BAB I PENDAHULUAN
1.1
Latar Belakang
Sepsis didefinisikan sebagai
respons tubuh terhadap penyakit infeksi
ditandai dengan disfungsi organ yang mengancam nyawa dan merupakan masalah kesehatan di dunia saat ini. Sepsis dimasukkan kedalam kategori penyakit darurat karena ada gangguan dalam pemasukkan oksigen dan nutrisi ke jaringan sehingga dibutuhkan penanganan kegawat daruratan segera. Hal tersebut yang menjadikan sepsis sebagai penyebab tersering perawatan pasien di unit perawatan intensif (ICU). Di Amerika insidensi sepsis berkisar 66-132 per per seratus ribu populasi. Sepsis berat hampir 25 % dirawat di ICU , umumnya diakibatkan usia lanjut, imunocompomise, imunocompomise, dan penyakit berat yang mendasarinya. mendasarin ya. Sepsis merupakan penyebab kematian kedua di ICU pada non-coronary disease. disease. Sepsis dapat mengenai berbagai kelompok umur. Pada dewasa, sepsis umumnya terdapat pada orang yang mengalami immunocompromise, yang immunocompromise, yang disebabkan karena adanya penyakit kronik maupun infeksi lainnya. Mortalitas sepsis di negara yang sudah berkembang menurun hingga 9%, namun tingkat mortalitas pada negara yang sedang berkembang, seperti Indonesia, masih tinggi yaitu 50-70% dan apabila berlanjut pada syok sepsis dan disfungsi organ multiple, multiple, angka mortalitasnya dapat mencapai 80%. 1.2
Rumusan Masalah
Dengan
berdasarkan
uraian
latar
belakang
diatas
maka
penulis
merumuskan masalah sebagai berikut : 1.
Bagaimana penegakkan diagnosis pada pasien laporan kasus?
2.
Bagaimana penanganan yang tepat pada pasien ini?
3.
Bagaimana prognosis pada pasien ini?
1
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1.3
Tujuan Penulisan
Berdasarkan rumusan masalah diatas maka didapatkan tujuan penulisan sebagai berikut:
Untuk mengetahui penegakkan diagnosis yang tepat pada pasien dengan sepsis
Untuk mengetahui penanganan yang tepat pada pasien dengan sepsis
Untuk mengetahui pada pasien dengan sepsis
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BAB II STATUS PASIEN
A. Identitas
Nama
: Ny. S
Umur
: 60 tahun
Alamat
: Dente teladas
Jenis Kelamin
: Perempuan
Ruang
: ICU
Diagnosis
: pneumonia dan syok sepsis
Tanggal Masuk RS
: 13 desember 2017
Tanggal Masuk ICU
: 16 desember 2017
Medical Record
: 315286
B. Anamnesis (Alloanamnesis)
Keluhan Utama
Penurunan kesadaran sejak siang hari Keluhan Tambahan
Pucat
Riwayat Penyakit Sekarang
Pasien datang ke ruang IGD RS.Jend. Ahmad Yani Metro rujukan dari RS Muhammadiyah Metro pada tanggal 13 Desember 2017 dengan keluhan penurunan kesadaran sejak siang hari, pusing disertai pucat. Sebelumnya keluarga pasien mengatakan bahwa pasien mengalami demam yang naik
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Metro dan dirawat kurang lebih selama 7 hari dan ada perbaikan sehingga dapat pulang kerumah. Setelah sekitar 2 minggu dirumah kemudian pasien mengalami penurunan kesadaran dan lemas dibawa ke RS Medika Bratasena dan dirujuk ke RS Muhammadiyah Metro disertai keluhan nyeri perut dan demam menggigil kemudian di Rujuk ke RS Jendral Ahmad Yani dengan penurunan kesadaran dan perut kembung.
Riwayat Anestesi
Riwayat hipertensi (-) Riwayat DM (+) Riwayat asma (-) Alergi makanan (-) Alergi obat (-) Riwayat merokok (-) Konsumsi alkohol (-) Gangguan pembekuan darah (-) Riwayat operasi sebelumnya (-)
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C. Pemeriksaan Fisik
Keadaan umum : tampak sakit sedang Berat badan
: 65 kg
Tinggi badan
: 150 cm
BMI
: 29 (overweight)
keadaran
: compos mentis, GCS 15
Tanda Vital
Tekanan darah : 100/60 mmHg Nadi
: 70x/menit
Pernafasan
: 22x/menit
Suhu
: 36,9°C
SpO2
: NK 97%-100%
Status Generalis
1) Kulit
:
warna kulit sawo matang, tidak ikterik, terdapat sianosispada
ekstrmitass bawah, turgor kulit buruk, capillary refill kurang kurang dari 2 detik dan teraba hangat. 2) Kepala : normosefali, rambut berwarna hitam, distribusi merata
Mata
: konjungtiva anemis (+/+), sklera ikterik (-/-), RCL
+/+, RCTL +/+, pupil isokor 2 mm/2 mm
Hidung
: deformitas (-), nyeri tekan (-), krepitasi (-), deviasi
septum (-), sekret (-/-)
Telinga
: Normotia (+/+), nyeri tekan (-/-), nyeri tarik (-/-),
sekret (-/-)
Mulut
: sudut bibir simetris, kering (+), sianosis (-), tidak
terdapat deviasi lidah
Tenggorokan : Trismus (-), arkus faring simetris, hiperemis (-), uvula di tengah (-)
3) Leher
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Palpasi
: tidak terdapat pembesaran KGB maupun kelenjar
tiroid, tidak terdapat deviasi trakea, tidak terdapat peningkatan JVP 4) Thoraks
Jantung -
Inspeksi
: tidak tampak iktus kordis
-
Palpasi
: iktus kordis tidak teraba
-
Perkusi
:
Batas atas kiri : ICS II garis parasternal sinistra bunyi redup Batas atas kanan : ICS II garis parasternal dekstra bunyi redup Batas bawah kiri : ICS V ± 1 cm medial garis midklavikula sinistra dengan bunyi redup Batas bawah kanan : ICS IV garis parasternal dekstra dengan bunyi redup
Auskultasi : Bunyi jantung I/II regular, murmur (-), gallop (-)
Pulmo -
Inspeksi
:
dinding
thoraks
simetris,
retraksi
otot-otot
pernapasan (-) -
Palpasi : simetris, vokal fremitus sama s ama kuat kanan dan kiri
-
Perkusi : sonor di kedua lapang paru
-
Auskultasi : suara napas vesikuler (+/+), ronki (-/-), wheezing (-/-)
5) Abdomen
Inspeksi
: perut datar, massa (-), pulsasi abnormal (-)
Auskultasi
: bising usus (+) normal
Perkusi
: timpani pada seluruh lapang abdomen, asites (-)
Palpasi
: supel, hepar dan lien tidak teraba, nyeri tekan (-),
massa (-) 6) Ekstremitas
terdapat jejas, bekas trauma, massa, dan sianosis (+/+)
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Pemeriksaan Fisik dan follow up (16 desember 2017)
a. Keadaan Umum
: Tampak sakit berat
b. Kesadaran
: Somnolen
c. Tanda Vital TD
: 80/50 mmHg
Suhu
: 36,50 C
Pernapasan
: 22 x/menit, reguler
Nadi
: 98 x/menit, reguler, tekanan cukup
SPO2
: NK 96%
(17 desember 2017)
a. Keluhan saat ini
: lemah badan
b. Keadaan Umum
: Tampak sakit berat, apatis
c. Tanda Vital TD
: 100/70 mmHg
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e. Leher
: tidak ditemukan pembesaran KGB, tidak ditemukan deviasi trakea, JVP normal
f. Thorax Anterior dan Posterior Normochest, bentuk dan gerak gerak simetris, tidak terdapat retraksi
Cor
Ictus cordis tidak terlihat dan teraba di ICS V linea midclavicula sinistra Batas jantung atas: ICS II Batas jantung kanan: ICS IV linea sternalis sinistra Batas jantung kiri: ICS V linea midclavicula sinistra Bunyi jantung I dan II normal, tidak ditemukan bunyi jantung III, Gallop (-), murmur (-) Cardiomegali (-)
Pulmo
Ekspansi dinding dada simetris, fremitus taktil dextra=sinistra Sonor di seluruh lapang paru
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Palpasi
: Nyeri tekan (-), Shifting dulness dulness (-), hepar tidak teraba, lien tidak teraba
Perkusi
: Timpani, pekak hepar (+)
h. Ekstremitas Ekstremitas atas dan bawah lengkap. Akral hangat dan tidak ditemukan edema.
(18 desember 2017)
a. Keluhan saat ini
: nyeri seluruh tubuh dan pusing
b. Keadaan Umum
: Tampak sakit sedang, compos mentis
c. Tanda Vital TD
: 100/60 mmHg
Suhu
: 36 0 C
Pernapasan
: 20 x/menit, reguler
Nadi
: 86 x/menit, reguler, tekanan cukup
SPO2
: NK 99%
d. Kepala
: normocephal, konjungtiva anemis, sklera tidak ikterik
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Cor
Ictus cordis tidak terlihat dan teraba di ICS V linea midclavicula sinistra Batas jantung atas: ICS II Batas jantung kanan: ICS IV linea sternalis sinistra Batas jantung kiri: ICS V linea midclavicula sinistra Bunyi jantung I dan II normal, tidak ditemukan bunyi jantung III, Gallop (-), murmur (-) Cardiomegali (-)
Pulmo
Ekspansi dinding dada simetris, fremitus taktil dextra=sinistra Sonor di seluruh lapang paru Vesikuler (+/+), rhonki (-/-), wheezing (-/-) g. Abdomen Inspeksi
: Datar
Auskultasi
: BU (+) N
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Pemeriksaan Penunjang
Darah Lengkap (13 desember 2017) Leukosit
: 22,12 x 103 /uL (H)
Eritrosit
: 1,42 x 106 /uL (L)
Hemoglobin
: 4,0 g/dL (LL)
Hematokrit
: 10,6 % (LL)
MCV
: 74,6 fL (L)
MCH
: 28,2 pg
MCHC
: 37,7 g/dL (H)
Trombosit
: 60 x 103 /uL (L)
Golda
:A+
Kimia Darah (13 desember 2017)
GDS
: 254 mg/dL (H)
Ureum
: 49,6 mg/dL (H)
Kreatinin
: 1,29 mg/dL (H)
Darah Lengkap (15 desember 2017) Leukosit
: 12,77 x 103 /uL (H)
Eritrosit
: 2,62 x 106 /uL (L)
Hemoglobin
: 7,0 g/dL (L)
Hematokrit
: 19,3 % (LL)
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Kimia Darah (15 desember 2017)
GDS
: 163 mg/dL (H)
Kimia Darah (16 desember 2017)
Ureum
: 76,1 mg/dL (H)
Kreatinin
: 1,21 mg/dL (H)
Albumin
: 1,79 mg/dL (L)
Imunologi (16 desember 2017) Hbsag
: non reaktif
Darah Lengkap (17 desember 2017) Leukosit
: 16,80 x 103 /uL (H)
Eritrosit
: 3,48 x 106 /uL
Hemoglobin
: 9,6 g/dL (L)
Hematokrit
: 27,6 % (L)
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Trombosit
: 23 x 103 /uL (LL)
Kimia Darah (18 desember 2017)
Albumin
: 2,34 mg/dL (L)
Foto BNO 3 posisi : (14 desember 2017) -
udara usus prominen
-
suspect large bowel obstruction
-
tak tampak batu radio opak
-
kompresi vertebrae thoraco lumbales
-
spondilosis VTH 1-VL 1
-
tak tampak pneumoperitoneum
USG abdomen : (18 desember 2017) - sludge pada vesica Felea - tak tampak kelainan pada hepar, lien, pancreas dan kedua ren
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BAB III TINJAUAN PUSTAKA
3.1
Definisi Sepsis
Surviving Sepsis Campaign (SSC) 2012, sepsis diartikan sebagai adanya infeksi yang disertai dengan manifestasi klinis dari infeksi sistemik. Sepsis juga merupakan komplikasi infeksi yang berpotensi mengancam nyawa. Sepsis berat merupakan keadaan sepsis yang diikuti dengan gangguan fungsi organ, hipotensi atau hipoperfusi jaringan. Sedangkan sepsis dengan hipotensi ialah sepsis dengan tekanan sistolik <90mmHg atau ratarata tekanan arteri (Mean Arterial Pressure) <70 mmHg atau penurunan tekanan sistolik >40mmHg. Perkembangan dari Multiple dari Multiple Organ Dysfunction / Dysfunction / Multiple Organ Failure (MODS/MOF) akan menyebabkan suatu keadaan yang dinamakan syok septik. Syok septik didefinisikan sebagai suatu keadaan kegagalan
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3.3
Etiologi Sepsis
Mayoritas kasus sepsis disebabkan oleh infeksi bakteri, beberapa disebabkan oleh infeksi jamur, dan sangat sedikit yang disebabkan oleh penyebab lain. Penyebab bakteri umum sepsis adalah basil gram negatif (misalnya, E. coli, P. aeruginosa, E. corrodens, corrodens , dan Haemophilus influenzae pada neonatus). Bakteri lain juga menyebabkan sepsis adalah S. aureus, Streptococcus Streptococcus spesies, spesies Enterococcus Enterococcus dan Neisseria. Neisseria. Namun ada sejumlah besar generasi bakteri yang telah diketahui menyebabkan sepsis. Spesies Candida adalah beberapa dari jamur yang paling sering menyebabkan sepsis. 3.4
Patofisiologi Sepsis
Baik bakteri gram positif maupun gram negatif dapat menimbulkan sepsis. Pada bakteri gram negatif yang berperan adalah lipopolisakarida (LPS). Suatu protein di dalam plasma, dikenal dengan LBP (Lipopolysacharide binding protein) yang disintesis oleh hepatosit, diketahui berperan penting dalam metabolisme LPS. LPS masuk ke dalam sirkulasi, sebagian akan diikat oleh faktor inhibitor dalam serum seperti lipoprotein, kilomikron
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akan mengaktivasi sel T dalam jumlah besar untuk memproduksi sitokin proinflamasi yang berlebih.
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Pada sepsis berbagai sitokin ikut berperan dalam proses inflamasi, yang terpenting adalah TNFTNF-α, α, IL-1, IL-1, IL-6, IL-8, IL-12 sebagai sitokin proinflamasi dan IL-10 sebagai s ebagai antiinflamasi. Pengaruh TNF-α TNF-α dan IL-1 IL-1 pada endotel menyebabkan permeabilitas endotel meningkat, ekspresi TF, penurunan
regulasi
trombomodulin
sehingga
meningkatkan
efek
prokoagulan, ekspresi molekul adhesi (ICAM-1, ELAM, V-CAM1, PDGF, hematopoetic growth factor , uPA, PAI-1, PGE2 dan PGI2, pembentukan NO, endothelin-1. endothelin-1.1 TNF-α, TNF-α, IL-1, IL-1, IL-6, IL-8 yang merupakan mediator primer akan merangsang pelepasan mediator sekunder seperti prostaglandin E 2 (PGE2), tromboxan A2 (TXA2), Platelet Activating Factor (PAF), peptida vasoaktif seperti bradikinin dan angiotensin, intestinal vasoaktif peptida seperti histamin dan serotonin di
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juga berkaitan dengan reaksi inflamasi karena dapat meningkatkan produksi sitokin proinflamasi, ekspresi molekul adhesi dan menghambat agregasi trombosit. Peningkatan sintesis NO pada sepsis berkaitan dengan renjatan septik yang tidak responsif dengan vasopresor.
d. Peran netrofil pada sepsis Pada keadaan infeksi terjadi aktivasi, migrasi dan ekstravasasi netrofil dengan pengaruh mediator kemotaktik. Pada keadaan sepsis, jumlah netrofil dalam sirkulasi umumnya meningkat, walaupun pada sepsis berat jumlahnya
dapat
menurun.
Walaupun
netrofil
penting
dalam
mengeradikasi kuman, namun pelepasan berlebihan oksidan dan protease oleh netrofil dipercaya bertanggung jawab terhadap kerusakan organ.
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dan mikrotrombus. Berbagai faktor lain yang ikut berperan adalah terdapatnya faktor humoral dalam sirkulasi ((myocardial myocardial depressant substance), substance), malnutrisi kalori-protein, translokasi toksin bakteri, gangguan pada eritrosit, dan efek samping dari terapi yang diberikan.
e. Tahap Perkembangan Sepsis
Infeksi Proses patologi yang disebabkan oleh invasi mikroorganisme patogenik ke jaringan tubuh yang yang normalnya steril.
Systemic inflammatory response syndrome (SIRS) syndrome (SIRS) Respons peradangan sistemik terhadap beragam serangan klinis yang berat. Respons ini berupa dua atau lebih dari kondisi-kondisi kondisi-kondisi berikut:
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3.5
Penegakkan Diagnosis Sepsis
a. Anamnesis Anamnesis mengenai riwayat penyakit akan memberikan informasi mengenai faktor resiko potensial terjadinya infeksi, berhubunagn dengan patogen spesifik pada area jaringan tertentu.
b. Pemeriksaan Fisis Pemeriksaan fisik meliputi keadaan umum pasien, tanda-tanda vital. Gambaran klasik sepsis berat adalah pasien hipermetabolik dengan temperatur
tinggi,
takikardia,
takipnea,
hiperdinamik, tekanan diastolik rendah.
sirkulasi
vasodilatasi
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(botol aerob dan anaerob), dengan satu diambil decara perkutaneus dan satu diambil vascular access device, device, jika device <48 jam digunakan. Darah ini dapat diambil bersamaan waktu jika diambil dari tempat yang berbeda. Kultur dapat dari urin, cerebrospinal fluid , luka, sekret pernafasan dan cairan tubuh lain yang mungkin menjadi penyebab infeksi. o
Gram stain Terutama untuk spesimen pernafasan, untuk menentukan adanya sel inflamatori.
o
Biomarker Level prokalsitonin dan C reactive protein meningkat untuk
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2. Variabel inflamasi -
Leukositosis (jumlah sel darah putih >12.000 µL)
-
Leucopenia (jumlah sel darah putih <4000 µL)
-
Jumlah sel darah putih normal disertai dengan >10% bentuk imatur
-
C-reactive protein plasma lebih dari 2 standar deviasi di atas nilai normal sesuai usia
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4. Kerusakan paru akut dengan PaO2/FiO2 <250 tanpa disertai dengan pneumonia sebagai sumber infeksi 5. Kerusakan paru akut dengan PaO2/FiO2 <200 disertai dengan pneumonia sebagai sumber infeksi 6. Kreatinin >2,0 mg/dL (178,8 µmol/L) 7. Bilirubin >2mg/dL (34,2 µmol/L)
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3.9
Tatalaksana Sepsis
Penatalaksanaan sepsis meliputi resusitasi inisial, terapi antimikroba yang sesuai, mengontrol sumber infeksi dengan tindakan drainase atau bedah bila diperlukan. Diperlukan pula terapi suportif, s uportif, seperti bila terjadi te rjadi respons imun maladaptif host terhadap infeksi dapat diberikan vasopresor dan inotropik, terapi suportif terhadap kegagalan organ, gangguan koagulasi koagulasi
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Untuk mencapai cairan yang adekuat pemberian cairan inisial kristaloid, minumun 30 ml/kg untuk dewasa dan tambahan albumin pada pasien yang membutuhkan cukup banyak kristaloid untuk mempertahankan cukup MAP. Sebaiknya menghindari hetactarh, karena koloid buatan tidak terbukti menguntungkan melainkan meningkatkan resiko gagal ginjal akut.
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- terapi antifungal empirik, seperti: echinocandin, triazoles (fluconazole, amfoterisin B). - Pemilihan terapi antibiotik definitif tergantung pada tipe patogen, karakteristik pasien, dan regimen terapi rumah sakit. Karena pasien dengan sepsis berat atau syok septik punya latar yang sedikit untuk menentukan terapi, maka terapi pilihan inisial harus spektrum luas
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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Trusted by over 1 million members
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