadar

gula darah kapiler untuk menyingkirkan hipoglikemia.

Stroke merupakan kondisi emergency sensitive terhadap waktu, khususnya pemakaian

intravena rt-PA (alteplase) untuk akut iskemia stroke dalam 3 jam onset gejala. Pasien

yang diduga stroke harus ditranspor dengan ambulance ke RS terdekat.

Defisit neurologis berhubungan dengan sakit kepala, mual, muntah dan penurunan

kesadaran dan peningkatan Tekanan Darah sering pada stroke perdarahan.

Terapi hipertensi pada akut stroke sering kontroversi dan terapi disesuaikan dengan

penyebabnya.

Tabel 1: Differential diagnosis stroke

Hipoglikemia/ hiperglikemiaPost epileptik(Todd’s) paralysisMigraine komplikataHipertensi ensefalopati

Trauma kepala(epidural/ subdural hematom)Tumor otak/ abses

Meningitis/ ensefalitisDiseksi aortaBell’s palsyKondisi fungsional (psikiatri)

Penatalaksanaan

Mempertahankan status fisiologis optimal, oksigenasi, hidrasi dan kadar gula darah.

Semua pasien initial dipuasakan, dan mulai maintenance IV isotonic saline. Demam

harus dicari penyebab infeksi dan dikontrol dengan antipiretik.

Diagnosis definitif stroke dan subtipe stroke (IS, ICH, atau SAH). Memerlukan CT scan

kepala pada semua pasien dengan kecurigaan stroke dalam 24 jam MRS.

Emergency CT Scan kepala di IRD:

1. Pasien Iskemia, kandidat terapi trombolitik atau antikoagulan, dalam 3 jam dari onset

gejala, atrial fibrillation.

2. Dugaan ICH, peningkatan tinggi TD, sakit kepala, muntah, gelisah, jumlah platelet

rendah, kegagalan waktu pembekuan, penggunaan antikoagulan atau adiksi obat

stimulan.

3. Dugaan SAH, seperti sakit kepala berat, meningism, atau kehilangan kesadaran.

4. Pasien dengan resiko perburukan , seperti stroke kortikal berat dengan hemiplegi,

deviasi mata, dan afasia atau hemineglect; curiga stroke pada fossa posterior.

5.Penderita datang dengan gejala stroke durasi <7hari, misalnya:

Kelemahan salah satu sisi tubuh Anggota gerak di satu sisi tidak dapat diperintah Kesulitan bicara Vertigo dengan kesulitan bicara Kebas di satu sisi tubuh Ketidakmampuan mengekspresikan pikiran, atau mengerti orang lain Kebutaan yang mengenai sebagian atau seluruh lapang pandang pada satu atau kedua

mata Penglihatan dobel atau kelemahan wajah dan/atau anggota gerak

Gambar 1: Alur kerja Stroke Klinis di ED

* Diduga SAH:

1. 2 dari 3 keadaan klinis: Sakit kepala, LOC, Meningismus dengan atau tanpa adanya defisit neurologis

2. Sakit kepala berat terlokalisir, mendadak, dan merupakan keluhan yang pertama kali

** Kriteria inklusi rt-PA:

1. Usia 18-80 tahun (usia di luar batas tersebut dapat berbeda penanganan tergantung institusi/dokter)

2. Stroke akut <3jam (waktu penanganan – waktu onset). Sebagian besar estimasi konservatif diambil, yaitu waktu onset = waktu pasien terlihat baik terakhir kali.

3. Defisit motoris, visual, atau bahasa dapat diukur

Penatalaksanaan hipertensi pada stroke akut.

Stroke perdarahan

Penurunan akut TD dapat mengurangi perdarahan ulang dan perluasan hematom.

Kontrol TD secara agresif dapat memperluas iskemia pada daerah hematom.

Penatalaksanaan TD pada pasien stroke perdarahan akut:

SBP < 180 mmHg tidak memerlukan terapi di IRD,

DBP < 105 mmHg terapi setelah MRS

SBP 180-220 mmHg Nitroglycerin transdermal 5-10 mg, atau

DBP 105-120 mmHg IV labetalol, esmolol, enalapril atau diltiazem pada dosis

kecil titrasi

SBP > 220 mmHg IV nitoglycerin 0,6-6 mg/ h

DBP > 120 mmHg

Stroke Iskemia

Tidak ada data menunjukkan manfaat dari mengontrol TD pada stroke iskemia akut.

Kebanyakan TD spontan meningkat pada jam pertama dan kembali ke nilai sebelumnya

dalam hari pertama setelah onset stroke.

Kebanyakan neurologis menyatakan bahwa penurunan TD dapat berbahaya dari

penurunan perfusi kolateral dalam daerah penumbra iskemia, menyebabkan perluasan

infark.

Kontrol TD pada kondisi sbb:

1. gagal jantung kongestif

2. akut myokard iskemia/ infark

3. gagal ginjal akut

4. hipertensi ensefalopati

5. diseksi aorta

6. terapi dengan trombolitik atau anti koagulan

Tujuan manajemen TD pada stroke iskemia akut

SBP < 220 mmHg jangan diterapi kecuali ada indikasi medis

DBP < 120 mmHg

SBP > 220 mmHg transdermal nitroglycerin 5-10 mg atau

DBP 121-140 mmHg IV labetalol 10-20 mg dengan monitoring ECG, diulangi

tiap 10 menit sampai dosis maksimum 100 mg/ jam, atau

IV enalapril 1,25 mg

DBP > 140 mmHg IV nitroglycerin 0,6-6 mg/ jam

Disposisi

Semua pasien stroke harus MRS untuk pemeriksaan lebih lanjut, terapi dan rehabilitasi.

Pasien stabil dengan infark lacunar > 48 jam dengan non progresif dan tanpa defisit

neurology dapat KRS jika pengawasan ketat dirumah.

Kebanyakan pasien TIA perlu MRS untuk tindak lanjut dan terapi medis awal. Rujukan

segera ke neurolog atau stroke center bila ada.

Penderita datang dengan gejala stroke durasi <7hari, misalnya:

Kelemahan salah satu sisi tubuh

Anggota gerak di satu sisi tidak dapat diperintah Kesulitan bicara Vertigo dengan kesulitan bicara Kebas di satu sisi tubuh Ketidakmampuan mengekspresikan pikiran, atau mengerti orang lain Kebutaan yang mengenai sebagian atau seluruh lapang pandang pada

satu atau kedua mata Penglihatan dobel atau kelemahan wajah dan/atau anggota gerak

Laporan Kasus Net Str62e He06rag52

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