BLOK NEUROBEHAVIOUR & SPECIFIC SENSE SYSTEMS (NBSS)

BUKU PANDUAN TUTORIAL

TIM BLOK NBSS2010

JURUSAN KEDOKTERANFAKULTAS KEDOKTERAN DAN ILMU-ILMU KESEHATANUNIVERSITAS JENDERAL SOEDIRMAN

a. Nama Blok : Neurobehaviour & Specific Sense Systems

b. Kode Blok : KU 356 A

c. Ruang lingkup : Mempelajari tentang struktur, fisiologi dan patofisiologi dalam sistem saraf

dan indera manusia serta keterampilan klinis, penegakan diagnosis dan

penatalaksanaan pada kelainan-kelainan sistem saraf dan indera manusia

(mata dan telinga).

d. SKS : 10 SKS

Blok Neurubehavior & Specific Sense Systems merupakan blok ke-24 dalam kurikulum berbasis kompetensi

Jurusan kedokteran, Fakultas Kedokteran & Ilmu-ilmu Kesehatan Universitas Jenderal Sudirman. Blok ini

dilaksanakan pada awal semester VI. Materi yang akan diberikan dalam blok ini meliputi sistem saraf secara

keseluruhan beserta kelainannya, dan indera manusia (mata dan tellinga) beserta kelainannya pula, sesuai

dengan kompetensi yang harus dicapai berdasarkan Standar Kompetensi Dokter. Blok ini akan berjalan selama 8

minggu, yaitu minggu pembelajaran selama 7 minggu, dan 1 minggu terakhir untuk ujian.

Anatomi Ilmu bedahHistologi Rehabilitasi MediKBiokimia RadiologiFisiologi Patologi AnatomiNeurologi Patologi KlinikMata ForensikTHT MikrobiologiIlmu Kesehatan anak ParasitologiFarmakologi

Ketua : dr. Anton Budi D., SpTHT, M.Kes

Sie Akademik : dr. Khusnul Muflikhah

Sie Evaluasi : dr. Sutrisno

Sekretaris blok : Sri Wahyuningsih, SH

Caraka : Wartam Tipang

Mahasiswa yang mengikuti Blok Neurobehaviour and Specific Systems (NBSS) TA 2009/2010 adalah mahasiswa semester VI sebanyak 131 mahasiswa, dan mahasiswa semester VIII sebanyak 19 mahasiswa (mengulang). Diharapkan, mahasiswa memiliki karakteristik sebagai berikut :1. Berbudi pekerti terpuji yang ditunjukkan dengan sikap menghargai sesama manusia, menghargai pendapat

orang lain, jujur, bersikap terbuka, sopan dalam tingkah laku dan dalam berbusana, memberikan apresiasi yang positif terhadap ilmu pengetahuan/ teknologi

2. Mau dan mampu bekerja secara mandiri maupun dalam sebuah tim3. Memiliki etos belajar yang tinggi 4. Taat pada peraturan akademik

DESKRIPSI BLOK

DEPARTEMEN TERKAIT

ORGANISASI BLOK

KARAKTERISTIK MAHASISWA

a. Pada akhir blok mahasiswa diharapkan mampu menentukan pengelolaan pasien dengan kelainan pada sistem saraf dan indera secara komprehensif berdasarkan landasan ilmiah kedokteran dengan memanfaatkan teknologi informasi.

b. Untuk mencapai sasaran pembelajaran akhir blok, diharapkan :i. Mahasiswa mampu menguraikan embriogenesis susunan saraf pusatii. Mahasiswa mampu menguraikan patologi embriogenesis susunan saraf pusat yang sering

terjadiiii. Mahasiswa mampu menghubungkan patologi embriogenesis dengan terjadinya anomali

kongenital susunan saraf pusativ. Mahasiswa mampu menguraikan gejala dan tanda anomali kongenital susunan sarafv. Mahasiswa mampu menguraikan gambaran radiologi anomali kongenital susunan saraf pusatvi. Mahasiswa mampu menginterpretasikan hasil pemeriksaan fisik anomali kongenitalvii. Mahasiswa mampu menentukan pemeriksaan penunjang untuk menegakkan diagnosis

anomali kongenital susunan saraf pusatviii. Mahasiswa mampu menentukan diagnosis banding anomali kongenital susunan saraf pusatix. Mahasiswa mampu mengidentifikasi struktur susunan saraf pusatx. Mahasiswa mampu menguraikan fungsi-fungsi susunan saraf pusat dari tingkat organ hingga

molekulerxi. Mahasiswa mampu menguraikan patofisiologi kelainan susunan saraf pusatxii. Mahasiswa mampu menguraikan gejala dan tanda kelainan susunan saraf pusatxiii. Mahasiswa mampu menguraikan gambaran radiologi kelainan susunan saraf pusatxiv. Mahasiswa mampu menguraikan gambaran patologi anatomi kelainan susunan saraf pusatxv. Mahasiswa mampu menguraikan gambaran patologi klinik susunan saraf pusatxvi. Mahasiswa mampu menginterpretasi hasil pemeriksaan kelainan susunan saraf pusatxvii. Mahasiswa mampu menentukan pemeriksaan penunjang untuk kelainan susunan saraf pusatxviii. Mahasiswa mampu menentukan diagnosis kelainan susunan saraf pusatxix. Mahasiswa mampu mengidentifikasi struktur indera penglihatanxx. Mahasiswa mampu menguraikan fungsi indera penglihatanxxi. Mahasiswa mampu menguraikan patofisiologi kelainan indera penglihatanxxii. Mahasiswa mampu menguraikan gejala dan tanda kelainan indera penglihatanxxiii. Mahasiswa mampu menguraikan gambaran patologi anatomi kelainan indera penglihatanxxiv. Mahasiswa mampu menguraikan gambaran radiologi kelainan indera penglihatanxxv. Mahasiswa mampu menginterpretasi hasil pemeriksaan kelainan indera penglihatanxxvi. Mahasiswa mampu menentukan pemeriksaan penunjang untuk kelainan indera penglihatanxxvii. Mahasiswa mampu menentukan diagnosis kelainan indera penglihatanxxviii. Mahasiswa mampu mengidentifikasi struktur indera pendengaranxxix. Mahasiswa mampu menguraikan fungsi indera pendengaranxxx. Mahasiswa mampu menguraikan patofisiologi kelainan indera pendengaranxxxi. Mahasiswa mampu menguraikan gambaran patologi anatomi kelainan indera pendengaranxxxii. Mahasiswa mampu menguraikan gambaran radiologi kelainan indera pendengaranxxxiii. Mahasiswa mampu menguraikan gejala dan tanda kelainan indera pendengaranxxxiv. Mahasiswa mampu menginterpretasi hasil pemeriksaan kelainan indera pendengaranxxxv. Mahasiswa mampu menentukan pemeriksaan penunjang untuk kelainan indera pendengaranxxxvi. Mahasiswa mampu menentukan diagnosis kelainan indera pendengaranxxxvii. Mahasiswa mampu mengidentifikasi obat yang digunakan untuk kelainan susunan saraf pusat,

indera penglihatan dan pendengaranxxxviii. Mahasiswa mampu menjelaskan farmakodinamik dan farmakokinetik obat yang digunakan

untuk kelainan susunan saraf pusat, indera penglihatan dan pendengaranxxxix. Mahasiswa mampu menguraikan indikasi, kontraindikasi dan efek obat yang digunakan untuk

kelainan susunan saraf pusat, indera penglihatan dan pendengaranxl. Mahasiswa mampu menentukan obat yang paling tepat digunakan untuk kelainan susunan

saraf pusat, indera penglihatan dan pendengaranxli. Mahasiswa mampu mengidentifikasi rehabilitasi medis yang digunakan untuk kelainan susunan

saraf pusat, indera penglihatan dan pendengaranxlii. Mahasiswa mampu menguraikan fungsi rehabilitasi medis yang digunakan untuk kelainan

susunan saraf pusat, indera penglihatan dan pendengaranxliii. Mahasiswa mampu menentukan rehabilitasi medis yang paling tepat digunakan untuk kelainan

susunan saraf pusat, indera penglihatan dan pendengaranxliv. Mahasiswa mampu menguraikan aspek bioetika pada kasus-kasus kelainan SSP, indera

pendengaran dan indera penglihatan.xlv. Mahasiswa mampu menjelaskan gambaran/tanda vital akibat kematian pada kelainan SSP

SASARAN PEMBELAJARAN

1. Mini Lecture / PerkuliahanMini Lecture adalah kegiatan perkuliahan tatap muka yang berlangsung maksimal 100 menit.

Tujuan dari minilecture meliputi :a. Memberikan informasi kepada mahasiswa dalam jumlah besar dalam waktu yang bersamaanb. Informasi yang diberikan berupa konsep atau prinsip dasar.

2. Praktikum Praktikum adalah kegiatan pengajaran dan pembelajaran dengan mengutamakan ketrampilan yang

menunjang pemahaman terhadap suatu materi atau informasi.Ketrampilan tersebut dapat dilakukan di dalam ruang kuliah,laboratorium,atau di luar ruangan baik di dalam lingkungan maupun di luar kampus.Jenis pelaksanaannya dapat terbagi dua yaitu praktikum basah dan praktikum kering.Praktikum basah dilaksanakan di laboratorium menggunakan alat dan bahan habis pakai serta orang/hewan coba (bila diperlukan).Praktikum kering dapat dilakukan di dalam atau di luar laboratorium tanpa menggunakan bahan habis pakai.Contoh dari praktikum kering adalah demonstrasi gambar-gambar patologi jaringan, dan penyusunan resep obat berdasarkan kasus yang disediakan. Tujuan kegiatan praktikum adalah untuk membantu mahasiswa memahami dan menguasai materi yang diberikan.

3. Problem Based Learning (PBL)a.Pengertian

PBL adalah metode pembelajaran dengan menggunakan masalah sebagai stimulus.Masalah tersebut akan diselesaikan dalam diskusi kelompok kecil mahasiswa di bawah pengawasan tutor.Tutor tidak berperan sebagai pemberi informasi,membenarkan atau menyalahkan pendapat mahasiswa.Peran tutor adalah memfasilitasi mahasiswa untuk mencapai tujuan diskusi.

b. Tujuan Mengembangkan kemampuan untuk mengidentifikasi masalah kesehatan dari skenario masalah

yang berisi patient problem. Melatih kemampuan generic learning skills, dan memahami serta menghubungkan basic sciences

dengan clinical sciences. Meningkatkan penguasaan soft skills yang meliputi kepemimpinan, profesionalisme, ketrampilan

komunikasi, kemampuan untuk bekerja sama dan bekerja dalam tim, ketrampilan untuk berpikir secara kritis,serta kemampuan untuk menyelesaikan masalah yang dihadapi (Cline,2005).

Melatih karakter student centred learning,self directed learning dan adult learning.

4. Clinical skills activities (Skill Lab)a. Pengertian

Clinical skills adalah ketrampilan/prosedur klinik yang harus dikuasai atau diketahui oleh mahasiswa sesuai dengan kompetensinya sebagai dokter umum.Pengajaran dan pembelajaran ketrampilan klinik tersebut dilakukan dalam skills laboratorium,menggunakan alat bantu peraga,film, dan pasien terstandarisasi atau pasien yang sesungguhnya.

b. TujuanMelatih mahasiswa untuk menguasai berbagai ketrampilan dan prosedur klinik yang lege artis serta relevan dengan kompetensi dokter umum.

5. Out Patient Encounter (OPE Lapangan)a. Pengertian (Kerfott and De Wolf,1979)

Outpatient Encounter (OPE) adalah strategi pembelajaran dan pengajaran yang menggunakan masalah pasien bukan rawat inap sebagai kasus yang harus dipecahkan. Mahasiswa melakukan kontak secara langsung dengan pasien.

b. Tujuan Mengembangkan kemampuan untuk berinteraksi dengan pasien. Mengembangkan kemampuan menyelesaikan masalah dengan mempertimbangkan aspek

etika,sosial,ekonomi dan budaya, serta pola pikir pasien dan keluarganya. Mengembangkan kemampuan melakukan ketrampilan/prosedur klinik dibawah bimbingan

preceptor lapangan. Menghubungkan pengetahuan dasar dan klinik dalam menyelesaikan masalah pasien.

c. Teknis Pelaksanaan OPE dilaksanakan pada minggu VII OPE yang digunakan berupa skrining kasus oftalmologi komunitas (skrining kebutaan) pada lansia. Kasus yang akan ditelusuri mahasiswa adalah kasus penurunan visus pada lansia yang sering terjadi

yaitu katarak dan gangguan refraksi. Mahasiswa dibagi menjadi 14 kelompok kecil, tiap kelompok dibimbing oleh 1 orang preceptor dari

fakultas.

METODE PEMBELAJARAN

Tiap kelompok mahasiswa diterjunkan ke acara posyandu lansia di tempat-tempat yang telah ditentukan, di bawah koordinasi puskesmas.

d. Tugas mahasiswa di lokasi Di awal acara, mahasiswa melakukan presentasi singkat di hadapan lansia yang hadir mengenai

kasus/gangguan oftalmologi yang sering terjadi pada lansia, tujuan dan teknik pelaksanaan kegiatan yang akan dilakukan.

Mahasiswa melakukan anamnesis dan pemeriksaan fisik oftalmologi terhadap seluruh lansia yang hadir (pemeriksaan visus dan refleks fundus).

Lansia yang memiliki visus < 3/60 dan atau refleks fundus negatif, dikelompokkan tersendiri, dan masuk dalam kriteria skrining.

Di akhir acara, mahasiswa mempresentasikan secara singkat hasil skrining yang telah dilakukan didepan seluruh yang hadir, dengan titik point yaitu mengenai bagaimana tindak lanjut dari lansia yang terjaring skrining, serta upaya pencegahan apa saja yang dapat dilakukan.

Mahasiswa diwajibkan membuat laporan perkelompok, yang dalam pembuatannya harus melalui bimbingan dengan preceptor. Format penyusunan laporan terlampir

Laporan dikumpulkan selambat-lambatnya 3 hari setelah OPE berlangsung.e. Tugas Preceptor

Memberikan pengarahan kepada mahasiswa tentang tugas-tugas yang harus dilaksanakan Mendampingi mahasiswa saat OPE, kecuali bila ada aktivitas akademik lain yang tidak bisa

ditinggalkan. Dalam hal ini, preceptor harus mencari pengganti. Melakukan pembimbingan dalam penyusunan laporan Memberikan penilaian kepada mahasiswa ( kontak dengan pasien, presentasi di lokasi, diskusi

dengan preceptor, laporan kelompok)

6. Pemutaran dan diskusi FilmReal out-patient yang telah distandarisasi kemudian dibuat dalam bentuk audiovisual (menjadi

patient substitutes) yang berisi proses prosedur diagnosis antara relevant clinician dengan real out-patient tersebut.

Tujuan Instruksional Khusus :Diharapkan setelah menyelesaikan metode pembelajaran ini, mahasiswa mampu : Melakukan pencatatan informasi/data penting berkaitan dengan kasus (Write Up) ke dalam form yang

telah tersedia dengan melakukan observasi terhadap film. Menjelaskan dasar dari hypotesis yang paling mungkin dan DD nya. Menjelaskan patogenesis dan patofisiologi gejala tanda yang ada. Menjelaskan indikasi pemeriksaan laboratorium penunjang dan interpretasinya. Menjelaskan prinsip penatalaksanaan dan pencegahannya. Pada tahapan ini terdapat 2 learning model yaitu : Observasi film

Mahasiswa mengamati film yang berisi medical interview dan physical examination antara relevant clinician dengan real out-patient tentang kasus tertentu. Kemudian mahasiswa menuliskan temuan baik informasi/data dari anamnesis maupun hasil temuan abnormal dari pemeriksaan fisik serta hasil pemeriksaan penunjang di dalam form yang telah tersedia, sampai dapat melakukan assesment dan plan sesuai dengan pemahaman basic mecanism yang mendasari.

The report-back model.Di dalam pendekatan ini, setelah mahasiswa mengamati film, dan telah menuliskan temuan-

temuan di dalam form, maka mahasiswa melaporkan hasilnya kepada Preceptor, yaitu dengan mempresentasikan temuan-temuan, menjelaskan hipotesis yang paling mendekati, dan prinsip penatalaksanaan berdasar pemahaman basic mecanism. Preceptor bertugas menilai dengan check list yang sudah tersedia dan memberikan bimbingan berupa feedback langsung terhadap mahasiswa.

Pelaksanaan The report-back model : Dilakukan setiap kali selesai pemutaran film dalam 1 kali pertemuan (@ 100 menit). Penilaian dilakukan secara bersama (peer review) untuk 2 orang mahasiswa /15 – 20

menit/subkelompok. Preceptor bertugas menilai sesuai check list (sebelumnya seluruh preceptor mengikuti briefing dengan

clinician dan melihat film serta mendapatkan preceptor guide tentang kasus tersebut). Memberikan feedback langsung yang bersifat konstruktif terhadap masing-masing mahasiswa. Mengembalikan form yang telah diberi feedback tertulis ke masing-masing mahasiswa.

7. Belajar mandiri. Belajar mandiri dilakukan di luar jam perkuliahan (jadwal) untuk mereview mata kuliah yang diajarkan.

Dalam melakukan belajar mandiri, mahasiswa hendaknya mengacu pada hal-hal yang ditekankan dalam perkuliahan (tujuan pembelajaran), yang tidak dapat dijelaskan secara detil dalam waktu perkuliahan yang sangat singkat. Jika mendapati adanya kesulitan, hendaknya mahasiswa mencatatnya, kemudian mencari jawabannya dengan pencarian referensi maupun konsultasi dengan narasumber atau staf akademis.

SKENARIO I

Tujuan pembelajaran

Pada akhir diskusi, mahasiswa diharapkan mampu :1. Menjelaskan anatomi serebrum2. Menjelaskan anatomi saraf kranialis3. Menjelaskan fungsi korteks serebri masing-masing lobus4. Menjelaskan perbedaan fungsi hemisfer serebri5. Menjelaskan fungsi saraf kranialis6. Menjelaskan jaras piramidalis7. Definisi dan insidensi stroke8. Mekanisme dan klasifikasi stroke9. Tanda dan gejala stroke10. Menjelaskan patofisiologi dari gejala dan tanda stroke11. Pemeriksaan fisik umum dan neurologis12. Skoring untuk penilaian jenis stroke13. Diagnosis etiologis dan diagnosis banding stroke14. Menentukan diagnosis topis berdasarkan keadaan klinis15. Faktor resiko dan pencegahan stroke16. Komplikasi stroke17. Penatalaksanaan stroke18. Rehabilitasi medik stroke19. Aspek psikososial stroke20. Prognosis stroke21. Aspek etik pada kasus stroke

Informasi

Ny.S, 65 tahun, dibawa ke IGD oleh keluarganya karena kelemahan anggota gerak bagian kanan yang dirasakan kira-kira setengah jam yang lalu, yaitu ketika bangun tidur jam 5 pagi.

Pasien tampak mengantuk, tidak merasakan nyeri kepala. Tidak ada mual atau muntah. Tidak ada kejang. Pasien sulit berkomunikasi. Sebelumnya pasien belum pernah sakit seperti sekarang.Riwayat kesehatan :Ny.S adalah penderita DM dan hipertensi, keduanya tidak terkontrol, kurang lebih 10 tahun, jarang berolahraga, dengan pola makan yang tidak teratur. Suami Ny.S seorang perokok berat, 15-20 batang per hari.

Pemeriksaan Fisik :KU : somnolenGCS : E3M6Vafasia

Tekanan darah : 160/100 mmHgDenyut nadi : 76x/menit, regulerRespirasi : 24x/menitSuhu tubuh : 36,5’CStatus internus : dalam batas normal

Pemeriksaan neurologisMeningeal Sign (-)N. Cranialis :Parese N VII kanan tipe sentralParese N XII kanan

Fungsi Motorik

Superior(D/S) Inferior (D/S)

Gerak / N / NKekuatan 2 / 5 3 / 5Refleks

fisiologis / N / N

Refleks patologis

-/- +/-

Tonus N/N N/NTrofi eutrofi eutrofi

Fungsi sensorik : hemihipestesia kanan

Fungsi vegetatif : dalam batas normal

Hasil laboratoriumHb 12,8 gr/dlLeukosit 7800/mm3

Trombosit 240.000/mm3

Dula darah puasa 140mg/dl, Gula darah2 jam PP 210 mg/dlKolesterol total 245 mg/dl,HDL 45 mg/dlLDL 170 mg/dlTrigliserida 190 mg/dlAsam urat 5,2 mg/dl

Pemeriksaan penunjang lain CT Scan kepala terdapat gambaran infark cerebri

Diagnosis Diagnosis klinis : - Hemiparese dekstra

- Afasia- Parese N.VII dan N.XII- Hemihipestesia dekstra

Diagnosis topis : hemisfer sinistraDiagnosis etiologis : Stroke Non Hemoragik

Penatalaksanaan - Bed rest- Obat anti agregasi platelet- Rehabilitasi

o Komunikasio Mobilisasio Aktivitas sehari-hari

Refferency

Ischemic Stroke

Essentials of Diagnosis Secondary to thrombosis or embolism Consider in acute neurologic deficit (focal or global) or altered level of consciousness No historical feature distinguishes ischemic from intracerebral hemorrhagic stroke, although headache,

nausea and vomiting, and altered level of consciousness are more common in intracerebral hemorrhagic stroke

Abrupt onset of hemiparesis, monoparesis, or quadriparesis; dysarthria, ataxia, vertigo; monocular or binocular visual loss, visual field deficits, diplopia

General ConsiderationsStroke is a cerebrovascular disorder resulting from impairment of cerebral blood supply by occlusion (e.g., by thrombi or emboli) or hemorrhage. It is characterized by the abrupt onset of focal neurologic deficits. The clinical manifestation depends on the area of the brain served by the involved blood vessel. Stroke is the most common serious neurologic disorder in adults and occurs most frequently after age 60 years. The mortality rate is 40% within the first month, and 50% of patients who survive will require long-term special care.Ischemic strokes, comprising thrombotic, embolic, and lacunar occlusions, account for over 75% of all strokes and result in cerebral ischemia or infarction. A variety of disorders of blood, blood vessels, and heart can cause occlusive strokes, but the most common by far are atherosclerotic disease (especially of the carotid and vertebrobasilar arteries) and cardiac abnormalities.

Stabilize Ventilation

Establish AirwayAssess adequacy of airway and ventilation in all stroke patients, especially in the presence of depressed level of consciousness, absent gag reflex, respiratory difficulty, or difficulty managing secretions.Consider IntubationPatients with inadequate ventilation (respiratory acidosis) or difficulty managing secretions will require intubation.

Search for Head TraumaStroke patients may sustain head injury due to incoordination or weakness. Conversely, patients with focal neurologic findings due to head trauma may be mistakenly diagnosed as suffering from stroke. If head injury is suspected from the history or clinical findings, immobilize the cervical spine. Refer to Chapter 20 for management.

Treat Cerebral Edemamedical therapy for cerebral edema (see Table 15–3) associated with ischemic stroke does not alter the outcome.

Treat Seizures(See Chapter 17 for management of seizures.) Consider prophylaxis for seizure. Give intravenous phenytoin, 15–18 mg/kg at a rate not greater than 50 mg/min, or fosphenytoin, 15–20 mg/kg PE (phenytoin equivalents) intravenously.

Treat HypoglycemiaOccasionally patients with hypoglycemia may have focal neurologic deficits that may mimic a stroke. Confirm the presence of hypoglycemia using a glucometer or reagent strips before giving 50 mL of 50% dextrose solution. Stroke patients with elevated serum glucose may have a worsened outcome.

Obtain Emergency CT ScanEmergency CT scan of the head should be obtained early. This is the most readily available method for reliably detecting the presence of hemorrhage and focal cerebral edema. MRI, especially diffusion weighted, has enhanced the diagnosis of ischemic stroke.

Further Evaluation of the Patient with Stroke

Accurate diagnosis and identification of the underlying cause of the stroke are important for appropriate evaluation and treatment. Conditions that predispose to strokes should be sought and corrected. A systematic approach to the evaluation of the patient with stroke is detailed below and can be modified depending on the urgency of the patient's condition.

HistoryDetermine Time Course of DeficitsThe goal is to determine the exact time of onset of symptoms since the current recommended window of opportunity for thrombolytic therapy is 3 hours. Patients who awake with symptoms are considered to have symptom onset at the time they were last "normal" neurologically; when they went to sleep.

Identify Risk FactorsHypertension, diabetes mellitus, TIAs, hyperlipidemia, smoking, family history, and use of oral contraceptives predispose to atherosclerotic disease. Cardiac disorders such as changing cardiac rhythms (especially atrial fibrillation), dyskinetic myocardium, and valvular heart disease are associated with increased risk for embolic strokes (Table 35–1). Bleeding dyscrasias, hypercoagulable states, blood disorders (especially sickle cell disease), and vascular disorders are also associated with a risk for stroke. Carotid artery bruits in patients with TIAs or stroke suggest the possibility of emboli derived from atheromatous plaques.Table 35–1. Sources of Emboli.

Cardiac Deterioration of neurologic status or the presence of brain-stem involvement (depressed sensorium, pupillary or extraocular movement abnormality, decorticate or decerebrate posturing) suggests significant cerebral edema and impending herniation. With the exception of temporizing measures prior to surgical decompression in cerebellar or superficial lobar hemorrhage,

Changing rhythms, especially atrial fibrillation

Valvular disease

Rheumatic heart disease

Valve prosthesis

Bacterial and fungal endocarditis

Myxomatous vegetation

Congenital heart disease

Mitral valve prolapse

Atrial tumor

Myocardial dysfunction

Myocardial infarction

Ventricular aneurysm

Noncardiac

Foreign body

Air, nitrogen, or other gases

Fat

Tumor

Atheromatous material

Thrombus

Physical ExaminationGeneralA thorough examination may reveal the underlying cause for the stroke and direct treatment.

Vital SignsRecord the body temperature. Hypertension is a risk factor for stroke, and systolic pressure above 200 mm Hg may require treatment.

HeadArteriovenous malformations may be detected by auscultation of the head for bruits. Palpate the temporal arteries for tenderness, nodularity, or absence of pulse suggestive of giant cell arteritis. Search for any evidence of trauma.

EyesExamination of the retina may reveal visible emboli in the retinal vessels.

NeckThe carotid arteries should be examined (one at a time) for presence of bruits and reduction of pulsation. Although these findings are not specific for carotid disease, further carotid studies may be warranted to evaluate for possible carotid endarterectomy.

HeartChanging cardiac rhythms and murmurs or valvular disease are associated with increased risk of embolization from the heart.

SkinEcchymosis and petechiae may suggest blood disorders or vasculitis as causative factors. Presence of recent needle tracks or subungual splinter hemorrhages suggests the possibility of septic emboli derived from infected heart values.

Lung SoundsAuscultate for possible aspiration pneumonia or pulmonary edema.

Neurologic ExaminationA rapid neurologic examination should be performed in the emergency department and should focus on (1) localizing the anatomic site of deficit as an aid in determining the specific stroke syndrome and (2) assessing the degree of neurologic impairment, from which improvement or worsening can be assessed.

Level of AlertnessReduced mental alertness can be a sign of extensive injury from hemorrhage, brain-stem infarction or herniation, or metabolic changes.

CognitiveAssess response to commands and fluency of speech. Aphasia and apraxia are associated with involvement of the cerebral cortex and anterior (carotid) circulation; lacunar infarction or disturbance of posterior (vertebrobasilar) circulation is unlikely.

Cranial NervesVisual field abnormalities exclude lacunar infarction. Abnormal pupillary reflexes and ocular palsies are brain-stem findings and are associated with disturbance of posterior circulation or impending brain herniation.

MotorHemiparesis can be associated with disturbance of the anterior or posterior circulation. Generally, in anterior circulation strokes, the face, hand, and arm are affected more than the leg. In lacunar infarction and posterior circulation strokes, this pattern is less common. Hemiparesis involving one side of the face and the other side of the body is due to disturbance of posterior circulation.

SensoryHemisensory deficits without associated motor involvement are usually due to lacunar infarcts. Astereognosis (inability to identify objects by touch) and agraphesthesia (inability to recognize figures traced on the skin) are cortical sensory deficits and are due to disturbance of anterior circulation.

CerebellarHemiataxia suggests involvement of the cerebellum or the brain stem, or lacunar infarction deep in white matter.Perform NIH Stroke ScaleThe NIH stroke scale (Table 35–2) is a 13-item scoring system integrating neurologic examination components, language, and levels of consciousness that indicate the severity of neurologic dysfunction. The maximum score is 42, signifying devastating stroke, and 0 is normal. Score of 1–4 is considered minor stroke, 5–15 moderate stroke, 15–20 moderately severe stroke, and >20 a severe stroke.Table 35–2. NIH Stroke Scale Summary.

1a. Level of consciousness 0 = Alert1 = Drowsy2 = Stuporous3 = Comatose

1b. LOC questions: Ask the month and the patient's age 0 = Answers both questions correctly1 = Answers one question correctly2 = Answers neither question correctly

1c. LOC commands: Close your eyes and make a fist 0 = Performs both tasks correctly1 = Performs one task correctly2 = Performs neither task correctly

2. Best gaze 0 = Normal1 = Partial gaze palsy2 = Forced deviation

3. Visual fields 0 = No visual loss1 = Partial hemianopia2 = Complete hemianopia3 = Bilateral hemianopia

4. Facial paresis 0 = Normal symmetrical movements1 = Minor paralysis2 = Partial paralysis3 = Complete paralysis

5-8. Best motor (repeat for each arm and leg) 0 = No drift1 = Drift2 = Some effort against gravity3 = No effort against gravity4 = No movement

9. Limb ataxia 0 = Absent1 = Present in one limb2 = Present in two limbs

10. Sensory (pinprick) 0 = Normal1 = Partial loss2 = Dense loss

11. Best language 0 = No aphasia1 = Mild-to-moderate aphasia2 = Severe aphasia3 = Mute

12. Dysarthria 0 = Normal1 = Mild-to-moderate dysarthria2 = Severe dysarthria

13. Neglect/Inattention 0 = No abnormality1 = Partial neglect2 = Complete neglect

Total score 0–42

Clinical FindingsThe neurologic deficits may evolve over minutes to hours and are typical for a specific vascular distribution. Motor

and sensory pathways are impaired. Headache and vomiting are rare. The diagnosis is made on the basis of the clinical findings and exclusion of hemorrhage by CT scan. MRI and repeat CT scan at 48–72 hours will often confirm the diagnosis when the initial study is normal.

Laboratory TestsBlood TestsThe following blood tests should be obtained in most patients with focal neurologic deficits:

Complete blood count and platelet count (to detect blood dyscrasias), and prothrombin time and partial thromboplastin time for coagulation disorders.

Glucose level, because both hyperglycemia and hypoglycemia may cause focal neurologic findings that can mimic stroke.

Erythrocyte sedimentation rate to detect vasculitis or arteritis. Serologic test for syphilis. Toxicologic screen if drug use is suspected.

ElectrocardiogramAn electrocardiogram may reveal new arrhythmias or conversion to a normal rhythm, both of which are associated with increased risk for emboli. Presence of myocardial infarction or persistent changes suggestive of a ventricular aneurysm also increases the risk for stroke.

CTThese studies are essential for localizing the lesion; distinguishing hemorrhagic from ischemic stroke; and identifying other intracranial disease, such as tumor or abscess, which can be confused with strokes. A CT scan should be obtained in any suspected stroke patient.

Treatment & DispositionIn 1996, the US Food and Drug Administration approved the use of thrombolytic therapy for acute ischemic stroke, and the American Heart Association and the American Academy of Neurology published guidelines for its use. Management of acute ischemic stroke is handled on a case-by-case basis. Intravenous tissue plasminogen activator (t-PA) can be used if the following criteria are met:

Ischemic stroke in patient >18 years old with a measurable deficit on the NIH stroke scale. The time of onset of the stroke is clearly defined, and treatment is started within 3 hours after the onset

of symptoms. A noncontrast CT scan has excluded hemorrhage prior to treatment. Systolic blood pressure is less than 185 mm Hg and diastolic blood pressure is less than 110 mm Hg. The patient has no history of intracranial hemorrhage. The patient has no history of intracranial surgery, head injury, or previous stroke in the preceding 3

months. Patient is not pregnant. The patient has not had major surgery within 14 days. Patient does not have post-myocardial infarction pericarditis. Patient has no evidence of active internal bleeding. Patient does not have a known arteriovenous malformation or aneurysm. Patient has no known bleeding diathesis, platelet count > 100,000/mm3, PT < 15 seconds, INR < 1.7, and a

normal PTT. Patient is not taking oral anticoagulants or had heparin within 48 hours.

Dosage and administration of t-PA: Give 0.9 mg/kg body weight of intravenous t-PA up to a maximum of 90 mg. Give 10% of the dose as a bolus and then administer the rest of the dose as a continuous infusion over

1 hour. Do not give anticoagulants or antiplatelet drugs for 24 hours after treatment.

Acute stroke patients should be admitted to either a monitored bed or intensive care setting depending on the clinical condition.

Hemorrhagic Stroke

Subarachnoid Hemorrhage

Essentials of Diagnosis

Sudden onset of severe headache Nausea and vomiting Photophobia, visual changes Loss of consciousness

General Considerations

Subarachnoid hemorrhage (SAH) occurs secondary to bleeding in the subarachnoid space. It is a medical emergency. Approximately 80% are due to saccular or berry aneurysms. The rest may be due to trauma or arteriovenous malformation. Risk factors include family history of SAH, autosomal dominant polycystic kidney disease, connective tissue diseases, hypertension, smoking, and heavy alcohol use.

Clinical Findings

Patients usually complain of "the worst headache of my life" or "thunderclap" headache. Commonly associated symptoms include nausea and vomiting, neck stiffness, and photophobia. Patients who present with stupor or coma are at high risk for mortality.

A high index of suspicion must be raised in patients presenting with early warning signs of a sentinel leak. They are frequently misdiagnosed and early diagnosis can be lifesaving. Grading of subarachnoid bleeds is based on the patient's condition on presentation. The World Federation of Neurological Surgeons grading scale is as follows:

Grade

Glasgow Coma Score

I 15

II 14 or 13 without focal deficit*

III 14 or 13 with focal deficit

IV 12–7

V 6–3

*Cranial nerve palsies are not considered a focal deficit.

A CT scan should be performed as the first diagnostic study (Figure 35–1). CT scan is up to 98% accurate within the first 12 hours. Lumbar puncture should be performed if the CT scan does not demonstrate blood but the suspicion for SAH remains high. Spinal fluid demonstrating xanthochromia is diagnostic. However, it takes 12 hours after the bleeding for the spinal fluid to become xanthochromic and it will remain xanthochromic for approximately 2 weeks. Blood in the CSF may be due to SAH or a traumatic lumbar puncture. The reliability of decreasing erythrocyte count to identify a traumatic lumbar puncture is questionable. If the diagnosis is still in doubt angiography may be indicated.

Conventional angiography is the gold standard for detecting aneurysms but the newer imaging modalities of MR angiography (MRA) and CT angiography (CTA) are improving. CTA is easier to perform in critically ill patients compared to MRA. Both modalities have a sensitivity of 85–98%.

Complications & TreatmentAneurysmal RebleedingAneurysmal rebleeding may be secondary to uncontrolled hypertension or aneurysmal clot fibrinolysis. Surgical

clipping or endovascular coiling is strongly recommended to reduce the rate of rebleeding.SeizureBecause seizures increase the risk of rebleeding after an SAH, prophylactic use of an anticonvulsant, for example, intravenous fosphenytoin or phenytoin, 15–20 mg/kg, is recommended.

Hypovolemia and HyponatremiaHypovolemia and hyponatremia can occur secondary to the syndrome of inappropriate secretion of antidiuretic hormone. Treatment involves intravenous hydration with isotonic crystalloid. A central intravenous monitor is desirable.HydrocephalusAcute Obstructive HydrocephalusThis form of hydrocephalus occurs in about 20% of patients after SAH. Ventriculostomy is recommended, although it may increase the risk of rebleeding or infection.Chronic Communicating Hydrocephalus

This form of hydrocephalus is a frequent occurrence after SAH. A temporary or permanent cerebrospinal fluid diversion is recommended in symptomatic patients.

Vasospasm

Vasospasm, or delayed cerebral ischemia, remains a frequent complication with high morbidity and mortality rates. Nimodipine, 60 mg orally every 4 hours, is strongly recommended.

Hypertension

The acute management of elevated blood pressure in SAH is controversial. There is no evidence that lowering blood pressure decreases rebleeding or the rate of cerebral infarction. Antihypertensive therapy should be reserved for severe blood pressure elevations with evidence of end-organ deterioration.

Neurosurgical Consultation

Seek neurosurgical consultation for definitive management, which may include surgical clipping or endovascular coiling depending upon the resources available.

Intracerebral Hemorrhage

Essentials of Diagnosis

No specific signs or symptoms reliably distinguish between intracerebral hemorrhage and ischemic stroke Symptoms vary depending on affected area and extent of bleeding Patients are more likely to exhibit signs of increased intracranial pressure; seizures more common Headache often severe and sudden Nausea and vomiting, hypertension, altered sensorium

General Considerations

Intracerebral hemorrhage is twice as common as SAH and even more likely to result in a major disability or death. Bleeding occurs primarily in the brain parenchyma, although blood may appear in the cerebrospinal fluid. Symptoms are due to mass effect of the hematoma with displacement and compression of adjacent brain tissue. The most common cause is advancing age and damage of intracerebral arterioles by long-standing systemic hypertension. Other causes include anticoagulation, alcohol abuse, thrombolytic therapy, bleeding diathesis, neoplasms, cerebral amyloid angiopathy, infections, and arteriovenous malformations.

Clinical Findings

Clinical findings depend on the site of the hemorrhage but occur abruptly and progress within minutes to a few hours. Headache and vomiting are frequent symptoms. Focal neurologic deficits are prominent, since most bleeding sites abut the basal ganglia, thalamus, and internal capsule. Abrupt onset of coma and prominent brain-stem findings (pinpoint pupils, absent extraocular movements) are characteristic of pontine hemorrhage. A CT scan is diagnostic and is the imaging study of choice (Figure 35–2). MRI, MRA, and CTA are useful in detecting structural abnormalities such as malformations and aneurysms.

Ataxia and cerebellar abnormalities, with absent or mild hemiparesis, are characteristic of cerebellar hemorrhage. It is particularly important to diagnose hypertensive intracerebellar hemorrhage rapidly, because fatal brain-stem

compression may occur rapidly. Emergency surgical decompression of intracerebellar hemorrhage can be lifesaving. Because the clinical differentiation from acute vestibular dysfunction may be difficult, patients with sudden onset of disequilibrium and vomiting require a CT scan of the brain to exclude cerebellar hemorrhage.

Treatment & DispositionAs with all other emergencies, initial management of a patient with intracerebral hemorrhage is directed toward airway, breathing, and circulation. A directed history and physical examination are essential to assess for underlying clues and deficits. If the patient exhibits need for airway protection, orotracheal intubation should be performed.

Blood pressure management is based on a theoretical rationale: lower the blood pressure and decrease the risk of ongoing bleeding from ruptured small arterioles. The converse theory therefore holds that aggressive treatment of blood pressure may decrease cerebral perfusion pressure and worsen brain injury. The American Heart Association Special Writing Group of the Stroke Council recommends that blood pressure levels be maintained below a mean arterial pressure of 130 mm Hg in patients with a history of hypertension.

TUJUAN PEMBELAJARAN

Pada akhir diskusi, mahasiswa diharapkan mampu :

1. Menjelaskan anatomi, histology dan fisiologi SSP2. Menjelaskan macam-macam infeksi SSP3. Mengetahui etiologi infeksi SSP (meningitis)4. Menjelaskan klasifikasi meningitis beserta gejala dan tanda patognomonisnya5. Menjelaskan patofisiologi terjadinya meningitis6. Menjelaskan diagnosis banding meningitis7. Menjelaskan faktor risiko terjadinya meningitis8. Menjelaskan teknik dan interpretasi pemeriksaan meningeal sign (nuchal rigidity, brudzinski I,II & III,

Kernig Sign )9. Menjelaskan teknik pelaksanaan pungsi lumbal dan interpretasi hasil10. Menjelaskan penatalaksanaan meningitis11. Mengidentifikasi komplikasi dari meningitis dan pencegahannya12. Menjelaskan macam-macam kejang 13. Menjelaskan patofisiologi terjadinya kejang14. Mengidentifikasi penyakit-penyakit yang dapat disertai kejang

Informasi

Jicko, seorang laki-laki usia 24 tahun datang ke UGD diantar oleh keluarganya karena keluhan sakit kepala berat. Menurut keluarganya, keluhan tersebut dirasakan sudah 2 hari. Jicko sudah tidak mampu lagi menahan badannya untuk berdiri sehingga ia segera dibaringkan di bed pasien.

Ketika dokter jaga UGD berbicara kepadanya, jicko hanya merintih-rintih. Mata jicko terpejam dan kelihatan sangat tidak nyaman. Dia terus memejamkan matanya menghindari cahaya dan bergerak hanya sesekali saja. Tiba2 jicko muntah menyemprot dan seluruh badannya kaku dengan kedua mata tertutup sangat rapat selama hampir 5 menitMenurut keluarganya, jicko sudah satu minggu tidak berangkat bekerja karena sakit panas. Semakin hari panasnya semakin tinggi, dan jicko hanya minum obat turun panas yang dibeli di warung. Jicko belum pernah mengalami sakit kepala sehebat ini. Riwayat trauma kepala disangkal

Pemeriksaaan Fisik :KU : gelisahGCS : E2M5V2

Suhu : 39,50CTD : 100/70 mmHgNadi : 100x/menitRR : 24x/menitStatus internus : dbn

Status neurologis :- Leher : kaku kuduk (+) Tes Brudzinski I (+)- Mata : conjungtiva palpebra tak anemis, sclera tak ikterik

: isokor, refleks cahaya +/+- Nn Cranialis : dbn

Fungsi Motorik Superior (D/S) Inferior (D/S)

SKENARIO II

Gerak Sulit dinilai Sulit dinilaiKekuatan Sulit dinilai Sulit dinilaiRefleks fisiologis / N / NRefleks patologis -/- +/-Tonus N/N N/NTrofi Eutrofi eutrofi

Sensorik : sulit dinilai

Pemeriksaan penunjang :

Hb : 11 g/dlHct : 34 vol%Eritrosit : 4,1 x 106 mmkLeukosit : 11000/mmk

Analisis LCS dari Pungsi lumbal :Sifat : keruhTekanan : 300 mmHg Protein : 75 mg/dlLeukosit total : 10/mlGlukosa : 100 mg/dl

DiagnosisKlinis : - penurunan kesadaran

- Cefalgia- Kejang

Topis : meningenEtiologi : meningitis bakterial

Penatalaksanaan :- Infus asering 16 tpm- O2 3 L/m- Injeksi Ceftriaxon 1 x 2 gram- Metil prednisolon 2 x 125 gram- Diazepam 10mg (bila kejang)- Parasetamol (prn)

Panduan Meningitis is an inflammation of the leptomeninges and underlying subarachnoid cerebrospinal fluid (CSF). It can be useful to divide symptom onset into acute, subacute, and chronic categories. Unlike subacute (1-7 d) or chronic (>7 d) meningitis, which have myriad infectious and noninfectious etiologies, acute meningitis (<1 d) is almost always a bacterial infection caused by one of several organisms. Depending on age and general condition, these gravely ill patients present acutely with signs and symptoms of meningeal inflammation and systemic infection of less than 24 hours' duration, and usually less than 12 hours duration. Patients with acute bacterial meningitis may decompensate very quickly and so they require emergency care, including antimicrobial therapy, ideally within 30 minutes of emergency department (ED) presentation. Most bacterial meningitis is not acute. Approximately 75% of patients with bacterial meningitis present subacutely with symptoms beginning several days prior. These ill patients still require urgent ED diagnosis and care to prevent further decompensation.The emergence of resistant strains has prompted changes in antibiotic protocols in some countries, including the US. Apart from dexamethasone, neuronal cell protectants still hold only future promise as adjunctive therapy.The challenges for emergency physicians when treating meningitis are (1) early identification and treatment of patients with acute bacterial meningitis, (2) assessing whether a treatable central nervous system (CNS) infection is present in those with suspected subacute or chronic meningitis, and (3) identifying the causative organism. Bacterial meningitis must be excluded.PathophysiologyA number of factors influence the development of acute and subacute bacterial meningitis, including virulence of the strain, host defenses, and bacteria-host interactions. Bacterial seeding usually occurs by hematogenous spread. In those without an identifiable source of infection, local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source. Rarely, infected contiguous structures invade via septic thrombi or osteomyelitic erosion; meningeal seeding also may occur with a direct bacterial inoculate during trauma, neurosurgery, or instrumentation. Meningitis in the newborn is transmitted vertically from colonized pathogens in the maternal intestinal or genital tract or horizontally from nursery personnel or caregivers at home.

Once in the CSF, the paucity of antibodies, complement components, and white blood cells (WBCs) allows the bacterial infection to flourish. Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated events that result in increased permeability of the blood-brain barrier, cerebral edema, and presence of toxic mediators in the CSF. Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process and account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose. Exudates extend throughout the CSF, particularly to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resultant hearing loss), obliterating CSF pathways (causing obstructive hydrocephalus), and inducing vasculitis and thrombophlebitis (causing local brain ischemia).As intracranial pressure (ICP) continues to rise and brain edema progresses, CNS autoregulatory processes begin to fail. This pivotal event may occur when the transient increase in cerebral blood flow (CBF) reverses and begins to decrease. CBF reduction correlates with the patient's decreasing alertness and changes in mental status.Without medical intervention, the cycle of decreasing CBF, worsening cerebral edema, and increasing ICP proceeds unchecked. Ongoing endothelial injury may result in vasospasm and thrombosis, further compromising CBF, and may lead to stenosis of large and small vessels. Systemic hypotension (septic shock) also may impair CBF, and the patient soon dies from systemic complications or from diffuse CNS ischemic injury.Emergency physicians should be aware that future therapies will be based on improved understanding of the pathogenesis of acute bacterial meningitis and may include caspase inhibitors, antioxidants, poly (ADP-ribose) polymerase inhibitors, inhibitors of lipid peroxidation, and metalloproteinase inhibitors, in addition to antibiotics and steroids.

The pathophysiologies of nonbacterial pathogens are less well understood. Fungal meningitis is thought to unfold in a manner similar to but less acute than bacterial meningitis.FrequencyUnited StatesThe incidence of bacterial meningitis declined from 1.9 to 1.5 cases per 100,000 from 1998 to 2003, in part, due to the introduction of the conjugate Haemophilus influenzae type b and pneumococcal conjugate vaccines. There continues to be an increased incidence of bacterial meningitis among persons aged 60 years and older, independent of other factors.1

InternationalMeningococcal meningitis is endemic in parts of Africa, India, and other developing nations. Periodic epidemics occur in the so-called sub-Saharan "meningitis belt" as well as among religious pilgrims traveling to Saudi Arabia for the Hajj. A significant increase in the incidence of penicillin-resistant S pneumoniae meningitis has occurred worldwide. The incidence of HIV infection worldwide has resulted in a corresponding increased frequency of meningitis caused by encapsulated organisms (primarily S pneumoniae), along with AIDS-related opportunistic organisms and tuberculosis.2

Mortality/MorbidityMorbidity and mortality depend on pathogen, patient's age and condition, and severity of acute illness.3

Among bacterial pathogens, pneumococcal meningitis causes the highest rates of mortality (21%) and morbidity (15%).

Mortality rate is 50-90% and morbidity even higher if severe neurologic impairment is evident at the time of presentation (or with extremely rapid onset of illness), even with immediate medical treatment.

RaceStatistically, blacks are at greater risk than other races, although race may not be an independent risk factor.SexIn neonates, male-to-female ratio is 3:1. No sex preference exists among adults.AgeAccording to the Centers for Disease Control and Prevention (CDC),4 the median age is 39 years. In 1986, it was 15 months.

Excluding meningococcal meningitis, patients younger than 5 years and older than 60 years are at increased risk.

Newborns are at highest risk for acute bacterial meningitis. After the first month of life, the peak incidence is in infants aged 3-8 months.

Clinical

HistoryDistinguishing acute, subacute, and chronic meningitis helps identify the pathogen. Approximately 25% of patients with bacterial meningitis present acutely, well within 24 hours of onset of symptoms. Other patients with subacute bacterial meningitis and most patients with viral meningitis present with neurologic symptoms developing over 1-7 days. Chronic symptoms lasting longer than 1 week suggest meningitis caused by some viruses as well as tuberculosis, syphilis, fungi (especially cryptococci), and carcinomatous meningitis.

Classic symptoms (not evident in infants or seen often in the elderly) include the following: o Headacheo Nuchal rigidity (generally not present in children <1 y or in patients with altered mental status)o Fever and chillso Photophobiao Vomiting

o Prodromal upper respiratory infection (URI) symptoms (viral and bacterial)o Seizures (30-40% in children, 20-30% in adults)o Focal neurologic symptoms (including focal seizures)o Altered sensorium (confusion may be sole presenting complaint, especially in elderly)

Symptoms in infants o Fevero Lethargy and/or change in level of alertnesso Poor feeding and/or vomitingo Respiratory distress, apnea, cyanosis

Partially treated meningitis: As many as 40% of patients with acute or subacute bacterial meningitis were treated previously with oral antibiotics (presumably due to misdiagnosis at time of initial presentation). In partially treated meningitis, seizures may be the sole presenting symptom; fever and changes in level of alertness or mental status occur less commonly than in untreated meningitis.

Low-grade ventriculitis associated with ventriculoperitoneal shunt: Patients may have a less dramatic presentation than those with acute bacterial meningitis, with headache, nausea, minimal fever, and malaise.

Fungal meningitis: Headache, low-grade fever, and lethargy are the primary symptoms; the course may be mild with fluctuating symptoms, especially in immunocompromised patients.

Tuberculous meningitis: Fever, weight loss, night sweats, and malaise, with or without headache and meningismus are common symptoms; this infection may follow a protracted course with vague, nonspecific presentation.

PhysicalOtherwise healthy patients within age extremes present with clinically obvious acute bacterial meningitis. In contrast, most patients with subacute bacterial meningitis present a diagnostic challenge. Systemic examination occasionally reveals a pulmonary or otitis media co-infection.

Signs of meningeal irritation o Nuchal rigidity or discomfort on neck flexiono Kernig sign: Passive knee extension in supine patient elicits neck pain and hamstring resistance.o Brudzinski sign: Passive neck or single hip flexion is accompanied by involuntary flexion of both

hips. Papilledema is present in only one third of meningitis patients with increased ICP; it takes at least several

hours to develop. Focal neurologic signs

o Isolated cranial nerve abnormalities (principally III, IV, VI, VII) in 10-20% of patientso Associated with a dramatic increase in complications from lumbar puncture (LP) and portends a

worse outcome Systemic findings

o Extracranial infection (eg, sinusitis, otitis media, mastoiditis, pneumonia, urinary tract infection) may be noted.

o Arthritis is seen with N meningitidis, less commonly with other bacteria.o Nonblanching petechiae and cutaneous hemorrhages are seen classically with N meningitidis;

however, these also can occur with other bacterial and viral infections.o Endotoxic shock with vascular collapse is characteristic of severe N meningitidis infection.

Altered mental status, from irritability to somnolence, delirium, and coma Infants

o Bulging fontanelle (if euvolemic)o Paradoxic irritability (ie, quiet when stationary, cries when held)o High-pitched cryo Hypotoniao Examine skin over entire spine for dimples, sinuses, nevi, or tufts of hair, which may indicate a

congenital anomaly communicating with the subarachnoid space.CausesMeningitis is caused by the following pathogens in each age group:

Neonates - Group B or D streptococci, nongroup B streptococci, Escherichia coli, and L monocytogenes Infants and children -H influenzae (48%), S pneumoniae (13%), and N meningitidis Adults -S pneumoniae, (30-50%), H influenzae (1-3%), N meningitidis (10-35%), gram-negative bacilli (1-

10%), staphylococci (5-15%), streptococci (5%), and Listeria species (5%) Risk factors

o Aged 60 years or oldero Aged 5 years or younger, especially children with diabetes mellitus, renal or adrenal insufficiency,

hypoparathyroidism, or cystic fibrosis o Immunosuppressed patients are at increased risk of opportunistic infections and acute bacterial

meningitis. Immunosuppressed patients may not show dramatic signs of fever or meningeal inflammation.

o HIV infection, in particular, predisposes to bacterial meningitis caused by encapsulated organisms, primarily S pneumoniae.

o Crowding (eg, military recruits and college dorm residents) increases risk of outbreaks of meningococcal meningitis.

o Splenectomy and sickle cell disease increase the risk of meningitis secondary to encapsulated organisms.

o Alcoholism and cirrhosis: Multiple etiologies of fever and seizures in these patients make meningitis challenging to diagnose.

o Diabetes o Recent exposure to others with meningitis, with or without prophylaxiso Contiguous infection (eg, sinusitis)o Dural defect (eg, traumatic, surgical, congenital)o Thalassemia major o Intravenous (IV) drug abuseo Bacterial endocarditis o Ventriculoperitoneal shunto Malignancy (increased risk of Listeria species infection)o Some cranial congenital deformities

Differential DiagnosesBrain Abscess Neoplasms, Brain

Delirium Tremens Pediatrics, Febrile Seizures

Encephalitis Pediatrics, Meningitis and Encephalitis

Herpes Simplex Subarachnoid Hemorrhage

Herpes Simplex Encephalitis

Other Problems to Be ConsideredAll causes of altered mental status and comaLeptospirosisSubdural empyemaWorkup

Laboratory Studies Complete blood count (CBC) with differential Serum electrolytes to determine dehydration or syndrome of inappropriate secretion of antidiuretic

hormone [SIADH]) Serum glucose as baseline for determining normal CSF glucose; may be low if glycogen stores are

depleted or high in infected patients with diabetes BUN and/or creatinine and liver profile to assess organ functioning and adjust antibiotic dosing Coagulation profile and platelets in patients with chronic alcohol use, liver disease, or if disseminated

intravascular coagulation (DIC) is suspected. (Patients may require platelets or fresh frozen plasma [FFP] prior to LP.)

Urinary electrolytes if SIADH is suspected Serum cryptococcal antigen, especially if baseline is known (less diagnostic than India ink and CSF

cryptococcal antigen) Cultures prior to instituting antibiotics may be helpful if diagnosis is uncertain: blood (50% positive in

meningitis caused by H influenzae, S pneumoniae, N meningitidis); nasopharynx, respiratory secretions, urine, and skin lesions.

Latex agglutination or counter immunoelectrophoresis (CIE) of blood, urine, and CSF for specific bacterial antigens is recommended occasionally if diagnosis is challenging or in patients with partially treated meningitis.

Serum test for syphilis is indicated if neurosyphilis is in differential diagnosis. (Cases have been documented of neurosyphilis CSF negative for Venereal Disease Research Laboratory test [VDRL].)

Imaging Studies Head CT scan with contrast or MRI with gadolinium

o Imaging is indicated in patients with evidence of head trauma, immunosuppression, altered mental status, or focal findings.

o Presence of papilledema and inability to fully assess fundi or neurologic status are indications for CT scan prior to LP.

o Obtain blood cultures and initiate treatment before imaging studies and LP in patients with suspected bacterial meningitis.

o Results may be normal or demonstrate small ventricles, effacement of sulci, and contrast enhancement over convexities.

o Late findings include venous infarction and communicating hydrocephalus.o Rule out brain abscess, sinus or mastoid infection, skull fracture, and congenital anomalies.

o Acute bacterial meningitis is shown in the CT and MRIs below. All of the images below are from the same patient.

Chest radiography o As many as 50% of patients with pneumococcal meningitis also have evidence of pneumonia on

initial chest radiograph.o This association occurs in fewer than 10% of patients with meningitis caused by H influenzae or N

meningitidis and in approximately 20% of patients with meningitis caused by other organisms.Procedures

Lumbar puncture (see Table 1 for interpretation of results) o Elevated opening pressure correlates with increased risk of morbidity and mortality in bacterial

and fungal meningitis.o Take tube #1 to chemistry lab for glucose and protein.o Take tube #2 to hematology lab for cell count with differential.o Take tube #3 to microbiology and immunology lab for Gram stain, bacterial culture, acid-fast

bacillus (AFB) stain and tuberculosis (TB) cultures, India ink stain and fungal cultures, CIE, VDRL, and cryptococcal antigen, if indicated.

o Hold tube #4 for repeat cell count with differential, if needed (or for other subsequent studies not initially ordered).

o Research correlates CSF cytokines in children with bacterial meningitis.o According to Seupaul, 3 diagnostic tests have clinically useful likelihood ratios for the diagnosis of

bacterial meningitis in adults: CSF/blood glucose ratio less or equal to 0.4, CSF WBC count greater or equal to 500/L, and CSF lactate level equal or greater than 31.53.5

General patterns in CSF pressure measurement and analysis in bacterial, viral, and fungal (cryptococcal) meningitis may support a diagnosis. The most important diagnostic tests in the ED to rule out bacterial meningitis are a well-performed Gram stain and, if available, polymerase chain reaction (PCR) on the CSF of patients with suspected herpes simplex encephalitis.

Table 1. Comparison of CSF Findings by Type of OrganismOpen table in new windowTable

Bacterial Meningitis Viral Meningitis* Fungal Meningitis**

Pressure5-15 cm H2 O

Increased Normal or mildly increased Normal or mildly increased in TB. May be increased in fungal. AIDS patients with cryptococcal meningitis have increased risk of blindness, death unless maintained at <30 cm.

Cell countpreterm: 0-25term: 0-22>6 months: 0-5mononuclearcells/mm3

No cell count result can exclude bacterial meningitis. Typically thousands of PMNs, but may be less dramatic or even normal (classically, in very early meningococcal meningitis and in extremely ill neonates). Lymphocytosis with normal CSF chemistries seen in 15-25%, especially when cell counts <1000 or if partially treated. Approximately 90% of patients with ventriculoperitoneal shunts have CSF WBC count >100 cells/mm3 are infected; CSF glucose usually normal, and organisms are less pathogenic. Cell count and chemistries normalize slowly (over days) with antibiotics.

Usually <500 cells, nearly 100% mononuclear. Up to 48 hours, significant PMN pleocytosis may be indistinguishable from early bacterial meningitis; this is particularly true with eastern equine encephalitis. Presence of nontraumaticRBCs in 80% of HSV meningoencephalitis, although 10% have normal CSF results

Hundreds of mononuclear cells

Microno organisms

Gram stain 80% effective. Inadequate decolorization may mistake H influenzae for gram-positive cocci. Pretreatment with antibiotics may affect stain uptake, causing gram-positive

No organism India ink 80-90% effective for fungi; AFB stain 40% effective for TB (increase yield by staining supernate from at least 5 cc CSF)

organisms to appear gram negative and decrease culture yield on average 20%.

Glucoseeuglycemia: >50% serumhyperglycemia: >30% serum wait 4 h after glucose load

Decreased Normal Sometimes decreased. Aside from fulminant bacterial meningitis, the lowest levels of CSF glucose are seen in TB, primary amebic meningoencephalitis, neurocysticercosis

Proteinpreterm: 65-150term: 20-170>6 months: 15-45mg/dL

Usually >150, may be >1000 Mildly increased Increased; >1000 with relatively benign clinical presentation suggestive of fungal disease

Bacterial Meningitis Viral Meningitis* Fungal Meningitis**

Pressure5-15 cm H2 O

Increased Normal or mildly increased Normal or mildly increased in TB. May be increased in fungal. AIDS patients with cryptococcal meningitis have increased risk of blindness, death unless maintained at <30 cm.

Cell countpreterm: 0-25term: 0-22>6 months: 0-5mononuclearcells/mm3

No cell count result can exclude bacterial meningitis. Typically thousands of PMNs, but may be less dramatic or even normal (classically, in very early meningococcal meningitis and in extremely ill neonates). Lymphocytosis with normal CSF chemistries seen in 15-25%, especially when cell counts <1000 or if partially treated. Approximately 90% of patients with ventriculoperitoneal shunts have CSF WBC count >100 cells/mm3 are infected; CSF glucose usually normal, and organisms are less pathogenic. Cell count and chemistries normalize slowly (over days) with antibiotics.

Usually <500 cells, nearly 100% mononuclear. Up to 48 hours, significant PMN pleocytosis may be indistinguishable from early bacterial meningitis; this is particularly true with eastern equine encephalitis. Presence of nontraumaticRBCs in 80% of HSV meningoencephalitis, although 10% have normal CSF results

Hundreds of mononuclear cells

Microno organisms

Gram stain 80% effective. Inadequate decolorization may mistake H influenzae for gram-positive cocci. Pretreatment with antibiotics may affect stain uptake, causing gram-positive organisms to appear gram negative and decrease culture yield on average 20%.

No organism India ink 80-90% effective for fungi; AFB stain 40% effective for TB (increase yield by staining supernate from at least 5 cc CSF)

Glucoseeuglycemia: >50% serumhyperglycemia: >30% serum wait 4 h after glucose load

Decreased Normal Sometimes decreased. Aside from fulminant bacterial meningitis, the lowest levels of CSF glucose are seen in TB, primary amebic meningoencephalitis, neurocysticercosis

Proteinpreterm: 65-150term: 20-170>6 months: 15-45mg/dL

Usually >150, may be >1000 Mildly increased Increased; >1000 with relatively benign clinical presentation suggestive of fungal disease

*Some bacteria (eg, Mycoplasma, Listeria, Leptospira species, Borrelia burgdorferi [Lyme], spirochetes) produce spinal fluid alterations that resemble the viral profile. An aseptic profile also is typical of partially treated bacterial infections (more than 33% of patients have received antimicrobial treatment, especially children) and the 2 most common causes of encephalitis — the potentially curable HSV and arboviruses.**In contrast, TB meningitis and parasites resemble the fungal profile more closely.

Treatment

Prehospital Care

Evaluate and treat patient for shock or hypotension. Infuse crystalloid until euvolemic. Consider seizure precautions. Treat seizures according to usual protocol. Consider airway protection in patients with altered mental status. For alert patients in stable condition with normal vital signs, administer oxygen, establish IV access, and

transport rapidly to the ED.

Emergency Department Care

Acute meningitis: Regardless of presentation, perform CSF examination in acute meningitis to identify the specific organism and susceptibilities. Institute treatment as early as possible in the disease course, since delay in instituting treatment may contribute significantly to morbidity and mortality.

Subacute meningitis: Most patients with subacute bacterial meningitis present more of a diagnostic challenge than those with acute illness. In these patients, CSF examination constitutes the critical step in documenting the presence or absence of a CNS infection and type of infecting organism. If the patient's condition is serious and antibiotics have been given (arguably masking symptoms and hindering growth of organisms on culture), assume a bacterial infection is present, provide adequate antibiotic coverage, and admit the patient.

The patient's condition and ED organization may warrant a watchful wait for 8-12 hours, then a reexamination of the CSF (sooner if patient's condition deteriorates). If initial granulocytosis changes to mononuclear predominance, CSF glucose remains normal, and patient continues to look well, the infection is most likely nonbacterial.

In acutely ill patients, perform an LP (if appropriate) and administer first dose(s) of antibiotics +/- steroids within 30 minutes of presentation to ED.

Consider instituting ED triage protocol to identify patients at risk. Initiate empiric therapy if LP cannot be performed within 30 minutes. Begin empiric therapy prior to head CT scan if a focal neurologic deficit is present. If no mass effect is

present, perform LP to obtain microbiology studies. Treat systemic complications of acute bacterial meningitis: hypotension and/or shock, hypoxemia,

hyponatremia (SIADH), cardiac arrhythmias and ischemia, cerebrovascular accident (CVA), and exacerbation of chronic diseases.

Look for signs of hydrocephalus and increasing ICP. o Manage fever and pain, control straining and coughing, avoid seizures, and avoid systemic

hypotension.o In otherwise stable patients, sufficient care includes elevating head and monitoring neurologic

status.o When more aggressive maneuvers are indicated, some authorities favor early use of diuresis (ie,

furosemide 20 mg IV, mannitol 1 g/kg IV), provided circulatory volume is protected.o Hyperventilation in intubated patients, with a goal of PaCO2 25-30 mm Hg, may briefly lower ICP;

hyperventilation with PaCO2 <25 mm Hg may decrease CBF disproportionately and lead to CNS ischemia.

o Consider placing an ICP monitor in comatose patients or in those with signs of increased ICP.o With elevated ICP, remove CSF until pressure decreases by 50% and maintain at less than 300

mm water. Seizure precautions in ED: Aggressively control seizures if present, since seizure activity increases ICP (ie,

lorazepam 0.1 mg/kg IV and IV load with phenytoin 15 mg/kg or phenobarbital 5-10 mg/kg). Controversy surrounds the administration of dexamethasone, which is given with or just before

antibiotics.6

o Dexamethasone may interrupt the cytokine-mediated neurotoxic effects of bacteriolysis, which are at maximum in the first days of antibiotic use.

o Recent meta-analysis of 10 years of clinical trials confirmed that dexamethasone decreases morbidity, especially incidence and severity of neurosensory hearing loss, for H influenzae

meningitis and suggested comparable benefit for S pneumoniae meningitis in childhood. No adequate adult studies exist, although the pathophysiology is presumably similar. Meta-analysis suggests that limiting dexamethasone therapy to 2 days may be optimal. More recent studies conducted in Europe continue to support the use of dexamethasone in developed (as opposed to developing) countries, perhaps related to the relative incidence of TB meningitis.

o Theoretically, anti-inflammatory effects of steroids decrease blood-brain barrier permeability and impede penetration of antibiotics into CSF.

Decreased CSF levels of vancomycin have been confirmed in steroid-treated animals yet not in human studies.

Many authorities believe that all other antibiotics achieve minimal inhibitory concentrations (MICs) in CSF regardless of steroid use.

Dexamethasone may not clinically impede even vancomycin.o In developing countries, the use of oral glycerol (rather than dexamethasone) has been studied

as adjunctive therapy in the treatment of bacterial meningitis in children. In limited studies, it appears to reduce the incidence of neurologic sequelae with few side effects.7

Ideal ED antibiotic therapy is based on a clearly identified organism on CSF Gram stain. Age and underlying conditions dictate empiric treatment in an ED patient without trauma or CNS instrumentation. Information presented in this article is taken from the 2003 edition of The Sanford Guide to Antimicrobial Therapy.

o In neonates to age 1 month, the most common microorganisms are group B or D streptococci, Enterobacteriaceae (eg, E coli), and L monocytogenes.

Primary treatment is a combination of ampicillin (age 0-7 d: 50 mg/kg IV q8h; age 8-30 d: 50-100 mg/kg IV q6h) plus cefotaxime 50 mg/kg IV q6h (up to 12 g/d).

Alternative treatment is ampicillin (age 0-7 d: 50 mg/kg IV q8h; age 8-30 d: 50-100 mg/kg IV q6h) plus gentamicin (age 0-7 d: 2.5 mg/kg IV or IM q12h; age 8-30 d: 2.5 mg/kg IV or IM q8h).

Most authorities recommend adding acyclovir 10 mg/kg IV q8h for herpes simplex encephalitis.

o In infants (1-3 mo), the most common microorganisms are those listed under neonates above and under older infant/child below.

Primary treatment is cefotaxime (50 mg/kg IV q6h, up to 12 g/d) or ceftriaxone (initial dose: 75 mg/kg, 50 mg/kg q12h up to 4 g/day) plus ampicillin (50-100 mg/kg IV q6h).

Alternative treatment is chloramphenicol (25 mg/kg PO or IV q12h) plus gentamicin (2.5 mg/kg IV or IM q8h).

If prevalence of cephalosporin-resistant S pneumoniae (DRSP) is >2%, add vancomycin (15 mg/kg IV q8h). Strongly consider dexamethasone (0.4 mg/kg IV q12h for 2 d or 0.15 mg/kg IV q6h for 4 d) starting 15-20 minutes before first dose of antibiotics.

o In older infants or young children (3 mo - 7 y), the most common microorganisms are S pneumoniae, N meningitidis, and H influenzae.

Primary treatment is either cefotaxime (50 mg/kg IV q6h up to 12 g/d) or ceftriaxone (initial dose: 75 mg/kg, then 50 mg/kg q12h up to 4 g/d). If prevalence of DRSP is >2%, add vancomycin (15 mg/kg IV q8h). In countries with low prevalence of DRSP, consider penicillin G (250,000 U/kg/d IM/IV in 3-4 divided doses). Due to DRSP, penicillin G is no longer recommended in the US.

Alternative treatment (or if severely penicillin allergic) is chloramphenicol (25 mg/kg PO/IV q12h) plus vancomycin (15 mg/kg IV q8h).

Strongly consider dexamethasone (0.4 mg/kg IV q12h for 2 d or 0.15 mg/kg IV q6h for 4 d) starting 15-20 minutes before the first dose of antibiotics.

o In an older child or an otherwise healthy adult (7-50 y), the most common microorganisms are S pneumoniae, N meningitidis, and L monocytogenes.

In areas where prevalence of DRSP is >2%, primary treatment is either cefotaxime (pediatric dose: 50 mg/kg IV q6h up to 12 g/d; adult dose: 2 g IV q4h) or ceftriaxone (pediatric dose: initial dose: 75 mg/kg, then 50 mg/kg q12h up to 4 g/day; adult dose: 2 g IV q12h) plus vancomycin (pediatric dose: 15 mg/kg IV q8h; adult dose: 750-1000 mg IV q12h or 10-15 mg/kg IV q12h). Some add rifampin (pediatric dose: 20 mg/kg/d IV; adult dose: 600 mg PO qd). If Listeria species is suspected, add ampicillin (50 mg/kg IV q6h).

Alternative treatment (or if severely penicillin allergic) is chloramphenicol (12.5 mg/kg IV q6h: not bactericidal) or clindamycin (pediatric dose: 40 mg/kg/day IV in 3-4 doses; adult dose: 900 mg IV q8h: active in vitro but no clinical data) or meropenem (pediatric dose: 20-40 mg/kg IV q8h; adult dose: 1 g IV q8h: active in vitro but few clinical data; avoid imipenem as it is proconvulsant).

In areas with low prevalence of DRSP, use cefotaxime (pediatric dose: 50 mg/kg IV q6h up to 12 g/d; adult: 2 g IV q4h) or ceftriaxone (pediatric dose: 75 mg/kg initial dose then 50 mg/kg q12h up to 4 g/d; adult: 2 g IV q12h) plus ampicillin (50 mg/kg IV q6h).

Alternative treatment (or if severely penicillin allergic) is chloramphenicol (12.5 mg/kg IV q6h) plus trimethoprim/sulfamethoxazole (TMP/SMX; TMP 5 mg/kg IV q6h) or meropenem (pediatric dose: 20-40 mg/kg IV q8h; adult dose: 1 g IV q8h).

Data are limited on the need for dexamethasone in adults, although there is support for its use in developed countries when S. pneumoniae is the suspected organism. Administer first dose of dexamethasone (0.4 mg/kg q12h IV for 2 d or 0.15 mg/kg q6h for 4 d) 15-20 minutes before first dose of antibiotics.

o In adults older than 50 years or adults with disabling disease or alcoholism, the most common microorganisms are S pneumoniae, coliforms, H influenzae, Listeria species, Pseudomonas aeruginosa, and N meningitidis.

Primary treatment if the prevalence of DRSP is >2% is either cefotaxime (2 g IV q4h) or ceftriaxone (2 g IV q12h) plus vancomycin (750-1000 mg IV q12h or 10-15 mg/kg IV q12h). If CSF Gram stain shows gram-negative bacilli, use ceftazidime (2 g IV g8h). In areas of low prevalence of DRSP, use cefotaxime (2 g IV q4h) or ceftriaxone (2 g IV q12h) plus ampicillin (50 mg/kg IV q6h).

Other options for treatment include meropenem, TMP/SMX, and doxycycline. Data are limited on the need for dexamethasone in adults, although there is support for

its use in developed countries when S pneumoniae is the suspected organism and suspicion for TB or fungal etiologies is low. Administer first dose of dexamethasone (0.4 mg/kg q12h IV for 2 d or 0.15 mg/kg q6h for 4 d) 15-20 minutes before first dose of antibiotics.

o In HIV-positive/AIDS patients, consider cryptococci, Mycobacterium tuberculosis, syphilis, HIV aseptic meningitis, and Listeria species. If the pathogen is unknown after an ED workup, draw a serum/CSF cryptococcal antigen and treat empirically as in adults older than 50 years (pending results of all blood and CSF tests) to cover the bacterial pathogens, particularly S pneumoniae and L monocytogenes, for which this patient population is most at risk .

o In patients who have had trauma or neurosurgery, the most common microorganisms are S pneumoniae (if CSF leak is present), Staphylococcus aureus, coliforms, and P aeruginosa.

Primary treatment is vancomycin (1 g IV q12h) plus ceftazidime (2 g IV q8h). Alternative treatment is meropenem (1 g IV q8h).

o In patients with infected ventriculoperitoneal (atrial) shunt, the most common microorganisms are Staphylococcus epidermidis, S aureus, coliforms, Propionibacterium acnes, and diphtheroids (rare). Consult a neurosurgeon, since early shunt removal is usually necessary for cure.

Pediatric dose - Either cefotaxime (50 mg/kg IV q6h) or ceftriaxone (50 mg/kg IV q12h if gram-negative bacillus) plus vancomycin (15 mg/kg/d IV q6h)

Adult dose - Vancomycin (1 g IV q12h) plus rifampin (600 mg PO qd). If CSF Gram stain shows gram-negative bacilli, use ceftazidime (2 g IV q8h) alone.

o In patients with aseptic meningitis (CSF pleocytosis and normal CSF glucose, negative bacteria on Gram stain), the most common microorganisms are enteroviruses, human herpesvirus-2 (HHV-2), lymphocytic choriomeningitis virus (LCM), HIV, and other viruses. Other etiologies include drugs (NSAIDs, metronidazole, IV immunoglobulin) and, rarely, leptospirosis.

Manage by repeating LP if necessary to rule out partially treated bacterial meningitis. Treatment options for leptospirosis are doxycycline (100 mg PO/IV q12h), penicillin G (5

million U IV q6h), or ampicillin (500 mg IV q6h).o For patients with symptoms lasting longer than 1 month with CSF pleocytosis, 40% have

tuberculous meningitis, 7% cryptococci, 8% neoplastic, and 34% remain undiagnosed. Defer ED treatment until organism is identified.

o Most authorities recommend adding vancomycin when treating patients of all ages in the US with suspected S pneumoniae meningitis to cover drug-resistant strains (36% of S pneumoniae, according to 1995 data).

o Use of vancomycin may affect the decision to include dexamethasone (see above).o Increase standard cefotaxime pediatric dosage by 50-100 mg/kg/d to overcome intermediate

cephalosporin resistance found in some S pneumoniae. Prophylaxis for close contacts of patients with (suspected) N meningitidis

o Indicated for those at increased risk, such as those who were in close contact with patient for at least 4 hours during the week before onset (eg, house mates, daycare center, cell mates) or were exposed to patient's nasopharyngeal secretions (eg, kissing, mouth-to-mouth resuscitation, intubation, nasotracheal suctioning). Spread is via respiratory droplets, not aerosols, hence close contact is required for prophylactic consideration.

o Rifampin (pediatric dose: children <1 mo - 5 mg/kg q12h; children >1 mo - 10 mg/kg q12h; adult dose: 600 mg PO bid) for 4 doses

o Alternative - Ciprofloxacin (adults) 500 mg PO single dose or ceftriaxone (<15 y: 125 mg; >15 y: 250 mg) IM single dose

o Primary treatment in many European countries - Spiramycin (pediatric dose: 10 mg/kg; adult dose: 500 mg) PO q6h for 5 days

o Administer meningococcal vaccine only in established epidemics or in travelers to countries where meningococcal disease is currently epidemic. Vaccination does not replace prophylaxis.

Prophylaxis for household or daycare contacts of patients with (suspected) H influenzae type b is controversial. Most authorities treat contacts to protect unvaccinated children, especially those younger than 4 years who are at risk.

o Indicated for those residing with the patient for at least 4 hours during the week before illness onset (if at least 1 unvaccinated child 4 years or younger, give prophylaxis to all except pregnant household contacts) or daycare contact with patient within 5-7 days (for single case: if all contacts at least 2 years, no prophylaxis; if unvaccinated children 2 years or younger attend, consider prophylaxis and vaccinate susceptible children. For 2 or more cases in 60 days: if unvaccinated children attend, prophylaxis recommended for children and personnel).

o Rifampin (pediatric dose: 10 mg/kg; adult dose: 600 mg) PO q12h for 4 doses.

TUJUAN PEMBELAJARAN

Pada akhir diskusi mahasiswa diharapkan mampu :1. Menjelaskan anatomi komponen penyusun rongga intrakranial2. Menyebutkan macam-macam nyeri kepala3. Menjelaskan karakteristik masing-masing jenis nyeri kepala4. Menjelaskan patofisiologi terjadinya nyeri kepala5. Mendiskusikan diagnosis banding nyeri kepala primer6. Mendiskusikan diagnosis banding nyeri kepala sekunder7. Menyebutkan penyakit-penyakit / faktor pencetus yang dapat menimbulkan gejala nyeri kepala8. Mengusulkan pemeriksaan penunjang yang diperlukan9. Menjelaskan penatalaksanaan nyeri kepala10. Menjelaskan prognosis nyeri kepala11. Mengetahui kegawat daruratan nyeri kepala12. Menjelaskan mekanisme peningkatan tekanan intrakranial

Informasi

Nona M, 17 tahun, datang ke poliklinik Saraf dengan keluhan nyeri kepala. Keluhan sudah dirasakan sejak 1 hari yang lalu. Sebelumnya, nona M juga beberapa kali mengalami nyeri kepala, namun sembuh setelah minum obat yang dibeli di warung sebelah rumahnya.

M pertama kali merasakan nyeri kepala kira-kira satu tahun yang lalu, dan hampir selalu muncul pada saat awal menstruasi. Nyeri dirasakan berdenyut, terutama di kepala sebelah kiri, walaupun kadang disebelah kanan, dengan lama serangan kira-kira 4-6 jam, dan didahului pandangan berkunang-kunang. Dalam 3 bulan ini,nyeri kepala muncul sampai10 kali. Pasien juga mengeluh mual, namun tidak muntah.

Pemeriksaan FisikKU : Baik, composmentis (GCS=E4M6V5=15)Tanda Vital : Tekanan darah : 120/80 mmHg

Nadi : 80 x/mnt Frekuensi pernafasan : 16x/mnt Temperatur : 37◦C

Status internus : dbnStatus neurologis :

- Mata : conjungtiva palpebra tak anemis, sclera tak ikterik : isokor, reflek cahaya +/+

- Nn Cranialis : dbn- Motorik : superior inferior

Gerak +/+ +/+Kekuatan 5/5 5/5Reflek fisiologis N/N N/NReflek patologis -/- -/-Tonus N/N N/NTrofi eutrofi eutrofi

- Sensorik : dbn

Hasil pemeriksaan penunjang - laboratorium (darah rutin) : dbn- Elektroensefalografi : gelombang dasar alfa, gelombang epileptik (-)

Diagnosis : Migrain tanpa aura

Terapi : - Asam mefenamat 500 mg (bila nyeri kepala) - Domperidon 30 mg bila mual

SKENARIO III

Panduan

Primary Headache Disorder Migraine, with or without aura Tension-type, infrequent, frequent, or chronic

Cluster and other trigeminal autonomic cephalgias (TACs)

Secondary Headache Associated with head and/or neck trauma Associated with cranial or vascular disorder, such as stroke Associated with nonvascular intracranial disorder, such as intracranial hypertension and seizures Associated with a substance (nitrate and alcohol) or its withdrawal (analgesics, caffeine, narcotics, and

alcohol) Associated with infection, such as meningitis and brain abscess Associated with metabolic disorder, such as hypoxia, hypercapnia, and hypoglycemia Associated with disorder of surrounding structures, including neck, eyes, ears, nose, sinuses, and teeth Associated with psychiatric disorder

Cranial neuralgias

To achieve these goals, the comprehensive management strategy may include the following: 1. Acute pharmacologic therapy 2. Nonpharmacologic therapy 3. Preventive therapy 4. Patient education

Acute Pharmacologic Therapy

Medications used range from a wide variety of nonspecific analgesics to specific agents directed toward rectifying the cause of the migraine. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen (Motrin, Advil), and naproxen (Aleve), as well as those in combination with acetaminophen, aspirin, and caffeine (Excedrin), have been proven to be superior to placebo in clinical trials for mild to moderate attacks, if used occasionally. A well-controlled study also showed the benefit of acetaminophen over placebo. Parenteral antiemetics, such as metoclopramide (Reglan) and prochlorperazine (Compazine) also have been shown to be superior to placebo in migraine headaches. Opioids such as meperidine (Demerol) and hydrocodone (Lorcet, Lortab) are commonly prescribed for migraines but should be used sparingly. The concern for physical dependence and addiction is real. Although ergot products are effective, their use has declined because of their significant adverse-effect profile and contraindications.

Box 65-2 Precipitating Factors in MigrainesBody_ID: B065002

Hormonal imbalance, such as during menses, pregnancy, and hormonal replacement therapy

Emotional factors Accident/Trauma Diet: see below Alcohol and medicines such as nonsteroidal antiinflammatory drugs Caffeine Hot or cold weather Exertion Smoking

Migraine Dietary Restrictions Dairy products: Aged cheeses (cheddar, Swiss), sour cream, chocolates Meats: Beef and chicken livers, unrefrigerated dry fermented sausage, fermented

bologna, salami, pepperoni, pickled fish, pickled herring, smoked fish, bacon Beverages: Red wine, caffeinated drinks, chi-anti, burgundy, beer, ale, sauternes Fruits: Avocados, overripe bananas

Vegetables: Fava beans, peanuts, snow pea pods, broad bean pods, sauerkraut

Food additives: Meat tenderizers, food containing monosodium glutamate (MSG) or brewer's yeast

Nonpharmacologic Therapy These briefly include biofeedback (self-regulation), cognitive/behavioral (stress management) therapy, and relaxation training.

Preventive Therapy Prophylaxis is frequently required in migraineurs who continue to have frequent attacks despite the described management. A variety of preventive medications are available (Table 65-2) including antidepressants, antihypertensives, and antiseizure medications. Amitriptyline, valproate, propranolol, and timolol have been proven most efficacious in clinical trials. The drug is chosen depending on the patient's comorbidity. It is important to understand that most prophylactic agents take at least 4 to 6 weeks before their benefit can be evaluated.

Patient Education

Table 65-2. Prophylactic Agents

Antidepressants Tricyclic antidepressants

Nonsedating Protriptyline, desipramine

Sedating Amitriptyline, nortriptyline, imipramine, doxepin

Selective serotonin reuptake inhibitors Fluoxetine, sertraline, paroxetine, fluvoxamine

Others Trazodone, bupropion, venlafaxine

Antihypertensives β-Blockers Atenolol, nadolol, propranolol, metoprolol, timolol

Calcium channel blockers Verapamil, nifedipine, diltiazem, nimodipine

ACE inhibitors Lisinopril

Alpha agonist Clonidine

Antiseizure Divalproex, gabapentin, topiramate

Others NSAIDs, MAOIs, methysergide, cyproheptadine, ergot derivatives, magnesium

ACE, angiotensin-converting enzyme; MAOI, monoamine oxidase inhibitor; NSAID, nonsteroidal anti-inflammatory drug.

Patient education is the cornerstone of migraine management. It is imperative that the patient understand that migraines can be managed but not cured. The goal of therapy is to reduce the migraine frequency and severity to an extent at which the patient can carry out regular physical activity and daily responsibilities with a decent quality of life. This is a chronic disorder, and lifestyle modification plays a great role. Maintaining a headache diary to track the pattern of headaches is often helpful and frequently helps the patient realize that many factors are associated with headaches. Education on avoiding the triggers and focusing on protective factors is immensely important, as the patient feels more in control of his or her condition. Support groups are helpful, as patients realize they are not alone out there.

Tension-type Headache

Tension-type headaches can be episodic or chronic. This is the most common type of headache, and most of us have had them at some time in life. Female patients are more frequently affected. The pain is typically a steady, nonthrobbing, dull, and bilateral ache, which does not worsen with routine physical activity (Table 65-3). Patients commonly describe it as a bandlike constriction around the head and a sensation of heaviness and tightening at the back of the head and neck. Nausea and vomiting are absent. Posterior neck muscles may be tender as well as contracted. The headaches are commonly associated with significant life stressors and emotional lability but are usually not disabling. Concomitant depression may be an ongoing process in these patients and must be evaluated further.

Treatment The moderate attacks are controlled well with the traditional NSAIDs . For severe attacks, triptans as well as narcotic analgesics are reserved. Muscle relaxants and osteopathic manipulative therapy also are frequently helpful because of the concomitant neck-muscle contraction associated with this type of headache. Prophylaxis may be warranted when frequent urgent therapy is required. The headaches may become disabling and long lasting, interfering with performance on a daily basis. Prophylactic agents are similar to those used mostly for migraines. Tricyclic antidepressants have shown proven benefit. Management of other associated conditions, as mentioned, is helpful and should be done in all cases.

Cluster Headache Table 65-3. Distinguishing Characteristics of Tension-type and Migraine Headaches

Tension-type Headache Migraine

No aura Aura present in 15%-25% of patients

Steady tightness or dull pain Throbbing and pulsating pain

Not aggravated with routine physical activity Aggravated with exertion or physical activity

Mostly bilateral Mostly begins as unilateral but may become bilateral

Mild to moderate pain Moderate to severe disabling pain

Usually not associated with nausea, vomiting, or photo/phonophobia

Usually associated with nausea, vomiting, photophobia, or phonophobia

Cluster headache is the least common of the primary headaches and often causes excruciating pain, which peaks quickly from the onset within 15 minutes and lasts up to 4 hours. Pain commences around an orbit, radiates to the rest of the face, and is associated with lacrimation, facial flushing, conjunctival injection, and nasal congestion. It affects smoking men in their second or third decade more often than women. The headaches tend to occur at the same time of the day continuously for many days, followed by remission, only to recur later in life in similar clusters. Attacks can be triggered by alcohol consumption as well as by sudden temperature changes when a patient is within a cluster series. During an attack, the patient is restless, agitated, and can be observed pacing in pain.

Treatment Inhalation of 100% oxygen from a tight-fitting mask at a flow rate of 5 to 10 L/min for 10 to 15 minutes during an attack is highly effective. Injectible or intranasal triptans as well as narcotic analgesics and traditional NSAIDs offer relief when given parenterally.

Summary

For the many individuals who have headaches, a primary care physician can begin by performing a comprehensive history and physical examination. This simple step helps to rule out a secondary cause for headache most of the time. The various diagnostic tests can be individualized and performed only if needed. Once a primary headache disorder is diagnosed, it becomes relatively simple to classify the headache type and treat accordingly. Often patients will have more than one primary headache type. As we understand today, considerable overlap occurs in treatment and prevention strategies of the primary headache disorders. The physician should use this fact to the advantage of the patient in the management, rather than ignoring it. Managing the chronic nature of headaches requires an ongoing healthy partnership between the physician and the patient.

TUJUAN PEMBELAJARAN

Pada akhir diskusi mahasiswa diharapkan mampu :1. Menjelaskan anatomi tulang belakang2. Menjelaskan anatomi medulla spinalis3. Menjelaskan fungsi jaras yang melalui medulla spinalis4. Menggambarkan area dermatom5. Menjelaskan patofisiologi terjadinya nyeri punggung 6. Menjelaskan definisi parese, monoparese, dan paraparese7. Menjelaskan patofisiologi terjadinya paraparese dan monoparese8. Menjelaskan peran saraf dalam defekasi dan berkemih9. Menjelaskan diagnosis banding nyeri punggung10. Menjelaskan penatalaksanaan nyeri punggung11. Menjelaskan epidemiologi Tuberkulosis12. Menjelaskan port d’entry M. Tuberkulosis13. Menjelaskan patogenesis terjadinya spondilitis TB14. Menjelaskan komplikasi spondilitis TB15. Menjelaskan penatalaksanaan spondilitis TB16. Menjelaskan prognosis spondilitis TB

INFORMASITn. SW (19 tahun) datang ke IGD RSMS dengan keluhan nyeri punggung dan lemah pada kedua kaki. Keluhan dirasakan sejak 3 bulan yang lalu

Riwayat penyakit :3 bulan yang lalu : Tn SW mulai merasa nyeri pada punggung. Nyeri mulai dirasakan seteleh ia jatuh terduduk. Setelah itu mulai merasa baal pada kedua kaki, mulai sulit berjalan, apabila memakai sandal mudah terlepas.1 bulan yang lalu : keluhan nyeri punggung menetap, tidak menjalar. Pasien semakin sulit berjalan, sehingga harus dipapah.Sejak 1 minggu yang lalu hingga saat ini, Tn.SW tidak mampu berjalan dan tidak mampu menggerakkan kedua kakinya. Rasa baal menjalar sampai ke perut.

Tn. SW mengatakan bahwa ia sering sakit-sakitan. Ia sering menderita sakit maag karena ia jarang makan (nafsu makan rendah). Ia juga sering menderita sakit batuk dan pilek.

Pemeriksaan FisikKU : sadar, GCS = E4M6V5TB : 169 cm BB 50 kgTanda Vital : Tekanan darah : 110/80 mmHg

Frekuensi Pernafasan : 20 x/mnt Nadi : 80 x/mnt Temperatur : 37◦C

Mata : conjungtiva palpebra tak anemis Sclera tak ikterik Isokor, reflek cahaya +/+

Status Internus : dbnStatus Neurologis:

- Nn Cranialis : dbn- Motorik : superior Inferior

- gerak : N/N ↓/↓- kekuatan : 5/5 1/1- Reflek fisiologis : N/N ↑/↑- Reflek Patologis : -/- +/+- Tonus : N/N ↑/↑- Trofi : eutrofi eutrofi- klonus : +/+

- Sensorik : hipestesi dari ujung jari kaki sampai umbilikus

Vegetatif : retensio urin et alvi

Status lokalis : gibus (+) regio lumbal

SKENARIO IV

Pemeriksaan PenunjangHb : 10 g/dlHematokrit : 39%Leukosit : 13.500 mmkTrombosit : 204.000 mmkLED : 36 mm/jamHitung jenis :

Eosinofil 3 Basofil 0 Batang 1 Segmen 42 Limfosit 54 Monosit 6

Kimia darahGDS : 90 g/dlSGOT : 13 IUlSGPT : 15 IUUreum : 40 mg/dlCreatinin : 0,8 mg/dl

Ro thorax : tampak gambaran fibroinfiltrat pada apex paruRo Vertebra Thoracolumbal : fr. Kompresi korpus vertebra Th X kesan spondilitis TBLumbal Pungsi : blok parsial aliran LCSMRI : kesan spondilitis TB

Diagnosis Klinis : paraparese inferior spastik, NPBTopis : Medulla spinalis segmen V.Th.XEtiologi : Spondilitis TB

Penatalaksanaan :Terapi farmakologi :

OAT Kortikosteroid : methylprednisolon 2x125 mg (tapering of)

Terapi operatif : stabilisasi interna corpus vertebra Th X Membersihkan perkejuan/debris yang ada

Panduan

Back Pain Overview

Pain in the lower back or low back pain is a common concern, affecting up to 90% of Americans at some point in their lifetime. Up to 50% will have more than one episode. Low back pain is not a specific disease. Rather, it is a symptom that may occur from a variety of different processes. In up to 85% of people with low back pain, despite a thorough medical examination, no specific cause of the pain can be identified.

Back pain can have many underlying reasons, but often no specific cause will be found and the pain will stop. This chapter tries to touch on many of the causes of back pain and proper evaluation and diagnosis. Please make sure to discuss your individual symptoms as well as the suggested treatments with your health-care provider to determine the appropriate diagnostic and treatment plan for your circumstances.

Low back pain is second only to the common cold as a cause of lost days at work. It is also one of the most common reasons to visit a doctor's office or a hospital's emergency department.

For 90% of people, even those with nerve root irritation, their symptoms will improve within two months no matter what treatment is used, even if no treatment is given.

Doctors usually refer to back pain as acute if it has been present for less than a month and chronic if it lasts for a longer period of time.

Back Pain Causes

Back pain is a symptom. Common causes of back pain involve disease or injury to the muscles, bones, and/or nerves of the spine. Pain arising from abnormalities of organs within the abdomen, pelvis, or chest may also be felt in the back. This is called referred pain. Many intra-abdominal disorders, such as appendicitis, aneurysms, kidney diseases, bladder infections, pelvic infections, and ovarian disorders, among others, can cause pain referred to the back. Normal pregnancy can cause back pain in many ways, including stretching ligaments within the pelvis, irritating nerves, and straining the low back. Your doctor will have this in mind when evaluating your pain.

Nerve root syndromes are those that produce symptoms of nerve impingement (a nerve is directly irritated), often due to a herniation (or bulging) of the disc between the lower back bones. Sciatica is an example of nerve root impingement. Impingement pain tends to be sharp, affecting a specific area, and associated with numbness in the area of the leg that the affected nerve supplies.

o Herniated discs are produced as the spinal discs degenerate or grow thinner. The jellylike central portion of the disc bulges out of the central cavity and pushes against a nerve root. Intervertebral discs begin to degenerate by the third decade of life. Herniated discs are found in one-third of adults older than 20 years of age. Only 3% of these, however, produce symptoms of nerve impingement.

o Spondylosis occurs as intervertebral discs lose moisture and volume with age, which decreases the disc height. Even minor trauma under these circumstances can cause inflammation and nerve root impingement, which can produce classic sciatica without disc rupture.

o Spinal disc degeneration coupled with disease in joints of the low back can lead to spinal-canal narrowing (spinal stenosis). These changes in the disc and the joints produce symptoms and can be seen on an X-ray. A person with spinal stenosis may have pain radiating down both lower extremities while standing for a long time or walking even short distances.

o Cauda equina syndrome is a medical emergency whereby the spinal cord is directly compressed. Disc material expands into the spinal canal, which compresses the nerves. A person would experience pain, possible loss of sensation, and bowel or bladder dysfunction. This could include inability to control urination causing incontinence or the inability to begin urination.

Musculoskeletal pain syndromes that produce low back pain include myofascial pain syndromes and fibromyalgia.

o Myofascial pain is characterized by pain and tenderness over localized areas (trigger points), loss of range of motion in the involved muscle groups, and pain radiating in a characteristic distribution but restricted to a peripheral nerve. Relief of pain is often reported when the involved muscle group is stretched.

o Fibromyalgia results in widespread pain and tenderness throughout the body. Generalized stiffness, fatigue, and muscle aches are reported.

Other skeletal causes of low back pain include osteomyelitis (infections of the bones of the spine). Noninfectious inflammation of the spine (spondylitis) can cause stiffness and pain in the spine that is particularly worse in the morning.

Tumors, possibly cancerous, can be a source of skeletal pain.Inflammation of nerves from the spine can occur with infection of the nerves with the herpes zoster virus

that causes shingles. This can occur in the thoracic area to cause upper back pain or in the lumbar area to cause low back pain

Tuberculous spondylitisPott disease, also known as tuberculous spondylitis, is one of the oldest demonstrated diseases of humankind, having

been documented in spinal remains from the Iron Age and in ancient mummies from Egypt and Peru.1 In 1779, Percivall Pott, for whom Pott disease is named, presented the classic description of spinal tuberculosis.2 Since the advent of antituberculous drugs and improved public health measures, spinal tuberculosis has become rare in developed countries, although it is still a significant cause of disease in developing countries. Tuberculous involvement of the spine has the potential to cause serious morbidity, including permanent neurologic deficits

and severe deformities. Medical treatment or combined medical and surgical strategies can control the disease in most patients.PathophysiologyPott disease is usually secondary to an extraspinal source of infection. The basic lesion involved in Pott disease is a combination of osteomyelitis and arthritis that usually involves more than one vertebra. The anterior aspect of the vertebral body adjacent to the subchondral plate is area usually affected. Tuberculosis may spread from that area to adjacent intervertebral disks.

In adults, disk disease is secondary to the spread of infection from the vertebral body. In children, because the disk is vascularized, it can be a primary site.3

Progressive bone destruction leads to vertebral collapse and kyphosis. The spinal canal can be narrowed by abscesses, granulation tissue, or direct dural invasion, leading to spinal cord compression and neurologic deficits. The kyphotic deformity is caused by collapse in the anterior spine. Lesions in the thoracic spine are more likely to lead to kyphosis than those in the lumbar

spine. A cold abscess can occur if the infection extends to adjacent ligaments and soft tissues. Abscesses in the lumbar region may descend down the sheath of the psoas to the femoral trigone region and eventually erode into the skin.FrequencyUnited StatesAlthough the incidence of tuberculosis increased in the late 1980s to early 1990s, the total number of cases has decreased in recent years.

The frequency of extrapulmonary tuberculosis has remained stable. Bone and soft-tissue tuberculosis accounts for approximately 10% of extrapulmonary tuberculosis cases

and between 1% and 2% of total cases. Tuberculous spondylitis is the most common manifestation of musculoskeletal tuberculosis, accounting

for approximately 40-50% of cases.4

International

Approximately 1-2% of total tuberculosis cases are attributable to Pott disease.In the Netherlands between 1993 and 2001, tuberculosis of the bone and joints accounted for 3.5% of all tuberculosis cases (0.2-1.1% in patients of European origin and 2.3-6.3% in patients of non-European origin).5

Mortality/Morbidity Pott disease is the most dangerous form of musculoskeletal tuberculosis because it can cause bone

destruction, deformity, and paraplegia. Pott disease most commonly involves the thoracic and lumbosacral spine. However, published series have

show some variation.6,7,8,9 Lower thoracic vertebrae is the most common area of involvement (40-50%),

followed closely by the lumbar spine (35-45%). In other series, proportions are similar but favor lumbar spine involvement.10

Approximately 10% of Pott disease cases involve the cervical spine.Race

Data from Los Angeles and New York show that musculoskeletal tuberculosis primarily affects African Americans, Hispanic Americans, Asian Americans, and foreign-born individuals.

As with other forms of tuberculosis, the frequency of Pott Disease is related to socioeconomic factors and historical exposure to the infection.

SexAlthough some series have found that Pott disease does not have a sexual predilection, the disease is more common in males (male-to-female ratio of 1.5-2:1).Age

In the United States and other developed countries, Pott disease occurs primarily in adults. In countries with higher rates of Pott disease, involvement in young adults and older

children predominates.Clinical

History

The presentation of Pott disease depends on the following: o Stage of diseaseo Affected siteo Presence of complications such as neurologic deficits, abscesses, or sinus tracts

The reported average duration of symptoms at diagnosis is 4 months7 but can be considerably longer, even in most recent series.11,9 This is due to the nonspecific presentation of chronic back pain.

Back pain is the earliest and most common symptom. o Patients with Pott disease usually experience back pain for weeks before seeking treatment.o The pain caused by Pott disease can be spinal or radicular.

Potential constitutional symptoms of Pott disease include fever and weight loss. Neurologic abnormalities occur in 50% of cases and can include spinal cord compression with paraplegia,

paresis, impaired sensation, nerve root pain, and/or cauda equina syndrome. Cervical spine tuberculosis is a less common presentation but is potentially more serious because severe

neurologic complications are more likely. o This condition is characterized by pain and stiffness.o Patients with lower cervical spine disease can present with dysphagia or stridor.o Symptoms can also include torticollis, hoarseness, and neurologic deficits.

The clinical presentation of spinal tuberculosis in patients infected with the human immunodeficiency virus (HIV) is similar to that of patients who are HIV negative; however, spinal tuberculosis seems to be more common in persons infected with HIV.12

Physical

The examination should include the following: o Careful assessment of spinal alignmento Inspection of skin, with attention to detection of sinuseso Abdominal evaluation for subcutaneous flank masso Meticulous neurologic examination

Although both the thoracic and lumbar spinal segments are nearly equally affected in persons with Pott disease, the thoracic spine is frequently reported as the most common site of involvement. Together, they comprise 80-90% of spinal tuberculosis sites. The remaining cases correspond to the cervical spine.

Almost all patients with Pott disease have some degree of spine deformity (kyphosis). Large cold abscesses of paraspinal tissues or psoas muscle may protrude under the inguinal ligament and

may erode into the perineum or gluteal area. Neurologic deficits may occur early in the course of Pott disease. Signs of such deficits depend on the level

of spinal cord or nerve root compression. Pott disease that involves the upper cervical spine can cause rapidly progressive symptoms.

o Retropharyngeal abscesses occur in almost all cases.o Neurologic manifestations occur early and range from a single nerve palsy to hemiparesis or

quadriplegia. Many persons with Pott disease (62-90% of patients in reported series6,7 ) have no evidence of extraspinal

tuberculosis, further complicating a timely diagnosis.

Information from imaging studies, microbiology, and anatomic pathology should help establish the diagnosis

TUJUAN PEMBELAJARAN

Pada akhir diskusi, mahasiswa diharapkan mampu :1. Membedakan penyebab mata merah dan visus turun2. Menjelaskan patofisiologi terjadinya mata merah dan visus turun3. Membedakan penyebab mata nyeri4. Menjelaskan patofisiologi terjadinya nyeri pada mata5. Menguraikan anatomi bola mata beserta bagian-bagiannya6. Menguraikan histologi mata7. Menjelaskan fungsi masing-masing bagian dari mata8. Menjelaskan definisi glaukoma9. Menjelaskan pembentukan dan aliran humor akueus10. Menjelaskan patofisiologi terjadinya glaukoma11. Menjelaskan klasifikasi glaukoma beserta masing-masing gejala dan tanda yang membedakannya12. Menjelaskan perjalanan penyakit glaukoma beserta kegawatan yang mungkin terjadi13. Menjelaskan penatalaksanaan awal glaukoma14. Menjelaskan pilihan obat-obat yang digunakan pada glaukoma15. Indikasi, kontraindikasi dan efek samping pemakaian obat16. Mengetahui sistem rujukan pada penyakit-penyakit mata

Informasi

Ny. Sayu, 35 tahun datang ke IGD dengan keluhan mata kanannya sakit. Keluhan dirasakan sejak 3 jam yang lalu. Pasien juga mengeluh pandangannya kabur.

Pada anamnesis lebih lanjut didapatkan bahwa sakit terasa disekitar mata kanan dan menjalar ke kepala sebelah kanan. Ny.Sayu juga mengeluhkan seperti melihat lingkaran pelangi di sebelah mata kanan saat ia melihat lampu. Saat bercermin, mata kanannya terlihat berwarna merah. Ny.Sayu merasa mual dan ingin muntah. Tidak ada riwayat sakit mata sebelumnya. Tidak ada riwayat trauma mata sebelumnya. Tidak ada riwayat operasi mata sebelumnya. Tidak ada riwayat memakai kacamata untuk melihat jauh sebelumnya, hanya kacamata baca. Tidak ada anggota keluarga yang menderita sakit seperti yang dialami Ny.Sayu.

Pemeriksaan FisikKeadaan umum : lemah, tampak kesakitan

SKENARIO V

Tekanan darah : 170/90 mmHgNadi : 80kali/menitRespirasi : 20 kali/menitTemperatur : 370C

Status internus : dalam batas normal

Status oftalmologisOD OS

1/~ (1/tak terhingga Visus 6/12Spasme Palpebra TenangHiperemis, injeksi silier Konjungitva TenangEdema Kornea JernihBulat, sentral diameter 6 mm, reflek (+) Iris/pupil Bulat sentral, diameter 3 mm, reflek (+)Dangkal, flare (+) COA Dangkal, jernihKesan jernih Lensa JernihSulit dinilai Fundus Dalam batas normalSulit dinilai Papila Dalam batas normalSulit dinilai Makula Dalam batas normalSulit dinilai Retina Dalam batas normal (digital) TIO Normalbebas MBO bebas

Diagnosis : OD Glaukoma Akut Sudut Tertutup PrimerTerapi :

Diamox 2 x 250 mg Timolol 0,5% Pilokarpin 2% Rencana tindakan bedah (trabekulektomi)

Panduan

Glaucoma is an acquired chronic optic neuropathy characterized by optic disk cupping and visual field loss. It is usually associated with elevated intraocular pressure. In the majority of cases, there is no associated ocular disease (primary glaucoma) (Table 11–1).

Table 11–1. Glaucoma Classified According to Etiology.

A. Primary glaucoma 3. Due to lens changes (phacogenic)

1. Open-angle glaucoma a. Dislocation

a. Primary open-angle glaucoma (chronic open-angle glaucoma, chronic simple glaucoma)

b. Intumescence

b. Normal-tension glaucoma (low-tension glaucoma)

c. Phacolytic

2. Angle-closure glaucoma 4. Due to uveal tract changes

a. Acute a. Uveitis

b. Subacute b. Posterior synechiae (seclusio pupillae)

c. Chronic c. Tumor

d. Plateau iris d. Ciliary body swelling

B. Congenital glaucoma 5. Iridocorneoendothelial (ICE) syndrome

1. Primary congenital glaucoma 6. Trauma

2. Glaucoma associated with other developmental ocular abnormalities

a. Hyphema

a. Anterior chamber cleavage syndromes b. Angle contusion/recession

Axenfeld's syndrome c. Peripheral anterior synechiae

Reiger's syndrome 7. Postoperative

Peter's syndrome a. Ciliary block glaucoma (malignant glaucoma)

b. Aniridia b. Peripheral anterior synechiae

3. Glaucoma associated with extraocular developmental abnormalities

c. Epithelial downgrowth

a. Sturge-Weber syndrome d. Following corneal graft surgery

b. Marfan's syndrome e. Following retinal detachment surgery

c. Neurofibromatosis 1 8. Neovascular glaucoma

d. Lowe's syndrome a. Diabetes mellitus

e. Congenital rubella b. Central retinal vein occlusion

C. Secondary glaucoma c. Intraocular tumor

1. Pigmentary glaucoma 9. Raised episcleral venous pressure

2. Exfoliation syndrome a. Carotid-cavernous fistula

b. Sturge-Weber syndrome

10. Steroid-induced

D. Absolute glaucoma: The end result of any uncontrolled glaucoma is a hard, sightless, and often painful eye.

About 60 million people have glaucoma. An estimated 3 million Americans are affected, and of these cases, about 50% are undiagnosed. About 6 million people are blind from glaucoma, including approximately 100,000 Americans, making it the leading cause of preventable blindness in the United States. Primary open-angle glaucoma, the most common form among blacks and whites, causes insidious asymptomatic progressive bilateral visual loss that is often not detected until extensive field loss has already occurred. Blacks are at greater risk than whites for early onset, delayed diagnosis, and severe visual loss. Angle-closure glaucoma accounts for 10–15% of cases in whites. This percentage is much higher in Asians and in Inuit. Primary angle-closure glaucoma may account for over 90% of bilateral blindness due to glaucoma in China. Normal-tension glaucoma is the most common type in Japan.

The mechanism of raised intraocular pressure in glaucoma is impaired outflow of aqueous resulting from abnormalities within the drainage system of the anterior chamber angle (open-angle glaucoma) or impaired access of aqueous to the drainage system (angle-closure glaucoma) (Table 11–2). Treatment is directed toward reducing the intraocular pressure and, when possible, correcting the underlying cause. Although in normal-tension glaucoma intraocular pressure is within the normal range, reduction of intraocular pressure may still be beneficial.

Table 11–2. Glaucoma Classified According to Mechanism of Intraocular Pressure Rise.

A. Open-angle glaucoma B. Angle-closure glaucoma

1. Pretrabecular membranes: All of these may progress to angle-closure glaucoma due to contraction of the pretrabecular membranes.

1. Pupillary block (iris bombé)

a. Neovascular glaucoma a. Primary angle-closure glaucoma

b. Epithelial downgrowth b. Seclusio pupillae (posterior synechiae)

c. ICE syndrome c. Intumescent lens

2. Trabecular abnormalities d. Anterior lens dislocation

a. Primary open-angle glaucoma e. Hyphema

b. Congenital glaucoma 2. Anterior lens displacement

c. Pigmentary glaucoma a. Ciliary block glaucoma

d. Exfoliation syndrome b. Central retinal vein occlusion

e. Steroid-induced glaucoma c. Posterior scleritis

f. Hyphema d. Following retinal detachment surgery

g. Angle contusion or recession 3. Angle crowding

h. Iridocyclitis (uveitis) a. Plateau iris

i. Phacolytic glaucoma b. Intumescent lens

3. Posttrabecular abnormalities c. Mydriasis for fundal examination

a. Raised episcleral venous pressure 4. Peripheral anterior synechiae

a. Chronic angle closure

b. Secondary to flat anterior chamber

c. Secondary to iris bombé

d. Contraction of pretrabecular membranes

Intraocular pressure can be reduced by decreasing aqueous production or increasing aqueous outflow, using medical, laser, or surgical treatments. Medications, usually administered topically, are available to reduce aqueous production or increase aqueous outflow. Surgically bypassing the drainage system is useful in most forms of glaucoma if there is a failure to respond to medical treatment. In recalcitrant cases, laser, cryotherapy, or diathermy can be used to ablate the ciliary body to reduce aqueous production. Improving access of aqueous to the anterior chamber angle in angle-closure glaucoma may be achieved by peripheral laser iridotomy or surgical iridectomy if the cause is pupillary block, miosis if there is angle crowding, or cycloplegia if there is anterior lens displacement. In the secondary glaucomas, consideration must always be given to treating the primary abnormality.

In all patients with glaucoma, the necessity for treatment and its effectiveness are assessed by regular determination of intraocular pressure (tonometry), inspection of optic disks, and measurement of visual fields.

The management of glaucoma is best undertaken by an ophthalmologist, but detection of asymptomatic cases is dependent on the cooperation and assistance of all medical personnel, particularly optometrists. Ophthalmoscopy to detect optic disk cupping and tonometry to measure intraocular pressure should be part of the routine ophthalmologic examination of all patients over 35 years of age. They are especially important in patients with a family history of glaucoma and in high-risk groups such as blacks, who should undergo regular screening every 2 years from age 35 and annually from age 50.

Physiology of Aqueous Humor

Intraocular pressure is determined by the rate of aqueous production and the resistance to outflow of aqueous from the eye.

Composition of Aqueous

The aqueous is a clear liquid that fills the anterior and posterior chambers of the eye. Its volume is about 250 L, and its rate of production, which is subject to diurnal variation, is about 2.5 L/min. The osmotic pressure is slightly higher than that of plasma. The composition of aqueous is similar to that of plasma except for much higher concentrations of ascorbate, pyruvate, and lactate and lower concentrations of protein, urea, and glucose.

Formation & Flow of Aqueous

Aqueous is produced by the ciliary body. An ultrafiltrate of p lasma produced in the stroma of the ciliary processes is modified by the barrier function and secretory processes of the ciliary epithelium. Entering the posterior chamber, the aqueous passes through the pupil into the anterior chamber (Figure 11–1) and then to the trabecular meshwork in the anterior chamber angle. During this period, there is some differential exchange of components with the blood in the iris.

Intraocular inflammation or trauma causes an increase in the protein concentration. This is called plasmoid aqueous and closely resembles blood serum.

Outflow of Aqueous

The trabecular meshwork is composed of beams of collagen and elastic tissue covered by trabecular cells that form a filter with a decreasing pore size as the canal of Schlemm is approached. Contraction of the ciliary muscle through its insertion into the trabecular meshwork increases pore size in the meshwork and hence the rate of aqueous drainage. Passage of aqueous into Schlemm's canal depends on cyclic formation of transcellular channels

in the endothelial lining. Efferent channels from Schlemm's canal (about 30 collector channels and 12 aqueous veins) conduct the fluid directly into the venous system. Some aqueous passes between the bundles of the ciliary muscle into the suprachoroidal space and then into the venous system of the ciliary body, choroid, and sclera (uveoscleral flow) (Figure 11–1).

The major resistance to aqueous outflow from the anterior chamber is the juxtacanalicular tissue adjacent to the endothelial lining of Schlemm's canal, rather than the venous system. But the pressure in the episcleral venous network determines the minimum level of intraocular pressure that can be achieved by medical therapy.

Pathophysiology of Glaucoma

The major mechanism of visual loss in glaucoma is retinal ganglion cell apoptosis, leading to thinning of the inner nuclear and nerve fiber layers of the retina and axonal loss in the optic nerve. The optic disk becomes atrophic, with enlargement of the optic cup (see below).

The pathophysiology of intraocular pressure elevation—whether due to open-angle or to angle-closure mechanisms—will be discussed as each disease entity is considered (see below). The effects of raised intraocular pressure are influenced by the time course and magnitude of the rise in intraocular pressure. In acute angle-closure glaucoma, the intraocular pressure reaches 60–80 mm Hg, resulting in acute ischemic damage to the iris with associated corneal edema and optic nerve damage. In primary open-angle glaucoma, the intraocular pressure does not usually rise above 30 mm Hg and retinal ganglion cell damage develops over a prolonged period, often many years. In normal-tension glaucoma, retinal ganglion cells may be susceptible to damage from intraocular pressures in the normal range, or the major mechanism of damage may be optic nerve head ischemia.

Clinical Assessment in Glaucoma

Tonometry

Tonometry is measurement of intraocular pressure. The most widely used instrument is the Goldmann applanation tonometer, which is attached to the slitlamp and measures the force required to flatten a fixed area of the cornea. Corneal thickness influences the accuracy of measurement. Intraocular pressure is overestimated in eyes with thick corneas and underestimated in eyes with thin corneas. This difficulty may be overcome by the Pascal dynamic contour tonometer. Other applanation tonometers are the Perkins tonometer and the Tono-Pen, both of which are portable, and the pneumatotonometer, which can be used with a soft contact lens in place when the cornea has an irregular surface. The Schiotz tonometer is portable and measures the corneal indentation produced by a known weight. (For further discussion of tonometry, see Chapter 2; for tonometer disinfection techniques, see Chapter 21.)

The normal range of intraocular pressure is 10–21 mm Hg (Figure 11–2). The distribution is Gaussian, but with the curve skewed to the right. In the elderly, average intraocular pressure is higher, giving an upper limit of 24 mm Hg. In primary open-angle glaucoma, 32–50% of affected individuals will have a normal intraocular pressure when first measured. Conversely, isolated raised intraocular pressure does not necessarily mean that the patient has primary open-angle glaucoma, since other evidence in the form of a glaucomatous optic disk or visual field changes is necessary for diagnosis. If the intraocular pressure is consistently elevated in the presence of normal optic disks and visual fields (ocular hypertension), the patient may be observed periodically as a glaucoma suspect.

Gonioscopy

The anterior chamber angle is formed by the junction of the peripheral cornea and the iris, between which lies the trabecular meshwork (Figure 11–3). The configuration of this angle—ie, whether it is wide (open), narrow, or closed—has an important bearing on the outflow of aqueous. The anterior chamber angle width can be estimated by oblique illumination with a penlight (Figure 11–4) or by slitlamp observation of the depth of the peripheral anterior chamber, but it is best determined by gonioscopy, which allows direct visualization of the angle structures (Figure 11–3). If it is possible to visualize the full extent of the trabecular meshwork, the scleral spur, and the iris processes, the angle is open. Being able to see only Schwalbe's line or a small portion of the trabecular meshwork means that the angle is narrow. Being unable to see Schwalbe's line means that the angle is closed.

Large myopic eyes have wide angles, and small hyperopic eyes have narrow angles. Enlargement of the lens with age narrows the angle and accounts for some cases of angle-closure glaucoma.

Optic Disk Assessment

The normal optic disk has a central depression—the physiologic cup—whose size depends on the bulk of the fibers

that form the optic nerve relative to the size of the scleral opening through which they must pass. In hyperopic eyes, the scleral opening is small, and thus the optic cup is small; the reverse is true in myopic eyes. Glaucomatous optic atrophy produces specific disk changes characterized chiefly by loss of disk substance—detectable as enlargement of the optic disk cup—associated with disk pallor in the area of cupping. Other forms of optic atrophy cause widespread pallor without increased disk cupping.

In glaucoma, there may be concentric enlargement of the optic cup or preferential superior and inferior cupping with focal notching of the rim of the optic disk (Figure 11–5). The optic cup also increases in depth as the lamina cribrosa is displaced backward. As cupping develops, the retinal vessels on the disk are displaced nasally (Figure 11–6). The end result of glaucomatous cupping is the so-called "bean pot" cup in which no neural rim tissue is apparent (Figure 11–7).

The "cup–disk ratio" is a useful way of recording the size of the optic disk in glaucoma patients. It is the ratio of cup size to disk diameter, eg, a small cup is 0.1 and a large cup 0.9. In the presence of visual field loss or elevated intraocular pressure, a cup–disk ratio greater than 0.5 or significant asymmetry between the two eyes is highly suggestive of glaucomatous atrophy.

Clinical assessment of the optic disk can be performed by direct ophthalmoscopy or by examination with the 78-diopter lens or special corneal contact lenses that give a three-dimensional view.

Other clinical evidence of neuronal damage in glaucoma is atrophy of the retinal nerve fiber layer, which precedes the development of optic disk changes. It is detectable by ophthalmoscopy or fundal photography, both aided by using red-free light, optical coherence tomography, scanning laser polarimetry, or scanning laser tomography.

Visual Field Examination

Regular visual field examination is essential to the diagnosis and follow-up of glaucoma. Glaucomatous field loss is not in itself specific, since it consists of nerve fiber bundle defects that may be seen in other forms of optic nerve disease; but the pattern of field loss, the nature of its progression, and the correlation with changes in the optic disk are characteristic of the disease.

Glaucomatous field loss involves mainly the central 30 degrees of field (Figure 11–8). The earliest change is baring of the blind spot. Contiguous extension into Bjerrum's area of the visual field—at 15 degrees from fixation—produces a Bjerrum scotoma and then an arcuate scotoma. Focal areas of more pronounced loss within Bjerrum's area are known as Seidel scotomas. Double arcuate scotomas—above and below the horizontal meridian—are often accompanied by a nasal step (of Roenne) because of differences in size of the two arcuate defects. Peripheral field loss tends to start in the nasal periphery as a constriction of the isopters. Subsequently, there may be connection to an arcuate defect, producing peripheral breakthrough. The temporal peripheral field and the central 5–10 degrees are affected late in the disease. Central visual acuity is not a reliable index of progress of the disease. In end-stage disease, there may be normal central acuity but only 5 degrees of visual field in each eye. In advanced glaucoma, the patient may have 20/20 visual acuity and be legally blind.

Various ways of testing the visual fields in glaucoma include the automated perimeter (for example, Humphrey, Octopus, or Henson), the Goldmann perimeter, the Friedman field analyzer, and the tangent screen. (For testing techniques, see Chapter 2.) Conventional automated perimetry, most commonly using the Humphrey perimeter, employs a white stimulus on a white background (white-on-white perimetry). Visual field defects are not detected until there is about 40% retinal ganglion loss. Refinements to detect earlier visual field changes include blue-on-yellow perimetry, also known as short-wavelength automated perimetry (SWAP), frequency-doubling perimetry (FDP), and high-pass resolution perimetry.

Treatment of Raised Intraocular Pressure

Medical Treatment

Suppression of Aqueous Production

Topical beta-adrenergic blocking agents may be used alone or in combination with other drugs. Timolol maleate 0.25% and 0.5%, betaxolol 0.25% and 0.5%, levobunolol 0.25% and 0.5%, metipranolol 0.3%, and carteolol 1% solutions twice daily and timolol maleate 0.1%, 0.25%, and 0.5% gel once daily in the morning are the currently available preparations. The major contraindications to their use are chronic obstructive airway disease—particularly asthma—and cardiac conduction defects. Betaxolol, with its relatively greater selectivity for 1

receptors, less often produces respiratory side effects, but it is also less effective at reducing intraocular pressure. Depression, confusion, and fatigue may occur with the topical beta-blocking agents. The frequency of systemic

effects and the availability of other agents has reduced the popularity of the beta-adrenergic blocking agents.

Apraclonidine (0.5% solution three times daily and 1% solution before and after laser treatment) is an 2-adrenergic agonist that decreases aqueous humor formation without effect on outflow. It is particularly useful for preventing rise of intraocular pressure after anterior segment laser treatment and can be used on a short-term basis in refractory cases. It is not suitable for long-term use because of tachyphylaxis (loss of therapeutic effect over time) and a high incidence of allergic reactions. Epinephrine and dipivefrin have some effect on aqueous production but are rarely used these days (see below).

Brimonidine (0.2% solution twice daily) is an -adrenergic agonist that primarily inhibits aqueous production and secondarily increases aqueous outflow. It may be used as a first-line or adjunctive agent, but allergic reactions are common.

Dorzolamide hydrochloride 2% solution and brinzolamide 1% (two or three times daily) are topical carbonic anhydrase inhibitors that are especially effective when employed adjunctively, although not as effective as systemic carbonic anhydrase inhibitors. The main side-effects are a transient bitter taste and allergic blepharoconjunctivitis. Dorzolamide is also available combined with timolol in the same solution.

Systemic carbonic anhydrase inhibitors—acetazolamide is the most widely used, but dichlorphenamide and methazolamide are alternatives—are used in chronic glaucoma when topical therapy is insufficient and in acute glaucoma when very high intraocular pressure needs to be controlled quickly. They are capable of suppressing aqueous production by 40–60%. Acetazolamide can be administered orally in a dosage of 125–250 mg up to four times daily or as Diamox Sequels 500 mg once or twice daily, or it can be given intravenously (500 mg). The carbonic anhydrase inhibitors are associated with major systemic side effects that limit their usefulness for long-term therapy.

Hyperosmotic agents influence aqueous production as well as dehydrate the vitreous body (see below).

Facilitation of Aqueous Outflow

The prostaglandin analogs—bimatoprost 0.003%, latanoprost 0.005%, and travoprost 0.004% solutions, each once daily at night, and unoprostone 0.15% solution twice daily—increase uveoscleral outflow of aqueous. They are highly effective first-line or adjunctive agents. In many countries but not the United States, latanoprost is available combined with timolol in the same solution for use once daily in the morning. All the prostaglandin analogs may produce conjunctival hyperemia, hyperpigmentation of periorbital skin, eyelash growth, and permanent darkening of the iris (particularly in green-brown and yellow-brown irides). These drugs have also been rarely associated with reactivation of uveitis and herpes keratitis and can cause macular edema in predisposed individuals.

Parasympathomimetic agents increase aqueous outflow by action on the trabecular meshwork through contraction of the ciliary muscle. Pilocarpine is not commonly used since the advent of prostaglandin analogs but can be useful in some patients. It is given as 0.5–6% solution instilled up to four times a day or as 4% gel instilled at bedtime. Carbachol 0.75–3% is an alternative cholinergic agent. Parasympathomimetic agents produce miosis with dimness of vision, particularly in patients with cataract, and accommodative spasm that may be disabling to younger patients. Retinal detachment is a serious but rare occurrence.

Epinephrine, 0.25–2% instilled once or twice daily, increases aqueous outflow with some decrease in aqueous production. There are several external ocular side effects, including reflex conjunctival vasodilation, adrenochrome deposits, follicular conjunctivitis, and allergic reactions. Dipivefrin is a prodrug of epinephrine that is metabolized intraocularly to its active state. Neither epinephrine nor dipivefrin should be used in eyes with narrow anterior chamber angles. Both agents have an adverse effect on the outcome of subsequent glaucoma drainage surgery.

Reduction of Vitreous Volume

Hyperosmotic agents render the blood hypertonic, thus drawing water out of the vitreous and causing it to shrink. This is in addition to decreasing aqueous production. Reduction in vitreous volume is helpful in the treatment of acute angle-closure glaucoma and in malignant glaucoma when anterior displacement of the crystalline lens (caused by volume changes in the vitreous or choroid) produces angle closure (secondary angle-closure glaucoma).

Oral glycerin (glycerol), 1 mL/kg of body weight in a cold 50% solution mixed with lemon juice, is the most commonly used agent, but it should be used with care in diabetics. Alternatives are oral isosorbide and intravenous urea or mannitol (see Chapter 3 for dosages).

Miotics, Mydriatics, and Cycloplegics

Constriction of the pupil is fundamental to the management of primary angle-closure glaucoma and the angle crowding of plateau iris. Pupillary dilation is important in the treatment of angle closure secondary to iris bombé due to posterior synechiae.

When angle closure is secondary to anterior lens displacement, cycloplegics (cyclopentolate and atropine) are used to relax the ciliary muscle and thus tighten the zonular apparatus in an attempt to draw the lens backward.

Primary Glaucoma

Primary Open-Angle Glaucoma

Primary open-angle glaucoma is the most common form in blacks and whites. In the United States, 1.29–2% of persons over age 40, rising to 4.7% of persons over age 75, are estimated to have primary open-angle glaucoma. The disease is four times more common and six times more likely to cause blindness in blacks. There is a strong familial tendency in primary open-angle glaucoma, and close relatives of affected individuals should undergo regular screening.

The chief pathologic feature of primary open-angle glaucoma is a degenerative process in the trabecular meshwork, including deposition of extracellular material within the meshwork and beneath the endothelial lining of Schlemm's canal. This differs from the normal aging process. The consequence is a reduction in aqueous drainage leading to a rise in intraocular pressure.

Juvenile-onset open-angle glaucoma (a familial primary open-angle glaucoma with early onset), about 5% of familial cases of primary open-angle glaucoma, and about 3% of nonfamilial cases of primary open-angle glaucoma are associated with mutations in the myocilin gene on chromosome 1.

Raised intraocular pressure precedes optic disk and visual field changes by months to years. Although there is a clear association between the level of intraocular pressure and the severity and rate of progression of visual loss, there is great variability between individuals in the effect on the optic nerve of a given pressure elevation. Some eyes tolerate elevated intraocular pressure without developing disk or field changes (ocular hypertension; see below); others develop glaucomatous changes with consistently "normal" intraocular pressure (low-tension glaucoma; see below). Nevertheless, higher levels of intraocular pressure are associated with greater field loss at presentation. When there is glaucomatous field loss on first examination, the risk of further progression is much greater. Since intraocular pressure is the only treatable risk factor, it remains the focus of therapy. There is strong evidence that control of intraocular pressure slows disk damage and field loss. For each 1-mm Hg reduction of intraocular pressure, there is an approximately 10% decreased risk of progression of glaucoma.

If there are extensive disk changes or field loss, it is advisable to reduce the intraocular pressure as much as possible, preferably to less than 15 mm Hg. A patient with only a suspicion of disk or field changes may need less vigorous treatment. In all cases, the inconveniences and possible complications of treatment must be considered. Many glaucoma patients are old and frail and may not tolerate vigorous treatment. In order to gain a perspective on the need for treatment, an initial period of observation without treatment may be necessary to determine the rate of progression of disk and field changes. There is no justification for subjecting an elderly patient to extremes of treatment when the likelihood of their developing significant visual loss during their lifetime is small.

Diagnosis

The diagnosis of primary open-angle glaucoma is established when glaucomatous optic disk or field changes are associated with elevated intraocular pressures, a normal-appearing open anterior chamber angle, and no other reason for intraocular pressure elevation. At least one-third of patients with primary open-angle glaucoma have a normal intraocular pressure when first examined, so repeated tonometry may be necessary before the diagnosis can be established.

Screening for Glaucoma

The major problem in detection of primary open-angle glaucoma is the absence of symptoms until relatively late in the disease. When patients first notice field loss, substantial optic nerve damage has already occurred. If treatment is to be successful, it must be started early in the disease, and this depends on an active screening program. Unfortunately, glaucoma screening programs are hampered by the unreliability of a single intraocular pressure measurement in the detection of primary open-angle glaucoma and the complexities of relying on optic disk or visual field changes. At present it is necessary to rely for early diagnosis predominantly on regular ophthalmologic

assessment of first-degree relatives of affected individuals.

Course & Prognosis

Without treatment, open-angle glaucoma may progress insidiously to complete blindness. If antiglaucoma drops control the intraocular pressure in an eye that has not suffered extensive glaucomatous damage, the prognosis is good (although visual field loss may progress despite normalized intraocular pressure). When the process is detected early, most glaucoma patients can be successfully managed medically. Trabeculectomy is a good option in patients who progress despite medical treatment (Figure 11–9).

Normal-Tension Glaucoma (Low-Tension Glaucoma)

Some patients with glaucomatous optic disk or visual field changes have an intraocular pressure consistently below 21 mm Hg. These patients have normal-tension or low-tension glaucoma. The pathogenesis may involve an abnormal sensitivity to intraocular pressure because of vascular or mechanical abnormalities at the optic nerve head, or this may be a purely vascular disease. There may be an inherited predisposition, normal-tension glaucoma being particularly common in Japan. A few families with normal tension glaucoma have an abnormality in the optineurin gene on chromosome 10. Some studies have shown an association with vasospasm. Disk hemorrhages are more frequently seen in normal-tension than in primary open-angle glaucoma and often herald progression of field loss.

Before the diagnosis of low-pressure glaucoma can be established, a number of entities must be excluded:

1. Prior episode of raised intraocular pressure, such as caused by anterior uveitis, trauma, or topical steroid therapy.2. Large diurnal variation in intraocular pressure with significant elevations, usually early in the morning.3. Postural changes in intraocular pressure with a marked elevation when lying flat.4. Intermittent elevations of intraocular pressure, such as in subacute angle closure.5. Underestimation of intraocular pressure due to reduced corneal thickness.6. Other causes of optic disk and field changes, including congenital disk abnormalities, inherited optic neuropathy, and acquired optic atrophy due to tumors or vascular disease.

Among patients diagnosed with normal-tension glaucoma, approximately 60% have progressive visual field loss, suggesting the possibility of acute ischemic events in the pathogenesis of those without progression. Reduction of intraocular pressure is beneficial in patients with progressive visual field loss, but this may not be achieved with medical therapy. Glaucoma drainage surgery with an antimetabolite may be required. The possibility of a vascular basis for normal-tension glaucoma has led to the use of systemic calcium channel blockers, but definite benefit from this intervention has yet to be demonstrated.

Ocular Hypertension

Ocular hypertension is elevated intraocular pressure without disk or field abnormalities and is more common than primary open-angle glaucoma. The rate at which such individuals develop glaucoma is approximately 1–2% per year. The risk increases with increasing intraocular pressure, increasing age, greater optic disk cupping, a positive family history for glaucoma, and perhaps myopia, diabetes mellitus, and cardiovascular disease. The development of disk hemorrhages in a patient with ocular hypertension also indicates an increased risk for development of glaucoma.

Patients with ocular hypertension are considered glaucoma suspects and should undergo regular monitoring (once or twice a year) of intraocular pressures, optic disks, and visual fields. It is likely that many ocular hypertensives who do not develop glaucoma have relatively thick corneas, producing an overestimation of intraocular pressure. Measurement of central corneal thickness may thus be useful to determine which patients do not require such careful monitoring. Conversely, many individuals with ocular hypertension may have glaucoma, but the retinal ganglion cell damage is not detectable with currently available techniques. Developments in perimetry and retinal nerve fiber layer imaging are addressing this issue.

Primary Angle-Closure Glaucoma

Primary angle closure occurs in anatomically predisposed eyes without other pathology. Elevation of intraocular pressure is a consequence of obstruction of aqueous outflow by occlusion of the trabecular meshwork by the peripheral iris. The condition may manifest as an ophthalmic emergency or may remain asymptomatic until visual loss occurs. The diagnosis is made by examination of the anterior segment and careful gonioscopy. Primary angle-closure glaucoma is the term that should be used only when primary angle closure has resulted in optic nerve

damage and visual field loss. Risk factors include increasing age, female gender, family history of glaucoma, and South-East Asian, Chinese, or Inuit ethnic background.

Acute Angle Closure

Acute angle closure ("acute glaucoma") occurs when sufficient iris bombé develops to cause occlusion of the anterior chamber angle by the peripheral iris. This blocks aqueous outflow, and the intraocular pressure rises rapidly, causing severe pain, redness, and blurring of vision. Angle closure develops in hyperopic eyes with preexisting anatomic narrowing of the anterior chamber angle, usually when it is exacerbated by enlargement of the crystalline lens associated with aging. The acute attack is often precipitated by pupillary dilation. This occurs spontaneously in the evenings, when the level of illumination is reduced. It may be due to medications with anticholinergic or sympathomimetic activity (eg, atropine for preoperative medication, antidepressants, nebulized bronchodilators, nasal decongestants, or tocolytics). It may occur rarely with pupillary dilation for ophthalmoscopy. If pupillary dilation is necessary in a patient with a shallow anterior chamber (easily detected by oblique illumination with a penlight [Figure 11–4]), it is best to rely on short-acting mydriatics, avoid constricting the pupil with pilocarpine, and advise the patient to seek attention immediately in the event of ocular pain or redness or increasingly blurred vision.

Clinical Findings

Acute angle closure is characterized by sudden onset of visual loss accompanied by excruciating pain, halos, and nausea and vomiting. Patients are occasionally thought to have acute gastrointestinal disease. Other findings include markedly increased intraocular pressure, a shallow anterior chamber, a steamy cornea, a fixed, moderately dilated pupil, and ciliary injection. It is important to perform gonioscopy on the fellow eye to confirm the anatomic predisposition to primary acute angle closure.

Differential Diagnosis

(See Differential Diagnosis of Common Causes of Inflamed Eye)

Acute iritis causes more photophobia than acute glaucoma. Intraocular pressure is usually not elevated; the pupil is constricted or irregular in shape and the cornea is usually not edematous. Marked flare and cells are present in the anterior chamber, and there is deep ciliary injection.

Acute conjunctivitis is usually bilateral, and there is little or no pain and no visual loss. There is discharge from the eye and an intensely inflamed conjunctiva but no ciliary injection. The pupillary responses and intraocular pressure are normal, and the cornea is clear.

Complications & Sequelae

If treatment is delayed, the peripheral iris may adhere to the trabecular meshwork (anterior synechiae), producing irreversible occlusion of the anterior chamber angle requiring surgery. Optic nerve damage is common.

Treatment

Acute angle closure is an ophthalmic emergency!

Treatment is initially directed at reducing the intraocular pressure. Intravenous and oral acetazolamide—along with topical agents, such as beta-blockers and apraclonidine, and, if necessary, hyperosmotic agents—will usually reduce the intraocular pressure. Pilocarpine 2% should be instilled one-half hour after commencement of treatment, by which time reduction of iris ischemia and lowering of intraocular pressure allow the sphincter pupillae to respond to the drug. Topical steroids may also be used to reduce secondary intraocular inflammation. Once the intraocular pressure is under control, laser peripheral iridotomy should be undertaken to form a permanent connection between the anterior and posterior chambers, thus preventing recurrence of iris bombé. This is most often done with the neodymium:YAG laser (see above). Surgical peripheral iridectomy is the conventional treatment if laser treatment is unsuccessful, but ALPI may be performed. The fellow eye should always undergo prophylactic laser iridotomy.

Subacute Angle Closure

The same etiologic factors operate in subacute as in acute angle closure except that episodes of elevated intraocular pressure are of short duration and are recurrent. The episodes of angle closure resolve spontaneously, but there is accumulated damage to the anterior chamber angle, with formation of peripheral anterior synechiae.

Subacute angle closure will occasionally progress to acute closure.

There are recurrent short episodes of unilateral pain, redness, and blurring of vision associated with halos around lights. Attacks often occur in the evenings and resolve overnight. Examination between attacks may show only a narrow anterior chamber angle with peripheral anterior synechiae. The diagnosis can be confirmed by gonioscopy. Treatment consists of laser peripheral iridotomy.

Chronic Angle-Closure Glaucoma

Patients with the anatomic predisposition to anterior-chamber angle closure may never develop episodes of acute rise in intraocular pressure but form increasingly extensive peripheral anterior synechiae accompanied by a gradual rise in intraocular pressure. These patients present in the same way as those with primary open-angle glaucoma, often with extensive visual field loss in both eyes. Occasionally, they have attacks of subacute angle closure.

On examination, there is elevated intraocular pressure, narrow anterior chamber angles with variable amounts of peripheral anterior synechiae, and optic disk and visual field changes.

Laser peripheral iridotomy should always be undertaken as the first step in the management of these patients. Intraocular pressure is then controlled medically if possible, but the extent of peripheral anterior synechia formation and sluggish outflow through the remaining trabecular meshwork make pressure control very difficult, so that drainage surgery is often required. Cataract extraction with intraocular lens implantation can be effective in controlling the intraocular pressure, provided no more than two quadrants of synechial angle closure are present. Epinephrine and strong miotics must not be used unless peripheral iridotomy or iridectomy has been performed because they will accentuate angle closure.

Plateau IrisPlateau iris is an uncommon condition in which the central anterior chamber depth is normal but the anterior chamber angle is very narrow because of an anterior position of the ciliary processes. Such an eye has little pupillary block, but dilation will cause bunching up of the peripheral iris, occluding the angle (angle crowding), even if peripheral iridotomy or iridectomy has been performed. Affected individuals present with acute angle closure at a young age, with recurrences after peripheral laser iridotomy or surgical iridectomy. Long-term miotic therapy or laser iridoplasty is required.

TUJUAN PEMBELAJARAN

Pada akhir diskusi, mahasiswa diharapkan mampu:

1. menjelaskan anatomi, histologi telinga (luar, tengah, dan dalam)2. menjelaskan fisiologi pendengaran3. menjelaskan fisiologi tuba auditiva4. menjelaskan etiologi terjadinya Otitis Media Supuratuf Kronik (OMSK) 5. menjelaskan faktor risiko kekambuhan OMSK6. menjelaskan stadium beserta gejala dan tanda OMSK7. menjelaskan cara pemeriksaan garpu tala (metode Rhinne, Weber, dan Schwabach) dan interpretasinya8. Menjelaskan cara pemeriksaan telinga dengan menggunakan otoskop dan interpretasinya9. mengusulkan pemeriksaan penunjang untuk penegakkan diagnosis OMSK10. menjelaskan diagnosis banding OMSK11. menjelaskan penatalaksanaan OMSK12. mengidentifikasi komplikasi OMSK

Informasi

Seorang anak laki-laki umur 10 tahun datang ke dokter U diantar oleh ibunya dengan keluhan utama keluar cairan dari telinga kiri. Keluhan tersebut dirasakan sejak 3 hari yang lalu. Cairan yang keluar berwarna putih kekuningan, kental dan tidak berbau. Ibu pasien mengeluh, pendengaran anaknya agak berkurang.

Kira-kira 3 bulan yang lalu, pasien pernah mengunjungi dokter U dengan sakit pada telinga kiri, disertai demam tinggi dan batuk pilek yang telah berlangsung selama 4 hari. Dokter U memberi 2 macam obat, namun tidak diminum karena pasien menolak minum obat.

Pemeriksaan Fisik :

SKENARIO VI

Keadaan umum : sedangKesadaran : Compos mentisSuhu axilla : 38,50C

Status Lokalis aurikula Kanan Kiri

Bentuk dan ukuran telinga normal normalTragus pain - +

Canalis auditorium eksterna kanan kiri

Serumen - -Otorrhoe - +Furunkel - -Edema - -Hiperemi - -Secret - Purulen, kental

Tes Pendengarankanan Kiri

Rinne + -Weber Lateralisasi ke kiriScwabach Sama dengan pemeriksa memanjang

Diagnosis pasien Otitis Media Supuratif Kronik aktif benigna dekstra

Terapi yang diberikan :Drainase secretAntibiotik topical 3x1 tetes

HEARING

The receptors of the cochlear duct provide us with a sense of hearing that enables us to detect the quietest whisper yet remain functional in a crowded, noisy room. The receptors responsible for auditory sensations are hair cells similar to those of the vestibular complex. However, their placement within the cochlear duct and the organization of the surrounding accessory structures shield them from stimuli other than sound.

In conveying vibrations from the tympanic membrane to the oval window, the auditory ossicles convert pressure fluctuations in air to pressure fluctuations in the perilymph of the cochlea. These fluctuations stimulate hair cells along the cochlear spiral. The frequency of the perceived sound is determined by which part of the cochlear duct is stimulated. The intensity (volume) of the perceived sound is determined by how many of the hair cells at that location are stimulated. We will now consider the mechanics of this remarkably elegant process.

The Cochlear Duct

In sectional view (Figures 17-27a , b and 17-28a , b ), the cochlear duct, or scala media, lies between a pair of perilymphatic chambers: the vestibular duct (scala vestibuli) and the tympanic duct (scala tympani). The vestibular and tympanic ducts are interconnected at the tip of the cochlear spiral. The outer surfaces of these ducts are encased by the bony labyrinth everywhere except at the oval window (the base of the vestibular duct) and the round window (the base of the tympanic duct).

The hair cells of the cochlear duct are located in a structure called the organ of Corti (Figures 17-27b and 17-28a, b ). This sensory structure sits on the basilar membrane, a membrane that separates the cochlear duct from

the tympanic duct. The hair cells are arranged in a series of longitudinal rows. They lack kinocilia, and their stereocilia are in contact with the overlying tectorial membrane. This membrane is firmly attached to the inner wall of the cochlear duct. When a portion of the basilar membrane bounces up and down, the stereocilia of the hair cells are pressed against the tectorial membrane and become distorted. The basilar membrane moves in response to pressure fluctuations within the perilymph. These pressure changes are triggered by sound waves arriving at the tympanic membrane. To understand this process, we must consider the basic properties of sound.

An Introduction to Sound

kanan kiriRetraksi - -Bulging - -Perforasi - + (tipe sentral)Conus of light + -

Membran timpani

Hearing is the detection of sound, which consists of waves of pressure conducted through a medium such as air or water. In air, each pressure wave consists of a region where the air molecules are crowded together and an adjacent zone where they are farther apart (Figure 17-29a ). These waves are sine waves—that is, S-shaped curves that repeat in a regular pattern—and travel through the air at about 1235 km/h (768 mph).

The wavelength of sound is the distance between two adjacent wave crests (peaks) or, equivalently, the distance between two adjacent wave troughs (Figure 17-29b ). Wavelength is inversely related to frequency, the number of waves that pass a fixed reference point in a given time. Physicists use the term cycles rather than waves. Hence the frequency of a sound is measured in terms of the number of cycles per second (cps), a unit called hertz (Hz). What we perceive as the pitch of a sound is our sensory response to its frequency. A high-frequency sound (high pitch, short wavelength) might have a frequency of 15,000 Hz or more; a very low-frequency sound (low pitch, long wavelength) could have a frequency of 100 Hz or less.

It takes energy to produce sound waves. When you strike a tuning fork, it vibrates and pushes against the surrounding air, producing sound waves whose frequency depends on the frequency of vibration. The harder you strike the tuning fork, the more energy you provide and the louder the sound. The loudness increases because the sound waves carry more energy away with them. The energy content, or power, of a sound determines its intensity, or volume. Intensity is reported in decibels. Table 17-2 indicates the decibel levels of familiar sounds.

When sound waves strike an object, their energy is a physical pressure. You may have seen windows move in a room in which a stereo is blasting. The more flexible the object, the more easily it will respond to sound pressure. Even soft stereo music will vibrate a sheet of paper held in front of the speaker. Given the right combination of frequencies and intensities, an object will begin to vibrate at the same frequency as the sound, a phenomenon called resonance. The greater the sound intensity, the greater the amount of vibration produced. For you to be able to hear, your thin, flexible tympanic membrane must vibrate in resonance with the sound waves.

The Hearing Process

The process of hearing can be divided into six basic steps, summarized in Table 17-3 and diagrammed in Figure 17-30a .

step 1: Sound waves arrive at the tympanic membrane. Sound waves enter the external auditory canal and travel toward the tympanic membrane. The orientation of the canal provides some directional sensitivity. Sound waves approaching the side of the head have direct access to the tympanic membrane on that side, whereas sounds arriving from another direction must bend around corners or pass through the auricle or other body tissues.

step 2: Movement of the tympanic membrane causes displacement of the auditory ossicles. The tympanic membrane provides the surface for sound collection, and it vibrates in resonance to sound waves with frequencies between approximately 20 and 20,000 Hz (in a young child). When the tympanic membrane vibrates, so do the malleus and, through their articulations, the incus and stapes. In this way, the sound is amplified.

step 3: Movement of the stapes at the oval window establishes pressure waves in the perilymph of the vestibular duct. Liquids are incompressible; if you push down on one part of a water bed, the water bed bulges somewhere else. Because the rest of the cochlea is sheathed in bone, pressure applied at the oval window can be relieved only at the round window. When the stapes moves inward, the round window bulges outward. As the stapes moves in and out, vibrating at the frequency of the sound arriving at the tympanic membrane, it creates pressure waves within the perilymph.

step 4: The pressure waves distort the basilar membrane on their way to the round window of the tympanic duct. The pressure waves established by movement of the stapes travel through the perilymph of the vestibular and tympanic ducts to reach the round window. In doing so, these pressure waves distort the basilar membrane. The location of maximum distortion varies with the frequency of the sound, owing to regional differences in the width and flexibility of the basilar membrane along its length. High-frequency sounds, which have a very short wavelength, vibrate the basilar membrane near the oval window. The lower the frequency of the sound, the longer the wavelength, and the farther from the oval window the area of maximum distortion will be (Figure 17-30b–d ). Thus, frequency information is translated into position information.

The amount of movement at a given location depends on the amount of force applied by the stapes. The amount of force is a function of the intensity of the sound. The louder the sound, the more the basilar membrane moves.

step 5: Vibration of the basilar membrane causes vibration of hair cells against the tectorial membrane. Vibration of the affected region of the basilar membrane moves hair cells against the tectorial membrane. This movement leads to the displacement of the stereocilia, which in turn opens ion channels in their cell membranes. A subsequent inrush of ions depolarizes the hair cells. The depolarization leads to neurotransmitter release and thus to the stimulation of sensory neurons.

The hair cells of the organ of Corti are arranged in several rows. A very soft sound may stimulate only a few hair cells in a portion of one row. As the intensity of a sound increases, not only do these hair cells become more active, but additional hair cellsÑat first in the same row, and then in adjacent rowsÑare stimulated as well. The number of hair cells responding in a given region of the organ of Corti thus provides information on the intensity of the sound.

step 6: Information about the region and intensity of stimulation is relayed to the CNS over the cochlear branch of the vestibulocochlear nerve (N VIII). The cell bodies of the bipolar sensory neurons that monitor the cochlear hair cells are located at the center of the bony cochlea in the spiral ganglion (Figure 17-28a ). From there, the information is carried by N VIII to the cochlear nuclei of the medulla oblongata for subsequent distribution to other centers in the brain.

Auditory Pathways

Hair cell stimulation activates sensory neurons whose cell bodies are in the adjacent spiral ganglion. Their afferent fibers form the cochlear branch of the vestibulocochlear nerve (N VIII) (Figure 17-31 ). These axons enter the medulla oblongata, where they synapse at the cochlear nucleus. From there, the information crosses to the opposite side of the brain and ascends to the inferior colliculus of the mesencephalon. This processing center coordinates a number of responses to acoustic stimuli, including auditory reflexes that involve skeletal muscles of the head, face, and trunk. These reflexes automatically change the position of your head in response to a sudden loud noise; you usually turn your head and your eyes toward the source of the sound.

Before reaching the cerebral cortex and your conscious awareness, ascending auditory sensations synapse in the medial geniculate nucleus of the thalamus. Projection fibers then deliver the information to the auditory cortex of the temporal lobe. Information travels to the cortex over labeled lines: High-frequency sounds activate one portion of the cortex, and low-frequency sounds activate another. In effect, the auditory cortex contains a map of the organ of Corti. Thus, frequency information, translated into position information on the basilar membrane, is projected in this form onto the auditory cortex. There, it is interpreted to produce your subjective sensation of pitch.

An individual whose auditory cortex is damaged will respond to sounds and have normal acoustic reflexes, but sound interpretation and pattern recognition will be difficult or impossible. Damage to the adjacent association area leaves the ability to detect the tones and patterns but produces an inability to comprehend their meaning.

Auditory Sensitivity

Our hearing abilities are remarkable, but it is difficult to assess the absolute sensitivity of the system. The range from the softest audible sound to the loudest tolerable blast represents a trillionfold increase in power. The receptor mechanism is so sensitive that, if we were to remove the stapes, we could in theory hear air molecules bouncing off the oval window. We never use the full potential of this system, because body movements and our internal organs produce squeaks, groans, thumps, and other sounds that are tuned out by central and peripheral adaptation. When other environmental noises fade away, the level of adaptation drops and the system becomes increasingly sensitive. For example, when you relax in a quiet room, your heartbeat seems to get louder and louder as the auditory system adjusts to the level of background noise.

Young children have the greatest hearing range: They can detect sounds ranging from a 20-Hz buzz to a 20,000-Hz whine. With age, damage due to loud noises or other injuries accumulates. The tympanic membrane gets less flexible; the articulations between the ossicles stiffen; and the round window may begin to ossify. As a result, older individuals show some degree of hearing loss.

Otitis media ialah peradangan sebagian atau seluruh mukosa telinga bagian tengah, tuba Eustachius, antrum mastoid dan sel-sel mastoid. Otitis media terbagi atas otitis media supuratif dan otitis media non supuratif. Masing-masing mempunyai bentuk akut dan kronis. Pada beberapa penelitian, diperkirakan terjadinya otitis media yaitu 25% pada anak-anak. Infeksi umumnya terjadi dua tahun pertama kehidupan dan puncaknya pada tahun pertama masa sekolah1.

OTITIS MEDIA SUPURATIF KRONIKOMSK adalah stadium dari penyakit telinga tengah dimana terjadi peradangan kronis dari telinga tengah dan mastoid dan membran timpani tidak intak ( perforasi ) dan ditemukan sekret (otorea), purulen yang hilang timbul. Sekret mungkin encer atau kental, bening atau berupa nanah dan berlangsung lebih dari 2 bulan. Perforasi sentral adalah pada pars tensa dan sekitar dari sisa membran timpani atau sekurang-kurangnya pada annulus. Defek dapat ditemukan seperti pada anterior, posterior, inferior atau subtotal. Menurut Ramalingam bahwa OMSK adalah peradangan kronis lapisan mukoperiosteum dari middle ear cleft sehingga menyebabkan terjadinya perubahan-perubahan patologis yang ireversibel,2,4.

KLASIFIKASI OMSKOMSK dapat dibagi atas 2 tipe yaitu2,11 :1. Tipe tubotimpani = tipe jinak = tipe aman = tipe rhinogen.Penyakit tubotimpani ditandai oleh adanya perforasi sentral atau pars tensa dan gejala klinik yang bervariasi dari luas dan keparahan penyakit. Secara klinis penyakit tubotimpani terbagi atas:1.1. Penyakit aktifPada jenis ini terdapat sekret pada telinga dan tuli. Biasanya didahului oleh perluasan infeksi saluran nafas atas melalui tuba eutachius, atau setelah berenang dimana kuman masuk melalui liang telinga luar. Sekret bervariasi dari mukoid sampai mukopurulen1,2. 1.2. Penyakit tidak aktif` Pada pemeriksaan telinga dijumpai perforasi total yang kering dengan mukosa telinga tengah yang pucat. Gejala yang dijumpai berupa tuli konduktif ringan. Gejala lain yang dijumpai seperti vertigo, tinitus,atau suatu rasa penuh dalam telinga1,4.2. Tipe atikoantral = tipe ganas = tipe tidak aman = tipe tulangPada tipe ini ditemukan adanya kolesteatom dan berbahaya. Penyakit atikoantral lebih sering mengenai pars flasida dan khasnya dengan terbentuknya kantong retraksi yang mana bertumpuknya keratin sampai menghasilkan kolesteatom. Kolesteatom dapat dibagi atas 2 tipe yaitu :1,3

a. Kongenitalb. Didapat. Pada umumnya kolesteatom terdapat pada otitis media kronik dengan perforasi marginal. teori itu adalah2,5 :1. Epitel dari liang telinga masuk melalui perforasi kedalam kavum timpani dan disini ia membentuk kolesteatom ( migration teori menurut Hartmann); epitel yang masuk menjadi nekrotis, terangkat keatas. 2. Embrional sudah ada pulau-pulau kecil dan ini yang akan menjadi kolesteatom.3. Mukosa dari kavum timpani mengadakan metaplasia oleh karena infeksi (metaplasia teori menurut Wendt).4. Ada pula kolesteatom yang letaknya pada pars plasida ( attic retraction cholesteatom). 1. Perforasi sentralLokasi pada pars tensa, bisa antero-inferior, postero-inferior dan postero-superior, kadang-kadang sub total1,2,4. 2. Perforasi marginalTerdapat pada pinggir membran timpani dengan adanya erosi dari anulus fibrosus. Perforasi marginal yang sangat besar digambarkan sebagai perforasi total. Perforasi pada pinggir postero-superior berhubungan dengan kolesteatom1,2,4

3. Perforasi atikTerjadi pada pars flasida, berhubungan dengan primary acquired cholesteatoma1,2,4.V. EPIDEMIOLOGIPrevalensi OMSK pada beberapa negara antara lain dipengaruhi, kondisi sosial, ekonomi, suku, tempat tinggal yang padat, hygiene dan nutrisi yang jelek. Kebanyakan melaporkan prevalensi OMSK pada anak termasuk anak yang mempunyai kolesteatom, tetapi tidak mempunyai data yang tepat, apalagi insiden OMSK saja, tidak ada data yang tersedia7,9.

VI. ETIOLOGITerjadi OMSK hampir selalu dimulai dengan otitis media berulang pada anak, jarang dimulai setelah dewasa. Faktor infeksi biasanya berasal dari nasofaring (adenoiditis, tonsilitis, rinitis, sinusitis), mencapai telinga tengah melalui tuba Eustachius. Fungsi tuba Eustachius yang abnormal merupakan faktor predisposisi yang dijumpai pada anak dengan cleft palate dan Down’s syndrom. Adanya tuba patulous, menyebabkan refluk isi nasofaring yang merupakan faktor insiden OMSK yang tinggi di Amerika Serikat. Kelainan humoral (seperti hipogammaglobulinemia) dan cell-mediated (seperti infeksi HIV, sindrom kemalasan leukosit) dapat manifest sebagai sekresi telinga kronis1,2.Penyebab OMSK antara lain1,2,5:1. Lingkungan2. Genetik3. Otitis media sebelumnya.4. Infeksi15

5. Infeksi saluran nafas atas6. Autoimun7. Alergi8. Gangguan fungsi tuba eustachius.Beberapa faktor-faktor yang menyebabkan perforasi membran timpani menetap pada OMSK1,2 :· Infeksi yang menetap pada telinga tengah mastoid yang mengakibatkan produksi sekret telinga purulen berlanjut.· Berlanjutnya obstruksi tuba eustachius yang mengurangi penutupan spontan pada perforasi.· Beberapa perforasi yang besar mengalami penutupan spontan melalui mekanisme migrasi epitel.· Pada pinggir perforasi dari epitel skuamous dapat mengalami pertumbuhan yang cepat diatas sisi medial dari membran timpani. Proses ini juga mencegah penutupan spontan dari perforasi.Faktor-faktor yang menyebabkan penyakit infeksi telinga tengah supuratif menjadi kronis majemuk, antara lain10 :1. Gangguan fungsi tuba eustachius yang kronis atau berulang.a. Infeksi hidung dan tenggorok yang kronis atau berulang.

b. Obstruksi anatomik tuba Eustachius parsial atau total2. Perforasi membran timpani yang menetap.3. Terjadinya metaplasia skumosa atau perubahan patologik menetap lainya pada telinga tengah.4. Obstruksi menetap terhadap aerasi telinga atau rongga mastoid. 5. Terdapat daerah-daerah dengan sekuester atau osteomielitis persisten di mastoid.6. Faktor-faktor konstitusi dasar seperti alergi, kelemahan umum atau perubahan mekanisme pertahanan tubuh.

VII. PATOGENESISPatogensis OMSK belum diketahui secara lengkap, tetapi dalam hal ini merupakan stadium kronis dari otitis media akut (OMA) dengan perforasi yang sudah terbentuk diikuti dengan keluarnya sekret yang terus menerus 1,6. Perforasi sekunder pada OMA dapat terjadi kronis tanpa kejadian infeksi pada telinga tengah misal perforasi kering. Beberapa penulis menyatakan keadaan ini sebagai keadaan inaktif dari otitis media kronis1.

VIII. PATOLOGIOMSK lebih sering merupakan penyakit kambuhan dari pada menetap. Keadaan kronis ini lebih berdasarkan keseragaman waktu dan stadium dari pada keseragaman gambaran patologi. Secara umum gambaran yang ditemukan adalah:1. Terdapat perforasi membrana timpani di bagian sentral. 2. Mukosa bervariasi sesuai stadium penyakit3. Tulang-tulang pendengaran dapat rusak atau tidak, tergantung pada beratnya infeksi sebelumnya. 4. Pneumatisasi mastoid7

OMSK paling sering pada masa anak-anak. Pneumatisasi mastoid paling akhir terjadi antara 5-10 tahun. Proses pneumatisasi ini sering terhenti atau mundur oleh otitis media yang terjadi pada usia tersebut atau lebih muda. Bila infeksi kronik terusberlanjut, mastoid mengalami proses sklerotik, sehingga ukuran prosesus mastoid berkurang1.

IX. GEJALA KLINIS1. Telinga Berair (Otorrhoe)Sekret bersifat purulen atau mukoid tergantung stadium peradangan. Pada OMSK tipe jinak, cairan yang keluar mukopus yang tidak berbau busuk yang sering kali sebagai reaksi iritasi mukosa telinga tengah oleh perforasi membran timpani dan infeksi. Keluarnya sekret biasanya hilang timbul. Pada OMSK stadium inaktif tidak dijumpai adannya sekret telinga. Pada OMSK tipe ganas unsur mukoid dan sekret telinga tengah berkurang atau hilang karena rusaknya lapisan mukosa secara luas. Sekret yang bercampur darah berhubungan dengan adanya jaringan granulasi dan polip telinga dan merupakan tanda adanya kolesteatom yang mendasarinya. Suatu sekret yang encer berair tanpa nyeri mengarah kemungkinan tuberkulosis2.2. Gangguan PendengaranBiasanya dijumpai tuli konduktif namun dapat pula bersifat campuran. Beratnya ketulian tergantung dari besar dan letak perforasi membran timpani serta keutuhan dan mobilitas sistem pengantaran suara ke telinga tengah. Pada OMSK tipe maligna biasanya didapat tuli konduktif berat8

3. Otalgia (Nyeri Telinga)Pada OMSK keluhan nyeri dapat karena terbendungnya drainase pus. Nyeri dapat berarti adanya ancaman komplikasi akibat hambatan pengaliran sekret, terpaparnya durameter atau dinding sinus lateralis, atau ancaman pembentukan abses otak. Nyeri merupakan tanda berkembang komplikasi OMSK seperti Petrositis, subperiosteal abses atau trombosis sinus lateralis1,2.4. VertigoKeluhan vertigo seringkali merupakan tanda telah terjadinya fistel labirin akibat erosi dinding labirin oleh kolesteatom. Vertigo yang timbul biasanya akibat perubahan tekanan udara yang mendadak atau pada panderita yang sensitif keluhan vertigo dapat terjadi hanya karena perforasi besar membran timpani yang akan menyebabkan labirin lebih mudah terangsang oleh perbedaan suhu. Penyebaran infeksi ke dalam labirin juga akan meyebabkan keluhan vertigo. Vertigo juga bisa terjadi akibat komplikasi serebelum4.

X. TANDA KLINISTanda-tanda klinis OMSK tipe maligna3 :1. Adanya Abses atau fistel retroaurikular2. Jaringan granulasi atau polip diliang telinga yang berasal dari kavum timpani.3. Pus yang selalu aktif atau berbau busuk ( aroma kolesteatom)4. Foto rontgen mastoid adanya gambaran kolesteatom.XI. PEMERIKSAAN KLINIK

Pemeriksaan Radiologi.Proyeksi SchullerMemperlihatkan luasnya pneumatisasi mastoid dari arah lateral dan atas. Foto ini berguna untuk pembedahan karena memperlihatkan posisi sinus lateral dan tegmen3.

Proyeksi Mayer atau Owen, Diambil dari arah dan anterior telinga tengah. Akan tampak gambaran tulang-tulang pendengaran dan atik sehingga dapat diketahui apakah kerusakan tulang telah mengenai struktur-struktur3.Proyeksi StenverMemperlihatkan gambaran sepanjang piramid petrosus dan yang lebih jelas memperlihatkan kanalis auditorius interna, vestibulum dan kanalis semisirkularis. Proyeksi ini menempatkan antrum dalam potongan melintang sehingga dapat menunjukan adanya pembesaran akibat2,3

Proyeksi Chause IIIMemberi gambaran atik secara longitudinal sehingga dapat memperlihatkan kerusakan dini dinding lateral atik. Politomografi dan atau CT scan dapat menggambarkan kerusakan tulang oleh karena kolesteatom3. BakteriologiBakteri yang sering dijumpai pada OMSK adalah Pseudomonas aeruginosa, Stafilokokus aureus dan Proteus. Sedangkan bakteri pada OMSA Streptokokus pneumonie, H. influensa, dan Morexella kataralis. Bakteri lain yang dijumpai pada OMSK E. Coli, Difteroid, Klebsiella, dan bakteri anaerob adalah Bacteriodes sp1,2. 1. Bakteri spesifikMisalnya Tuberkulosis. Dimana Otitis tuberkulosa sangat jarang ( kurang dari 1% menurut Shambaugh). Pada orang dewasa biasanya disebabkan oleh infeksi paru yang lanjut. Infeksi ini masuk ke telinga tengah melalui tuba. Otitis media tuberkulosa dapat terjadi pada anak yang relatif sehat sebagai akibat minum susu yang tidak dipateurisasi3. 2. Bakteri non spesifik baik aerob dan anaerob.Bakteri aerob yang sering dijumpai adalah Pseudomonas aeruginosa, stafilokokus aureus dan Proteus sp. Antibiotik yang sensitif untuk Pseudomonas aeruginosa adalah ceftazidime dan ciprofloksasin, dan resisten pada penisilin, sefalosporin dan makrolid. Sedangkan Proteus mirabilis sensitif untuk antibiotik kecuali makrolid. Stafilokokus aureus resisten terhadap sulfonamid dan trimethoprim dan sensitif untuk sefalosforin generasi I dan gentamisin2

XII. PENATALAKSANAANPrinsip pengobatan tergantung dari jenis penyakit dan luasnya infeksi, dimana pengobatan dapat dibagi atas :1. Konservatif2. Operasi2,3

OMSK BENIGNA TENANGKeadaan ini tidak memerlukan pengobatan, dan dinasehatkan untuk jangan mengorek telinga, air jangan masuk ke telinga sewaktu mandi, dilarang berenang dan segera berobat bila menderita infeksi saluran nafas atas. Bila fasilitas memungkinkan sebaiknya dilakukan operasi rekonstruksi (miringoplasti, timpanoplasti) untuk mencegah infeksi berulang serta gangguan pendengaran.

OMSK BENIGNA AKTIFPrinsip pengobatan OMSK adalah3 :1.Membersihkan liang telinga dan kavum timpani.2.Pemberian antibiotika : – topikal antibiotik ( antimikroba)

- sistemik.

Pemberian antibiotik topikalPemberian antibiotik secara topikal pada telinga dan sekret yang banyak tanpa dibersihkan dulu, adalah tidak efektif. Bila sekret berkurang/tidak progresif lagi diberikan obat tetes yang mengandung antibiotik dan kortikosteroid.4 Mengingat pemberian obat topikal dimaksudkan agar masuk sampai telinga tengah, maka tidak dianjurkan antibiotik yang ototoksik misalnya neomisin dan lamanya tidak lebih dari 1 minggu. Cara pemilihan antibiotik yang paling baik dengan berdasarkan kultur kuman penyebab dan uji resistesni3.Antibiotika topikal yang dapat dipakai pada otitis media kronik adalah3 :1. Polimiksin B atau polimiksin EObat ini bersifat bakterisid terhadap kuman gram negatif, Pseudomonas, E. Koli Klebeilla, Enterobakter, tetapi resisten terhadap gram positif, Proteus, B. fragilis Toksik terhadap ginjal dan susunan saraf.2. NeomisinObat bakterisid pada kuma gram positif dan negatif, misalnya : Stafilokokus aureus, Proteus sp. Resisten pada semua anaerob dan Pseudomonas. Toksik terhadap ginjal dan telinga.3. KloramfenikolObat ini bersifat bakterisid

Pemberian antibiotik sistemikPemberian antibiotika tidak lebih dari 1 minggu dan harus disertai pembersihan sekret profus. Bila terjadi kegagalan pengobatan, perlu diperhatikan faktor penyebab kegagalan yang ada pada penderita tersebut. Antimikroba dapat dibagi menjadi 2 golongan. Golongan pertama daya bunuhnya tergantung kadarnya. Makin tinggi kadar obat, makin banyak kuman terbunuh, misalnya golongan aminoglikosida dengan kuinolon. Golongan kedua adalah antimikroba yang pada konsentrasi tertentu daya bunuhnya paling baik. Peninggian dosis tidak menambah daya bunuh antimikroba golongan ini, misalnya golongan beta laktam.

B. fragilis KlindamisinAntibiotika golongan kuinolon (siprofloksasin, dan ofloksasin) yaitu dapat derivat asam nalidiksat yang mempunyai aktifitas anti pseudomonas dan dapat diberikan peroral. Tetapi tidak dianjurkan untuk anak dengan umur dibawah

16 tahun. Golongan sefalosforin generasi III ( sefotaksim, seftazidinm dan seftriakson) juga aktif terhadap pseudomonas, tetapi harus diberikan secara parenteral. Terapi ini sangat baik untuk OMA sedangkan untuk OMSK belum pasti cukup, meskipun dapat mengatasi OMSK. Metronidazol mempunyai efek bakterisid untuk kuman anaerob. Menurut Browsing dkk metronidazol dapat diberikan dengan dan tanpa antibiotik ( sefaleksin dan kotrimoksasol) pada OMSK aktif, dosis 400 mg per 8 jam selama 2 minggu atau 200 mg per 8 jam selama 2-4 minggu1,2,6.

OMSK MALIGNAPengobatan untuk OMSK maligna adalah operasi. Pengobatan konservatif dengan medikamentosa hanyalah merupakan terapi sementara sebelum dilakukan pembedahan. Bila terdapat abses subperiosteal, maka insisi abses sebaiknya dilakukan tersendiri sebelum kemudian dilakukan mastoidektomi3.Ada beberapa jenis pembedahan atau tehnik operasi yang dapat dilakukan pada OMSK dengan mastoiditis kronis, baik tipe benigna atau maligna, antara lain3:1.Mastoidektomi sederhana ( simple mastoidectomy)2.Mastoidektomi radikal3.Mastoidektomi radikal dengan modifikasi4.Miringoplasti5.Timpanoplasti6.Pendekatan ganda timpanoplasti ( Combined approach tympanoplasty)

Tujuan operasi adalah menghentikan infeksi secara permanen, memperbaiki membran timpani yang perforasi, mencegah terjadinya komplikasi atau kerusakan pendengaran yang lebih berat, serta memperbaiki pendengaran. Pedoman umum pengobatan penderita OMSK adalah Algoritma berikut2,7.KOMPLIKASITendensi otitis media mendapat komplikasi tergantung pada kelainan patologik yang menyebabkan otore. Walaupun demikian organisme yang resisten dan kurang efektifnya pengobatan, akan menimbulkan komplikasi. biasanya komplikasi didapatkan pada pasien OMSK tipe maligna, tetapi suatu otitis media akut atau suatu eksaserbasi akut oleh kuman yang virulen pada OMSK tipe benigna pun dapat menyebabkan komplikasi1,2.Komplikasi intra kranial yang serius lebih sering terlihat pada eksaserbasiakut dari OMSK berhubungan dengan kolesteatom1,2.

A. Komplikasi ditelinga tengah :1. Perforasi persisten2. Erosi tulang pendengaran3. Paralisis nervus fasial

B. Komplikasi telinga dalam1. Fistel labirin2. Labirinitis supuratif3. Tuli saraf ( sensorineural)

C. Komplikasi ekstradural1. Abses ekstradural2. Trombosis sinus lateralis3. Petrositis

D. Komplikasi ke susunan saraf pusat1. Meningitis2. Abses otak3. Hindrosefalus otitis

Perjalanan komplikasi infeksi telinga tengah ke intra kranial harus melewati 3 macam lintasan1,2 :1. Dari rongga telinga tengah ke selaput otak2. Menembus selaput otak.3. Masuk kejaringan otak.