Diagnosa Banding Penurunan Kesadaran Manajemen

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DIAGNOSA BANDING PENURUNAN KESADARAN MANAJEMEN
Dipresentasikan oleh Jofizal Jannis | Neurologist| National Brain Centre
pada PIT VI IDI Kota Bogor | 10 Nopember 2013

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Diagnosa Banding Penurunan Kesadaran Manajemen

  1. 1. Jofizal Jannis Neurologist National Brain Centre
  2. 2. Kesadaran adalah : is the body’s state of arousal or awareness of self and environment Koma : keadaan tidak sadar total terhadap diri dan lingkungan meski di stimulasi dengan kuat. Diantara sadar dan koma terdapat variasi status gangguan kesadaran. Klinis dapat ditentukan dengan bedside.
  3. 3. OBJEKTIF • Dokter mampu melakukan stabilisasi, diagnosis, mengatasi dan evaluasi pasien koma. • Dokter dapat mengatur prioritas pendekatan secara berurutan
  4. 4. Objektif Primer • • • • • • Airway Breathing Circulation Terapi progresif cepat (koma hipoglikemik) Evaluasi TTIK atau lesi massa Terapi TTIK, kemungkinan intervensi bedah
  5. 5. Objektif Sekunder • Dokter mengenal perbedaan koma struktural dan metabolik toksik • Dokter mengerti dan mengenal • Koma • TTIK • Sindrom Herniasi • Tanda lesi massa supratentorial • Tanda lesi massa infra tentorial
  6. 6. Dua (2) komponen kesadaran : formasio retikularis dan hemisfer serebral Formasio retikularis : a diffuse collection of neurons that extends throughout the brainstem (terpusat pons. Dari mes, pons dan m.o). Reticular Activating System : a diffuse collection of neuron in the reticular formation, plays an essential role in keeping the concious brain. ARAS : Blocking jaras asending antara formatio reticular dan korteks serebri menyebabkan tidak sadar
  7. 7. Supra orbital Sternum Kuku jari Sendi temporo mandibular
  8. 8. WHAT YOUR FIND
  9. 9. PENILAIAN PENURUNAN KESADARAN PENURUNAN KESADARAN KUALITATIF APATIS SOMNOLEN KUANTITATIF SOPOR GLASGOW COMA SCALE KOMA EYES OPEN 4. Spontan 3. Bicara 2. Nyeri 1. None MOTORIK 6. Ikut Perintah 5.Nyeri lokal 4.Menolak 3.Fleksi 2.Ekstensi 1. None VERBAL 5. Orientasi baik 4. Bingung 3. Kata kata 2. Suara 1. None
  10. 10. DIAGNOSIS PENURUNAN KESADARAN KOMA STRUKTURAL KOMA METABOLIK TANDA LATERALISASI (+) LATERALISASI (-) Kelainan difus Ingat SAH
  11. 11. ETIOLOGI KOMA GANGGUAN METABOLIK GANGGUAN STRUKTURAL Kerusakan RAS Langsung Perdarahan Infark Trauma tumor Infeksi Tidak Langsung Herniasi Metabolisme energi Aktivitas neuronal membran Multifaktor Iskemi, anoksia, hipoksia Hipoglikemi Hiper/ hipotermia Imbalans elektrolit Gangguan asam basa Hiper/ hipoosmolar Kejang umum Kegagalan organ Hepatik Renal Pulmoner Pankreatik Keracunan Infeksi
  12. 12. Koma Struktural Selamat Meninggal Tidak Sadar Komplikasi Sadar Mati Otak Pemulihan PVS Disabilitas Menolak dibantu MCS Disabilitas ringan Disabiltas Berat
  13. 13. WHAT IT MEANS
  14. 14. Vaskular Infeksi Trauma Alkohol PENYEBAB PENURUNAN KESADARAN Metabolik Imunitas Neoplastik
  15. 15. Kesadaran (arousal) • Asending RAS, dari sisi bawah pons ke pons ke talamus ventromedial • Sel yang berasal dari sistem ini menduduki area paramedian di brainstem Korteks serebral TALAMUS HJPOTALAMUS RAS
  16. 16. Consciousness
  17. 17. Kesadaran normal
  18. 18. Wakefulness
  19. 19. Awareness
  20. 20. BRAIN DEATH
  21. 21. Minimally Conciousness
  22. 22. DIAGNOSIS DIFERENSIAL KOMA LOCK IN SYNDROME VEGETATIVE STATE PSIKIATRI
  23. 23. Koma
  24. 24. VEGETATIVE STATE
  25. 25. Vegetative
  26. 26. Vegetative state (coma vigil, apallic syndrome) Pasien tertolong dari koma, tapi berkembang keadaan persistent unresponsif, tapi sleep– wake cycles kembali. • Setelah cedera kepala berat, fungsi brainstem kenbali mengalami sleep–wake cycles, membuka mata respons terhadap stimuli verbal dan kontrol pernafasan normal. •
  27. 27. Lock-in Syndrome
  28. 28. Locked-in
  29. 29. Locked in syndrome • Pasien awake and alert, tapi tidak sanggup bergerak atau bicara • Lesi Pontine mempengaruhi pergerakan mata ke lateral dan kontrol gerak. • Lesi sering spare vertical eye movements and blinking.
  30. 30. Psikogenik unresponsif • Pasien, walau tampak tidak sadar, biasa menunjukkan beberapa respons stimuli eksternal • Refleks kornea menyebabkan kontraksi otot orbikularis okuli • Ditandai oleh resistensi gerak pasif tungkai dan tanda penyakit organik tidak ada
  31. 31. PENILAIAN KLINIS PENURUNAN KESADARAN PERNAPASAN PUPIL Soma (isokor) Anisokor Midriasis Miosis TENTUKAN SECARA KUALITATIF DAN KUANTITATIF N. KRANIAL N. Okuler N. Facial MOTORIK Lateralisasi
  32. 32. DIAGNOSIS PENURUNAN KESADARAN ANAMNESIS History Riwayat makan obat Trauma Infeksi PEMERIKSAAN FISIK Tekanan darah Suhu Pernapasan Sklera PEMERIKSAAN NEUROLOGI Lateralisasi
  33. 33. Keadaan Perubahan Level Kesadaran Gambaran Koma DVS Brain Death LOS Akinetik Mutisme Self awareness - - - + + Sleep wave cycle - + - + + Fungsi motorik - - - Terbatas +++ Fungsi pernafasan  + - + + EEG  Polimortik Teta Delta Slow  - ~ Nonspesific slow wave <50% <5% -   Cerebral metabolisme
  34. 34. BILA MENGALAMI DELIRIUM SEGERA ASES PENYEBAB NYERI RETENSIO URINE HIPOKSIA HIPOTENSI DEHIDRASI
  35. 35. Abnormalitas pernafasan dapat membantu lokalisasi tetapi tidak selalu dalam konteks tanda lain seperti hiperpnea refleks sentral (midbrainhipotalamus) Apneustik, kluster, ataksik,(pons bawah) Hilangnya pernafasan otomatis (medula)
  36. 36. Abnormalitas Penafasan Deskripsi Lokalisasi Cheyne – Stokes Pola pernafasan kresendo dekresendo diiluti oleh apnue atau hipobnea, menetap selama tidur Bihemisfer (unilateral / bilateral), atau brainstem Cluster Ireguler pernafasan diikuti periode apnue yang lamanya bervariasi Bihemisfer /pons Ataxic or irregular Kecepatan pernafasan yang tidak teratur irama dan amplitudo diputus oleh apnue Tidak terlokalisasi atau medula dorsomedial Apneustic Inspirasi panjang dengan 2-3 detik berhenti kemudian ekspirasi. Tekmentum lateral dari pons bawah Central neurogenetic hiperventilation Hiperventilasi terus terusan kecepatan pernafasana tidak melebihi 40 kali/menit Bihemisfer pons dan midbrain
  37. 37. Pernafasan cheyne stok Hiperventilasi neurogenik sentral apnestik Pernafasan cluster & pernafasan ataxic Apnoe
  38. 38. Spektrum abnormalitas pupil dan penyebab Pupil normal Anisokor di pupil karena herniasi Oval pupil (gambaran awal mati otak) Midriasis (ansietas, delirium, kejang, obat-obat seperti atrofin, NE, dopamin) Midposisi (mati otak, lesi mesenfalon) Sindrom Hordner Miosis (opioid, lesi pons akut, hiperkapni, hiperglikemi non ketotik
  39. 39. WHAT TO DO
  40. 40. Pendekatan DD Unresponsif ABCs Glucosa, ABG, Lytes, Mg, Ca, Tox, ammonia Y IV D50, narcan, Brainstem at tanda Fokal Y CT N Unconscious N Disfungsi otak difus Metabolik / infeksi Lesi fokal Tumor, ICH/SAH/ infark Pseudo-Coma Psikogenik, Lo oked-in, NM paralysis LP± CT
  41. 41. Koma Intubasi –ventilasi/stabilisasi tekanan darah Sindrom Neurologi Pencitraan otak CT otak CT otak Abnormal Hasil Penyebab Stroke TBI Bedah Evakuasi Kraniektomi Rx ICP Abnormal Normal Massa Tumor Pilihan pengobatan Intrinsik batang otak Jaringan Otak dan pergeseran batang otak Basilar embolus arteri ICH TBI Massa Trombolisis Pengambilan bekuan Perawatan medik Perawatan medik Biopsi Infeksi
  42. 42. Resusitasi, memakai ABC Neurologi N A B C D – – – – – Neck Airway Breathing Circulation Diabetes Drug E F G H I – – – – – Epilepsi Fever GCS Herniation Investigate
  43. 43. Manajemen Gangguan Kesadaran Kesadaran menurun
  44. 44. Neuroprotektan
  45. 45. Neuroproteksi Tujuan untuk melindungi jaringan otak yang hampir rusak. Beberapa obat yang pernah dipakai  Citicholin  Piracetam  Piritinol
  46. 46. Jaringan Saraf  Lipid : 51-54%  Komponen lipid terdiri:  Phospholipid : 28% (lecithins, cephalins & sphingomyelin)  Kolesterol : 10%  Cerebroside (galactolipids) : 7%  Lipid mengandung sulfur, aminolipid : 9%
  47. 47. Level lesithin pada trauma kapitis - Secara eksperimental - Pada sisi cedera : 3 hari pertama cedera terjadi penurunan lecithin - Pada sisi lain tidak terjadi perubahan
  48. 48. FARMAKODINAMIK SITIKHOLIN  Bekerja langsung pada SSP  Mengaktifkan for. retikularis di Batang Otak sehingga menurunkan ambang rangsang reaksi arousal untuk membantu membangkitkan kesadaran  Mengaktifkan fungsi pyramidal dan ekspiramidal yang tersisa  Menurunkan ambang rangsang evoke muscular discharge shg merangsang aktivitas system piramidal yang berkaitan dg fungsi motorik
  49. 49. Efek sitikholin pada CDP Kholin sinthetase endogen dan penggunaan FFA CDP Kholin (sitikholin) Sistidin kholin FOSFATIDIL KHOLIN MEMBRAN SEL FFA Sistidin CTP kholin FOSFORIL KHOLIN DYACYL GLYCEROL + SITIKHOLIN
  50. 50. Mekanisme kerja citikholin  Sebagai derivate asam nukleat melakukan biosintesis lecithin dan stabilisasi membran sel  Memperbaiki aktivitas membrane ATP ase  Mengaktifkan kembali metabolisme serebral  Memperbaiki sirkulasi serebral secara selektif  Pembentukan neurotransmitter  Mencegah akumulasi asam lemak toksik shg mencegah luas infark dan kerusakan jaringan
  51. 51. Terapeutik Window citikholin 24 – 48 jam  Citikholin mempunyai efek neuroproteksi  Mengurangi lesi pada membran saraf dengan cara meningkatkan sintesis fosfolipid dan mengurangi kadar asam lemak bebas  Beberapa studi membuktikan bahwa citikholin mempunyai.terapeutik window 24 – 48 jam
  52. 52. Treatment of acute cerebral infarction with a choline precursor in a multicenter A multicenter double-blind placebo-controlled study of cytidine 5'diphosphocholine (CDP-choline) was conducted to evaluate possible clinical benefits of the drug in patients with acute, moderate to severe cerebral infarction. The patients included also suffered from moderate to mild disturbances of consciousness, and all were admitted within 14 days of the ictus. Patients were allocated randomly to treatment with either CDP-choline (1,000 mg/day i.v. once daily for 14 days) or with placebo (physiological saline). One hundred thirty-three patients received CDP-choline treatment, and 139 received placebo. The group treated with CDP-choline showed significant improvements in level of consciousness compared with the placebo-treated group, and CDP-choline was an entirely safe treatment. (Stroke 1988; 19:211-216)
  53. 53. Oral Citicoline in Acute Ischemic Stroke An Individual Patient Data Pooling Analysis of Clinical Trials Treatment with oral citicoline within the first 24 hours after onset in patients with moderate to severe stroke increases the probability of complete recovery at 3 months. (Stroke. 2002;33:2850-2857.)
  54. 54. Citicoline Preclinical and Clinical Update 2009–2010 Abstract—Citicoline is a neuroprotectant and neurorestorative drug that is used in the treatment of acute ischemic stroke in some countries. The research with this compound continues. In this review, we focus on the latest publications or communications or both and on the major ongoing experimental and clinical projects involving citicoline in stroke recovery. (Stroke. 2011;42[suppl 1]:S36-S39.)
  55. 55. Citicoline in the treatment of acute ischaemic stroke: an international, randomised, multicentre, placebo-controlled study (ICTUS trial) Results 2298 patients were enrolled into the study from Nov 26, 2006, to Oct 27, 2011. 37 centres in Spain, 11 in Portugal, and 11 in Germany recruited patients. Of the 2298 patients who gave informed consent and underwent randomisation, 1148 were assigned to citicoline and 1150 to placebo. The trial was stopped for futility at the third interim analysis on the basis of complete data from 2078 patients. The fi nal randomised analysis was based on data for 2298 patients: 1148 in citicoline group and 1150 in placebo group. Global recovery was similar in both groups (odds ratio 1ÅE03, 95% CI 0ÅE86–1ÅE25; p=0ÅE364). No significant diff erences were reported in the safety variables nor in the rate of adverse events.
  56. 56. The Role of Citicoline in Neuroprotection and Neurorepair in Ischemic Stroke Advances in acute stroke therapy resulting from thrombolytic treatment, endovascular procedures, and stroke units have improved significantly stroke survival and prognosis; however, for the large majority of patients lacking access to advanced therapies stroke mortality and residual morbidity remain high and many patients become incapacitated by motor and cognitive deficits, with loss of independence in activities of daily living. Citicoline has therapeutic effects at several stages of the ischemic cascade in acute ischemic stroke and has demonstrated efficiency in a multiplicity of animal models of acute stroke. Long-term treatment with citicoline is safe and effective, improving post-stroke cognitive decline and enhancing patients’ functional recovery. Prolonged citicoline administration at optimal doses has been demonstrated to be remarkably well tolerated and to enhance endogenous mechanisms of neurogenesis and neurorepair contributing to physical therapy and rehabilitation.

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