Catatan Residen Bedah Umum - Catatan Ilmu Bedah

CATATAN RESIDEN BEDAH
DIGESTIF - ONKOLOGI - ANAK - ORTHOPEDI - VASKULAR
HAPPY HEART TEAM - Edited by MIY

Terima kasih kepada teman - teman seperjuangan
“Happy Heart Team” Bedah UHJanuari 2019 - ASSASSIN
dr. Hans
dr. Uga
dr. Fitran
dr. Arfan
dr. Arief
dr. Deo
dr. Arham
dr. Fatma
dr. Hasnah
dr. Teguh
dr. Robert
dr. Firman
dr. Ikhlas

ANATOMI
1. KOLON :
A. STRUKTUR :
* 3 TAENIA : (MOL) MESOCOLICA, OMENTALIS, LIBERA
* Terdapat Haustra dan Incisura (Otot longitudinal dan sirkuler)
* Appendices Epiploica
* Tidak ada mucosal vili
B.PEMBAGIAN :
* Caecum berdiameter terbesar +/- 8.5 cm
* Ascenden terletak di retroperitoneum sepanjang 15 cm
* Transversum sepanjang 50 cm dan
mobile
* Descendens terletak di retroperitoneum
sepanjang 20 cm
* Sigmoid sepanjang 40 cm, diameter
tersempit 2.5 cm
C.DINDING : 6 Lapisan
1.Mukosa : Kripta Lieberkuhn
2.Muskularis Mukosa
3.Submukosa
4.Muskularis propria
5.Subsereosal fat
Arc of Riolan berjalan
6.Serosa dari A. colica media ke
A. Colica Kiri
D.VASKULARISASI
- MIDGUT → SMA ;- A.Ileokolika → A.Appendikularis,A. Caecalis Anterior & Posterior
- A. Kolika Dekstra → Colon Ascendens
- A. Kolika Media → Cabang kanan dan Kiri →Colon Transversum
- HINDGUT → IMA : - A. Kolika Sinistra → Cabang Ascenden → Distal transversum
→ Cabang Descenden → Colon Descenden
- A. Sigmoidalis
- A. Hemoroidalis Superior → Rektum Proximal
* Sepanjang tepi kolon terdapat A. Marginalis / Drummond
* Vena mengikuti arteri ke vena porta ( Hindgut melewati V.Splenica lalu ke Vena Porta)

E. LIMFATIK
- Aliran mengikuti vena
- KGB colon : - Epiploika (serosa kolon)
- Perikolika (1-2 cm luar kolon, drummond)
- Intermediate ( cabang utama a.mesentrica)
- Principal (SMA/IMA)
F. FISIOLOGI
- Metabolisme : pemecahan karbohidrat pada proximal, protein pada distal
- storage ; reservoir
- absorbsi air terutama pada proximal
- absorbsi Na dan Cl, Sekresi HCO3 dan K pada proximal.
2. REKTUM
- Batas atas/panjang : Batas fusi 2 taenia mesenterik dengan promontorium

- Pada Sigmoidoskopi : Jarak 15 cm dari anal verge
- Pembagian :
* 1/3 proximal : 12 cm dari anal verge, dibungkus peritoneum di anterior dan lateral
* 1/3 media : 6-12 cm dari anal verge, dibungkus peritoneum di anterior
* 1/3 distal : <6 cm , tidak terbungkus peritoneum
- Pada bagian posterior dibungkus fascia propria.
- Refleksi peritoneum +/- 11 cm dari anokutan di rektum media.
- Terdiri dari 5 lapisan : - Mukosa
- Muskularis mukosa
- Submukosa
- Muskularis propria
- Serosa-fascia perirektal
- VASKULARISASI :
- Rectum proximal : A. Hemoroidalis Superior cabang IMA
- Rectum Media dan Distal : A. Hemoroidalis media+inferior cabang dari A.
Iliaca Interna

- LIMFE :
Rectum proximal → KGB mesentrika inferior
Rectum media → KGB iliaca interna
Rectum Distal → iliaka interna dan inguinal
- INERVASI sekitar rektum :
Nervus Erigentes
Untuk ereksi dan
Nervus Hipogastrikus ejakulasi
Trunkus Nervus Simpatikus
- FISIOLOGI
* Defekasi :
* plexus myenterikus berperan dalam distensi rektum → peristaltik meningkat →
relaksasi sfingter ani
* Plexus sacralis parasimpatis → Reflex defekasi
- Anal canal : Distal dari M.Levator Ani

HERNIA
Dinding Canalis Inguinalis
- Anterior : Aponeurosis MOE
- Posterior : Fascia Transversalis
- Medial : Conjoint tendon - MOI + M. Transversus abdominis
- Inferior : Ligamentum Inguinale
- Superior : MOI + M. Transversus abdominis
Isi Canalis Inguinalis
- Funiculus Spermaticum : - Vas deferens
- A. Testicularis
- V. Testicularis
- A. Cremasterica
- Limfe
- N. Ilioinguinalis → Femoris proximal dan medial, scrotum dan radix penis (di
annulus)
- N. iliohipogastrik → Regio Pubis (di floor hernia)
- N. Genitofemoralis
Pada Cranio lateral tempat annulus internus yang merupakan bagian terbuka dari
aponeurosis musculus transversus abdominis sedangan annulus eksternus
merupakan bagian terbuka dari aponeurosis musculus obliqus externus.
Hernia direct/medial yang menonjol pada trigonum hasselbach, batas medial nya yaitu
rectus abdominis, tepi lateral nya arteri epigastrik inferior dan batas inferior nya
ligamentum inguinale.

Laparoscopy : TAPP , TEP
- TAPP : Trans Abdominal Pre Peritoneal
- TEP : Totally Extra Peritoneal

ILEUS OBSTRUKSI
Gangguan aliran normal usus akibat hambatan mekanik yang

mengakibatkan serangkaian masalah berupa gangguan cairan, imbalance
elektrolit akibat dari peningkatan tekanan intralumen.
PENINGKATAN TEKANAN INTRALUMEN

↓
MENEKAN SALURAN LIMFATIK PADA MUKOSA
↓
EDEM LIMFATIK
↓
PENINGKATAN TEKANAN HIDROSTATIK INTRALUMEN
↓
MENARIK CAIRAN ELEKTROLIT AND PROTEIN KE LUMEN USUS
↓
DEHIDRASI
↓
MUNTAH DAN GANGGUAN ABSORBSI MENYEBABKAN DEHIDRASI MAKIN
PARAH
↓
SIRKULASI MENURUN → SYOK HIPOVOLEMIK
↓
GANGGUAN PERFUSI
↓
METABOLISME ANAEROB
↓
ASAM LAKTAT MENINGKAT → ASIDOSIS METABOLIK
- Dehidrasi merangsang reabsorbsi bikarbonat pada tubulus proximal ginjal,

bikarbonat meningkat → Alkalosis metabolik
- Hipertensi vena terus menerus disertai peningkatan tekanan intralumen
menyebabkan penekanan makrovaskular dan mikrovaskular menyebabkan iskemia +
nekrosis yang menyebabkan perforasi.

CAUSA OBSTRUKSI :
EKSTRAMURAL / EKSTRINSIK :- Adhesi
- Hernia
- Karsinomatosis
- Endometriosis
- Volvulus
- Congenital Band
- Sindrom SMA
INTRAMURAL :- Malignancy
- Stenosis / striktur (Pasca anastomosis)
- Hematom (trauma, antikoagulan)
- Inflamasi (chron, divertikulitis)
- Polip
- Invaaginasi
- Hirschsprung
- Radiasi
INTRALUMEN : - Impaksi
- Polip
- Benda asing
- Gallstone ileus
- Mekonium
ONSET : Akut, Subakut, Kronis

Derajat : Parsial, komplit
Progresifitas : Open/close loop, Sederhana/Strangulasi

Anamnesis
1. Gejala Umum : Kembung / Gangguan buang air besar dan flatus
2. Progresifitas : - Onset Sejak kapan?
- Semakin memberat ?
- Sebelum nya ada gejala apa? Sudah minum obat diare?
- Apakah ada nyeri saat BAB? demam ? mual dan muntah ?
- Perubahan pola BAB ? Diare atau konstipasi?
- Feses berwarna hitam/berdarah? Disertai Lendir?
- Feses berukuran kecil seperti pensil atau kotoran kambing?
- Rasa tidak puas setelah BAB?
- Penurunan Berat Badan?
- Apakah ada benjolan di ketiak, bahu kiri, lipat paha atau perut?
3. Gejala Metastasis : - Nyeri kepala?
- Kejang?
- Kesadaran menurun?
- Sesak?
- Kuning?
- Nyeri tulang belakang?
- Hematuria ?
4. Riwayat : - Riwayat Pengobatan sebelumnya? Operasi atau radiasi?
- Riwayat penyakit sebelumnya? Komorbid?
- Riwayat Keluarga?
- Life style? Konsumsi daging merah, rendah serat, alkohol,
merokok
Gejala Khas pada Kolon Kanan : - Anemia yang tidak jelas sumbernya
- Lemas, penurunan berat badan
- Benjolan perut kanan
- Rasa tidak nyaman perut kanan
Gejala Khas pada kolon kiri : - Obstipasi, konstipasi, diare
- Diameter feses kecil/ feses kambing
- Gejala obstruksi

PEMERIKSAAN FISIK
1. STATUS GENERALIS : Sakit ringan/sedang/berat, gizi cukup, sadar

2. STATUS VITALIS
3. STATUS PERFORMANCE
4. HEAD TO TOE : Anemis, ikterik, dehidrasi (turgor, mulut kering), KGB
5. STATUS LOKALIS :
- INSPEKSI : a.Distensi abdomen
B. Bekas luka operasi
C. Massa abdomen
D. Darm steifung dan darm contour
E. Massa abdomen
- AUSKULTASI : - metalic sound
- peristaltik meningkat
- PERKUSI : - Timpani KGB :
INGUINAL (blummer) → RECTUM DISTAL
- PALPASI : - Nyeri tekan
SUPRAKLAVIKULA KIRI → VIRCHOW
- Nyeri lepas UMBILIKUS → SISTER MARY JOSEPH
Axilla Kiri - IRISH NODE
- Massa
- KGB
- RT : - Darah
- Tumor → batas atas dan bawah, ukuran, mobile, bentuk
- Skibala
RESEKTABILITAS :
- Ampula kolaps
FO ; MOBILE
- Nyeri FR ; FIXED RESEKTABLE
FNR ; UNRESEKTABLE
- Tonus sfingter ani

KLINIS :
- PROGRESIFITAS : Perubahan pola defekasi > 6 minggu
* Perdarahan (Hematokezia)
* Frekuensi BAB meningkat - sering pada colon ascenden
- INFILTRATIF :
* infiltratif colon dapat mengenai organ ; duodenum → melena
* infiltratif rektum :
- sfingter ani → nyeri anus konstan atau waktu BAB atau inkontinensia
- Vesika urinaria → Hematuria
- Ureter → Hidronefrosis
- Vagina → Fistula
- Prostat
- METASTASIS
* Hepar (60%) → Hepatomegali, Ikterus
* Paru (10%) → Batuk dan sesak
* Peritoneum
* Ovarium
* Tulang → Spine → Nyeri (sering pada rectum > colon)
* Otak → nyeri kepala, kejang, kesadaran menurun
* KGB Supraclavicula kiri (virchow node), Umbilicus (Sister mary node)
Metastasis dapat melalui beberapa jalur :
- Direct extension : *Sirkuler → Obstruksi
* Longitudinal
* Radier→Perkontinuitatum→infiltrasi organ sekitar
- Limfogen
- Hematogen : Vena porta → hepar
Vena Cava Inferior → Paru (rektum distal)
Pleksus Venosus Vertebra → Vertebra
Vena Hipogastrika → ovarium (rektum)
- Transperitoneal : IntraOp (iatrogenik)

- Intra Lumen → Feses (gravitasi), bila tumor proximal lebih besar dari
distal mungkin suatu metastase
- Serabut Saraf
COLON ASCENDEN COLON REKTUM

DESCENDEN
TIPE Besar, Fungating Kecil, Stenotik Infiltratif,
TUMOR Ulceratif
GEJALA Kolitis, Massa iliaca Obstruktif, Proktitis
dextra, Dull pain Kolik
supraumbilikal
DEFEKASI Diare Konstipasi Tenesmus,
Darah, Lendir
FECAL mikroskopis Mikro/makro makroskopis
BLOOD
ANEMIA Hampir selalu lambat lambat
KLINIS :
- Progresifitas : Hematokezia
Diare
BAB Kecil-Kecil
Tenesmus
Massa
Anemia
- Infiltrasi : Melena
Inkontinensia Alvi
Hematuria
Hidronefrosis
Nyeri BAB
- Metastasis : Hepar, Paru, Otak, Tulang, Peritoneum, KGB
- Faktor Resiko : Polip, IBD, Riwayat Keluarga, Riwayat radiasi
- Komorbid
- Life Style : Konsumsi daging, kurang serat, alkohol, merokok

COLON DESCENDENS MUDAH OBSTRUKSI KARENA ;
1. Tumor anuler/melingkar/skirus
2. Diameter colon kecil
3. Feses padat
COLON ASCENDENS JARANG OBSTRUKSI KARENA ;

1. Tinja masih cair
2. Diameter colon besar
3. Dinding tipis dan distensibel
4. Tumor polipoid sehingga penyerapan air terganggu dan muncul diare
5. Produksi mukus meningkat sehingga terjadi diare
Pada Ca. Rektum gejala tenesmus, dan kaliber feses mengecil, KGB biasanya
teraba pada inguinal.
LABORATORIUM :
- Persiapan operasi
- Sepsis Campaign : Laktat
Curiga bakteri : - procalcitonin, CRP, kultur
Curiga jamur : Galactomannan
- Kontrol elektrolit

Radiologi
- Foto polos abdomen 3 Posisi
- Usus halus
A. Dilatasi > 3 cm
B. Air fluid level >2.5 cm
C. Multiple air fluid level
D. Dilatasi gaster
E. Gas tidak sampai ke distal
F. String of pearl sign → posisi tegak
dan lateral
G. Herring bone

Kolon
A. Dilatasi kolon
B. Udara tidak sampai distal obstruksi
C. Kolaps kolon distal
D. Hilangnya haustra
E. Air fluid level
- CT scan bila diagnosis belum definitif, Non kontras → kontras

* Mencari zona transisi
* Halo sign : edem mukosa
* Dinding usus menebal >3mm
* Kongesti vena mesentrika
* Edem mesentrium
* Cairan bebas
* Pneumatosis
- FLUOROSKOPI : - pada pasien stabil
- Konservatif tidak berhasil
- Obstruksi parsial
- Kontras larut air (gastrografin)
- Kontras dalam rektum setelah 24 jam → resolusi spontan
COLON IN LOOP : Gambaran Stenosis, Stopping, Deviasi
Untuk melihat topografi, persiapan minimal, dan untuk melihat
level tumor (batas atas dan batas bawah).
- MRI : Kontras, lebih sensitif dibanding CT Scan.
NCCN initial workup/staging : Chest, Abdomen, Pelvic CT untuk evaluasi ekstensi

tumor atau infiltrasi jaringan sekitar dan menilai keterkaitan limfe node dan metastasis.
Bila tidak dapat CT kontras dapat dilakukan MRI dengan gadolinium based.
Bila tidak dapat dengan kontras, dilakukan MRI tanpa kontras/ CT Scan /PET Scan.
Rektum sebaiknya dilakukan MRI.

STAGING
Setelah diagnosis tegak → staging → tentukan resektabilitas & metastasis

- Xray Thorax
- Usg Abdomen
- CT Scan Kontras
→ KGB dan Resektabilitas
→ Nilai : *Kondisi tumor → lihat fat line tumor, nilai ekstensi, letak, batas
dan resektabilitas
* Infiltrasi → Kolon : Duodenum, hepar, gaster
Rektum : Buli, Ovarium, ureter
* Metastasis
- MRI : Bila kontraindikasi CT kontras, akurat untuk staging N
- PET SCAN : metastasis
TNM Colon :
T 1 - Submukosa
T 2 - Muskularis Propria
T 3 - Perikolorektal
T 4 - a) Peritoneum visera
b) Organ lain
N 1 - 1-3 KGB regional positif (≥ 0.2mm)
a) 1 KGB regional
b) 2-3 KGB regional
c) Tumor deposit pada subserosa, mesentrium, perikolik, perirectal
N 2 - ≥ 4 KGB
a)4-6 kgb
b)≥ 7 kgb
M1 - a) 1 organ tanpa metastasis peritoneum
b) 2 organ tanpa metastasi peritoneum
c) metastasis peritoneum

STADIUM :
1 ; T1-T2
2 : T3-T4
3 : N1,N2
4 : M1
High-Rrisk factors for recurrence : (exclusive of those cancers that are MSI-H):
- Poorly differentiated/undifferentiated histology
- Lymphatic/vascular invasion
- Bowel obstruction
- <12 lymph nodes examined
- Perineural invasion (PNI)
- Localized perforation;
- Close, indeterminate, positive margins; or high-tier tumor budding.

TNM REKTUM :
T1 ; Submukosa
T2 : Muskularis propria
T3 : Subserosa/ Mesorectal Fat/Pericolorectal
T4 : a) Peritoneum
B) Organ lain
N1 a) 1 lymph node
B. 2-3 Lymph node
C. Perirectal tissue/mesenterium
N2 a) 4-6 KGB
b. 7
M1 a: 1 organ
B: >1 organ
STADIUM
I ; T1,T2
II : T3,T4b
III : N1,N2
IV : M1

HISTOPATOLOGI
- Makroskopik : Jenis reseksi
Panjang reseksi
Lokasi Tumor
Bentuk Tumor
Ukuran Tumor
Kedalaman
Batas sayatan proximal dan distal
- Mikroskopik :
a) Tipe :
-Adenokarsinoma → Well / Moderate (low grade) / poorly differentiated ( High Grade)
-Signet Ring Cell Ca
-Squamous cell ca
-Undifferentiated Ca
-Carcinoid → Neuroendokrin dif. Baik
B) Derajat differensiasi / grading ;
WHO → I : kelenjar > 95% dari massa
II : Kelenjar 50-95%
III : Kelenjar 5-50% / Signet
IV : Kelenjar <5 %
C) Kedalaman :
- Mukosa
- Submukosa
- Muskularis propria
- Serosa
- Organ berdekatan
D) Jumlah KGB yang positif ( minimal 12 KGB yang diperiksakan)
E) Status Margin
F) Invasi Limfovaskular
G) Evaluasi patologi molekuler :
- KRAS ( Kirsten Rat Sarcoma Protooncogen)
* Bila (+) tidak respon dengan anti EGFR

* Bila (+) diterapi dengan anti VEGFR (Bevacizumab)
* Kombinasi FOLFOX/CAPEOX/FOLFIRI/FOLFOXIRI
- BRAF
* Bila (+) prognosis buruk
* terapi 1st line anti EGFR (Cetuximab)
* Kombinasi Folfox/Folfoxiri
- MSI (Microsatellite instability)
NCCN : dianjurkan periksa mutasi RAS dan BRAF pada pasien metastasis.

TERAPI
1. LOCOREGIONAL : - Operasi
- Radioterapi (Rektum)
- Kemoterapi
2. SISTEMIK : - Kemoterapi
- Target terapi : anti EGFR dan anti VEGFR
- Radioterapi
- Operasi (reseksi primer + metastasektomi)
- Paliatif
- TENTUKAN RESEKTABILITAS (STAGING)

→ Yes (Resektable) → Definitif → Reseksi En Block
→ No (St.3&4)→Neoadjuvant →konversi resektable→operasi
→ tidak konversi → sistemik / operasi bypass
NCCN 2014 & KKR 2014
- Ca. Colon :
Stadium 0 (TisNoMo) → Eksisi lokal/polipektomi/en bloc segmental
Stadium 1 (T1-2, N0, M0) → Colectomy → Anastomosis → tidak ct adj.
Stadium 2 (T3-4, N0, M0) →Low risk→Colectomy→Anastomosis→pertimbangkan
C
kemoterapi adjuvan
→ High Risk→ Colectomy→ Anastomosis→Kemo adjuvan
- Folfox atau
- Capeox
Stadium 3 (N1,N2) → Colectomy → Anastomosis → CT Adjuvan → FOLFOX atau
Cek MSI terutama colon kanan CAPEOX atau

Stadium 4 : Ada 3 pilihan pada metastasis yang resektable
A) Colectomy dan metastasectomy lanjut kemoterapi 6 bulan FOLFOX
atau CAPEOX
B) Kemoterapi +/- Targeting terapi 2-3 bulan, lanjut colectomy dan
metastasectomy dan kemoterapi short course
C) Colectomy lanjut kemoterapi +/- targeting terapi 2-3 bulan kemudian
metastasektomi dan kemoterapi short course.
Pada metastase yang unresektable :

- Kemoterapi +/- Targeting terapi +/- Colectomy/Diversi (bila resiko obstruksi)
dan evaluasi 2 bulan, bila resektable → colectomy + metastasektomi + kemoterapi
adjuvan. Bila tetap unresektable lanjut ke kemoterapi advanced disease.
Pada metastase peritoneal :

- Tanpa obstruksi = kemoterapi advanced disease
- Obstruksi = Bypass/ Colostomy / Colectomy lanjut kemoterapi advanced disease.
KEMOTERAPI NEOADJUVAN → Bila metastase → Cek Oncogen / mutasi ALL RAS,

BRAF, MSI → Target Terapi + FOLFOX/CAPEOX/FOLFOXIRI
↓
1/2 Siklus
↓
Lihat Respon Terapi
↓
Recist → Stable, Progresive, Partial, Complete

AGEN KEMOTERAPI
- Alkilating agent → Kerusakan DNA/menyebabkan kerusakan secara langsung
→ Mencegah pembelahan sel → Apoptosis sel kanker
* Alkilating klasik : Cyclophosphamide
* Nitrosureas : Camustine
* Misc. DNA binding : Carboplatin, Cisplatin
- Anti Metabolit → Spesifik pada siklus sel → fase S

→ Untuk fraksi pertumbuhan tinggi : methotrexate, capecitabine,
gemcitabine
-Antibiotik antitumor→merusak sintesi DNA/RNA,untuk tumor pertumbuhan lambat

* Bleomycin
* Doxorubicin
- Alkaloid → menghambat siklus mitosis ; vincristine, Taxane ( Paclitaxel, docitaxel)

- Topoisomerase inhibitor → Hambat transkripsi dan replikasi ; irinotecan.

KEMOTERAPI KOLOREKTAL
- 5 FU ( Fluorodeoxyuridine)
→ Analog pirimidine → hambat sintesis timin → golongan anti metabolit
* Efek samping bolus : ekstravasasi, penurunan cepat blood cell
- Leucovorin
→ Calcium Folinat
→ Diberikan Bersama 5FU meningkatkan efek terapi pada Ca. Colorectal
→Mengurangi efek toksik methotrexate
- Capecitabine
→ Pro drug fluoropirimidin yang di metabolisme menjadi 5FU dalam tiga proses
( golongan antimetabolit)
* cara pemberian : ditelan dengan air setelah makan, dosis 1000-1250 mg/m2 dalam
2x sehari selama 14 hari selang 7 hari kemudian diberikan lagi.
- Oxaliplatin
→ Golongan Platinum (anti alkilating), banyak efek samping
- Irinotekan
→ pada stadium lanjut, kombinasi dengan 5FU dan Leucovorin (FOLFIRI, FOLFOXIRI)
* Dosis 180 mg/m2 iv 2 minggu sekali.
TARGETING TERAPI
Menargetkan sel kanker tanpa mempengaruhi sel normal, mekanisme nya
memicu kematian sel tumor, membantu imun menghancurkan sel kanker, hentikan
pertumbuhan sel kanker, dan mengurangi asupan hormon pertumbuhan.
- Anti EGFR:Cetuximab →Ca.Colorectal metastatic (BRAF +)

- Anti VEGFR : Bevacizumab → KRAS (+)
- HER2 inhibitor : Transtuzumab
- MSI High : Pembrolizumab

CAPEOX :
Oxaliplatin 130 mg/m2 iv hari pertama
Capecitabine 1000mg/m2, 2 kali sehari, selama 14 hari, istirahat 7 hari
Tiap 3 minggu
Cetuximab : 500 mg/m2 iv hari pertama, siklus tiap 2 minggu

Bevacizumab : 7.5 mg/KgBB iv hari pertama, siklus 3 minggu
FOLFOXIRI : irinotecan 180 mg/m2 IV hari pertama, siklus tiap 2 minggu.
NCCN
- Colorectal non metastase
A) Tumor colon → Resektable → Kolektomi reseksi en bloc → Adjuvan Terapi
→ Unresektable → Sistemik Neoadjuvant
→ Polip → Margin bersih , Histologi baik → Observasi
Indikasi Adjuvan Terapi :
- Stadium 2 high risk
- Stadium 3 keatas
- PA mucinous dan SCC
Kriteria High Risk :
1. Klinis : A. Riwayat Obstruksi
B. Riwayat Perforasi
C. KGB yang diambil kurang dari 12
2. PA : A. Poorly differentiated / High Grade
B. Invasi limfovaskular
C. Margin tidak clear
D. Perineural invasion
B) Rektum → cT1N0 → Transanal local eksisi → High Risk → Kemoradiasi

→ cT1-2, N0 → Reseksi transabdominal → Adjuvant kemo

STADIUM PATOLOGIS
- Tis, cT1, N0, M0 → Observasi

cT2 N0 M0
(STADIUM 1)
- cT3N0M0 dan low risk (STADIUM 2 LOW RISK) → Observasi atau pertimbangkan
single agent capecitabine atau 5fu/leucovorin 6 bulan.
- cT3N0M0 atau T4 dan High Risk (STADIUM 2 HIGH RISK) → Adjuvant kemoterapi
FOLFOX 6 bulan atau CAPEOX 3 bulan atau single agent Capecitabine 6 bulan atau
5FU/Leucovorin 6 bulan.
High Risk : - MSS (Microsatellite Stability)
- T4
- Histopatologi tidak berdiferensiasi
- Invasi Limfovaskular
- Lesi perforasi lokal
- Margin dekat, tidak jelas
- Nodul < 12 KGB yang diambil
- Riwayat Obstruksi usus
STADIUM 3 :
- Resiko Rendah : pT1-3, N1 → FOLFOX 6 bulan, CAPEOX 3 bulan.
- Resiko Tinggi : pT4, N2 → FOLFOX 6 Bulan (kategori 1), CAPEOX 3-6 bulan
atau Capecitabine tunggal, 5fu/leucovorin bila tidak cocok oxaliplatin.
- T4b atau bulky node → Neoadjuvant FOLFOX/CAPEOX → Reseksi
- Ca. Colon metastatik → Cek biomarker KRAS/RAS, BRAF, HER2, MSI
- Metastasis hepar → tidak dianjurkan debulking (R1/R2), terapi operasi harus

mencapai R0, terapi lainnya berupa embolisasi vena porta, ablatif (TACE).

- RESEKTABEL METASTASIS :
A) Kolektomi dan reseksi metastasis 1 tahap/bertahap
B) Neoadjuvan 2-3 bulan (FOLFOX/ CAPEOX/FOLFIRI/FOLFOXIRI kemudian
lanjut kolektomi dan metastasektomi
C) Kolektomi kemudian kemoterapi 2-3 bulan
(FOLFOX/CAPEOX/FOLFIRI/FOLFOXIRI) kemudian lanjut metastasektomi
Lanjut adjuvan FOLFOX/CAPEOX/Capecitabine/5FU+Leucovorin selama 6

bulan
- UNRESECTABLE : Tidak dapat dilakukan CME

* CAPEOX / FOLFOX / FOLFOXIRI / FOLFIRI +/-
(Bevacizumab/Cetuximab/Panitumumab) → Evaluasi ulang 2 bulan
kemudian jika resektable lanjut operasi dan adjuvan sistemik terapi, jika
unresektable lanjut terapi sistemik FOLFOX/CAPEOX/ FOLFIRI/FOLFOXIRI
+/- Targeting Terapi.
- RESIDIF
* Tidak pernah kemoterapi → Reseksi → Adjuvan 6 bulan
FOLFOX/CAPEOX/5FU/Leucovorin
→ Unresektabel → Neoadjuvan 2-3 bulan
- Kapan kemoterapi adjuvan ; Segera setelah operasi, tidak lebih dari 8

minggu.
-NCCN first line → FOLFOX
FOLFOX VI ; - Oxaliplatin 85 mg/m2 iv (Tiap 2 minggu)
- Leucovorin 400 mg/m2 iv ( Tiap 2 minggu)
- 5FU 400 mg/m2 iv habis dalam 2 jam (Hari 1 Bolus)
- 5 FU 1200 mg/m2 (Hari 1 & 2 Kontiniu) Tiap 2 minggu
* Bedanya dengan FOLFOX VII, tidak ada bolus 5FU 400 mg di hari 1 pada
FOLFOX VII.

CAPECITABINE : 1000-1250 mg/m2 oral, 2x1, selama 14 hari, tiap 3 minggu
selama 24 minggu.
CAPEOX : - Oxaliplatin 130 mg/m2 iv hari 1

- Capecitabine 1000 mg/m2 oral, 2x1, 1-14 hari, tiap 3 minggu
selama 24 minggu, 8 Siklus.
5FU/Leucovorin : - Leucovorin 400 mg/m2 iv dalam 2 jam, diulang per

minggu selama 6 minggu
- 5FU 400mg/m2 iv bolus 1 jam setelah leucovorin, 6x
seminggu, 4 siklus tiap 8 minggu.
NCCN 2023 – Advanced or Metastatic

Initial therapy recommended :
- FOLFOX ± Bevacizumab (Bila RAS +) atau

- CAPEOX ± Bevacizumab (Bila RAS +) atau
- CAPEOX / FOLFOX ± Cetuximab/Panitumumab (Left Side Tumor Only
atau KRAS/NRAS/BRAF Wild Type) (WT – Wild Type = No Mutation)
- Atau FOLFIRI ± Bevacizumab
- Atau FOLFIRINOX ± Bevacizumab
- Atau FOLFIRI/FOLFIRINOX ± Cetuximab/Panitumumab (Left side tumor
atau Wild Type).

KEMORADIASI ;
REKTUM 5FU+RT
CAPECITABINE + RT
* Nilai CRM melalui MRI 5FU/LV + RT
- pT1 Low risk → Observasi
- pT1 High Risk → Reseksi transabdominal → lanjut kemo

(FOLFOX/CAPEOX/5FU+LV) + Radioterapi
→ Kemoradiasi (capecitabine + RT / 5FU + RT atau 5FU+LV+RT)

→ Reseksi → Adjuvan FOLFOX/CAPEOX
- pT3, N0, M0 (STADIUM 2) → Kemoradiasi long course 5FU + RT atau

Capecitabine + RT kemudian kemoterapi FOLFOX/CAPEOX atau Kemoterapi
Dahulu kemudian Kemoradiasi. Selama 12-16 minggu
Stadium 3
Terdapat beberapa pilihan terapi adjuvant
→ RT + 5FU-Leucovorin atau RT + Capecitabine long course 25 siklus lanjut

kemoterapi FOLFOX/CAPEOX.
→ Kemoterapi FOLFOX/CAPEOX kemudian Kemoradiasi long course 25

siklus.
→ Kemoterapi FOLFOX/CAPEOX Saja
Neoadjuvan kemoterapi 12-16 minggu : pada kasus unresektabel atau T4 –

N any ; (NCCN 2023)
1. Long course kemoradiasi dengan capecitabine atau

infus 5FU kemudian kemoterapi 12-16 minggu dengan
FOLFOX / CAPEOX / FOLFIRINOX lalu restaging.
2. Atau Kemoterapi dengan FOLFOX / CAPEOX /
FOLFIRINOX selama 12 – 16 minggu kemudian
kemoradiasi lalu restaging.

ESMO
SISTEMIK ;
- Neoadjuvan untuk : FOLFOX
CAPEOX
- Stadium lanjut 5FU+LV
CAPECITABINE
- Metastasis KGB
- Margin tidak dapat clear
- Pilihan regimen : 1) Capecitabine + RT / 5FU+RT / 5FU+LV + RT
2) Kemoterapi 12-16 minggu

FOLFOX/CAPEOX/CAPECITABINE/5FU+LV
3) RT siklus pendek + Kemoterapi 12-16 minggu
- Setelah itu staging ulang, nilai resektabilitas
METASTASIS PADA CA REKTUM

- Resektable
→ CRM aman → Sistemik terapi FOLFOX / CAPEOX / 5FU+LV /

CAPECITABINE kemudian Radioterapi siklus pendek / 5FU + RT/
Capecitabine + RT/ 5FU+LV+RT kemudian reseksi
→ CRM tidak aman→
1) Sistemik terapi kemudian Kemoradiasi kemudian reseksi
2)Radioterapi pendek kemudian sistemik kemudian reseksi
3)Kemoradiasi kemudian sistemik kemudian reseksi
- Unresektable
→ FOLFIRI/FOLFOX/CAPEOX/FOLFOXIRI +/- Bevacizumab/Cetuximab
→ Bila konversi resektabel bisa lanjut RT pendek/Kemoradiasi → Reseksi
→ Tetap unresektable → Progresif → RT paliatif → sistemik
→ Tidak progresif → sistemik

OPERASI
COLON
Elektif → Prinsip→ Segmentektomi mengikuti pola vaskularisasi /
drainase limfatik secara en bloc.
→ Minimal reseksi 10 cm proximal dan 5 cm distal pada colon
→ Pada Reseksi ileum diusahakan seminimal mungkin
→ Minimal KGB lebih dari 12 yang diperiksa
* Ca. Caecum / Colon descendens → Hemikolektomi dextra
- Ligasi A. Colica kanan
- Ligasi A. Ileokolika
- Ligasi A. Colica Media cabang kanan → buka peritoneal

reflexion di paracolica, Lakukan Partial omentectomy, End
to end anastomosis menggunakan benang 3-0 chrome
pada mukosa, lalu secara interuptus dengan benang silk 3-
0 pada seromuskular.
* Tumor di Flexura hepatika → Extended hemikolektomi dextra

Hemikolektomi dextra + Ligasi A. kolika media di pangkal (Cabang
Utama) di proximal colica kiri
* Tumor di Colon Transversum → Transverse colectomy atau

Extended Hemicolectomy Dextra
* Tumor di Flexura lienalis → Extended Hemikolektomi Sinistra

atau extended hemikolektomi dextra et sinistra → Selanjutnya
Anastomosis ileum - colon descendens.

* Tumor di Colon descendens → Hemicolectomy sinistra,
- Ligasi A. Colica Sinistra di Proximal keluarnya dari IMA,
- Ligasi A. colica Media cabang kiri dan
- Ligasi IMV didasar pankreas.
Perhatikan ligamentum Splenocolica, Phrenocolica, Pancreaticocolica

di Flexura lienalis, identifikasi ureter kiri dan duodenum.
* Tumor di Colon Sigmoid → anterior resection,
- Ligasi IMA di Proximal keluarnya A. Colica Sinistra
- Ligasi A. Sigmoidalis.
Approach dari lateral (white line) atau dari medial (mesocolon)
Bebaskan keatas hingga flexura lienalis agar tidak tension.
Perforasi dapat terjadi di sekitar tumor (sentral nekrosis), proximal

tumor dan di caecum (tekanan tinggi).
* Loop Colostomy : insisi transversal 4-6 cm, pada border lateral rectus
abdominis, split anterior rectus, rectus abdominis dan posterior sheath,
maturasi pakai vicryl 4-0.
* End Colostomy : Left Lower quadrant, insisi bulat, 4-5 cm colon keluar
kulit.

REKTUM
- Tentukan resektabilitas melalui ; Rectal Touche, CT SCAN atau MRI
- Margin reseksi 5 cm proximal dan 2 cm distal.
- Kriteria Unresektable bila:
Schiatic Pain
Destruksi Tulang S1/S2
Obstruksi ureter
Terfiksasi di dinding pelvis
Ekstra pelvic disease
- Letak tumor dari anal verge/ intersfingteric groove
A) 1/3 proximal → anterior reseksi → diatas peritoneal reflexion
B) 1/3 Mid → LAR → Dibawah peritoneal reflexion, ligasi SHA
dan MHA, mobilisasi rectosigmoid dengan bebaskan peritonium
hingga flexura lienalis, bebaskan kebawah hingga promontorium
dan presacral, diseksi dekat dinding posterior, hati-hati Nervus
hipogastrikus sejajar ureter kiri.
C) 1/3 distal
→ Stadium dini → eksisi lokal → Trans Anal Local Excision,
Syarat : Ukuran tumor < 3 cm, Margin > 3mm, < 30% lingkar rektum,
tumor mobile, T1N0 , dalam jarak 15 cm dari anal verge

→ Stadium lanjut → ELAR, ULAR (Sfingter Saving) → Colonic pouch
ULAR → Stripping mukosa anus mulai dari linea dentata ke proximal
lalu anastomosis coloanal.
Mile’s procedure : Batas reseksi proximal 5 cm dan distal 2 cm.
* Preservasi : Ureter, Vasa iliaka, N. Simpatikus / Parasimpatikus dan
Presakral.
* Ligasi : Superior Hemoroidalis Arteri, High Ligasi IMA 1-2 cm dekat
aorta, IMV dekat treitz jika KGB diluar pelvis
* Fase Abdominal : Extended left colectomy, diseksi presakral,
mobilisasi rektum, kolostomi.
* Fase Perineal : Ligasi pudendal vessel, pisahkan prostat dari rectum,
pisahkan muscle levator, tutup perineum.
- Bila Invasi ke presacral fascia → not curable / unresectable
- Perhatikan Batas Reseksi : - Warna jaringannya bagus

- Hindari Perdarahan
- Hindari hematom
- Bersihkan jaringan lemak
- Epiploica

- Faktor anastomosis leakage :
A) Teknis : - Anastomosis kurang dari 6 cm dari anal verge
- Mobilisasi inkomplit flexura lienalis
- Tegangan jahitan
- Suplai darah
B) Non Teknis : - Sepsis
- Komorbid
- Obese
- Umur
- Malnutrisi
- Merokok

ATLAS OF INTESTINAL STOMA
Under normal conditions, approximately 90% of nutrients are absorbed

within the first 150 cm of small intestine. In the intact gastrointestinal tract, 9–10 L
of endogenous fluid enters the small bowel daily. This fluid is composed of saliva
and bile (approximately 1 L each) and gastric and pancreatic juices (1.5–3 L
combined).
Nearly 6 L of enteric contents are absorbed in the jejunum and 2.5 L in the ileum.
This absorptive pattern results in approximately 1.5 L of contents entering the colon
daily. Ninety percent of the liquid entering the cecum is absorbed in the colon, leaving
approximately 0.1 L of fluid in the feces.
The ideal location for most ileostomies is in the right lower quadrant
through the rectus muscle, sufficiently away from the midline incision to allow proper
placement of the stoma appliance. The infraumbilical fat mound over the rectus muscle
sheath is generally an ideal location because it is away from the umbilicus, skin creases,
or bony prominences.
The best site is on either side of the midline overlying the rectus muscle, 5 cm
away from the umbilicus and any scars, bony prominences and, hopefully, the
beltline. Additionally, the mark must be checked with the patient sitting to avoid any
crevicesand folds that may not be noted in the supine or standing positions [ 2 ] (Fig.
11.1 ).

SHORT BOWEL SYNDROME
- MALABSORBSI : SIGN - Diare

- Imbalance Elektrolit
- Malnutrisi
- Dehidrasi
- Panjang usus halus 3-8 meter, SBS terjadi bila panjang reseksi 50-80% usus
halus atau sisa usus halus 180 cm (1/3).
*Duodenum 25-30 cm
*Jejunum 2/5
*ileum 3/5
- Penyerapan cairan terbanyak berada di 150 cm pertama pada usus halus.
- Terapi :
TPN
Enteral Diet : - Elemental, Polymeric, Isoosmolar, Jumlah Kecil (50 ml/Jam)
H2R + PPI
Anti Diare
Somatostatin

BOWEL PREPARATION
DAY 1 : Diet susu
DAY 2 : Diet susu
Klisma 1000 ml Nacl
Fleet enema 1 botol
Fleet phosposoda 1/2 + air 3/4 gelas (2x)
DAY 3 : Diet sari buah
Klisma 1000ml Nacl
Fleet enema 1 botol
Fleet phosposoda 1/2 + air 3/4 gelas (2x)
Bowel Preparation pada pasien rencana Colon in Loop:

- 48 Jam sebelum tindakan : diet lunak
- 18 Jam sebelum tindakan : laksatif oral
- 4 Jam sebelum tindakan : laksatif enema , Puasa Rokok, Makan, Bicara.
FOLLOW UP POST TERAPI

- Anamnesis + Pemeriksaan Fisik + CEA tiap 3 bulan selama 2 tahun pertama,
kemudian tiap 6 bulan selama 5 tahun.
- Kolonoskopi / barium enema 1 tahun post operasi atau 3-6 bulan pada riwayat
obstruksi.
- XRAY thorax tiap tahun
- CT SCAN tiap tahun
- PET SCAN bila CEA meningkat tapi CT SCAN dan kolonoskopi negatif.

COLON NCCN

Stadium II high risk → Adjuvant → Folfox 6 bulan / Capeox 3 bulan
High Risk : T4
Poorly differentiated
Limfovaskular
Obstruksi
Perforasi
Positive margin

OBSTRUKSI LETAK RENDAH (LBO)
- Causa : Tersering ;-Kanker kolorektal

-Volvulus sigmoid, caecum, transversum
- Divertikulitis
Jarang; - Invaginasi
- Hernia
- Chrohn
- Tumor ekstralumen
- Impaksi
- Corpus alienum
DD : Ogilvie syndrome (Acute pseudoobstruction/ACPO)

- Dilatasi akut kolon oleh karena perubahan inervasi otonom
tanpa adanya obstruksi mekanis, biasanya pada usia diatas 60 tahun dan sakit
berat. Diterapi dengan konservatif ; endoskopi, neostigmine.
DCS :
ILEUS OBSTRUKSI LETAK RENDAH KOLEKTOMI KANAN +
ILEOSTOMI TERMINAL
NO ATAU
CA. COLON KANAN HEMODINAMIK LOOP ILEOSTOMI
STABIL
YES
TATALAKSANA AWAL ; NO - KOLEKTOMI KANAN

KURATIF
- Rehidrasi DENGAN ATAU TANPA
- Pantau Hemodinamik ANASTOMOSIS
- Pantau Urin ATAU
- Pantau Elektrolit
YES
- BYPASS INTERNAL
- Dekompresi ATAU
- Resusitasi Sepsis KOLEKTOMI KANAN - ILEOSTOMI SEMENTARA
- Antibiotik spektrum luas ATAU
DENGAN ANASTOMOSIS
- Anti Emetik - STENT METALIC
- Pemeriksaan LAB
DAN INTRAOPERATIF
- Pemeriksaan Radiologi STAGING
- Puasa

CA COLON KIRI
Ya Tidak HARTMANN
ATAU
STABIL
LOOP KOLOSTOMI
Ya
LOOP KOLOSTOMI
Tidak ATAU
KURATIF
STENT
Ya
- RESEKSI ANASTOMOSIS
DAN LAVASE INTRA OP +/-
DIVERTING STOMA
ATAU
- HARTMANN PROCEDURE
LESI EKSTRAPERITONEAL REKTAL → Loop Kolostomi
KOLOREKTAL
DIAGNOSIS :
Secara Klinis ;
- Tumor, Ciri suatu keganasan (Progresif, infiltratif, metastasis)
- Faktor resiko (genetik, lingkungan, life style)
- Komorbid
- Riwayat pengobatan sebelumnya
- Radioterapi
LAB : FOBT → (+) pada kanker colon/gaster/peptic ulcer
Tumor Marker CEA → menilai respon terapi dan prognosis, nilai normal
<5 ng/ml, periksa 4-8 minggu setelah operasi dan diulang tiap 3-6 bulan.

LOWER ENDOSKOPI / KOLONOSKOPI (Gold Standar)
RADIOLOGI : Colon in loop (bila tidak ada endoskopi)
Gambaran tumor kolon :
Arrest/Stopping
Stenosis
Filling Defect, apple core, shoulder sign
Deviasi
ERUS → Menilai Invasi Tumor (Staging)

CT scan kontras → Menilai Resektabilitas dan Staging setelah diagnosis
USG dan Xray → Metastasis dan staging setelah diagnosis
PATOLOGI
SCREENING :
- RESIKO SEDANG : Rekomendasi
FOBT tiap 1 tahun
Usia >50 tahun Kolonoskopi tiap 10
tahun
Adenoma/KKR > 60 tahun Sigmoidoskopi tiap 5
tahun
- RESIKO TINGGI :
Rekomendasi
Riwayat polip adenomatosa Kolonoskopi <3 tahun
Riwayat KKR (telah reseksi kuratif) setelah polipektomi
Riwayat keluarga KKR Kolonoskopi 1 tahun

setelah reseksi
Riwayat IBD

BIMBINGAN dr. BOY
- Indikasi kemoterapi :
* PA jenis mucinous dan SCC
* Stadium 3 keatas
* Stadium 2 high risk → 1.Klinis: Obstruksi
Perforasi
Margin tidak clear
2.PA: Poorly Differentiated
Invasi Limfovaskular
KGB < 12
- Pada Colon Kanan - Caecum
* Cek MSI (Dominan pada 85% colon kanan)
- Bila High (+) → tidak respon 5FU → terapi dengan imunoterapi→
Pembrolizumab
- Low / MSS → Respon 5FU
- Pada stadium IV metastasis

* Cek All RAS (KRAS, NRAS, HRAS) & BRAF
- RAS (+) → tidak respon cetuximab → berikan bevacizumab
- Pada guideline NCCN, disarankan untuk periksa semua oncogen (MSI, RAS, BRAF)
- Kemoterapi colorectal → Periode 6 bulan / 3 bulan
* CAPEOX siklus 3 minggu (8 siklus) : Capecitabine 1000mg/m2, 2x1, 14 hari
Oxaliplatin 130mg/m2, hari pertama
* FOLFOX VI siklus 2 minggu (12 siklus): 5FU bolus 400mg/m2, hari pertama
5FU kontiniu 1200mg/m2, hari I & II
Leucovorin 400 mg/m2
Oxaliplatin 85 mg/m2
- Workup : Colonoscopy, bisa colon in loop
Biopsi - MSI testing - Gen tumor (RAS, BRAF, HER2) bila metastasis
Xray, USG abdomen, CT abdomen Kontras (Staging)

OBSTRUKSI
→ Letak Tinggi / Small Bowel Obstruction (SBO)
↓
- Malignancy
- Adhesi : Peritoneal → Kongenital / didapat → respon trauma peritoneum
- Hernia : a. Hernia eksterna inkarserata ↓
Causa Lain : ↓ Paska Laparotomi

-Volvulus (jarang)
-Crohn - Inguinal
-Invaginasi - umbilikal
-Askariasis
-Gallstone ileus - Insisional
-Sindrom SMA
-Striktur ec. - Femoral
*Radiasi
*Anastomosis - Parastoma
B. Hernia interna inkarserata : - Hernia paraduodenal
- Hernia perisaekal
- Hernia winslow (foramen epiploica)
- Hernia obturator
H
Hernia Winslow
- Hernia Strangulata : Iskemia dan nekrosis usus

- Nyeri terus menerus
- Takikardia
- Demam Pada BNO
bisa tampak
- Leukositosis Gasless
abdomen -
terisi penuh
- Defans muskular cairan
- Asidosis metabolik

- Gallstone Ileus
Fistula empedu ke duodenum (Cholecystoenteric Fistula) yang menyebabkan
batu tersumbat di valvula ileosaekal.
* Radiologi : Rigler Triad
- Pneumobilia
- SBO
- Ectopic Gallstone
- Sindrom Superior Mesenteric Artery

(SMA)
Obstruksi letak tinggi oleh karena
penekanan duodenum pars 3 diantara aorta
dan A. Mesentrika superior (Aortomesenteric duodenal compression atau Wilkie’s
syndrome)
* Faktor Resiko :
-Penurunan BB yang cepat ;
A. Penipisan bantalan lemak
B. Operasi bariatrik
C. Keganasan,malabsorbsi,
anoreksia
- Kelainan Anatomis
- Aneurisma aorta abdominalis
- Operasi skoliosis
* Diagnosis :
- Ada faktor resiko
- Small Bowel Obstruction
- Muntah Hijau
- Nyeri kolik setelah makan
- Keluhan berkurang jika prone
* Radiologi : CT Kontras
- Sudut aortomesenterik <22 derajat, Jarak aorta <8 mm & dilatasi duodenum

BOLOGNA ASBO GUIDELINE

- SBO AKIBAT ADHESI PASCA OPERASI
*Dapat konservatif
→ 24-48 jam maximal 5 hari
→ Kondisi stabil dan tidak ada tanda strangulasi dan iskemia usus
→ Tidak ada peritonitis
* Nutrisi parenteral
* Dekompresi
* Anti biotik
* Dapat dilakukan foto kontras water soluble ( Gastrografin / Methylglucamine
Diatrizoat) pada obstruksi parsial yang tidak resolusi dalam 24-48 jam
↓
Contrast di colon setelah 24-36 jam → Lanjutkan NOM
- Indikasi Operasi :
* Peritonitis
* Perforasi
* Nyeri Hebat
* Bowel Ischemia
* Strangulasi
* Gagal Nom : Obstruksi >72 jam, CRP >75, intraperitoneal fluid, WBC 10000,
Nyeri Perut yang semakin berat.

GASTER
Faktor resiko keganasan pada gaster :

Usia 50-70 tahun, Laki-laki > Wanita, 2 : 1
Lesi pra maligna :
- Adenoma
- Displasia
- Metaplasia
- Gastritis Atrofik
Anatomi : Bagian → Cardia, Fundus, Corpus, Antrum Pylorus

Curvatura → Mayor, Minor
Lapisan → Longitudinal, Sirkuler, Oblique (luar ke dalam)
Sel → Musin (lendir)
Utama → Pepsinogen
Parietal → Hcl dan Castle (pengikat B12)
Trunkus Celiacus
Vaskularisasi : bercabang 3 :
- A. Hepatika Komunis
- A. Gastrica sinistra → pada kurvatura minor cabang celiacus
- A. Gastrika sinistra
- A. Gastrica dextra → Cabang A. Hepatica Comunis -A .Gastroduodenale
- A. Gastroepiploica Dextra → cabang a. gastroduodenal pada curve mayor

- A. Gastroepiploica Sinistra → A. lienalis
A. Hepatika Komunis
- A. Gastroepiploika = A. Gastro-Omentalis bercabang menjadi :
-A.Gastrika kanan
- A. Gastrika Brevis pada fundus -A.Gastroduodenale
-A.Hepatika propria

Sistem barier mukosa gastroduodenal :
- Pre epitel berisi mukus bikarbonat
- Epitel menghasilkan mukus (pertahankan PH 6-7)
- Subepitel → mikrovaskular
Lokasi keganasan : cardia (25%), corpus (30%), antrum (40%)
Histologi :
- Adenokarsinoma (95%)
- Squamous cell carcinoma
SEL EPITEL
- Small cell carcinoma
- Carcinoid
- GIST → Sel Cajal (stroma)
- Limfoma
- Signet Cell
Tumor Lokasi → Proximal / GEJ → Siewert Type

* Siewert I : esofagus mencapai kardia
* Siewert II : True junction (2 cm dari junction)
* Siewert III : Subcardia

Operasi : Menurut letak tumor
I → Ivor Lewis / McKeown
II/III → Total/Subtotal gastrektomi
Midbody→TotalGastrektomi→ Esofagojejunostomy Roux en Y
Distal→ Subtotal → Bilroth 1-2, gastrojejunostomy Roux en Y
Adjuvan terapi : ECF - Epirubicin, Cisplatin, 5FU
Rekonstruksi Bilroth :
- Resection of gastrocolic omentum
- Ligation of right gastric, Right gastroepiploica, left gastric artery.
- Removal lymph node and mesentery
- Resect 2 cm proximal duodenum
- Proximal margin are 6 cm from tumor

Anamnesis :
- Muntah
Faktor Resiko :
- Early satiety Diet daging asap
Rokok
- Anorexia Infeksi H. Pylori
Radiasi
- BB menurun Genetik
- Disfagia
- Hematemesis melena Lokasi Ulkus curiga keganasan :
- Ulkus 1-2 cm sepanjang curva mayor
- Anemia - Ulkus pylorus
- Ulkus yang besar dan tembus ke posterior
KGB :
- Virchow node → Supraclavicula sinistra (Troisier sign)
Staging :
- Irish node → Axilla sinistra T1 - Submucosa
T2a- Muscularis Propria
- Sister Mary Joseph → Umbilikus T2b- Subserosa
T3 - Serosa
- Blummer node - Inguinal T4 - Invasi Struktur Sekitar
Examination : N1 - 1-6 KGB

N2 - 7-15 KGB
- Gold Standar → Endoskopik N3 - >15 KGB
- Barium meal double kontras Stadium :
I : T1, T2
- EUS
II : N1, N2, T3
- CT Scan Abdomen III : T4, T3-N1, T2-N2
IV : T4-N1, M1
- Thorax & USG
Dumping syndrome : Karena aliran cepat Chime / karbohidrat ke usus halus

- Early : Diaphoresis, Palpitasi, Diare, Sinkop (Pelepasan vasoaktif intestinal peptide
dan Serotonin)
- Late : Hipoglikemia, Hiperinsulinemia
Terapi : Diet tinggi serat, Diet rendah karbohidrat, Octreotide sc 2x100 ng
(somatostatin)

GIST → berasal dari sel intestinal cajal (regulator motilitas usus) → Sering terjadi di
lambung, usus halus dan rektum.
Gejala Klinis : Massa Abdomen, Nyeri, Perdarahan, metastasis ke liver
Pada CT scan (30 HU pre kontras dan 50 HU post kontras)
- Tumor <5 cm batas jelas, homogen
- Tumor >10 cm tepi irreguler, heterogen - curiga malignancy
PA : Bentuk homogen 3 tipe : spindel, epiteloid, campuran

PERFORASI GASTER

Operasi elektif ulkus peptikum : Vagotomi → menurunkan sekresi asam oleh sel
parietal yang distimulasi oleh asetilkoline dari vagus dan gastrin pada antrum.
Jenis vagotomy : Truncal Vagotomy, Selective Vagotomy, Highly Selective Vagotomy.
- Prediktor Mortalitas terbaik : Hipoalbuminemia

- Komplikasi Operasi pada gaster : Early Satiety, Dumping
Syndrome, Risk for Gastric Cancer, Gastritis.

ACHALASIA
Aperistaltik yang menyebabkan lower esofageal shincter kontraksi patologis
dan dilatasi esofagus proximal akibat dari tidak adanya ganglion pada plexus
myenterikus & aurbach.
Gejala :
- Disfagia progresif
- Makanan padat bisa turun, Makanan cair sulit turun.
- Cairan hangat bisa turun
- Heartburn, regurgitasi, BB turun, Rasa penuh dibelakang sternum.
Pemeriksaan gold standar dengan manometri untuk menilai tekanan LES,
patologis bila >35 mmhg juga untuk menilai tipe 1,2,3 (tipe paling berat)
- XRay thorax : pelebaran mediastinum,
kelainan paru akibat aspirasi, bisa
tampak air fluid level.
- Barium swallow (150-250cc) tampak
dilatasi esofagus proximal (>3 cm) dan
gambaran bird beak
- UGIE : tampak sisa makanan dan
mukosa rapuh + ulserasi
Terapi medikamentosa dengan injeksi
botox (botolinum), oral dengan calcium
blocker, sildenafil.Terapi operatif dengan
Heller Myotomy disertai funduplikasi
(nissen) → cegah GERD
Terapi minimal invasif dengan POEM → Per Oral Endoskopi Myotomy

Esofagus
- 3 Lapisan : Sel epitel squamous tanpa keratin
Submukosa (paling kuat untuk anastomosis)
Muskularis eksterna
- Part : Servikal - krikoid ke jugular notch
Upper thorakal - notch ke karia
Middle - Karina ke pertengahan antara EGJ dan karina
Lower - sampai ke hiatal
Vaskularisasi :
- Cervical (thoracal inlet) dari a. thyroidea inferior

- Thoracal atas dan Tengah (10cm dari GEJ) dari aorta
- Thoracal bawah dan abdominal dari a. gastrika sinistra dan frenikus inferior.
TUMOR ESOFAGUS
Gejala : Disfagia (tidak bisa makan makanan padat), Muntah, Suara serak (N.
Laringeus Rekuren)
Penunjang : Esofagografi, Endoskopi, EUS, CT Scan.
- Malignancy barium swallow : shoulder sign, filling defect - irregularity

KGB Esofagus Regional :
- Cervical : Jugular interna, Supraclavicula, Scalenus
- Intrathoracal
- GE Junction : Celiac, Gastric Sinistra, Perikardial, Diafragmatik
Terapi :
Stadium Dini (T1-T2) = Reseksi
Locally Advance (T3-4, N1-3) = SCC – Kemoradiasi lalu reseksi, Adenocarcinoma –
Kemoterapi lalu reseksi.
Operasi :
McKeown – 3 insisi (Laparotomi, Torakotomi Kanan, Servikal Kiri) pada kasus tumor
esofagus letak servikal, torakal atas dan Tengah
Ivor Lewis – 2 Insisi (Torakotomi kanan, Laparotomi) pada kasus tumor letak Tengah

TRAUMA ABDOMEN
- Prinsip ATLS : (Edisi 10th)

- Primary survey - 24 jam pertama
- ABCDE
- IV Line, Gastric Dekompresi, Kateter Urine
- Grading shock ; Tatalaksana 1 liter cairan atau 20cc/KgBB pada
anak <40 Kg, target MAP ≥ 65
The definition of shock—an abnormality of the circulatory system that results

in inadequate organ perfusion and tissue oxygenation.
Any injured patient who is cool to the touch and is tachycardic should be
considered to be in shock until proven otherwise (ATLS 10th).

- Secondary survey : Head to Toe, Nilai anterior dan posterior
thoracoabdomen, nilai flank, nilai pelvis, nilai perineum, scrotum, meatus
urethra dan perianal. Setelah pemeriksaan selimuti pasien.
- Nilai respon resusitasi : Normal BP, Normal HR, Normal Pulse Pressure, CNS,
Skin color, Urine Output merupakan indikator utama (0.5 ml/KgBB/Jam dewasa,
1 Ml/KgBB/Jam pada Anak)

- Masif transfusi darah yaitu transfusi darah >10 unit/24 jam atau 4 Unit
dalam 1 jam.
- Damage control resusitasi , pRBC : Plasma : Platelet (1:1:1)
- Some jurisdictions administer tranexamic acid in the prehospital setting
to severely injured patients in response to recent studies that demonstrated improved
survival when this drug is administered within 3 hours of injury. The first dose is
usually given over 10 minutes and is administered in the field; the follow-up dose of
1 gram is given over 8 hours.
The anterior abdomen is defined as the area between the costal margins
superiorly, the inguinal ligaments and symphysis pubis inferiorly, and the anterior
axillary lines laterally
The thoracoabdomen is the area inferior to the nipple line anteriorly and the
infrascapular line posteriorly, and superior to the costal margins. This area
encompasses the diaphragm, liver, spleen, and stomach, and is somewhat protected
by the bony thorax
The flank is the area between the anterior and posterior axillary lines from
the sixth intercostal space to the iliac crest.
The back is the area located posterior to the posterior axillary lines from the
tip of the scapulae to the iliac crests. This includes the posterior thoracoabdomen.
Musculature in the flank, back, and paraspinal regio.

MEKANISME TRAUMA TUMPUL
- Kompresi
- Shearing → Akselerasi - deselerasi
- Bursting → tekanan intralumen naik saat trauma
INDIKASI CT SCAN
- Penetrasi - Perubahan GCS
No No - Gross hematuria
PERITONITIS FAST
- Fraktur Pelvis
Yes - Abdominal Tendernes
HEMODINAMIK - HCT <35%
STABIL Yes bleeding
No FAST (+) LAPAROTOMI
Gagal
NOM NOM
TRAUMA PENETRANS
- STABIL → Luka Tembak → - Flank Belakang →→ CT Scan Abdomen

- Quadran Kanan Atas → →
- Anterior Abdomen → Explorasi Laparotomi
→ Luka Tusuk → Flank Belakang → → CT SCAN ABDOMEN

→ Anterior Abdomen → Lokal Wound Eksplorasi
→ Peritonitis, Eviserasi → Laparotomi Eksplorasi
Indikasi Laparotomi Eksplorasi Trauma

Tumpul
- Hipotensi menetap setelah resusitasi
( hemodinamik tidak stabil, No response,
transient response)
- Ongoing bleeding
- Udara bebas
- Peritonitis
- Ruptur Diafragma
Indikasi Laparotomi Trauma Penetrans
- Hipotensi
- Hemodinamik tidak stabil
- Peritonitis
- Tembus peritoneum
- Eviserasi organ
Thus, indications for laparotomy in

patients with penetrating abdominal
wounds include :
• Hemodynamic abnormality
• Gunshot wound with a transperitoneal
trajectory
• Signs of peritoneal irritation
• peritoneal penetration (e.g., evisceration)
ATLS 10th
KRITERIA TIDAK STABIL :
-BP < 90,
-HR >120,
-SKIN VASOKONSTRIKSI (AKRAL DINGIN, CRT MENURUN),
-KESADARAN MENURUN (GCS) DAN ATAU SESAK
ATAU
-TENSI >90 TAPI MEMBUTUHKAN TRANSFUSI >4 KANTONG
RBC DAN ATAU MEMBUTUHKAN VASOPRESSOR.

- Abdomen packing : awal mulai packing dari zona 1,2,3 → buka packing zona 3,2,1
zona retro cattell braasch

Manuver Cattel-Braasch : mobilisasi colon kanan ke medial untuk eksposure
infrahepatik vena cava inferior (Zona 1)
Manuver Kocher : untuk ekspose ginjal kanan dan vasa renalis kanan
Manuver Mattox : mobilisasi kolon kiri ke medial untuk eksposure aorta abdominalis

SPLEEN
- Trunkus soleakus → A. Lienalis → 6 cabang pada hilus lienalis

→ V. Mesentrika Superior → V. porta
- 8 Ligamen Fiksasi Lien :

- Gastrosplenika
- Splenorenal
- Splenophrenika
- Splenokolika
- Pancreaticocolica
- Pancreaticosplenica
- Phrenicocolica
- Pre Splenic Folds

Gejala ; Hipotensi, Nyeri LUQ, Nyeri Tekan (Diffuse peritonitis), Nyeri Alih ke
bahu kiri saat inspirasi (KEHR SIGN)
I : Agen
hemostatik
( Fibrn Glue)
II : Splenorafi
(matras Chrom
2.0), Hemostatik
III : Splenorafi,
Hemostatik
IV : Partial
Splenektomi
V : Splenektomi,
Splenosis pada
omentum mayor
Benang 0 monofilament simple running
suture
Indikasi Splenektomi :
- Pasien tidak stabil
- Multiple Trauma
- Grade V
- Gagal NOM
Non Operative Managemen :

- Stabil setelah resusitasi
- Grade I,II,III
- Tidak ada trauma lain
Gagal NOM :
- Perdarahan Berlanjut
- Butuh transfui 4 unit pRBC
- OVERWHELMING POST SPLENECTOMY INFECTION (OPSI) : Tidak mampu

fagositosis bakteri gram (+) berkapsul, sebaiknya vaksin pneumococcal.

TRAUMA HEPAR
- Batas liver pada superior setinggi Costa V, dan pada hemithorax kanan setinggi kosta
VII dan VIII di hemithorax kiri. Hepar di fiksasi oleh ligamentum falsiform, lig. Teres, lig.
Triangular, lig. Koronarium dan omentum minus.

NOM CRITERIA :
Curiga Trauma Hepar :

- Hemodinamik Stabil - Jejas abdomen kanan atas
- Setelah resusitasi hemodinamik stabil - BOA sign : nyeri menjalar ke bahu
- Tidak ada nyeri abdomen menetap

- Tidak ada hemoragik aktif
- Hemoperitoneum <500 ml Kenapa NOM ?
Trauma hepar tumpul biasanya
- Transfusi <2 kantong mengenai vena (tekanan
- Tidak ada tanda peritonitis rendah). Perdarahan berhenti
jika ada clotting
- Tidak ada defans muskular
- Tidak ada trauma organ abdomen lain
- Gr. I-III (95% NOM)

- As noted earlier, most blunt hepatic trauma causes venous injuries that are
low pressure (3–5 cm H2 O); therefore, hemorrhage usually stops once a
clot forms on the area of disruption.
- With grade III and IV hepatic injuries, Coimbra et al documented a reduced
mortality with nonoperative management. Richardson has recommended
that hemodynamically stable patients who have received less than 4 units
of blood can be safely managed nonoperatively. Unlike the spleen, which
can be easily removed, liver-related bleeding can be made worse by
operative intervention.(Mattox)
Monitoring :
- Gejala
- USG
- Lab Serial
- Batasi aktifitas 8 minggu

Indications for surgery :
- Haemodynamically unstable patient

- Multiple transfusions required to maintain haemodynamic stability
- Signs of peritonitis, or development of peritonism on serial abdominal
examinations
- Active arterial blush on CT; interventional techniques (angiographic
embolization) have failed
- It should be emphasized that evidence of blood in the peritoneal
paracolic gutters, in the pelvis, or tracking along the periportal triads
is suggestive of a more significant injury than the liver anatomy may
indicate and mandates exploration. (maingot)
- Liver sumber perdarahan , kontrol dengan :

→ Klem pedikel hepar ( Pringle Manuver) (lig. Gastohepatik) → Oklusi V. Porta,
A. Hepatika dan CBD, lepas tiap 20 menit.
→ Kompresi posterior dengan packing, perihepatic packing → lepas setelah 48
jam
→ Manual kompresi
→ Total oklusi vascular (heaney manuver) → (Infrahepatic IVC, Suprahepatic
IVC, + Pringle manuver )
Jika perdarahan berhenti setelah pringle manuver, kemungkinan asal

perdarahan dari cabang vena porta dan cabang dari arteri hepatika, jika
perdarahan tidak berhenti, kemungkinan berasal dari retrohepatik inferior vena
cava atau vena hepatik mayor.

- Pada laserasi hepar dijahit dengan chromic 2-0 atau 0 absorbable,
blunt/tapered needle secara horizontal matras atau figure of 8.
- Batas reseksi hepar yaitu 25% ( resectional debridement) pada jaringan non
viable
- Gall bladder dapat di jahit primer ataupun cholecystectomy.
- Pada cedera bile duct dapat dilakukan pemasangan T-Tube, jahit primer
dengan benang 4-0 hingga 6-0 monofilament absorbable. Bila transeksi dapat
dilakukan choledocojejunostomy.
MASSIVE TRANSFUSION PROTOCOL :

4 unit PRC , 2 unit FFP, 1 unit PLT, Tranexamat 15 mg/kgbb/iv bolus, maintenance
2mg/Kgbb/Jam dan calcium gluconas 0.3 ml/kgbb. Diberikan pada kasus trauma
hepar dengan hemodinamik tidak stabil AAST 4-5 dan pada Syok Grade 4.

PANKREAS
- Organ retroperitoneal sehingga cedera pada pankreas sering disertai cedera

organ lain
-Curiga cedera pankreas pada :

- Trauma tumpul : Hematoma retroperitoneal, cairan retroperitoneal, edema
pankreas.
- Trauma penetrans : perdarahan atau cairan pankreas/bile, retroperitoneal
hematom.
- MRCP dan ERCP dapat membantu menegakkan diagnosis
MANAGEMENT :
1&2 : Pasang drain dan
kontrol perdarahan,
NOM bila diagnosis pre
operasi.
3 : Distal
pankreatektomi
4 : Kontrol bleeding,
debridement, pasang
drain
5 : Damage kontrol
dengan drain atau
pancreaticoduodenecto
my
Treatment ;
I & 2 : Pasang
drain dan
kontrol
perdarahan,
NOM bila
diagnosis Pre
operatif

Indikasi Konservatif : Observasi 72 Jam
- Trauma tumpul dengan hemodinamik stabil
- CT scan tidak menunjukkan adanya : - Fraktur parenkim pankreas
- Hematom Parenkim
- Parenkim Edema
- Cairan di lesser sac atau retroperitoneal
Indications of exploratory laparotomy include :

◼ Peritonitis
◼ Penetrating injury in region of pancreas
◼ Hypotension in combination with a positive FAST
◼ Positive abdominal lavage following blunt trauma
◼ Pancreatic duct disruption based on CT or ERCP
Body and Tail

◼ Duct intact: non operative drainage
◼ Duct involved:
• Distal pancreatectomy/pancreaticojejunostomy + closure of proximal
duct end
Head of the pancreas :

◼ No duct injury : closed drainage
◼ Duct injury : Central pancreatectomy + Roux-en-Y
Pancreaticojejunostomy
◼ Destructive injury : Whipple pancreaticoduodenectomy

Indikasi Whipple Pada Trauma : Masif injury pada caput pancreas dan
ductus pancreaticus, Avulsi ampulla vater, Kerusakan duodenum Pars II.

GASTER
AAST
Grade 1 : Kontusio / Hematom Intramural → Observasi
Grade 2 : Laserasi GE Junction < 2 cm → Jahit Primer
Laserasi 1/3 Proximal <5 cm
Laserasi 2/3 Distal <10 cm
Grade 3 : Laserasi GEJ > 2 cm → Jahit Primer + Piloroplasti
1/3 Proximal > 5 cm → Total gastrektomi pada GEJ
2/3 Distal > 10 cm
Grade 4 : Devaskularisasi <2/3 gaster → Subtotal/Total Gastrektomi
Grade 5 : Kehilangan Jaringan >2/3 gaster → Total Gastrektomi
USUS HALUS
AAST
Grade 1 : Hematom / Laserasi tanpa perforasi
Grade 2 : Laserasi perforasi <50% sirkumferensial
Grade 3 : Perforasi >50% tanpa transeksi
Grade 4 : Transeksi usus halus
Grade 5 : Kehilangan jaringan + Devaskularisasi
Hemodinamik tidak stabil : cuci abdomen dan eksteriorisasi
KOLON DAN REKTUM

AAST
Grade 1 : Kontusio
Grade 2 : Laserasi < 50%
Grade 3 : Laserasi >50%
Grade 4 : Full thickness sampai peritoneum
Grade 5 : Devaskularisasi

DUODENUM
- DUODENAL HEMATOM → Vomit setelah blunt trauma

→ Pada pemeriksaan barium → coiled sign
→ Non operatif management
- Dilakukan manuver kocher untuk menilai duodenum, nilai grade injury :

1. Grade I : NOM, Nasojejunal Tube, Bowel Rest, IV resusitasi, Oral hari ke 5.
2. Grade 2 : Jahit primer Interuptus, Prolene/PDS 3.0/4.0, Jahit Transversal
3. Grade 3 & 4 : D1 Gastrojejunostomy-duodenojejunostomy-Roux en Y
4. Grade 4&5 : Pancreaticoduodenectomy
- Perforation → Primary Repair

- Zona 1 → Debridement dan anastomosis
- Zona 2 → Roux en Y
- Zona 3 & 4 → Reseksi → Roux en Y
- Setelah itu pylorus disumbat
AAST DUODENUM INJURY :

I : Hematom Simple, Laserasi 1/2 ketebalan
II : Laserasi <50% Sirkumferensial
III : Laserasi 50-75% D2, 50-100% D3
IV : >75% D2, Mengenai ampula vater/CBD
V : Rusak parah duodenopancreatic complex, Devaskularisasi
- Duodenum tidak ada serosa, sehingga memiliki resiko untuk bocor setelah
anastomosis lebih besar, jangan di refresh - jahit primer.
- Bilroth 1 lebih fisiologis
- Roux en Y → Gastrojejunostomy, duodenojejunostomy

If the patient is hemodynamically stable or a transient responder, a
computed tomography (CT) should be performed to determine the extent of
the duodenal injury and any other significant injuries. The hallmarks of duodenal
injury on CT are peri-duodenal emphysema, free fluid in the cavity and/or
retroperitoneal hematoma. CT with intravenous contrast has a sensitivity of
86% and a specificity of 88% for detecting duodenal lesions 14 - 16.
However, patients with peritoneal signs and/or hemodynamic
instability (sustain systolic blood pressure (SBP) <90 mmHg) should be
transferred immediately to the operating room (OR) for the appropriate
staging of the injury according to the AAST classification during the initial
exploratory laparotomy.
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8216054/)
Our surgical management per AAST Grade is as follows:
AAST Grade I: Non-operative management (NOM), nasojejunal tube

placement for early enteral feeding, bowel rest and intravenous (IV) fluid
resuscitation. Attempt oral feeding on hospital day 5.
AAST Grade II: Primary repair with debridement of the lesion if necrotic tissue
is suspected or present. The repair is performed using 3-0 or 4-0 PDS
absorbable suture as a continuous or interrupted suture line depending on
the surgeon’s preference. A nasojejunal tube is placed manually by the surgeon
prior to definitive repair of the injury for early enteral feeding, followed by
bowel rest and IV fluid resuscitation. Oral feeding is attempted on
postoperative day 5.
AAST Grade III: D1 injuries that involve between 50 to 100% of the bowel
circumference should be repaired when possible by resection plus
terminal end to end anastomosis using 3-0 or 4-0 PDS absorbable suture as a
continuous or interrupted suture line and/or stapler device.
If anastomosis couldn’t be done, then The patient is then transferred to

the ICU for correction of the lethal diamond and in 24 to 48 hours later, the
patient should be taken back to the OR for definitive care. Duodenal

reconstruction should then be performed via a gastroenteric anastomosis
Roux-en-Y
DD2 injuries involving 50 to 75% of the bowel circumference should

undergo appropriate staging by making sure that the ampulla or distal common
bile duct are not involved. Primary repair with debridement of the lesion
should be considered as the first option of surgical approach via a terminal
end to end anastomosis using 3-0 or 4-0 PDS absorbable suture as a
continuous or interrupted suture line and/or stapler device.
However, if the anastomosis is technically difficult, then the duodenal

ends should be left in discontinuity and a nasogastric tube inserted
following damage control principles. The patient is then transferred to the ICU
for correction of the lethal diamond and in 24 to 48 hours later, the patient should
be taken back to the OR for definitive care. Duodenal reconstruction should
then be performed via a side to side anastomosis

D3 and D4 injuries involving between 50 to 100% of the bowel
circumference a Cattel Brash Maneuver with a Kocher extension and a
ligament of Treitz release should be done to properly mobilize the bowel and
adequately evaluate its viability. When possible, a side to side anastomosis
should be performed using 3-0 or 4-0 PDS absorbable suture as a continuous
or interrupted suture line and/or stapler device.
AAST Grade IV: D2 duodenal injuries encompassing more than 75% of the
bowel circumference and/or involving the ampulla or distal common bile duct
should undergo DCS. This consists of the over-sewing of the duodenal ends,
ampulla and/or distal common bile duct. followed by nasogastric and
cholecystostomy tube placement, abdominal packing and an open abdomen with
a negative pressure dressing. Then the patient should be transferred to the ICU for
correction of the lethal diamond, and between 24 to 48 hours later, taken back to
the OR for definitive reconstruction. Duodenal reconstruction should then be
performed via a choledochal-jejunal, gastro-jejunal anastomosis Roux-en-Y
plus cholecystectomy.

AAST Grade V: Duodenal injuries with massive destruction of the
duodenal pancreatic complex and/or devascularization of the duodenum
require DCS. These patients are associated with extremely high mortality rates
and the main objective is to isolate the pancreatoduodenal complex via cross
suturing with 3-0 non-absorbable monofilament continuous locking suture of the
exposed pancreatic tissue for appropriate hemorrhage control. The duodenal ends,
pancreatic duct and distal common bile duct should be over-sewn. All other
significant associated injuries should be addressed, followed by nasogastric and
cholecystostomy tube placement, abdominal packing and an open abdomen with
a negative pressure dressing. Then the patient should be transferred to the ICU for
correction of the lethal diamond, and between 24 to 48 hours later taken back to
the OR for definitive reconstruction
Indications for a Whipple Procedure in trauma include:
Massive injury to the head of the pancreas with pancreatic duct involvement
Avulsion of the ampulla of Vater
Destruction of the second portion of the duodenum
The main complication of these injuries are duodenal leaks that evolve into
fistulas because it sees approximately 5 liters of fluid per day (gastric acid, bile,
pancreatic juice and saliva).

HEPATOBILIER
HEPAR → Hipokondrium Kanan, Sebagian di Epigastrium, terdiri 8 segmen

anatomis
- Fiksasi Hepar
- Ligamentum Teres
- Ligamentum Falciforme di ventral
- Ligamentum Triangulare di lateral medial
- Omentum Minus / Lesser Omentum di caudomedial

VASKULARISASI :
- A. Trunkus Coeliacus → A. Hepatica Comunis (25%) → bercabang menjadi

a.sistikus dan arteri hepatika kanan, kiri dan tengah yang berjalan di
ligamentum duodenale bersamaan vena porta.
- Vena Porta (75%)
- Vena Hepatika
- Inferior vena cava → Vena hepatika kiri segmen 2,3,4
→ Vena hepatika tengah segmen 4,5,8
→ Vena hepatika kanan segmen 5,6,7
- TRUNKUS COELIACUS → A. Gastrika sinistra, A. Hepatika comunis,

A.Lienalis.
FISIOLOGI :
- Mengandung hepatosit
- Sebagai pusat metabolisme → produksi dan pemecahan karbohidrat, lemak,

protein
- Menghasilkan cairan empedu 600-1000 cc/24 Jam
- Tekanan vena porta 7-10 mmHg
- Glikogenesis → glikogenolisis
- Pembekuan darah
- Metabolisme vitamin
- Detoksifikasi
- Produksi Albumin, Globulin,

Bilirubin, PT/APTT (Fungsi
Essensial hati)

EMPEDU
- Disekresi oleh hepatosit
- Berfungsi untuk pencernaan dan absorbsi lemak.
- Kolesterol dipecah oleh hepatosit menjadi asam empedu primer (asam cholat
dan chenodeoxycholat) selanjutnya diubah oleh glycine dan taurine ( larut air)
dan diekskresi ke empedu (bile) lalu masuk ke usus halus dan kolon membantu
absorbsi lemak dan vitamin ADEK, dan diubah oleh bakteri usus menjadi
sterkobilin.
- pemecahan hemoglobin menjadi biliverdin diubah menjadi bilirubin

terkonjugasi /direct (larut air) di dalam liver kemudian menjadi sterkobilin dan
urobilin.
- Kontraksi gallbladder dirangsang oleh cholecystokinin ang terletak di sel epitel

usus halus utamanya duodenum. (pengaruh makan lemak-nyeri)
- Peningkatan bilirubin terkonjugasi akibat dari :
- Gangguan ekskresi intrahepatik (cholestasis intrahepatik)
- Obstruksi
Sterkobilin <5-6 mg/hari → Obstruksi
SGOT : tidak spesifik pada hepar
SGPT : Spesifik (sel hati)
GGT : Spesifik penyakit hati, untuk mengetahui hepatitis kronik dan cholestasis,
meningkat lebih awal dibanding ALP
- peningkatan GGT berkorelasi dengan obstruksi
ALP : sistem hepatobilier, meningkat pada sirosis bilier primer.
- meningkat 10X pada obstruksi empedu ekstra hepatik oleh tumor
- meningkat 3-10X pada obstruksi batu.

IKTERUS OBSTRUKSI
- Kuning di sclera (bilirubin >3) atau seluruh tubuh (Kulit >5 mg/dl)
• Sejak kapan (Onset dan progresiftasnya)
• Sifatnya terus menerus atau hilang timbul (Jika Causa Batu bisa hilang
timbul)
• Malignant Jaundice (icterus di mana kadar bilirubinnya >17-20 gr/dl dengan
tanda-tanda cholangitis), ada gatal atau tidak → malignant jaundice
menyebabkan pelepasan histamin
• Disertai nyeri, atau riwayat nyeri sebelumnya. Sifat nyerinya hilang timbul
(jika batu) dan pada tumor nyeri tidak signifikan.
Nyeri menjalar (Kehr sign), jika nyeri dipengaruhi perubahan posisi, pemicu
nyeri jika habis makan makanan yang berlemak
• Tanyakan tanda infeksi: demam, sejak kapan, sifat demamnya
• Mual dan muntah → dipengaruhi oleh klinis oleh kolik, jika tumornya bisa
menyebabkan Gastric outlet obstruction (GGO), bahkan bisa bilious
• Jika mengarah ke tumor cari khas tumor → infiltrasi, progresifitas, dan
metastasis
• Jika tumor (duodenum) tanyakan Riwayat melena
• BAB acholic → tidak ada stercobilin
• Urine → teh pekat (urobilinogen)
• Pola makan
• Riwayat Penuruan berat badan
• Riwayat Komorbid (sickle cell anemia, DM, HT)
• Riwayat berobat sebelumnya
• Riwayat tirah baring
- Trias Charcot : Demam, Jaundice, RUQ pain
- Penta Raynaud : Charcot + Kesadaran menurun dan syok
- Gangguan koagulasi terjadi akibat terganggunya penyerapan

vitamin K
- Gatal akibat pelepasan histamin pada subcutis akibat adanya
garam empedu (chenodeoxycholate dan deoxycholate)

PEMERIKSAAN FISIK :
- Hepatomegali
- Splenomegali (schuffner)
- Ascites, Edem perifer
- Spider Nevi
- Kaput medusa
- Ginecomasti
- Courvosier sign (teraba massa yang tidak nyeri disertai ikterus)
- Murphy sign
- Sklera dan telapak tangan ikterus.
LAB :
- Darah Rutin (Hb, PLT, WBC)
- CRP
- Alkali fosfatase
- GGT
- SGOT
- SGPT
- Bilirubin Total dan Direk
- Albumin
- Faktor Pembekuan darah
- Kultur Darah

RADIOLOGI :
- USG ; CBD melebar, Apakah ada Batu / causa obstruksi?
- CT ABDOMEN
- MRCP
- ERCP
Management :
- ERCP + Sphicterotomi (untuk melebarkan sphincter oddi untuk

ekstraksi batu dan mengalirkan bile)
- Laparscopy
- Open
• Jika tumor caput → Whipple (Pancreaticoduodenectomy) atau jika paliatif
dapat dilakukan drainase interna (bypass biliodigestive:
choledocoduodenostomy, choledocojejunostomi, cholesistojejenunostomi,
hepaticojejunostomy + gastrojejunostomy
(braun anastomosis atau roux en way, jaraknya 40-60 cm dari bypass
mencegah GGO)
Kontraindikasi Whipple

Cholangiocarcinomas are epithelial neoplasms that originate from
cholangiocytes and can occur at any level of the biliary tree.
These lesions are broadly classified into intrahepatic cholangiocarcinoma,

hilar cholangiocarcinoma, and distal extrahepatic bile duct tumors.
Ultrasonography is the imaging technique of choice for the diagnosis of

cholangiocarcinoma with obstructive jaundice. The presence of
dilated ducts without clear communications within a liver lobe indicates the
extension of tumor into the segmental bile ducts.
MRI with concurrent magnetic resonance cholangiopancreatography (MRCP)

is the radiologic technique of choice for assessing the extent of disease.
Treatment :
In patients with obstructive jaundice who have cholangio carcinoma,
especially hilar cholangiocarcinoma, preoperative biliary drainage has been
recommended to improve liver function before surgery and to reduce
postoperative complications.
Percutaneous transhepatic biliary drainage (PTBD) In patients with
hilar cholangiocarcinoma, drainage is currently performed only for liver lobes
that will remain after resection and for areas of segmental cholangitis.

Extended hemihepatectomy, with or without
pancreatoduodenectomy, plus extrahepatic bile duct resection and regional
lymphadenectomy has recently been recognized as the standard curative
treatment for hilar bile duct cancer. Pancreatoduodenectomy is the choice of
treatment for middle and distal bile duct cancer. Intrahepatic
cholangiojejunostomy has been performed in patients with unresectable
malignant biliary obstruction.

ABSES HEPAR
Jaringan nekrotik pada hati causa infeksi amoeba histolitika/infeksi

banal
- Ada 2 bentuk : pyogenik dan amoeba
- Piogenik berasal dari vena porta akibat dari infeksi GIT atau pelvis (ascending
infeksi)
- Infeksi saluran empedu akibat obstruksi - Kolangitis
- infeksi dari organ yang berdekatan
- Amuba sering pada lobus kanan, superfisial dan tunggal. Akibat dari higiene
yang buruk, khas berwarna kecoklatan (anchovy paste)
- Gejala : - Demam, Menggigil
- Nyeri kuadran kanan atas
- Malaise
- Anoreksia
- Jaundice
- Nyeri sendi
- Pemfis : - Hepatomegali
- Nyeri kuadran kanan atas
- Asites, efusi pleura
- Teraba massa
- Treatment : antibiotik
Operasi : - Resiko ruptur abses
- Abses lobus kiri
- Tidak respon medikamentosa
- Sepsis

HEPATOCELLULAR CARCINOMA
Etiologi : Hepatitis B dan C (kronis) , sirosis hepar
Patologi : 90% keganasan hepar (HCC), 5% kolangiokarsinoma
Penyebaran : 4 Jalur : Sentrifugal, parasinusoidal, via vena porta, metastasis

jauh.
Klinis :
Stadium lanjut : - Nyeri tumpul namun persisten pada perut atas
- Massa perut kanan atas
- Anoreksia
- Penurunan BB
- Ascites
- Hipertensi porta
- Ikterus
Pemeriksaan Fisik :
- Hepar berbenjol-benjol, keras dan nyeri tekan
- Tanda sirosis : caput medusa, spider nevi, eritema palmaris, ginekomasti
Lab : Marker spesifik AFP (>20), Curiga ganas bila >200 - 400
Radiologi : USG tampak hipoekhoik , CT Scan Trifasik - enhance pada fase

arterial
STAGING OKUDA :
- Ukuran tumor >50% dari hepar Stadium 1 (-)
- Ascites Stadium 2 (1-2)
- Albumin <3 gr Stadium 3 (3-4)
- Bilirubin >3

Kriteria Diagnosis :
A. Penyakit Hati yang mendasari
B. Tumor Marker (AFP ≥ 200)
C.Radiologi
TREATMENT :
TACE - Kemoterapi intraarterial, Oklusi arteri hepatika-nekrosis tumor
Surgery ; Margin 1 cm - Wedge Resection, Segmentektomi, Lobektomi,

Trisegmentektomi
Kemoterapi : Doxorubicin, epirubicin dan cisplatin.

TOKYO GUIDELINE 2018
- Suspek Acute Biliary infection :

- Demam Vital Sign Acute Cholangitis
- Menggigil Physical examination or
- Nyeri Perut Lab + Radiologi Cholecystitis
- Ikterus Diagnostic
- Mual dan muntah
- Penurunan Kesadaran Nilai Severitas→ Terapi
- LABORATORIUM :
- WBC
- CRP
- PLT
- Pt/Aptt/Inr
- Albumin
- Bilirubin Total - Direct
- ALP
- GGT
- SGOT/SGPT
- BUN/Cr
- AGD
- Kultur darah
- Imaging :
- USG
- CT abdomen
USG : Cholecystitis
- pembesaran gallbladder (ukuran)
- Penebalan dinding
- Pericholecystic fluid
- Sludge Debris
- Murphy sign on USG
: Cholangitis
- Dilatasi duktus
- Kongesti ec Stenosis atau oklusi
- Biliary Calculus

Kriteria Diagnosis Cholecystitis : A-B-C
A. Tanda inflamasi lokal : - Murphy Sign

- Massa/Nyeri/Nyeri tekan RUQ
B. Tanda Sistemik : - Demam
- CRP meningkat
- WBC meningkat
C. Imaging : - Temuan kolesistitis
Suspek Cholecystitis : 1A + 1B
Definitif Cholecystitis : 1A + 1B + 1C

Kriteria severitas akut cholecystitis :
- Grade III (Disfungsi Organ) :-Cardiovaskular (hipotensi butuh

vasopresor)
- Kesadaran menurun
- Distres Nafas (PF ratio <300)
- Gangguan Ginjal (oligouria, Cr >2)
- Disfungsi Hepar (Pt, INR >1.5)
- Hematological disorder (Plt <100.000)
- Grade II (minimal 1) :
- WBC meningkat (>18.000)
- Massa teraba pada RUQ
- Durasi > 72 jam
- Lokal Inflamasi (Gangrenous, Abses
perikolesistik, abses hepar, peritonitis
bilier, emfisematous cholecystitis)
- Grade I (Mild) : tidak memenuhi kriteria II dan III (Orang

sehat yang menderita kolesistitis)

Kriteria Diagnosis Akut Cholangitis : A-B-C
A) Tanda inflamasi Sistemik : - Demam > 38℃ atau menggigil

- Laboratorium-inflamasi
(WBC <4 atau > 10 , CRP ≥ 1)
B)Tanda Kolestasis : - Jaundice (Bil. Total ≥ 2)

- Lab - Abnormal Liver Function
(ALP, GGT,AST,ALT > 1.5X)
C)Imaging : - Dilatasi Bilier

- Etiologi terbukti (striktur, batu. Stent)
Suspek : 1A+1B/1C
Definitif : 1A+1B+1C

Kriteria Severitas Akut Cholangitis
- Grade III (disfungsi organ) : - Cardiovaskular (Hipotensi butuh
support)
- Kesadaran menurun
- Disfungsi nafas (PF ratio <300)
- Gangguan ginjal (kreatinin >2, oligouria)
- Hepar (Pt, INR >1.5)
- Hematologi (PLT <100.000)
- Grade II (minimal 2) :
- WBC Abnormal (>12 atau <4)
- Demam tinggi ≥ 39℃
- Umur ≥ 75 tahun
- Hiperbilirubin ( Total ≥ 5)
- Hipoalbuminemia

Terapi :
Initial : IV fluid, Antibiotic, Analgetik

Hindari pemberian Opioid : menyebabkan kontraksi sphincter oddi
sehingga tekanan bilier naik.

PANKREATITIS
- Inflamasi non bacterial akibat aktifasi dan autodigesti sel enzim pancreas
- ETIOLOGI : I GET SMASHED (Idiopatic, Gallstone, Ethanol, Trauma, Steroid, Mumps,
Autoimun, Scorpion, Hiperalcemia, ERCP, Drugs).
- Gejala : Nyeri abdomen menjalar ke bahu diantara scapula, Cullen Sign (Ekimosis sekitar
umbilicus), Grey turner sign (Ekimosis di pinggang), Fox sign (Ekimosis inguinal),
Amilase dan Lipase meningkat (Lipase lebih spesifik).
- Diagnosis 2 dari 3 gejala : Nyeri akut abdomen atas, Peningkatan enzim pancreas,
radiologi (CT SCAN – BALTHAZAR)
- CT SCAN BALTHAZAR criteria, melihat peripancreatic fluid collection
- Operasi : Drainase Nekrotomi

SEPSIS
Disfungsi organ yang mengancam nyawa akibat dari disregulasi respon host
terhadap infeksi
Kriteria Klinis :
- Suspected infection
- SOFA score ≥ 2
Sepsis
Guideline 2021 - qSOFA ≥ 2 → Hipotensi (≤100), GCS ≤ 13, Takipnea ≥ 22.
menyarankan
pemakaian - SIRS : 2 dari 4 → Temperatur <36 c atau >38 c
SIRS, NEWS,
MEWS Nadi >90x/ menit
dibandingkan
qSofa Pernafasan >20x/ menit
WBC <4000 , >12.000
SOFA SCORE NILAI :
1. Otak : GCS
2. Paru : P:F Ratio <400
3. Jantung : MAP <70 atau dengan bantuan vasopressor
4. Liver : Bilirubin >1.2
5. Renal : Kreatinin >1.2
6. Koagulasi : Plateler <150.000

SYOK SEPSIS :
Episode sepsis dimana sirkulasi dan abnormalitas metabolik cukup untuk
meningkatkan mortalitas
Kriteria klinis :
Sepsis + Terapi vasopressor untuk mempertahankan MAP ≥ 65 mmHg +
Laktat >2 mmol/L meskipun resusitasi adekuat.
Manifestasi klinis sepsis :
1. Paru : ARDS → Kapiler Bocor
2. Myokardium → Peningkatan pelepasan NO
3. CNS menurun akibat dari menurunnya sirkulasi
4. Ginjal → Oligouria
5. Metabolisme meningkat menyebabkan hiperglikemia+Katabolisme otot
1 HOUR BUNDLE :
Laktat 1. Ukur laktat (> 2 mmol/L)

meningkat
akibat dari
2. Kultur Darah
pembakaran
glukosa
3. Antibiotik broadspektrum (cephalosporin based + metro)
terhambat oleh
sitokain
4. Rapid cristalloid 30 ml/kgBB jika hipotensi atau laktat ≥4
sehingga mmol/L (dalam 3 jam), bisa dilakukan fluid challenge 4ml/kg.
piruvat Gunakan kristalloid dibandingkan NaCl karena efek samping
berubah membuat renal vasoconstriction dan AKI.
menjadi laktat
5. Vasopressor selama atau setelah resusitasi dengan target
MAP ≥ 65 mmHg, Norepinephrine pilihan pertama.
6. Setelah itu dilakukan SOURCE CONTROL
Timing of Source control :
- SSC guideline : as soon as medically and logistically practical after diagnosis
(6-12 jam)
- RCSE guideline ; 6 Jam
ELEMENT OF DAMAGE CONTROL SURGERY :
- Resection without anastomosis
- Temporary drainage
- Abdominal Packing
- Temporary closure.

Mengukur Respon Terapi :
- Hemodinamik Monitoring
- Temperatur ekstremitas
- CRT
- Procalcitonin
- Passive leg raise atau fluid challenge 4ml/KgBB
Biomarker untuk respons terapi dan diagnosis dini :

* Procalcitonin
* Galactomannan & B-D Glucan untuk Jamur
* Sitokin (IL-6,8,10), TNF-a
* Laktat dengan target penurunan mendekati normal
Vasoaktif :
- Norepinephrin : 0.05-1 mcg/KgBB/menit (encerkan 4mg/50cc)
- Dopamin : 2-20 mcg/kgbb/menit
- Dobutamin : 2-20 mcg/kgbb/menit
-ANTIBIOTIK :
- Karbapenem
- Penicilin / B-Lactam inhibitor
Ditambahkan antibiotik gram (-)
Bila MRSA diberikan Vancomycin
Bila infeksi jamur diberikan Amphotericin B
-TRANSFUSI :
Transfusi darah bila Hb <7.0
Transfusi PLT bila PLT <10.000
<20.000 Bila perdarahan
≥50.000 bila perdarahan akut dan akan operasi

-Ventilasi mekanik :
Pada ADRS dengan PF Ratio ≤ 300 sebagai lung protective strategi dengan
Volume Tidal 6ml/KgBB dan PEEP tinggi (permissive hiperkapnia)
-Kontrol Gula Darah Rutin dengan target < 180
- Bila curiga DVT diberikan LMWH (Enoxaparin) 1mg/kgBB SC q12Hr (5 hari)

dengan target INR 2-3x
- Cegah stress ulcer dengan pemberian PPI atau H2R blocker
- Nutrisi diberikan :
- Kalori : 25 Kcal/kgBB/Hari
- Glukosa : 4-5 ml/KgBB/menit
- Protein : 1-1.5 gr/KgBB/Hari
- Lemak : 25-30% dari kalori
- Immunonutrisi : omega 3
- Asam amino essensial : Glutamin 0.5 gr/kgbb/hari

NUTRISI
- Malnutrisi yaitu kekurangan intake disertai peningkatan uptake.
- Pengukuran status malnutrisi dapat menggunakan NRS atau SGA.
- Tentukan kebutuhan volume dan kalori dalam 24 jam
A) Pada pasien under weight hitung berat aktual
B) Pada pasien over weight hitung berat ideal
- Kebutuhan 24 jam :
A) Volume : 30-50 ml/KgBB/24 Jam
B) Kalori : 20-25 Kcal/KgBB/24 Jam (sakit berat x60)
C) Protein : 1 gr/KgBB/24 Jam (x4 = kcal)
D) Karbohidrat (dextrose) : 4gr/KgBB/24 jam atau

Kalori-protein-fat = x Kcal
E) Kalium : 1 mEq/KgBB/24 Jam
F) Natrium : 3 mEq/KgBB/24 Jam
G) Fat : 1 gr/KgBB/24 Jam (x10 = Kcal)
- Critically ill (pasien ICU >48 jam) memiliki resiko malnutrisi, segera
dimulai intervensi gizi.
- Rute pemberian gizi secara short term <4 minggu melalui NGT dan
pada long term >4 minggu melalui percutaneus feeding.
- Jika ada intoleransi pada enteral feeding dapat diberikan agen

prokinetik; 1. Eritromicin 100-250 mg/8 jam (2-4 hari), atau 2.
Metoclopramide 10 mg 2-3 kali per hari. Jika masih intoleransi dapat
dicoba post pyloric feeding.

- Enteral feeding harus ditunda bila :
- Syok belum teratasi (dapat dimulai jika stabil dengan

vasopressor)
- Tanda bowel iskemia
- Hipoksemia
- Residu >500 cc
- Kontraindikasi absolut :(dapat dimulai TPN jika ada

kontraindikasi)
- Bowel obstruksi
- Bleeding GIT
- Iskemia bowel
- Tidak ada akses ke GIT
- Abdominal kompartemen sindrom
- Muntah, Residu >500 cc / 6 jam
- Anastomosis yang tidak aman
- Sebaiknya diberikan nutrisi parenteral 3 in 1 : asam amino, fat dan

glukosa.
- Lemak berfungsi sebagai pengangkut vitamin ADEK, dan pada

pasien sakit berat membutuhkan sumber energi dari lemak,
karbohidrat dan protein.
- Perhatikan osmolaritas cairan iv:>900 mOsm/L harus vena

sentral

- Oligometric Formula Categories
Makronutrient facilitate digestion and absorbtion
Component :
- Asam amino : glutamine, arginine
- Peptide
- Monosakarida
- Disakarida
- MCT
- Vitamin & Mineral
Indikasi :
- IBD
- Malabsorbsi
- Short Bowel Syndrome
- Radiation Enteritis
- Early Enteral Feeding
- Pancreatic Insufficient
- Enteral Feeding :
- 250-500 ml formula (5-8x daily)
- hari 1 : 1000 ml
- hari 2 : 1500 ml
- hari 3 : sesuai kebutuhan

- Tujuan Early Feeding :
- Mempertahankan integritas mukosa
- Menurunkan morbiditas
- Nutrisi selama stres metabolik.

INTRA ABDOMINAL HIPERTENSION
Pengukuran menggunakan kateter urine dengan cairan 20-50cc
dikonversi ke mmhg dengan mengalikan 0.74
GRADE IAH:
1 12-15 mmHg
2 16-20 mmhg → oligouri
3 21-25 → Anuria +/- ↓ Cardiac Output
4 >25 → Anuria +/- ↓ Cardiac Output
ACS : >20 mmHg dengan disfungsi organ
Respon terhadap IAP > 20 mmHg :
- Vena Cava Tertekan → menurunkan Cardiac Output
- Tekanan Diafragma meningkat → gangguan ventilasi
- V. Renalis tertekan → Oligouria → AKI
- Aorta Tertekan → Hipoperfusi Ekstremitas
- Hipoperfusi Splanknik → Iskemia organ intraabdomen
ASIDOSIS METABOLIK MODS

ETIOLOGI :
1. Penurunan komplians abdomen : - Luka bakar
- Penutupan abdomen ketat
- Ventilator mekanik
2. Peningkatan isi lumen : - ileus
- Volvulus
3. Peningkatan tekanan intra abdomen : - Laparoskopi
- Pneumoperitoneum
- Tumor
4. Bocor Kapiler : - Resusitasi Masif
- Pankreatitis

Management :
- Evakuasi konten intralumen
- Evakuasi lesi intra abdomen
- Meningkatkan komplians abdomen
- Optimalisasi Cairan
- Optimalisasi perfusi organ

PENYAKIT USUS IRITATIF
Crohn Disease :
Segmental / discontinous location of inflammation, dapat terjadi di

sepanjang saluran cerna, mulut hingga anus.
- Gejala : Nyeri abdomen, Diare berdarah dan berlendir, BB menurun, arthralgia,

demam, konjungtivitis, uveitis, koagulopati.
- Colon in loop : Skip lesion
- Colonoscopy : Cobble-stone appearance, Asimetric

eritema, apthous ulcer
- PA : Minimal goblet cell mucin depletion, vasculitis,

fibrous and strictur, apthoid ulcer.
- Terapi : kortikosteroid (prednison 10-40mg/hari),

sulfasalazin 2-8gr/hari p.o
Kolitis Ulseratif:
Continuos lesion terbatas sepanjang colon
- Gejala : Diare frekuen, nyeri kolik, urgensi dan tenesmus
- Colon in loop : haustra menghilang, tampakan seperti pipa

(lead pipe appearance)
- Colonoscopy : Ulserasi, granular, Pola vaskuler

menghilang.
- PA : mucosal inflammation, loss of mucosa with retention

of crypt, Deeper submucosa inflamation.
- Terapi : Steroid lokal (enema), sistemik 60 mg/hari,

sulfasalazin 2-8 gr/hari p.o

DIVERTICKEL COLON
- Protrusi dinding colon berbentuk kantong
→ True divertikel : Seluruh lapisan dinding colon (biasanya kongenital)
→ False : Mukosa dan submukosa yang herniasi, tidak disertai lapisan

muskular,
- Lokasi tersering di sigmoid (95%)
- Patofisiologi : Peningkatan tekanan intralumen, mendorong mukosa ke

defek dinding usus. Tekanan tertinggi terdapat di sigmoid. Hukum Laplace -
Tekanan pada dinding lumen sebanding dengan radius dan tekanan
intralumen
- Klasifikasi : Divertikulosis - Asimptomatik
Divertikulitis akut - keluhan dengan inflamasi
Simple : Terlokalisir
Complex : Disertai fistula, obstruksi, striktur.
- Gejala : 80% asimptomatik
Nyeri Abdomen terutama pada kiri bawah
Diare
Obstipasi
Massa iliaka sinistra
- Diagnosis : Foto polos abdomen, Barium enema, Endoskopi, CT-Scan
- Klasifikasi Hinchey : stadium I : Abses perikolik
II : Abses pelvis
III : Peritonitis Purulen
IV: Peritonitis Fekal

- Stadium I dan II : One stage opertion, Stadium III dan IV : two stage
operation
- Terapi : Diet tinggi serat
NPO pada kasus akut
Antibiotik
Operatif (one stage atau two stage) bila ; peritonitis, obstruksi,

perdarahan.
- Komplikasi : perdarahan, perforasi, abses, fistel, striktur, obstruksi

• International Anaesthetic Societies recommend a 6-h pre-
operative fast for solids and a 2-h fast for clear liquids,
including carbohydrate drinks.

FISTULA ANI
- Anamnesa :
- Keluar cairan purulen
- Benjolan anus
- Pruritus ani
- Nyeri saat defekasi / batuk
- Riwayat abses
- demam
- Pemeriksaan Fisik :
- RT : Bidigital - teraba tract seperti tali dan Nilai eksternal opening
- Penunjang :
- Fistulografi
- MRI
- Anuskopi - Injeksi methilen Blue

- Klasifikasi PARKS :
-Superficial fistula (simple)
-Intersfingterik (Parks tipe 1, Simple)
-Transsphincteric (Tipe 2, Kompleks)
-Suprasphincteric (Tipe 3)
-Ekstrasphincteric (Tipe 4)
Complex : Muara multiple, melewati otot sfingter.
- TREATMENT : Fibrin plug, Fistulotomy, Fistulectomy, Seton Procedure

(kompleks), Laser. Post op : Sith batz, Stool softener, Penyembuhan 6 minggu.

HEMOROID :
Prolaps anal cushion menyebabkan dilatasi plexus hemoroidalis.
Management :
- Non Invasif :
Hidrosmin
MPPF → Ardium → 3x1000 selama 4 hari, 2x1000 3 hari, 2x500 2 bulan
Merupakan suatu venotonik : 1. efek mikrosirkulasi - menurunkan permeabilitas
kapiler, 2. efek meningkatkan tonus vena, 3. efek hemoreologi - menurunkan
agregasi platelet.
Laksatif
Diet tinggi serat
Hindari mengedan lama
- Invasif : Stappler, HALRAR, Open hemorroidektomi.
- Klisma pre operasi

- Dilatasi manual
- Klem arah jam 3,7,11
- insisi hingga base hemoroid/ linea pectinea
- tutup dengan chromic 0/3-0
- metode open/closed : white head, ferguson, stone, milligan morgan (tidak
ditutup)

FISTULA ENTEROCUTANEUS
- Low Output <200 ml/hari

- Moderate 200-500 ml/hari
- High output > 500 ml/hari (diberikan Normal saline + 10 meq KCl)
- Causa tidak menutup : FRIEND

F : Foreign Body
R : Radiation
I : Infection / Immunodefisiensi
E : Epitelialisasi
N : Neoplasma / Nutrisi
D : Distal obstruksi
- Management : SNAP
S : Sepsis Management (Antibiotik, Drainase Abses)
N : Nutrisi (Koreksi Cairan dan Elektrolit, Parenteral feeding)
A : Anatomi fistula
P : Procedure (Planing)
- Konservatif : menutup spontan 30 hari - 8 minggu , pemberian somatostatin
analog bolus 250 mg iv selama 5 hari (kalau octreotide 50 U/hari), untuk
menurunkan output, mengurangi motilitas dan menghambat sekresi hormon.
- Dapat juga diberikan anti diare (loperamide), PPI atau H2R blocker atau
sukralfat.

Definitive repair of the ECF should be planned if no spontaneous closure
occurs by 12 weeks after sepsis control, nutritional optimization, and
establishing wound cares.
(Enterocutaneous Fistula: Proven Strategies and Updates. Clin Colon Rectal
Surg 2016;29:130–137.)

KOREKSI ELEKTROLIT :
KOREKSI NATRIUM :
PRIA : (140-X) x 0.6 x BB
WANITA : x 0.5
Dengan NaCl 3% (1000 cc = 512 mEq)
Jika sadar 0.5 mEq/Jam, Jika kesadaran menurun 1 mEq/jam
Bila terlalu cepat dapat terjadi myelisis pontin
KOREKSI HIPOKALIUM :
(4-X) x 0.3 x BB
KCl 25 mEq → 1 cc = 1 mEq
Maximal 10 mEq/Jam
Maximal 60 mEq dalam 1000cc NaCl 0.9%
KOREKSI HIPERKALEMIA :
Ca. Glukonas 1 ampul (1 kali)
D40% (25 ml) + 2 U actrapid (insulin) → bisa diulang 3x dalam 1 jam
Maintenance : 1 flacc D10% + 20 U insulin / 24 jam
KOREKSI ALBUMIN :
(4-x) x 0.8 x BB = X gr → rubah ke ml (20% - X gr dikali 5)(25% - X gr dikali 4)
KOREKSI DEFISIT CAIRAN :

- 0,4 x BB x (Na/140-1)
- Defisit cairan + IWL + Urine (24 Jam)
- IWL = 10cc/KgBB/24 Jam, 15xBB/24 jam = X cc/Jam
DARAH :
WB : ∆ Hb x BB x 6
PRC : ∆ Hb x BB x 3
TC : 10ml/KgBB
FFP : 10-20 ml/KgBB (1 cc/KgBB/Jam)

NILAI LABORATORIUM
HB : 12-16
HCT : 40-55
WBC : 4-11
PLT : 150-400.000
SGOT : 10-40
SGPT : 10-50
ALBUMIN : 3-4.5
GGT : 5-40 (meningkat kerusakan hepar)

ALP : 20-140 (Enzim hati yang masuk ke empedu)
Bil. Dir : <0.4

Bil. Total : <1.2
AFP : < 20
Amilase : 50-120
CRP : <10 mg/L atau <1mg/dL

Procalcitonin : 0.05
Cr : 1.3
Ur : 10-50
Na : 135-145
K : 3.5-5
Cl : 94-111
Ca 153 : 0-30
Ca 199 : 0-37 (Pankreas)

CEA : 0-3.4
LDH : 110-210
PSA : 0-4
Laktat : <2
Calcitonin : 2-26

BENANG
ABSORBABLE
Braided Polyglicolic acid (Dexon) - Rapid
Polyglactin (Vicryl) - Rapid
Gut
Monofilamen Polyglecaprone (Monocryl)
Polydiaxone (PDS) - Slow absorb
Polygliconat (Maxon) - Slow
NON ABSORBABLE
Braided Silk
Polyester
Monofilament Nylon (Ethilon)
Polypropylene (Prolene)
Tutup perut pakai nomor 0/1 slowly resorbable monofilament

TIROID
Struma Nodosa Toksik/Non-Toksik (Nodul tiroid)
Klasifikasi :
1. Well Differentiated (90%) ;
A. Papillary Carcinoma (80%, terbanyak) : metastase via limfogen
B. Follicular Carcinoma (10%) : metastase via hematogen -- metastase
jauh ke tulang pipih menimbulkan lesi blastik (tampakan radioopaque pada
xray/biasanya teraba benjolan)
C. Hurtle cell tumor
2. Undifferentiated (5%) ; Anaplastik
3. Medullary thyroid carcinoma (4%) ; sifatnya familial, berasal dari sel
parafolikuler, cenderung metastase jauh
4. Miscellaneus (1%) ; Lymphoma

PERKENALKAN DIRI, MENANYAKAN IDENTITAS, UMUR, ALAMAT
Anamnesis :
1. GEJALA UTAMA : Benjolan pada leher, nyeri pada leher, luka pada leher
2. ONSET : sejak kapan, benjolan awal sebesar apa, saat ini sebesar apa
3. GEJALA PENYERTA : Nyeri pada leher, sulit menelan, sulit bernafas, sesak,
demam, suara serak
4. METASTASIS : Sesak, Nyeri Kepala, Nyeri Dada, Kesadaran Menurun, Nyeri
tulang/benjolan, rasa penuh di perut
5. GEJALA FUNGSI TIROID : berdebar, keringat, gemetar, sulit tidur, berat badan
turun, diare (Hipertiroid), muka bengkak, mudah lelah, konstipasi, obesitas (Hipotiroid)
6. FAKTOR RESIKO : riwayat radiasi, riwayat keluarga (Meduler)
7. RIWAYAT PENYAKIT DAHULU/PENGOBATAN : radiasi, riwayat tumor
8. RIWAYAT DIET : Kurang konsumsi iodium (goiter/hipertiroid)
9. TEMPAT TINGGAL :Pegunungan (folikuler), pantai (papiler), tetangga penyakit
sama (endemik)
10. AKTIFITAS FISIK : Bekerja, merawat diri (karnofski)

PEMERIKSAAN FISIK :
1. STATUS GENERALIS
2. STATUS VITALIS
3. STATUS PERFORMANCE
4. PERIKSA HEAD TO TOE
5. STATUS LOKALIS :
PASIEN POSISI DUDUK DENGAN KEPALA SEDIKIT EKSTENSI
Inspeksi : Benjolan ikut gerak menelan, warna kulit, luka, benjolan di daerah lain (KGB)
Palpasi dari belakang : konsistensi (solid/kistik/mix), lokasi, ukuran, batas, mobile,
permukaan, nyeri tekan, cek KGB level 1-6, bandingkan
kontralateral
Perkusi : manubrium sterni -- normal nya sonor (ekstensi
tiroid ke thorax)
Auskultasi : Bruit pada benjolan (hipervaskularisasi)
6. PEMERIKSAAN TAMBAHAN :
Pemberton Sign (obstruksi thoracic inlet)
Kocher Test : tekan benjolan muncul stridor (Penyempitan Trakea)
Berry Sign : tidak teraba a.carotis (massa mendorong/meng-encase)
Horner Syndrome : miosis, ptosis, enoptalmus, anhidrosis (penekanan saraf simpatis)
Kista tiroglosus : menjulurkan lidah , benjolan tertarik (ada foramen caecum)
Differential Diagnosis : Limfoma Maligna, Kista ductus tiroglosus
KLINIS CURIGA MALIGNANT NODUL TIROID :

Usia Muda 20-30 tahun atau usia diatas Benjolan padat, terfiksir dan irreguler
60 tahun
Pria Vokal paralisis / serak
Tumbuh Cepat Limfadenopati
Perubahan suara, menelan dan

bernafas
Riwayat Radiasi
Riwayat Keluarga

1. Congenital : agenesis, hipoplasia, ektopik, kista duktus
tiroglosus
2. Inflamasi : subakut (dequervain) akibat virus, hashimoto
(autoimun)-- hipotiroid (painless enlargement)
3. Gangguan Fungsi :
A. Hipotiroid : creatinisme (anak),
Mixedema (dewasa)
B. Hipertiroid : tirotoxicosis
Causa : - Graves disease (struma difusa toxic) trias tiroid
membesar, mata menonjol, tungkai bengkak
- Goiter (endemik) kekurangan iodium
Laboratorium :
Cek FT4 dan TSH
FT4 = kenapa di cek, Free tiroid yang ada ditubuh setelah T3 habis/terpakai lebih dahulu.
Nilai normal : FT4 (0.8-2.8 ng/ml), TSH (0.4-4.0 U/ml)
HASIL LAB KLINIS RENCANA Tx
TSH meningkat, FT4 hipotiroid subklinis (terkompensasi atau FNAB
normal dalam pengobatan)
TSH meningkat, FT4 turun hipotiroid FNAB
TSH menurun, FT4 normal hipertiroid subklinis Scintigrafi /
medikamentosa
TSH menurun FT4 naik hipertiroid Scintigrafi /
medikamentosa
TSH dan FT4 turun secondary hipotiroid, pituitary problem diagnostik
Cek Calcitonin jika curiga medullare

Cek Tiroglobulin hanya untuk follow up rekurensi (penanda tumor) setelah 6 bulan, target 0

RADIOLOGY : USG, CT-SCAN, Thorax X-Ray, USG Abdomen
USG Thyroid :
Curiga ganas ; A. Hipoechogen
B. Mikrokalsifikasi sentral
C. Irreguler border
D. Absence periferal halo
E. Vaskularisasi intranodul
F. Ratio AP:transversal >1
FNAB / BAJAH
Selain FNAB bisa Core Biopsy, FNAB hanya melihat citology, FNAB melihat
histopatologi
Keterbatasan FNAB ; sampel tidak adekuat dan pada jenis folikuler neoplasia

STAGING
T1 ≤ 2 Cm terbatas di tiroid (st.I)
T2 >2-4 Cm terbatas di tiroid (st.I)
T3a >4 Cm terbatas di tiroid (st.II)
T3b ekstensi ekstra tiroid hanya pada strap muscle (sternohyoid, sternothyroid,
thyrohyoid and omohyoid muscle)
T4a ekstensi ke subcutan, laring, trakea (Kocher Sign), esofagus atau N. laringeus
(Serak) (st.3)
T4b Ekstensi fascia prevertebra / a. carotis (Berry Sign) / mediastinal vessel
(Pemberton Sign) (IVa)
N1 Regional Node : 1a level VI/VII, 1b level I-V (st.II)
M1 distant Metastase (IVb)

1. Pada jenis differentiated lihat usia dibawah 55
tahun hanya ada 2 stadium, stadium 1 tanpa
metastase dan stadium 2 dengan metastase (M1)
2. Usia diatas 55 tahun ada 4 stadium, T1-2

(stadium 1), T3a/T3b - N1 (stadium 2), T4a
(stadium 3), T4b (stadium 4a), M1 (stadium 4b)
3. Pada anaplastik langsung stadium IV (a,b,c)
ADA 3 ALGORITMA PENATALAKSANAAN , PILIH SALAH SATU MENURUT

KETERSEDIAAN SARANA
- Algoritma triple diagnostik (klinis,usg,fnab)
- Algoritma Frozen Section
- Algoritma Sidik Tiroid/ Scintigrafi
Setelah triple diagnostik , tentukan resiko nya dengan AGES/AMES/MAGES (Risk of
Death), lalu setelah operasi total tiroid tentukan resiko rekurensi dengan ATA/ETA.

NCCN

Indikasi total tiroid :
- nodul bilateral Nodul jinak :
<2 cm : observasi/supresi
- ekstensi ekstratiroid
levotiroksin mulai dosis kecil
- metastase nodul atau metastasis jauh 1 mcg/kgbb lalu follow up 6
bulan jika membesar lakukan
- tumor >4cm, poorly differentiated ismolobektomi
- karsinoma papiler high risk
>2 cm : ismolobektomi
- folikuler
- meduler
- anaplastik

Terapi :
Operasi :
PRIMER : - Lobektomi NECK DISSECTION :
- Ismolobektomi - SND (Selective)
- Near Total -RND(tumorprimer
resectable)
- SubTotal tiroidektomi -Central Dissection(KGB level VI)
- Total Tiroidektomi -Lateral Dissection (KGB Lateral)
I. Lobektomi :
• Incisi kulit collar ( sesuai lipatan kulit ) diatas tumor

• Incisi diperdalam sampai sub platysma dengan ligasi
vena jugularis anterior
• Dibuat flap keatas sampai polus superior thyroid dapat
dicapai
• Dibuat flap kebawah sampai 1 jari diatas incisiura
jugularis
• Buka garis tengah (inter muscularis Sterno hyoid)
• M. Sterno hyoid & sterno thyroid disisihkan ke lateral, bila sulit ke 2 musculus
tersebut dipotong
• Thyroid dibebaskan ke medial - ligasi pembuluh darah kecil. Bebaskan para
thyroid
• Polus superior dibebaskan dengan ligasi a. thyroidea superior & preservasi n.
laryngeus externus. (SILK 3.0)
• Polus inferior dibebaskan dengan ligasi a. & v. thyroidea inf. preservasi
n.recurrens laryngeus unilateral & dilakukan lobectomy - kontrol perdarahan.
• Jahit otot bila dipotong – pasang drain hisap aproximasi m. sterno hyoid
II. Untuk Isthmolobectomy

Sama seperti diatas, tambahan dilakukan pengangkatan kel. Isthmus &
kel. pyramidalis.
III. Total Thyroidectomy
• Incisi diperdalam sampai sub platysma dengan ligasi v. jugularis anterior
• Dibuat flap keatas sampai polus superior dapat dicapai
• Dibuat flap ke bawah sampai I jari diatas incisiura jungularis
• Buka garis tengah (inter musculare sterno hyoid stemo thyroid disisihkan ke
lateral bila sulit ke 2 musculus tersebut dipotong
• Thyroid dibebaskan ke medial – ligasi p. darah bebaskan parathyroid
• Polus superior dibebaskan dengan ligasi a & v. thyroidea superior preservasi n.
laryngeus externus.
• Polus inferior dibebaskan dengan ligasi a & v. thyroidea inf.
• Preservasi n. recurrens laryngeus inferior
• Demikian seterusnya dilakukan sesuai diatas pada lobus sebelahnya
• Selanjutnya dilakukan pengangkatan lobus isthmus & pyramid sampai terlihat
trachea
Near Total : Jika terdapat infiltrasi, berfungsi sebagai organ saving, 1-2 gr
Sub Total : mempertahanan fungsi, dipertahankan sebesar jempol/ 5 gr, pertahankan
lobus superior disuplai dari a.thiroidea superior

Kelenjar paratiroid
berwarna keemasan dan
tenggelam di NaCL. Dapat
ditanam di
sternocleidomastoideus
atau deltoideus
Cara mengidentifikasi n. laringeus recurrent ;

TUBERKULUM ZUCKERCANDLE dekat paratiroid superior
dibawahnya terdapat nervus laryngeus recurrent dan bersilangan
dengan A. thiroidea inferior dapat juga disusuri sulkus
tracheoesofagus.
Bisa juga menggunakan alat intraoperative neural monitoring.
N. Laryngeus Superior terbagi 2 cabang :

- cabang interna sebagai sensoris pada mukosa laring (jika cedera resiko aspirasi/tersedak saat minum)
- cabang eksterna mengakibatkan suara low pitch/ lemah
N.Laryngeus Inferior (Rekuren) : paralisis vocal cord (serak). sesak pada cedera ipslateral dan
obstruksi nafas pada bilateral.
Functional Neck Dissection : mempertahankan 3 organ penting

SND : mempertahankan m.sternocleidomastoideus, n. accesorius, dan
jugularis interna.
RND, 3 tipe : I. preservasi N.Accesorius, II. Preservasi Jugularis, III. Preservasi
ketiganya (fungsional)

Komplikasi :
-Trakeomalasia : dilakukan delayed ekstubasi (5-7 hari) dan pemberian ca. Gluconas,
bisa sampai trachestomy
-Hemoragik
-Obstruksi nafas
-N.Laringeus rekurent palsy dan perubahan suara
-insufisiensi tiroid
-infeksi luka operasi
-scar
-Paratiroid insuffisiensi = hipokalsemia (chvostek sign, carpopedal spasm,
aritmia)
Terapi dengan calcium gluconas intravena : 1 ml/kgBB (10% ca.gluconas 1
amp=10ml) Dalam 500 ml D5% selama 8 jam.
Post Operasi :
* Lihat resiko rekurensi sesuai ATA/ETA, jika resiko sedang atau tinggi lanjut ke
sidik tiroid (max. 3 bulan post operasi) jika ada residu lanjutkan ke ablasi I-131 bila
tidak ada residu lanjut ke terapi supresi, jika resiko rendah lanjutkan terapi supresi.
* Pada terapi supresi levotiroksin terdapat target TSH pada kunjungan follow up
sesuai resiko.
- resiko rendah :0,5-2 U/mL
- resiko sedang : 0,1-0,5 U/mL
- resiko tinggi : <0,1 U/mL
Dosis awal bisa 1x50 mcg
Supresi vs Substitusi :
- Supresi pada kasus maligna (1x100 mcg)
- substitusi pada kasus jinak atau kasus ganas yang selesai pengobatan (1x50 mcg)

Adjuvant :
Hormonal (supresi/substitusi)
RAI (I-131)
Radiasi Eksterna
Targeting Terapi (sorafenib)
Kemoterapi
*Pada kasus metastase berdiferensiasi buruk
* Radioiodine Ablative (RAI)

- ablasi sisa jaringan tiroid dan mikroskopik residual
- untuk high risk (ATA/ETA)
- tidak pada low risk
- direkomendasikan pada diferensiasi baik yang metastasis jauh yang menyangat
ablasi
- metastasis KGB
- ekstensi ekstratiroid dan ukuran >4cm
Thyroid gland
mengabsorbsi
iodin dan
bertujuan untuk
radiasi sel kanker
Persiapan :
- diet rendah iodium
- puasa levotiroksine 3 minggu (target TSH>30), dilanjutkan 3 hari setelah radiasi
- bisa injeksi rekombinan TSH pada pasien yang tidak puasa levotiroksine
- dosis ablasi 100-200 mCi

* Radiasi Eksterna
- Paliatif Unresectable
- Obstruksi SVC (pemberton sign)
- medullary tiroid
- anaplastik tiroid
- cervical/mediastinal bulky nodes
* Hipertiroid
Pada sidik tiroid didapatkan hot nodul diberikan medikamentosa :
- lugolisasi : untuk memadatkan tiroid agar vaskularisasi kurang (7 hari preop dosis 3
dd 2 gtt)
- tiamazole 20 mg/hari
- PTU 100-150 mg/8 jam
- b-blocker 5-40mg - 4x1
Atau RAI atau tiroidektomi subtotal bila gagal terapi medikamentosa

TIROID STORM : imbalance hormon tiroid akibat tubuh terbiasa dengan kadar tiroid
tinggi tiba-tiba rendah.
MEDULLARY THYROID CARCINOMA
- Asal dari parafolikuler

- Cek calcitonin, CEA, Calcium pre-operasi
- Management :
1. Tanpa KGB : TT + Bilateral central lymph node diseksi
2. KGB (+) : TT + LND (level II,III,IV,V)
TT + Diseksi KGB sentral (Level 6) ----> cek calcitonin basal (>150

lakukan usg/pet scan tiap 3 bulan)
Bila residif -> locoregional -> radioterapi
Tidak residif -> levotiroksin + staging per tahun.
ANAPLASTIC THYROID CARCINOMA
- Paling agresif
- Management :
Resectable : TT + Radiasi Eksterna
Unresectable : Radiasi eksterna, Targeting terapi, tracheostomy.

BREAST CANCER
1. PERKENALKAN DIRI, MENANYAKAN IDENTITAS, UMUR, DAN TEMPAT

TINGGAL
2. ANAMNESIS :
- KELUHAN UTAMA : Benjolan di payudara/ketiak, Luka, keluar cairan dari

puting, perubahan warna kulit, Nyeri
- PROGRESIFITAS = * ONSET : Doubling time (membesar dengan cepat /2

kali lipat dalam 100 hari)
* INFILTRASI : muncul luka pada kulit payudara, perubahan

warna kulit, keluar cairan dari putting, puting tertarik kebelakang,lengan
bengkak.
* METASTASIS : Nyeri tulang belakang (tersering karena

aliran vena terlebih dahulu ke vena vertebralis), sesak, nyeri kepala atau
rasa penuh pada perut (hepar)
- GEJALA PENYERTA : Demam, Nyeri (curiga mastitis) dan apakah ada

benjolan di tempat lain (axilla).
- FAKTOR RESIKO : ADA 3 ; GENETIK , HORMONAL, LINGKUNGAN/Life

style
ETIOLOGI : * Paparan Hormon Estrogen ;

Congenital
Inflamasi
Neoplasma
1. Usia menarche ; resiko bila menarche <12 tahun
Trauma
Acquired 2. Usia menikah, apakah ada anak ; resiko bila nullipara
3. Usia anak pertama ; usia saat melahirkan >30 tahun
4. Riwayat menyusui berapa lama,
5. Riwayat kontrasepsi hormonal ; resiko bila oral >10 tahun

6. Late menopause >55 Tahun
* Riwayat Keluarga ; menderita penyakit tumor payudara atau ovarium.

* Riwayat life style ; diet kolesterol, obesitas, alkohol, merokok,
olahraga/aktifitas fisik saat ini
- PENYAKIT LAIN : Komorbid DM/HT/CHF
- PENGOBATAN SEBELUMNYA / RIWAYAT TRAUMA
3. PEMERIKSAAN FISIK
- STATUS GENERALIS : Sakit Sedang/Gizi Cukup/Compos Mentis
- STATUS VITALIS
- STATUS PERFORMANCE
- HEAD TO TOE : periksa sklera ikterik, konjungtiva anemis, benjolan pada

leher/ketiak/inguinal, udem ekstremitas, abdomen dan thorax.
- STATUS LOKALIS : CEK KONTRALATERAL JUGA !
Posisi pasien duduk dan baring, posisi tangan di samping/di angkat/di

pinggang/di belakang kepala.
INSPEKSI : 1. SIMETRIS ATAU TIDAK : Jarak papila ke garis tengah
2.PAPILA : apakah ada discharge, retraksi, ulkus
3.KULIT : apakah ada ulkus, warna kulit, dimpling (infiltasi

ligamentum cooper), udem, peau d’orange, scar post op

4.NODUL : tumor, nodul satelit, lihat payudara dan axilla nya
PALPASI : MULAI DARI SISI SEHAT
DESKRIPSIKAN TUMOR : Lokasi (Quadran), Ukuran, Konsistensi

padat/kenyal, batas tumor, permukaan, ekstensi / perlekatan / mobile (tangan
pasien di pinggang jika ikut kontraksi melekat di pectoralis), nyeri.
PERIKSA KGB : AXILLA, MAMMARIA INTERNA, INFRAKLAVIKULA,

SUPRAKLAVIKULA
PERIKSA KONTRALATERAL

4. RADIOLOGI
- USG MAMMAE bila usia <35 tahun (Jaringan

mammae masih padat)
Curiga keganasan bila terdapat :
1. Permukaan/batas irreguler
2. Taller than wider
3. Tepi hiperekhoik
4. Vaskularisasi meningkat
5. Echo interna heterogen
- Mammografi pada usia >35 tahun dan ukuran tumor ≤3 cm (kepadatan

payudara kurang)
- posisi CC (craniocaudal)
Curiga keganasan bila terdapat :
1. Stellata sign
2. Mikrokalsifikasi clustered (berkelompok)
3. Massa irreguler
4. Densitas meninggi
5. Translusen disekitar tumor

KRITERIA BIRADS

-XRAY THORAX untuk menilai metastase pada paru, terlihat coin lesion
berupa nodul metastase dengan ciri permukaan reguler dan kebanyakan
berada di apex
-USG ABDOMEN
- CORE BIOPSI
-XRAY VERTEBRA ↓
- Biopsi insisi >3 cm
5. HISTOPATOLOGI ↓
- Biopsi eksisi <3 cm
↓
TUJUAN : 1. DIAGNOSIS
- IHK (ER,PR,HER2,KI-67)
2. MORFOLOGI
3. GRADING : IHK UNTUK MENILAI 1. INVASI LIMFOVASKULAR

(MIKRO METASTASE), 2.MITOTIC TIME, 3. TUMOR INVASI
LIMFOSIT
4. TERAPI
5. PROGNOSIS
JENIS :
*NON INVASIVE EPITELIAL :
- LOBULAR CARCINOMA (biasanya pada kanker payudara

bilateral) - DUCTAL CARCINOMA/INTRADUCTAL
*INVASIVE EPITELIAL ( infiltratif keluar dan menembus membrana

basalis ductal) :
- INVASIVE LOBULAR
- INVASIVE DUCTAL
* MIXED CONNECTIVE & EPITHELIAL TUMOR :
- PHYLOIDES (ciri khas venektasi dan permukaan berbenjol-benjol)
- ADENOCARCINOMA

- Moderate dan Poorly differentiated memberikan respon kemoterapi yang baik
karena mitotic count nya cepat.
- Ki-67 melihat mitotic count, luminal a tidak terlalu respon dengan kemoterapi
karena ki-67 rendah (<14%).
HASIL PA GANAS
POLIMORFIK
HIPERKROMASI
POLIKROMASI
ANAPLASTIK
INTI BESAR
MITOSIS BERTAMBAH

Laboratorium
SGOT/SGPT prediksi metastasis liver
ALP, kalsium prediksi metastasis tulang
Tumor marker
Molekul protein berupa antigen, enzim, hormon, dsb yang dalam keadaan
normal tidak / hanya sedikit sekali diproduksi oleh sel tubuh.
Untuk menetukan rekurensi dan belum merupakan penanda diagnostik
maupun skrining.
Tumor marker untuk Ca mamae :
CEA ( Carcino Embryonic Antigen ) N : < 2,5 mcg/L tidak
direkomendasikan
CA 15-3 ( Cancer Antigen ) N : < 30 U/mL
CA 27.29

6. STAGING
Tumor primer :
T1 : <2 cm (a.<0.5 , b.0.5-1, c.1-2 cm)
T2 : 2-5 cm
T3 : >5 cm
T4 : Ekstensi ke jaringan sekitar ;
a. Infiltrasi ke dinding dada (intercosta, serratus anterior, costa)
b. Infiltrasi ke kulit (ulkus)
c. A+B
d. Mastitis karsinomatosa (Hiperemis, hangat, 2/3 dari payudara)
Nodes :
N1 : axilla ipsilateral, tidak terfiksir
N2 : a.) axilla ipsilateral terfiksir, b.) mammaria interna
N3 : a)infraklavikula, b)axilla dan mammaria interna,

c)supraklavikula
Metastase : M1 metastasis jauh

STADIUM TNM KETERANGAN
I (A,B) T1 / N1mic STADIUM DINI (EBC)
II (A,B) T1-2/N1, T2-T3/N0 STADIUM DINI
III (A,B,C) N2-N3, T4, T3-N1 LANJUT LOKAL (LABC)
IV M1 MBC
LABC :
- T3-T4
- Ekstensi dinding dada
- Nodul satelit
- N2-N3

7. RENCANA TERAPI :
TUJUAN : Kuratif atau paliatif
Tentukan dahulu RESEKTABILITAS : Terfiksir atau Ulkus luas atau

bisa memakai kriteria haagensen untuk kontraindikasi mastektomi.
KRITERIA HAAGENSEN : Paliatif - sistemik terapi
- Edem lengan Jika dari unresektable berubah

menjadi resektable setelah terapi
neoadjuvan perulu diberikan
- Edem luas permukaan payudara >1/3 radiasi adjuvant
- Nodul satelit kulit IBC : Clinical Syndrome

- Eritem
- Nodul parasternal - Edem >1/3 (Peau d’orange)
+ Cek CBC
- Metastase supraklavikula (skip metastase) + MRM + RT Chest+Regional Node
- Metastase jauh
- IBC (T4d)
- Melekat dinding dada
- Komorbid berat
Pembedahan dengan tujuan kuratif :
1. BCS
2. MRM (Patey (kgb level 1-3), Scanlon (kgb level 1-3),Madden(kgb

level 1-2 tanpa memotong pectoralis minor)
3. Radical mastectomi (Halsted-mengangkat pektoralis)

1. BCS : mempertahankan bentuk kosmetik payudara
terdiri dari 3 tindakan.
- Eksisi tumor (wide eksisi, lumpektomi, quadrantektomi) -

syarat harus free margin dengan frozen section.
- Diseksi axilla
- Radiasi (BCT)
Syarat : fasilitas untuk frozen section + radioterapi dan

proporsi tumor memadai
Indikasi : -Lesi yang dapat dieksisi (<5 cm)
- Stadium II atau early breast cancer
- T1 - T2
- Jarak >2 cm dari kulit
- Sebaiknya tipe luminal
- kalau Her2/TNBC :
*kalau tumor di nipple dilakukan skin sparring surgery
* Kalau di medial dilakukan nipple sparring surgery
Kontraindikasi : radioterapi saat hamil dan mikrokalsifikasi luas dan

multisentris (mammografi), letak tumor sentral dan dibawah, ukuran mammae
kecil.
2. Mastektomi :
A. Simple mastektomi : angkat jaringan payudara, kulit,

fascia pectoralis mayor, nipple areola complex tanpa
mengangkat KGB.
B. Radical mastektomi : (Halsted) total mastektomi +

KGB level I,II,III dan memotong pectoralis major dan
minor
C. MRM :

- (Patey) total mastektomi + KGB level 1-3 + potong pectoralis minor
- (Scanlon) total mastektomi + KGB 1-3 + insisi pectoralis minor
- ( Madden) total mastektomi + KGB 1-2 tanpa memotong pectoralis minor
VOLUME REPLACEMENT : Flap perforator atau TRAM flap atau silicon

atau LD flap.
Teknik Operasi :
• Dibuat flap sampai batas mamma

- Superior ICS II
- Uniperon ICS VI atau VII
- Medial parasternal
- Lateral m. latissimus dorsi (garis tengah axilla)
• Dilakukan mastektomi dengan mengangkat fascia m pektoralis major
• Dilanjutkan dengan deseksi kelenjar rotter
(interpectoral), ke sub scapularis, kelenjar mammaria
externa dan kel. axilla level I dan level II bawah v.
axillaris
• A.V.N. thoracodorsalis n.thoracalis lateralis
dipreservasi, n. intercostobrachialis (kalau bisa)
• Kel. lymphe yang (+) membesar dihitung pada level mana
• Kontrol perdarahan
• Pasang 2 drain isap (Sub mamma & Axilla)
PRESERVASI :
N.THORACALIS LONGUS = M. Serratus Anterior - wing scapula
N.THORACODORSALIS = M. Latissimus Dorsi - tidak bisa angkat tangan
N.INTERCOSTOBRACHIALIS = Sensoris kulit lengan medial

Vaskularisasi :
- Arteri Subclavia - A. Mammaria interna - cabang

perforantes
- Arteri Axillaris :
- A. thorakoakromialis
-A. Thorakalis lateralis
-A. Thorakodorsalis - cabang dari

A.subskapularis
- Arteri interkostalis 3,4,5 - cabang dari aorta
LIMFATIK :
- KGB Axillaris : level 1 (lateral pektoralis), level 2 (posterior), level 3 (medial)
- KGB Mammaria interna
- KGB Interpectoralis (Rotter)
KOMPLIKASI OPERASI :
- PERDARAHAN
- HEMATOM
- FLAP NEKROTIK
- WOUND DEHISENSI
- SEROMA
- INFEKSI
- LYMPHEDEMA
- WING SCAPULA

RADIOTERAPI
- Menurunkan rekurensi lokoregional dan meningkatkan survival
Indikasi : -T3-T4 (>5 cm)
- LABC/MBC
- Residual disease
- Positive margin
- IBC
- KGB axilla >3 node positif
- BCS (mandatory)

Adjuvan Radiasi :
- R1-R2
- Residu (+)
- Unresektable
- Paliatif
KEMOTERAPI
Indikasi :
- Tumor >1 cm
- All node positive 1-3
- Poor prognostik factor
- Advanced breast cancer
- Inflammatory breast cancer
- Resiko tinggi pada pasien EBC (HER2, ER/PR (-), KGB 1-3 positif,
KI-67 tinggi)
Neoadjuvant :
- Stadium lokal lanjut (IIIA-IIIC)
- Triple negative
- HER2 (neoadjuvant+transtuzumab)
Pre OP sistemic terapi :
- Inoperable
- IBC
- Bulky node N2,N3
- T4

HORMONAL TERAPI
Indikasi : ER/PR positive
Status menopause : 1. Pre Menopause : SERM (Tamoxifen 20mg/hari

P.O), Ablasi (OVB), GnRH/LHRH Agonist (Goserelin 3.6 mg SC/28 hari)
2.Post menopause : AI (Letrozole, Anastrozole,

Exemestane) (letrozole 2.5 mg P.O/hari), SERM/SERD
(Fulvestran)
- Diberikan selama 5 tahun
- Non steroid dulu lalu steroid pada golongan aromatase inhibitor

TARGETING TERAPI
HER2 +
ACTH :
- Blokade sel kanker spesifik Antracycline
Cyclofosfamide
- HER2 positif Taxane
Transtuzumab
- Transtuzumab diberikan selama 1 tahun +/- Pertuzumab
- Rekuren
- contoh kasus HER2 (+), ER/PR (-) : regimen AC lanjut T + transtuzumab +/-
pertuzumab (kardiotoksik, EF bagus)
Antracycline + Cyclofosfamide dilanjutkan Taxan + Transtuzumab ---

Transtuzumab tiap 7 hari selama 1 tahun
- contoh kasus
1. Stadium 1 & 2 : MRM +/- kemoterapi adjuvant bila high risk (Her2, KGB
+,ER/PR (-), Ki-67 high)
2. Stdium IIIa : MRM + kemoterapi adjuvant (CAF, CMF, CEF, T-A selama 6
siklus) + RT
3. Stadium IIIb : Kemoterapi neoadjuvant (CAF,CEF,T-A 3x) +/- RT lalu MRM

lalu kemo adjuvant.

Neoadjuvant → 3 siklus = stable disease → operasi→R1-R2, KGB >4 (+),
TNBC, HER2→adjuvant kemoterapi
→3 siklus = Partial response → habiskan 6 siklus
Syarat metastasektomi : tumor primer harus bisa diangkat + single nodule
NCCN
Locoregional T1-T3 : Mastektomi Total : *axillary node (-) → No Radioterapi
Tumor <5 cm
Margin >1 mm
* Margin (+)→ Consider RT to chest wall +/-RNI
Tumor >5 cm
*KGB (+) → RT to chestwall + RNI
Ductal/NOS → ER/PR (+) → HER2 (+) Luminal B2 → pT1-3, pN0,N+→ adj.

HT+CT+TT
Lobular → HER2 (-) Luminal A,B1 →pT1-3,pN0,N+→adj.HT+CT,supresi

ovarium bila pre menopause
Mixed → ER/PR (-) → HER2 (+) → pT1-3, N0,N+ → Adj.kemo + TT
Metaplastic → HER2 (-) TNBC → Adj.Kemo (AC-T)

HER2 Type
PERABOI
FOLLOW-UP
- Tumor Marker ; CA-153 ; kalau meningkat, tambah obat (mis. Ai)
- Cek tiap bulan pada tahun pertama
- Cek tiap 3 bulan pada tahun kedua
- USG dan Thorax Xray tiap 3 bulan pada tahun pertama

SKIN CANCER
- Melanoma Maligna atau Non Melanoma
1. Melanoma Maligna
Berasal dari ectoderm lapisan antara basalis dan papilare, merupakan

neoplasma maligna dari sel melanosit terdapat pada kulit dan mukosa.
Adanya mutasi pada kromosom 1,6,7,9,10 dan 11 serta 9p21 (familial).
FAKTOR RESIKO :
A. Eksposur UVa & UVb (pekerjaan)
B. Tinggal di daerah ketinggian
C. Riwayat luka bakar akibat sinar matahari
D. Lesi kulit kongenital (Nevus)
E. Riwayat menderita melanoma sebelumnya
F. Riwayat keluarga menderita melanoma
LAB : LDH
Diagnosis : (ABCDEF)
Secara klinis :
A : Asimetris
B : Border Irreguler
C : Color Variation --> Seperti hematom
D : Diameter >6 mm
E : Existing melanocytic nevi with change of color, size, shape. (nevus
berubah)
F : Finding a new pigmen lesion, especially person > 40 tahun
PEMFIS :
- Status Generalis
- Status Vitalis
- Status Performance
- Head to toe :
- Periksa telapak kaki, tangan dibawah kuku (Acral lentigenous melanoma)
- Periksa rongga mulut, mukosa anorektum, vulva dan vagina (melanoma
maligna kutaneus)
- Periksa KGB
- Status Lokalis : ABCDEF
Staging :
TNM (ketebalan) STADIUM :
I : T1-2a
T1 = <1 mm a) without ulcer, b) with ulcer II : 2b-4b
IIIA : N1-N2a
T2 = 1-2 mm a) without ulcer, b) with ulcer
IIIb/c : N1b-N2b-N3
T3 = 2-4 mm a) without ulcer, b) with ulcer
IV : M1
T4 = >4mm a) without ulcer, b) with ulcer

N1 = 1 KGB/Skip metastase , a) mikro b) makro
N2 = 2-3 KGB/1 KGB + Skip metastase , a)mikro b) makro c)satelit lesion
N3 = >4 KGB
M1 = a) distant skin
B) Lung
C) All other viscera
Selain TNM ada klasifikasi histopatologis :

- Clark’s Level : level kulit (1-5) I. Epidermis
II.Dermis Papilare
III. Antara dermis papilare dan retikulare
IV. Dermis retikulare (Trunkus dari pembuluh
darah dan limfatik)
V. Subkutan
- Breslow : level 1-3 (kedalaman <0,76, 0,76-1,5, >1,5)
Histopatologi :
- Melanoma insitu
- Lentigo malignant melanoma (LMM)
- Nodular malignant melanoma
(NMM)
- Acral lentigous melanoma (ALM)
- Superficial spreading melanoma
(SSM) -> tersering (70%)
FAKTOR PROGNOSTIK :
- Ketebalan tumor (Breslow)
- Clark’s level
- Ulserasi
- Mitotic Count
- Lesi satelit
- Angiolimfatik invasion
- Tumor infiltratif limfosit
PEMERIKSAAN PENUNJANG
- Xray Thorax
- USG Abdomen : atas -> melihat
hepar, bawah-> KGB paraaorta dan
parailiaka
- CT Scan
- MRI
- PET Scan - 3 bulan post operasi
untuk mencari skip
metastase/rekurensi
- Laboratorium : fungsi hati dan LDH

TERAPI : KURATIF VS PALIATIF
- Lesi >2 cm = Punch biopsi/ biopsi insisi

- Lesi <2 cm = eksisi biopsi -> margin 1-2 cm
- Prinsip kuratif harus free margin.

- Margin pada extremitas dan trunk : T1-T2 = 1 cm, T3-T4 = 2 cm.
- Pada wajah dilakukan mohs surgery
- setelah terbukti free margin baru dapat dilakukan rekonstruksi dengan
graft/flap.
- Adjuvan terapi berupa : kemoterapi, radiasi, target terapi, interferon alfa.
- Kemoterapi dengan DARTHMOTH : Cisplatin, Dacarbazin, Kasnosfin,
Tamoxifen.
- Radiasi bila R1-R2.
- Target terapi dengan anti PDL-1 : Pembrolizumab
- Adjuvan terapi dengan interferon alfa dosis tinggi (unresectable)

2. NON MELANOMA
- Faktor Resiko :
A. Pria > wanita = 3:1
B. Paparan UV
C. Immunosupresion (HIV)
D. Keturunan
- DD : Seboroik keratosis , Actinic Keratosis
- Basal Cell Carcinoma (BCC) / Basalioma : berasal dari sel basal

epidermis atau del folikel rambut
- Predileksi pada wajah dan hidung
- Tumbuh lambat dan resiko metastasis rendah tetapi mengakibatkan
destruksi lokal.
- Histopatologi : a. Nodular : Pink Nodul, Pigmentasi , ulserasi
B. Superficial : Berskuama
Ulkus Sentral.
ANAMNESIS : Hiperpigmentasi di tepi.
Sisi tidak rata (gigitan tikus)
- Lesi seperti tahi lalat yang berubah warna dan semakin membesar
Berdarah
- Gatal
- Nyeri
- Berdarah / lesi borok yang tidak sembuh-sembuh
- ulkus :
Ulkus rodent -> seperti gigitan tikus (sisinya tidak rata), ulkus ditengah,
hiperpigmentasi di tepi.
Nodulo-ulseratif -> papul (meninggi), permukaan mengkilap, ulseratif sentral,
skuama halus.
STAGING :
STADIUM :
T1 ≤ 2 cm I = T1
II = T2
T2 >2-4 cm
III = T1-3, N1
T3 >4 cm IV = M1
T4 invasi kartilage, tulang

N1 Regional Lymph Node
M1 Distant Metastase
High Risk :
Penunjang : Lesi selain di ekstremitas
dan badan
Xray Lesi >2 cm
USG Invasi perineural
Rekuren
CT-Scan : Luas Invasi ke tulang
Terapi :
- Eksisi luas dengan margin (2 cm)
- Jika radikalitas tidak tercapai dilakukan kemoterapi.
- sistemik terapi/ Targeting terapi : Vismodegib/sonidegib

KARSINOMA SEL SKUAMOSA (SCC)
- Berasal dari keratinizing cell/keratinosit epidermis, terbagi menjadi 2 :

Keratinizing (PA : Mutiara Bertanduk) yang merupakan jenis kemoresisten
dan Non Keratinizing.
- Biasanya tumbuh cepat dan berpotensi untuk metastasis.
FAKTOR RESIKO :
A. Sinar UV
B. Jaringan Parut
C. Ulkus Kronis
D. Luka Bakar
E. Virus HPV
ANAMNESIS :
- Keluhan utama
- Progresifitas : Onset, infiltrasi, metastasis (limfogen dan hematogen).
- Gejala penyerta
- Riwayat lesi sebelumnya
- Riwayat pekerjaan/tempat tinggal (eksposur UV)
- Riwayat trauma (luka bakar/luka kimia/ sunburn)
- Riwayat keluarga
- Riwayat penyakit terdahulu (komorbid DM/PJK/HIV)
- Riwayat pengobatan (Radiasi)
PEMERIKSAAN FISIK :
a. STATUS GENERALIS
b. STATUS VITALIS
c. STATUS PERFORMANCE
d. HEAD TO TOE : KGB & Metastasis Jauh
e.STATUS LOKALIS :
- Fungating -> lesi bunga kol
- Ulserasi
- Mudah berdarah

STAGING : STADIUM :
T1 kedalaman ≤ 2 cm I : T1
II : T2-T3
T2 2-5 cm III : T4 & N1
IV : M1
T3 > 5 cm
T4 Infiltrasi kartilago, tulang
N1 Regional node
M1 distant
- Biopsi insisi dihindari pada SCC dan BCC

- sebaiknya punch / shave biopsy
- Biopsi eksisi untuk lesi <2 cm, margin 1 cm
- CT scan dan MRI untuk menilai kedalaman.
- terapi sistemik : KEMOTERAPI : Cisplatin / Cisplatin + 5 FU + Carboplatin
- Targeting terapi : Cetuximab
SCC dengan infiltrasi (kartilago, dst) --> Compound Eksisi --> radioterapi jika
margin (+)
Lesi penis --> partial/total penektomi
Lesi SCC --> inoperable --> radioterapi

HIGH RISK :
Ukuran >2 cm
Lesi selain di ekstremitas
dan trunk
Rekuren
Gejala neurologis
Kedalaman 2-6 mm

SOFT TISSUE SARCOMA
- Asal Jaringan embrionik mesoderm, pada jaringan ikat, lemak, pembuluh

darah, saraf dan otot polos.
- Tumor jinak -> OMA, Tumor ganas -> Sarcoma
- Benjolan terkadang tidak nyeri dan disertai gejala metastasis (paru, hepar)
pada stadium lanjut.
- Lokasi : Lower extremity 46%
Upper extremity 15%
Retroperitoneal 15%
Head & Neck 8%
- Faktor Resiko : -Radiasi

-Bahan kimia (Asbes, Arsenik)
-Virus
-Trauma
-Genetik
- Imaging : Xray
USG
CT Scan (retroperitoneal)
MRI (Batas tumor)
STAGING : Stadium :
T1 <5 cm a) superficial, b)deep I : T1-2
T2 >5 cm a) superficial, b) deep II : G3
III : G3,T2b
IV : N1, M1
N1 Regional lymph node
Margin minimal
M1 distant metastasis reseksi 2-5 cm
- wide eksisi
FNCLCC - kompartemen eksisi
- amputasi
G1 low grade - limb sparing surgery
G2 Moderate - debulking
G3 High Grade
Tentukan diagnosis -> core biopsi -> staging dengan MRI,CXR,USG

Stage 1-Low grade -> resection
Stage 2 ≤ 5 cm - High grade -> resection +/- radiation
Stage 3 >5 cm - high grade + Nodal disease -> resection + radiation +/-
kemoterapi
Stage 4 -> kemoterapi +/- resection

RADIOTERAPI :
Indikasi : positive margin, high grade
Tidak perlu radiasi : ukuran kecil, stadium 1, low grade, wide eksisi batas 2
cm.
KEMOTERAPI :
- stadium lanjut
- neoadjuvant/adjuvant
- regimen CYVADIC (EORTC)
Cyclophospamide 500 mg/m2
Vincristin 1,4mg/m2
Doxorubicin 50mg/m2
Decarbazin 250mg/m2
Diulang tiap 21 hari

KELENJAR SALIVARIUS
Neoplasma jinak atau ganas yang berasal dari sel epitel/myoepitel

kelenjar liur.
3 Salivarius mayor : - Parotis -> tersering 85% -> 75% jinak (pleomorfik
adenoma)
- Submandibularis -> 50% ganas
- Sublingualis
Salivarius minor : mukosa traktus aerodigestivus atas dan sinus

paranasal
- Faktor Resiko : eksposure radiasi -> tipe mucoepidermoid carcinoma

Eksposure debu kayu -> adenocarcinoma
- parotis berukuran 5-6 cm pada parotid compartment berdekatan dengan

nervus VII facialis yang membagi lobus superficial dan lobus profunda dengan
dasar berupa muskulus masseter
- glandula submandibula terletak pada trigonum submandibula yaitu pada

margo inferio mandibula dan m. digastricus, dekat dengan n.lingualis dan
n.hipoglosus. Ductus excretorius (warthon) diantara m.myelohyoid dan
m.hyoglossus dan bermuara dibawah lidah.
- glandula sublingualis berada dibawah lidah pada paramedian, dengan

muara ductus rivinus.
Histopatologi :
- Jinak : pleomorfik adenoma
Monomorfik adenoma
Papillary cystadenoma
limfomatosum (warthin)
- Ganas : mucoepidermoid carcinoma
Adenocarcinoma
Small cell ca.
Lymphoma
Grade :
Low grade : acinic cell carcinoma
Mucoepidermoid carcinoma
High grade : Adenocarcinoma

SCC
Malignant mixed tumor
Adenoid cystic carcinoma

ANAMNESIS :
- Keluhan utama
- progresifitas ( onset, nyeri, gejala infiltrasi)
- rasa tidak nyaman pada telinga
- nyeri atau tidak (keterlibatan N.Trigeminus)
- Lumpuh (N. Facialis -> curiga maligna)
- disfagia/ nyeri tenggorok / gangguan pendengaran
- paralisis (horner syndrome)
- benjolan di tempat lain (KGB)
- Faktor resiko (pekerjaan, keluarga, radiasi)
- Penyakit lain
PEMERIKSAAN FISIK :
STATUS GENERALIS
STATUS VITALIS
STATUS PERFORMANCE
HEAD TO TOE
STATUS LOKALIS
PERIKSA NERVUS FACIALIS
TRISMUS -> INOPERABLE
Radiologi :
USG : gambaran maligna -> lesi heterogen hipoekoik, tepi ireguler, nekrosis
sentral, KGB
Xray thorax (metastasis)
Xray mandibula/maxilla
CT Scan/MRI
PET SCAN
Biopsi terbuka pada kasus inoperable

Bila operable dianjurkan tidak biopsi
Bisa menggunakan FNAB
STAGING : TNM
T1 ≤ 2 cm STADIUM :
T2 >2-4 cm I : T1
T3 >4 cm II : T2
T4 a) invasi muscle, sinus, kulit, tulang III : T3/N1
IV : N2N3/T4/M1
B) Invasi basis tengkorak, encase arteri carotis interna
N1 single ipsilateral , ≤3 cm
N2 multiple/kontralateral >3-6 cm
N3 >6 cm
Usg direkomendasikan

Bila ada invasi ke tulang/destruksi = ct scan
Tidak dianjurkan biopsi insisi, merupakan pilihan terakhir
SURGERY (Gold Standar)
- superficial parotidektomi/subtotal
* preservasi nervus VII (landmark ; tragal pointer, tympanomastoid,
digastric muscle)
* Insisi anterior helix ke inferior 2 cm dari margo inferior mandibula
* tembus platysma dan fascia superficial
* flap anterior dan posterior
* susuri N.VII
Parotidektomi superficial --> Ganas --> Total parotidektomi + KGB --> Meta
KGB --> RND
Glandula submandibularis :
- Insisi 2 jari dari angulus mandibula
- tembus platysma, ligasi a.v facialis
- hindari n. hypoglossus diantara gl.submandibula dan digastric muscle.
- preservasi n. lingualis dan warthon duct.
- tutup dan pasang drain.

KANKER RONGGA MULUT
Berasal dari epitel mukosa rongga mulut dan kelenjar ludah , sering
dijumpai pada kasus SCC, predileksi terbanyak pada pria dibandingkan pada
wanita. Faktor resiko berupa merokok dan alkohol, virus EBV dan HPV.
STAGING : T1 ≤ 2 cm
T2 >2-4 cm Stadium :
T3 >4 cm / ekstraparenkim ekstension I : T1
II : T2
T4 a) infiltrasi kulit, mandibula,nerve III : T3,N1
IV : T4,N2,M1
B)infiltrasi skull, a.carotis
N1 single ipsilateral, <3 cm

N2 multiple kontralateral >3cm
N3 >6 cm

Maintenance with Holliday Segar Method
RESUSITASI BEDAH ANAK
Loading Fluid Normal Saline 20 ml/KgBB

Selanjutnya tentukan Derajat Dehidrasi
Rehidrasi : Dehidrasi Ringan - x 60 ml
Dehidrasi Sedang - x 80 ml
Dehidrasi Berat - x 100 ml
Lalu diberikan cairan selama 24 jam dalam bentuk ;
6 jam 1 : 1/2 Rehidrasi + 1/4 Maintenance
18 Jam 2 : 1/2 Rehidrasi + 3/4 Maintenance

ANAMNESIS
FAKTOR RESIKO :
1. Riwayat Kehamilan :
- Hamil Usia Muda
- Konsumsi Obat saat hamil ; Dekongestan, Methimazole (Obat Tiroid), Riw. Pil KB
lama
- Riwayat Alkohol, merokok saat hamil
- Riwayat ANC ? Riwayat USG kehamilan?
- Penyakit saat hamil
- Polihidramnion
2. Riwayat Persalinan :
- Lahir Normal?
- Cukup Bulan?
- Langsung Menangis?
3. Riwayat Keluarga :
- Penyakit yang sama
OBSTRUKSI :
- Buang air besar bagaimana? Riwayat konstipasi? Sering menggunakan laksatif?
- Riwayat Mekonium terlambat >48 Jam?
- Riwayat BAB menyemprot?
- Muntah ?
- Berwarna hijau?
- Segera saat minum atau beberapa saat?
- Kembung?
- Air liur banyak?
- Feses ada? Warna ? disertai darah?
- Urin berwarna apa? Bercampur feses?
- Apakah Ada Benjolan di Inguinal
- Apakah masih menangis atau lemas
- Nyeri perut?
- GEJALA SISTEMIK : Demam, Sesak (Bibir sianosis), Kelainan VACTERL lainnya,
Gizi kurang?

- Riwayat Penyakit Sebelumnya?
Atresia Esofagus - Tracheoesofageal fistula
Faktor Resiko : - Riwayat Konsumsi methimazole saat hamil

- Riwayat Konsumsi Pil KB lama
- Trisomi 18-21
Klinis :
- Hipersalivasi → Pneumonia → Respiratory Distress
- NGT kinking
-Riwayat Polihidramnion
Treatment :
- Head Up - Body Up
- Suction Berkala
- Gastrostomi Dekompresi
- Fistula harus ditutup
- Cari VACTERL
Waterson Classification

Surgery :
- Lihat waterson criteria
- Kriteria lainnya (Buku Grosfeld) :
- Bila Gap fistula <2 vertebra → Primary Suture
- Gap >2-6 → Delay, Tutup Fistula dulu
- >6 Vertebra → Graft
CHPS
Faktor Resiko : Pria > Perempuan 4:1

Riwayat Keluarga
Usia muda kehamilan
Anak Pertama
Pola Makan
Klinis :
Muntah Proyektil Non Bilous
Usia 2-8 Minggu
Muntah setelah minum susu (Muntah berwarna
susu)
Terkadang datang dalam kondisi dehidrasi →
Somnolen
Peristaltik wave terlihat pada epigastrium dan
hipokondrium kiri
Massa Teraba dibawah tip liver → Bayi harus relax → Flexi lutut dan pinggul dan telah
di dekompresi
Bila menyebabkan gangguan metabolik : Hipokloremia, Hipokalemia, Metabolik
Alkalosis.
OMD : String Sign

USG : Ketebalan otot >3 mm
Panjang Pyloric ≥ 14 mm
Diameter ≥ 14 mm

Treatment :
- Resusitasi 20ml/KgBB Normal Saline
- Jika Hipokalemia → D51/2Ns + 20-30 Meq KCL →
Cek tiap 6 jam
- Pasang OGT dekompresi
- Rawat NICU rawat Inkubator
- Cegah dehidrasi
- Cegah Imbalance elektrolit
Operasi :
Pyloromiotomi
- Insisi transversal kuadran kanan atas

- Insisi longitudinal serosa pylorus 2 mm proximal dari junction duodenum hingga 5
mm anterior gaster di bagian avaskular.
- Dibuat seperti hernia hiatal.
Post Operasi : Feeding 80 gr per 3 jam
Komplikasi : Perforasi → Repair → Buat ulang sisi lain
Infeksi luka
Hernia incisional
Prolonged Emesis
DD : GERD
Peningkatan TIK
Gastroenteritis
Atresia Pilorik
Gastric Volvulus
ATRESIA DUODENUM
- Lebih sering pada Pria > Wanita

- Trisomi 21
- Terdapat cardiac malformation
- Terdapat anomali gastrointestinal
- Riwayat lahir prematur
- Riwayat Polihidramnion
Klinis :
-Muntah bilous
- Distensi Abdomen
- Aspirasi NGT >20 ml cairan gastrik (normal <5 ml)
Radiologi :

Double Bubble Appearance → Dekompresi dulu baru masukkan udara 40 cc
dan di klem.
No distal bowel gas
Tipe : Incomplete obstruction (web/diafragma-stenosis) dan complete obstruction
(atresia)
I : Web/Diafragma
II : Obliterasi → Terhubung dengan jaringan fibrous
III : Complete separation
Operasi : Duodeno-duodenostomy side to side (diamond)

ATRESIA JEJUNOILEAL
- Insidensi lebih sering pada pria > wanita

- Riwayat Lahir Prematur
Patofisiologi : Intrauterine iskemia pada midgut (segmental) menyebabkan

nekrosis dan akhirnya terjadi disintegrasi
Klinis : Obstruksi → Muntah bilous, Distensi Abdomen

Mekonium tetap keluar, dapat disertai darah
Dapat terjadi perforasi hingga peritonitis
Tipe : Stenosis / Tipe I - Ada web pada intralumen

Tipe II - Tersambung pada mesentrium
Tipe IIIa - Terpisah dan berbentuk V-Shaped
Tipe IIIb - Apple Peel
Tipe IV - Kombinasi I-III atau multiple
Operasi :
Approach pada transversal supra/infra umbilikus, setelah reseksi di evaluasi
segmen distal - irigasi untuk menyingkirkan distal obstruction atau bisa dengan

kontras enema. Distal dipotong oblique pada antimesentrium selanjutnya
dianastomosis menggunakan benang 5-0 atau 6-0. Bila peritonitis diharuskan
untuk eksteriorisasi.
Normal panjang small bowel 250 cm, minimal diperlukan 100 cm untuk intake
oral.
Post Operasi :
- TPN segera dan dilanjutkan hingga toleransi enteral
- Enteral mulai jika Gastric Outlet minimal dan Bayi sudah BAB, Mulai dengan 20
ml/KgBB/Hari susu.
- Jika sadar dan bisa 8ml/jam melalui tube - lanjut pemberian per oral

Although a primary anastomosis is the preferred method of treatment, this
method is inadvisable in certain circumstances. In the setting of an atresia with a
volvulus when the vascular integrity of the intestine is in question, or in severe
cases of meconium peritonitis, the creation of an enterostomy is warranted.
The most expeditious procedures are either a side-by-side (modified Mikulicz)
double-barrel enterostomy brought out through the wound or separate proximal and
distal stomas brought out at opposite ends of the wound and fixed to the abdominal wall
with a minimal number of interrupted 5-0 or 6-0 absorbable sutures. Depending on
anatomy, as well as the surgeon’s preference, the location of the enterostomy and the
mucous fistula can also be positioned outside of the wound.
POST OP : Maintaining fluid and electrolyte balance is a key component of postoperative

care. Intravenous fluids (10% dextrose in 0.25% normal saline along with 2 to 3
mEq/kg/day of potassium chloride) are administered, with a total fluid volume goal of
approximately 100 mL/kg/day. If the gastric output is clear and greater than 30
mL/kg/day, it is replaced with 0.45% normal saline.

ATRESIA COLON
- Dapat menyerupai gambaran pneumoperitoneum pada xray

- Operasi dengan staged approach
1. Colostomy : Proximal stenosis di exteriorisasi, distal
jadi mucous fistula
2. Reseksi distal end / segmen patologis
3. Biopsi Rektum
4. 3-6 Bulan berikutnya tutup stoma

ATRESIA ANI - MALFORMASI ANOREKTAL
Kelainan Penyerta :
- Down Syndrome ( Low set ear, Round Face, Flat Nasal Bridge, Protruding tongue,
Single palmar crease)
- Cardiovaskular anomali
- Gastrointestinal anomali - Malrotasi dan TEF
Anamnesis : - Keluhan Utama ? Sejak kapan diketahui ? Usia anak sekarang ?
- Ada BAB?
- Ada kembung ? Mual dan muntah ?
- Ada Urin ? Feses pada urin ?
- Minum bagaimana ? Tersedak ? Muntah ? Hipersalivasi ?
- Sesak ? Bibir kebiruan ? Kelainan lain ? Jari tangan dan kaki?
(VACTERL)
- Demam ?
- Riwayat Kehamilan ? Riwayat kelahiran ? Cukup bulan ? lahir
normal ? menangis ?
- Riwayat Keluarga ?
Pemeriksaan Fisik :
- Status Generalis
- Status Vitalis
- Status Dehidrasi
- Head To Toe (VACTERL) - Low set ear → Down Syndrome
- Lokalis : Anal Region → Flat Bottom? Anal Dimple ? Fistula ? Midline raphe / Bucket
handle?Penis ? Vagina ? Pada perempuan lihat lubang kemaluan (1/2/3)

Tatalaksana :
OGT Dekompresi
IV Line resusitasi 20 ml/KgBB asering
Pasang kateter, Nilai Urine
XRAY Babygram
XRAY 24 Jam setelah lahir pada pasien tanpa fistula - Cross table lateral dengan knee-
chest position, menilai udara sampai coccyx.
Jika udara tidak sampai coccyx atau mekonium pada urine atau sacrum abnormal atau
flat bottom, segera dilakukan colostomy dan PSARP 3 bulan kemudian.

Dapat dilakukan USG perirectal untuk melihat jarak udara terakhir pada rectum.
Anus Anterior : Varian normal, letaknya dianterior perineum, dikelilingi muscle complex
(sfingter), kalibernya normal
Perineal fistula : terletak di perineum dan tidak dikelilingi muscle complex secara
lengkap.
COLOSTOMY DIVIDED
Pada Proximal Sigmoid
PSARP DILATOR 2
(Tidak terlalu pendek - sulit kali sehari,
PSARP) 3 Bulan /2 Minggu Sebelumnya 2Minggu Sampai
dilakukan distal tercapai
(Tidak terlalu panjang - target
cologram/lopografi
Pada fistula rectourethra -
urine tertampung)
(Loop Dihindari karena
Lanjut Dilatasi 7 Bulan 8-12 mgu
spillage - megarektum) - 1 x per hari dalam 1 bulan
- 1 x per 3 hari dalam 1 bulan Tutup
- 2 x per minggu dalam 1 bulan Colostomy
- 1 x per minggu dalam 1 bulan
- 1 x per bulan dalam 3 bulan
Distal Lopografi : dilakukan dengan high pressure agar rectum menggembung dan
ujung fistula terlihat

Dilatasi dapat dimulai 2 minggu post PSARP
The anus is calibrated, and a dilator that fits snugly is initially used to dilate
the anus twice a day. Every week, the size of the dilator is increased by one unit until
the desired size is reached.
Once the correct size is reached, the colostomy can be closed, which is
usually 8 to 12 weeks after the reconstruction.Dilatations must continue after closure
(6 months). Once the dilator can be inserted easily, the schedule is reduced to once
a day for 1 month, twice a week for 1 month, once a week for 1 month, and then
once a
week for
3
months.

API :
Anal Position
Index (Jarak
Fourchette
atau Skrotal ke center anus/Jarak Fourchette ke tip coccyx) , Normal nya >0.34 pada
wanita dan >0.43 pada pria.
It is important to not make a decision about a colostomy or a primary

operation before 20 to 24 hours of age. The reason for waiting is that significant
intraluminal pressure is required for meconium to be forced through a fistula, which is
the most valuable sign of the location of distal rectum in these babies. If meconium is

visualized on the perineum, it is evidence of a rectoperineal fistula. If there is
meconium in the urine, the diagnosis of a rectourinary fistula is obvious.
Radiologic evaluations do not show the real anatomy before 24 hours because the
rectum is collapsed by the muscle tone of the sphincters that surround its lower part.
Therefore radiologic evaluations done too early (before 24 hours) will likely reveal a
“very high rectum” and therefore yield a false diagnosis.
During the first 24 hours, the newborn should receive intravenous fluids, antibiotics,
and nasogastric decompression to prevent aspiration. The clinician should use
these hours to evaluate for the presence of associated defects such as cardiac
malformations, esophageal atresia, and urologic problems. An echocardiogram
can be performed, and the baby should be checked for the presence of
esophageal atresia. A plain radiograph of the lumbar spine and sacrum should be
taken to evaluate for hemivertebrae and sacral anomalies. A spinal ultrasound helps
screen for tethered cord and other spinal problems. Ultrasonography of the abdomen
evaluates for the presence of hydronephrosis.
The descending or upper sigmoid colostomy has advantages over a right or

transverse colostomy. It is important to have a relatively short segment of
defunctionalized distal colon, but not too short as to interfere with the subsequent pull-
through.
The ideal location is just at the point where the proximal sigmoid comes off the
left retroperitoneum.
In the baby with a large rectourethral fistula, the baby
may pass urine into the colon, and a more distal colostomy
allows urine to escape through the distal stoma without
significant absorption. With a more proximal colostomy, the
urine remains in the colon and is absorbed, which can lead
to metabolic acidosis. A loop colostomy allows passage of
stool from the proximal stoma into the distal bowel, which can
lead to urinary tract infections, distal rectal pouch dilation, and
fecal impaction, which can lead to severe constipation later in life.

Bila stoma terlalu proximal (terlalu panjang), resiko segmen distal disuse/atrofi juga
panjang. Pada fistula rektourinarius, urin lebih banyak masuk ke kolon dan berisiko
terjadinya hipokloremia dan akan mengakibatkan asidosis metabolik. Komplikasi
lainnya yaitu dapat terjadi megarektum yang akan mengakibatkan konstipasi
dikemudian hari.
Komplikasi : - Striktur
- Infeksi
- Konstipasi
- Soiling
- Prolaps mukosa rektum
- Transient nerve femoral palsy - ec excessive pressure on groin

Cloaca : sebagian besar mempunyai kelainan urologi - refluks vesikoureter,
agenesis/displasia ginjal.
Screening VACTERL :
- Babygram
- Usg Abdomen : Hidronefrosis
- Echocardiografi : TOF
- Xray Vertebra, Sacrum, Pelvis.

OMPHALOCELE
- Umbilical cord terhubung ke sac → Kegagalan Viscera kembali ke cavum
abdomen.
- Sac merupakan lapisan dari Peritoneum, Wharton Jelly, Amnion
- Dapat didiagnosis pada fase prenatal : - Peningkatan AFP
- USG pada usia 18 minggu dapat terdiagnosa
- Setelah lahir, segera diperiksa kelainan penyerta : Echocardiografi, USG
Renal, dan Paru
- Sering disertai anomali kongenital lainya : Down syndrome, Kriptokismus dan
PJB.
- Dapat disertai kelainan Pentalogy of Cantrell (Disertai kelainan Jantung)
- Bila defek besar >4 cm, dapat berisi liver.
- Tatalaksana : IV fluid resusitasi 175 ml/kgbb
NGT Dekompresi
Tutup Kasa Saline Steril
- Operasi : Primary Closure atau Staged Closure
Immediately Primary Closure : Defek kecil <1.5 cm dapat
direpair secepatnya. Buka sac, tutup fascia dan skin.
Delayed Staged Closure :
Menggunakan silastic bag dan dijahit ke rektus fascia atau fullthickness ke
abdominal wall.
- Scarification Treatment : Merupakan Non Operative Management
Jika defek besar, dilakukan pemberian silver sulfadiazine sebagai
escharification pada amnion sac, selanjutnya diterapi sebagai hernia ventral.
Dapat juga diberikan triple agent ; Silver sulfadiazine, Povidone Iodine,
Neomycin atau polymixin/bacitracin.

- Hernia ventral ditutup 1 tahun kemudian.
GASTROSCHIZIS
- Faktor Resiko pada Kehamilan Muda, Usia <21 Tahun, merokok, konsumsi COX
inhibitor (Aspirin & Ibuprofen), Konsumsi dekongestan.
- Patofisiologi : Gestasi pada minggu ke-6 terjadi herniasi midgut ke umbilical cord
kemudian elongasi dan rotasi diluar abdomen selama 4 minggu, pada minggu ke-
10 organ kembali ke cavum abdomen, pada gastroschizis terjadi kegagalan
pembentukan mesoderm di anterior wall (kegagalan migrasi dari lateral fold -
tersering di sisi kanan dari umbilikus).
- Kenapa di sisi kanan ? kegagalan reabsorbsi vena umbilikalis kanan yang
menghilang akibat obliterasi sehingga thrombosis vena omphalomesentrik
menyebabkan nekrosis dinding abdomen.
- Diagnosis pre - natal pada usia kehamilan 20 minggu melalui USG tampak
floating bowel.
- Treatment : Resusitasi 175 ml/kgbb/24 jam, Nilai Usus : edema, Peel, Nekrotik.
Silo Bag.
- Operative : Primary repair dan delayed closure
- Goal : Returning the viscera to abdomen, Hindari peningkatan IAP.
- Peningkatan IAP diatas 10-15 mmHg menurunkan perfusi renal dan
intestinal, >20 mmHg mengakibatkan organ disfungsi. Perhatikan juga penurunan
saturasi pada saat penutupan.
- Staged Closure : Silo Bag - lalu lanjut definitif closure

- Closure dapat dengan berbagai cara : - Insisi perlebar ke cranial dan caudal
- Stretching muscle
- Undermining
- Skin to skin closure atau hingga Multiple insisi .

MALROTASI
- Pada masa kehamilan terjadi elongasi midgut menyebabkan malrotasi

ataupun non rotasi dan incomplete rotasi
- Gejala Klinis : Muntah bilous yang tiba - tiba merupakan suatu cardinal sign
Distensi abdomen
Bisa Peritoniis - Eritem abdomen dan syok
Failure to thrive
Early satiety
Tersering pada usia beberapa minggu
Nyeri tekan abdomen
Hematochezia
- XRAY : Barium Meal merupakan gold standar - gambaran coil
spring/corkscrew
- Color Doppler USG : Whirlpool sign

Treatment :
- Resusitasi
- NGT dekompresi
- AB broadspektrum
- Operatif - LADD procedure

INVAGINASI - INTUSSUSCEPTION
- Insidensi pada usia <2 tahun.

- Letak Tersering pada ileocolica (85%) dan Ileoileal (10%).
- Gejala klinis :
- Nyeri Abdomen Periodik : High Pitch Crying - Anak tiba-tiba
terbangun dan menangis akibat nyeri hingga mengangkat kaki, kemudian
anak bisa tenang / tidur kembali.
- Muntah
- Red Currant Jelly Stool ( Pembuluh darah mesentrium
terkompresi, edem lokal pada segmen usus yang masuk (intussusceptum)
dan mengakibatkan kompresi vena, kongesti dan stasis
mengakibatkan produksi mukus dan darah dari intussusceptum).
- Teraba massa abdomen (Sausage shape pada RUQ)
- Dance Sign
- Patofisiologi :
Idiopatik / Non PLP : Infants mempunyai banyak jaringan
limfoid, Peyer Patches (biasanya di antimesentrium) pada distal ileum peyer
patches berada di seluruh keliling usus, pada infeksi virus menyebabkan
hipertrofi dan hiperplasia dengan peristaltik meningkat menyebabkan
terjadinya intussusepsi. Infeksi virus akibat Adenovirus (ISPA) dan Rotavirus
(Diare).
PLP : Meckel Diverkulum
Polip Intestinal
Periappendicitis
Abdominal Trauma
Malignant Tumor

- XRAY Abdomen : Meniscus sign
Absent Cecal Gas
- USG : Massa diameter 3-5 cm
Target sign / Donut sign
Pseudokidney (Longitudinal view)

- Treatment :
NOM : Hemodinamik stabil dan tidak ada tanda perforasi, <72 jam.
Menggunakan pneumatik dan hidrostatik (rule of 3) - (Tinggi
3 kaki, tidak lebih 3x)
Kontraindikasi : Dehidrasi, Syok , Peritonitis.
Operatif : Milking dari distal intussusceptum seperti menjepit odol lalu di

iliopexy.
Red currant : iskemia mukosa menyebabkan produksi mukus berlebih, strangulasi

mengakibatkan laserasi mukosa darah.
Intussuceptum ; segmen yang masuk
Intussuscipiens : segmen yang dimasuki

HIRSCHSPRUNG DISEASE ( Congenital Megacolon)
- Tidak terdapat sel ganglion pada plexus myenterik dan submukosa.

(Aganglionik)
- Terdapat 3 plexus di colon : meisner, henle, auerbach - berfungsi untuk
ekskresi, absorbsi , motilitas usus.
- Kelainan terkait hirschsprung :
- Trisomi 21 (Down Syndrome)
- Neurofibromatosis
- Neuroblastoma
- Heart disease
- Urinary Tract
- CNS
- Patofisiologi : Sel ganglion bermigrasi dari krista neuralis pada minggu ke
13 ke GI tract lalu menjadi sel ganglion matur - Gagal migrasi krista neuralis.
- Klinis :
- Abdominal distension
- Muntah Bilous
- Delay Meconium pada 24 jam pertama
- Feeding intolerance - Failure to thrive
- Konstipasi kadang butuh enema.
- Xray Polos Abdomen :
Dilatasi Usus
- Water soluble kontras enema :
Melihat 3 zona, zona spastik, zona transisi, zona dilatasi
Foto ulang 24 jam kemudian → ada retensi kontras
Pada rectosigmoid lebih jelas terlihat pada foto lateral.

- Rectal Biopsy Full Thickness (Gold Standart) : Absen sel ganglion pada plexus
meisner
>1 - 2 cm diatas linea dentata Hipertrofi nerve trunk
- Dapat digunakan suction rectal biopsi pada anak usia <1 tahun, ambil di
2,3,5 cm dari linea dentata
- Pewarnaan : Hematoxylin + Eosin → asetilkolin esterase → IHC - Calretinin
- Hematoxylin eosin : absence ganglion cell, hipertrofi nerve trunk

- asetilkolin esterase : lebih jelas melihat nerve trunk memanjang ke mukosa
- Kalretinin : melihat sel ganglion imatur.
- Anorectal Manometry : Melihat recto anal inhibitory reflex → refleks
relaksasi dari sfingter ani interna saat distensi balon di rektum.

- Treatment : Resusitasi IV fluid
Antibiotik Broadspectrum + Metronidazole
NGT Dekompresi
Rectal Dekompresi dengan irigasi / stimulasi rektum.
Leveling Colostomy : Pull through 3-12 bulan kemudian.
Left lower quadrant oblique incision, cari zona transisi,
proximal dari zona transisi.
indikasi ; - Enterocolitis
- Perforation
- Malnutrisi
- Masif dilatasi usus
- HAEC : Stasis akibat obstruksi → Overgrow bakteri
Clostridium difficile / Rotavirus
Klinis : Demam, Distensi abdomen, Diare. Radiologi - Lab
Treatment :
Ringan - AB Oral Cephalosporin +
Metronidazole
Berat - AB iv
DD : Meconium ileus , Meconium Plug, atresia

ileum
Meconium Ileus : sumbatan pada ileum distal
akibat perlengketan mekonium karena
komposisi air sedikit biasanya akibat
insufisiensi enzim pankreas.
Meconium Plug : obstruksi kolon akibat
mekonium menggumpal, riwayat penggunaan
magnesium saat hamil (Pasien PEB). diterapi
dengan kontras water soluble (gastrografin).

OPERASI
1. Swenson : Remove colon aganglinic all layer, lalu anastomosis end to
end diatas sfingter
2. Duhamel : Approach abdominoperineal → anastomosis dari posterior
aganglionik
3. Soave : Menghindari cedera struktur pelvis, diseksi submukosa
endorektal (mukosektomi), anastomosis didalam cuff aganglionik.
4. Rehbein-State : Anastomosis end to end pada rectum
5. Martin - Kimura : Pada TCA

Post operasi :
Dilatasi dengan jari 1-2 minggu post operasi
Komplikasi :
- Ongoing Obstruksi - Mechanical striktur
- Soiling
- Enterocolitis
- Stenosis
- Leakage anastomosis
TCA : Biopsi di 3 tempat, Rektum - Transversum - Appendix.

Pada pemeriksaan colon in loop tampak microcolon - haustra tidak ada
DD : Atresia jejuno ileal
Barium Enema : Mencari 3 zona, pakai spuit tanpa kateter, tidak boleh
manipulasi dalam 24 jam
Colon in Loop : sampai caecum

TRAUMA MASA KECIL
Loss of more than 207 mL/kg of blood from the chest with continued bleeding
should be addressed surgically.
WSES : Hemodinamik stabil SBP > 70 mmhg + (umur dalam tahun x 2)
WSES : bolus 20ml/kgbb harus diberikan sebelum transfusi darah.

HERNIA DIAPHRAGMATICA
During the early development of the diaphragm, the midgut is herniated into the
yolk sac. If closure of the pleuroperitoneal canal has not occurred by the time the
midgut returns to the abdomen during gestational weeks 9 and 10, the
abdominal viscera herniate through the lumbocostal trigone into the ipsilateral
thoracic cavity. The resulting abnormal position of the bowel prevents its normal
counterclockwise rotation and fixation. No hernia sac is present if the event
occurs before complete closure of the pleuroperitoneal canal, but a
nonmuscularized membrane forms a hernia sac in 10% to 15% of CDH patients.
Although some claim the herniation can occur late in gestation or be
intermittently present as a dynamic process, in most cases the defect is
established by gestational week 12.The subsequent postnatal problems relate to
the effects of the herniated viscera on the developing heart and lungs.

The diagnosis of a CDH is often made on a prenatal ultrasound (US)
- Polyhydramnios
- Because of the small size of the neonate’s chest, breath sounds may or may
not be present on the side of the defect.
- Mediastinal compression with shift into the contralateral thorax may cause
deviation of the trachea away from the side of the hernia and also result
in obstruction to venous return with the hemodynamic consequences of
hypotension and inadequate peripheral perfusion.
- The signs of respiratory distress may include cyanosis, gasping, sternal
retractions, and poor respiratory effort.
- heart sounds will be heard best over the right chest;

The diagnosis of a CDH can be confirmed by a plain chest radiograph that
demonstrates loops of intestine in the chest.
The location of the gastric bubble should also be noted, and its position can
be confirmed by placement of an orogastric
tube
After the birth of the infant and confirmation of the diagnosis of CDH, all
efforts should be made to stabilize the cardiorespiratory system while inducing
minimal iatrogenic injury from therapeutic interventions. It is essential to
consider that the CDH is a physiologic emergency and not a surgical
emergency.
Resuscitation begins with endotracheal intubation and nasogastric tube
insertion. Ventilation by mask and Ambu bag is contraindicated to avoid
distention of the stomach and intestines that may be in the thoracic cavity.
Arterial and venous access should be acquired through the umbilicus.After
confirming the diagnosis, initial postnatal therapy is targeted at resuscitation
and stabilization of the infant in cardiopulmonary distress.
A nasogastric tube should be inserted to avoid gastric and intestinal
distention. Arterial and venous access is nec
essary for resuscitative maneuvers. Acid–base balance and oxygenation–
ventilation status should be carefully
monitored.

The type of mechanical ventilator can be successfully managed with a simple
pressurecycle ventilator, using a combination of high rates (100 breaths per
minute) and modest peak airway pressures (18 to 22 cm H2O and no PEEP)
or lower rates (20 to 40 breaths
per minute) and higher pressures (22 to 35 cm H2O, 3 to 5 cm PEEP). The
goal of such ventilatory support is to maintain minute ventilation while
obtaining a preductal PO2 greater than 60 mm Hg (SaO2 90% to 100%) with
a corresponding PCO2 of less than 60 mm Hg. pH and PCO2 levels have
been shown to be important in modifying pulmonary vascular toneInfants
should be properly sedated, and any combination of agents, including
midazolam, fentanyl, or morphine, can be used.
New management strategies for treating persistent pulmonary hypertension

now undergoing clinical evaluation include various calcium channel blockers,
prostacyclin derivatives, endothelin receptor antagonists, and
phosphodiesterase-5 inhibitors such as sildenafil.
The optimal timing of operative repair when using a strategy of delayed repair
also remains undetermined. The period of preoperative stabilization has
varied from several days to several weeks. Some authors have reported
waiting until the infant is successfully weaning off mechanical ventilation and
requiring low ventilator settings. Others follow the severity of pulmonary
hypertension with serial echocardiographic examinations and wait until the
hypertension has abated or at least stabilized
Foramen of Morgagni Hernia

The diaphragmatic hernia of Morgagni is located anteromedially on either side
of the junction of the septum transversum and the anterior thoracic wall. The
defect occurs through the embryologic space of Larrey. Occasionally, bilateral
Morgagni hernias communicate in the midline, constituting a large anterior
diaphragmatic defect extending all the way across the midline from right to
left. Typically, a sac is present, and herniation of the colon or small bowel is
usually discovered to the right or left ofthe midline. Morgagni hernias account

for lessthan 2% of diaphragmatic defects. Althoughthis defect may be
observed in neonates, it usually presents more commonly in older children or
adults. Associated anomalies may be present and include malrotation, cardiac
defects, and trisomy 21.379,379a An anterior midline deficiency in the
diaphragm, with or without the other elements of the pentalogy of Cantrell,
with free pericardial and peritoneal communication may allow herniation of
intestine into the pericardium. The hernia is often discovered incidentally as a
mass or air–fluid level on a chest radiograph. A barium enema or a CT scan
may confirm the diagnosis. Operative correction is easily performed through
an upper transverse abdominal incision. The diaphragm is sutured to the
underside of the posterior rectus sheath at the costal margin after reduction of
the hernia and resection of the sac. Laparoscopic and thoracoscopic
techniques have also been used to repair this defect, but the laparoscopic
approach is generally favored.

After reduction of an incarcerated hernia, a delay of 24–48 hours to allow
resolution of the edema prior to open repair has historically been recommended

We believe the ideal time to complete penile reconstruction in the child is
between 6 and 8 months of age. The anesthetic risk is low and, at this age,
postoperative care is much easier for the parents than it is when the child
is a toddler or toilet trained.78 In postpubertal patients, the complication
rates are significantly higher, which reinforces the concept of performing
hypospadias repairs early in life
OBJECTIVES OF REPAIR
The objectives of hypospadias correction are divided into the following
categories:
1. Complete straightening of the penis
2. Locating the meatus at the tip of the glans
3. Forming a symmetric, conically shaped glans
4. Constructing a neourethra uniform in caliber
5. Completing a satisfactory cosmetic skin coverage

VASKULAR - ORTHOPEDI

VASKULAR TRAUMA
TRAUMA EKSTREMITAS
↓
HEMODINAMIK STABIL → TIDAK STABIL→ OR
↓
STABIL
↓
TANDA TRAUMA VASKULAR
↓
1.NO SIGN 2. SOFT SIGN 3.HARD SIGN
↓ ↓
- Trauma tumpul -ABI <0.9 Imaging CTA
- High Energy YES -Abnormal US doppler YES
- Penetrating
Di OR pakai
C-Arm untuk
NO NO NO
ontable
angiografi
RAWAT JALAN untuk pasien
multileve
penetrating
dan blunt
trauma
Hard Sign : Soft Sign :

- Palpable thrill - Defisit neurologis
- Audible bruit - Riwayat syok/hipotensi
- Expanding hematom - Luka pada ekstremitas
- Perdarahan pulsatil - Non expanding hematom
- Tanda iskemik 6P - Non pulsatile bleeding
- Nadi lemah

STATUS VASKULAR :
Inspeksi : Warna kulit, Perdarahan aktif, deformitas, saturasi
Palpasi : Suhu/akral dingin, nyeri tekan, sensasi, crt, pulsasi
Neuro : Sensorik dan motorik
BANDINGKAN KONTRALATERAL !
- Thrombectomy dengan fogarty no.4 / 5 pada proximal dan distal pada

mayor trauma disertai heparinisasi
- AAST gr. 4 dan 5, dipilih untuk primary anastomosis end to end secara
free tension.
- Jika pasien unstable dan vena tidak dapat direpair, ligasi dapat
dilakukan, diikuti dengan fasciotomy profilaksis atau monitor serial
tanda kompartemen.
- Amputasi pada pasien yang tidak stabil dengan MESS > 7
Repair Vaskular :
1. Anastomosis end to end : Defek panjang <2 cm
Diameter maximal 1 cm
Tidak infeksi/kotor
Dijahit secara interuptus benang tapper monofilamen non absorbable →
propylene
2. Bypass, Interposisi, Patch : Defek >2 cm
Pemberian heparin post repair vaskular : pemberian inisial

dengan 80IU/KgBB bolus dilanjutkan dengan 18 U/KgBB sebagai
maintenance. Selanjutnya kontrol APTT .

GRADING AAST VASCULAR INJURY
- Grade I : A/V digital, Plamar, Dorsal-Plantar pedis
- Grade II : V. Basilika/Cephalica, Saphenous, A. Radial/Ulnar
- Grade III : V. Axillary, Femoral, Poplitea, A. Brachialis, Tibialis,
Peroneal
- Grade IV : A. Femoral, Poplitea
- Grade V : A. Axillary, Common Femoral
Non operative management :

AAST grade 1 & 2 tanpa adanya perdarahan aktif atau tanda iskemia
distal
TRAUMA NECK :
Zona 1 : Clavicula sampai cricoid

Zona 2 : Cricoid sampai sudut mandibula (angulus)
Zona 3 : Diatas angulus mandibula
Pada Trauma :
Zona 1 + Stabil : Dilakukan angiografi, esofagogram, esofagoskopi,
alternatif ct scan
Zona 2 + tidak stabil : Eksplorasi (hard sign/airway tidak clear).
Stabil : Observasi 12 jam
Zona 3 : Carotid + vertebral angiografi

TRAUMA VASKULAR :
1. Primary Survey - ABCDE
2. Resusitasi 1 liter, kontrol perdarahan (Bebat Tekan) , pasang

kateter, NGT, iv line 2 cabang
3. Nilai Respon resusitasi - Rapid, Transient, No respon
4. Secondary survey : Head to toe, Status vaskuler

5. AMPLE
6. Tidak stabil - Eksplorasi
7. Bila pasien Stabil → lihat Hard sign / Soft sign
8. Hard sign positif → Eksplorasi

9. Soft sign - Ukur ABI, Jika <0.9 → imaging → eksplorasi jika
POSITIF

LIMB ISKEMIA
-Terbagi menjadi akut, chronic dan akut on kronik (CLTI)

- Etiologi akut akibat thromboemboli - ada faktor resiko
- Etiologi kronik akibat atherosklerosis dan inflamasi
- Jika emboli (akut) : onset nya menit-jam hingga menghitam,
ditandai dengan 6P
- Jika thrombus (akut) : onset nya jam-hari, masih ada kollateral
- Faktor resiko : DM, Penyakit jantung, Hipertensi, dislipidemia, stroke,
smoking
- Digunakan klasifikasi Fontaine atau Rutherford

- Pada ALI menggunakan :
- Pada CLI menggunakan Fontaine atau Rutherford :

- Fontaine 1 : Keluhan minimal, hanya sering kaki letih.
- Fontaine 2 : Klaudikasio intermitten (<200 m dan >200m)
- Fontaine 3 : iskemik rest pain
- Fontaine 4 : Gangrene

KAKI atau JARI menghitam :
- Sejak kapan, Pucat atau biru sejak kapan? Berubah ke hitam
berapa lama?
- Awal nya dari mana? Ujung jari naik keatas?
- Riwayat hilang timbul? Akibat perubahan suhu?
- Riwayat bilateral/unilateral?
- Nyeri? Terus menerus? Kesemutan?
- Riwayat nyeri saat berjalan? Membaik saat istirahat?
- Apakah ada Riwayat luka? Trauma?
- Ada keluhan mati rasa? Sulit digerakkan ?
- Demam, sesak ?
- Riwayat pengobatan ?

- Faktor predisposisi, riwayat penyakit : dm, hipertensi,
kolesterol, PJK, stroke
- Life style : Diet, merokok, olahraga
- Riwayat keluarga
Pada pemeriksaan fisik :
- Status generalis
- Status vitalis
- Head to toe
- Status vaskular (cek kontralateral)
Inspeksi - Perubahan warna, luka , ulkus, marble white foot
pada plantar pedis, motorik bagaimana
Palpasi - Nilai pulsasi, crt, suhu, nyeri tekan, nyeri gerak
pasif, sensoris bagaimana
Auskultasi - Bruit
Motorik & Sensorik
Saturasi ekstremitas
Cek ABI

Penanganan :
- Pasang iv line resusitasi
- pasang kateter menilai urine
output
- Periksa Laboratorium : DR,
Pt/Aptt, GDS, Kolesterol, AGD,
Ur/Cr
- USG doppler
- CT Angiografi atau angiografi
- antibiotik
- analgetik
- iv Heparin bolus 80 U/KgBB, Maintenance 18 U/KgBB/Jam INDIKASI
- Terapi anti platelet, vasodilator, neurotropik AMPUTASI :
- Dead Limb
- Revaskularisasi ( Nilai rutherford criteria) - Disuse
- Danger
-Amputasi - Damn nuisance
- Modifikasi life style

- USG doppler pada proximal lesi masih memberikan gambaran trifasik,
pada distal lesi akan memberikan gambaran wave melemah jika ada
stenosis/atherosklerosis dan tidak akan memberikan gambaran wave
jika lesi emboli. Bisa juga diberikan colour pada arteri

USG Doppler
- CVI: cari refluks, kompresi bagaimana → bisa ada trombus
non compressible, cari setinggi mana refluks terjadi, vena
tidak ada spektranya.
- Arteri: cari spektranya, trifasik/bifasik/monofasik. Bila spektra
menurun/melemah → penyempitan (hitung berapa persen
penyempitannya, parsial atau total). Bila total sudah tidak ada
spektra/monofasik.
- Bila ada 20-40% penyempitan → parsial. Bila sudah stenosis →
sudah ada stenosis sudah ada penurunan flow dan klaudikasio
(penyempitan biasanya <20%). ABI sudah pasti <0,9.
- Bila sudah rest pain pasti sudah di bawah 0,6. Penyebab
stenosis adalah aterosklerosis (fibrosis di tunica intima sd media).
Di tunica intima ada pempuluh darah yang memperdarahi dinding
→ turun oksigennya dan agregasi platelet di dinding pembuluh
darah. Bila sudah klaudikasio sudah pasti dinding pembuluh darah
aterosklerosis → aliran arteri turbulensi sehingga risiko trombus di
perifer meningkat → dasar heparinisasi (mencegah terjadi klot
intravaskular akibat agregasi platelet, bukan memecah
trombus tapi agar fibrin stabil).
- Aspilet menipiskan dinding platelet, bukan kerja di intravaskular.
Hanya heparin kerja di intravaskular. Komplikasi: klot ke otak
stroke, ke tungkai nekrosis.
- Pseudoaneurima: Yin dan Yang (aliran yang masuk dan keluar).

CT angiography
- Indikasi: curiga AVM (masih muda misalnya tapi varises besar2).
- Trombus/oklusi: gambaran kontras tidak kontinu, ada bagian yang
menghilang. Terapi: bypass/ballooning/stenting.
CT venography
Tatalaksana
- Cilostazol mengurangi reperfusion injury (vasodilatasi + blood
thinner).
- Debridement dengan konsep sharp debridement sesuai dengan
jumlah kompartemen yang terlibat.
- Revaskularisasi setelah infeksi hilang, bila tidak ada luka,
revaskularisasi bisa dilakukan lebih awal.
o Endovaskular bisa sarana memadai.
o Open surgery: total oklusi → bypass kalo di atas femoral.
▪ Bila di iliaka → endovaskular, balon/stent.
▪ Bila di femoral → multipel dan segmental bypass
dengan GSV. endovaskular, balon/stent 50:50
▪ Below the knee → endovaskular.

▪ TRANSATLANTIC KONSENSUS.
- Rekonstruksi
- Bila sudah ada rest pain, ulkus, sistemik → CLI (biasanya lebih dari
14 hari sudah pasti ada ulkus, iskemik, gangren). Buerger yang
non immune disease masuk CLI non diabetik. CLI = chronic limb
ishcemia. Yang tipe dingin disebut → Critical limb ischemia (sama
dengan CTLI).
- PAD = PAOD (Penyakit obstruktif arterial disease)

DM dengan luka di telapak kaki
CLI dengan ulkus pedis.
Kalo belum USG jangan bilang PAD.
Bila sudah gangren di pedis → lihat poplitea.
Usahakan bisa amputasi below knee. Syarat below the knee: pulsasi
arteri poplitea (+), otot gastrocnemius masih utuh. Bila pasien
bedridden/OA → boleh langsung pilih above knee.
Revaskularisasi sebelum amputasi (untuk mencegah terjadi mayor
amputasi) → ct angiography dulu → angiography balon/stent.
- Inflow harus baik dari CT angiography (dari aorta dan iliaka).
- Arteriografi → ada sumbatan open.
- Bila di daerah → usg doppler saja untuk menentukan level oklusi.
- Trombektomi hanya untuk yg akut. Jangan bicarakan pada yg
kronik → kronik pasti BYPASS.
- Bila pada lansia → heparinisasi saja (jangan TROMBEKTOMI
karena risiko rekurensi tinggi).
-
Jelaskan rehabilitasi → goal apa dari amputasi (bisa saja pasien
sebelumnya masih bisa berjalan), bagaimana prostesis.
DM dengan luka di betis

Harus tau vena/arteri. Anamnesis/pfisik
Vena → bengkak, usg: flow baik
Arteri → kering, usg: flow kurang
Boleh juga CT angiografi.
Bila belum ada diagnostic: diabetic foot ulcer wagner berapa
Bila sudah ada diagnostic: CLI, gangren pedis, DM tipe 2, HT, CAD, HHD,
Riwayat stroke.

Evaluasi penderita diabetes dengan luka pada kaki terbagi tiga,
yakni: 1. Keadaan umum secara keseluruhan (misalnya: fungsi kognitif,
metabolik, status hidrasi, dll); 2. Ekstremitas atau kaki yang terluka
(misalnya: adanya neuropati atau insufisiensi vaskuler); dan 3. Daerah
luka yang terinfeksi.
Diagnosis klinis dapat ditegakkan dengan ditemukannya minimal 2
tanda lokal inflamasi, yaitu eritema, kalor, nyeri, edema, dan sekret
purulen. Tanda lain (sekunder) infeksi meliputi adanya jaringan nekrosis,
granulasi, sekret non-purulen, bau busuk, atau luka yang gagal sembuh
dengan perawatan adekuat.
Tanda-tanda ini berguna jika tanda lokal ataupun sistemik tidak
ditemukan akibat neuropati perifer atau iskemi.2,4,10 Semua luka harus
diteliti melalui inspeksi, palpasi, dan pemeriksaan lainnya baik saat awal
maupun follow up.

Example : To exemplify: a 56-year-old man, without diabetes, has ischemic pain at
rest, but no wounds. His ABI is 0.36 and there are no signs of local or systemic
infection. He could be classified as wound 0, ischemia 3, and foot infection 0, or
WIfI 030. His clinical stage would be 2 (low risk of amputation at 1 year) and
revascularization benefit would be moderate

GRADING CEAP :
C : Clinical classification
E : Etiologi, Congenital, Primary, Secondary, No cause
A : anatomic, Superficial , Perforating, Deep vein
P : Patofisiologi, Reflux, Obstruction, Pr,o (keduanya)

Tatalaksana :
- pemberian heparin intravena selama 5-7 hari, UFH atau LMWH
(enoxaparin) selanjutnya antikoagulan oral selama 6-12 minggu

- USG wave pada thrombus vena
- Normal USG pada vena menghasilkan gelombang searah

ULTRASOUND
Duplex ultrasound (DUS) is an integral component of diagnostic

testing for the evaluation and management of arterial disease. This
technology, which combines the acquisition of blood flow (pulsed Doppler
spectral analysis) and anatomic (B-mode and color Doppler imaging)
information.
There are two types of Doppler ultrasound displays. In one form, a
color-flow Doppler image shows the flow velocity distribution over a wide
area displayed as a color-encoded map superimposed on the gray-scale
B-mode tissue image. The second type, often referred to as spectral
Doppler, shows the time varying flow velocity distribution at a selected
sample volume.
Spectral Doppler provides quantitative information on the peak
velocity within the sample volume, whereas color-flow Doppler provides
semiquantitative information on the distribution of velocities over an entire
region.

Color Doppler Imaging
Color Doppler imaging refers to pixel encoding of blood flow based
on a color bar that depicts both flow direction (toward and away from the
transducer) and mean velocity (MV). The examiner adjusts the velocity
scale, color priority, and saturation of the color bar as well as instrument
color gain to show the appearance of normal, laminar arterial flow as
homogeneous regions varying in color-coded pixels during the pulse
cycle.
Arterial stenosis is recognized by color Doppler imaging as a
reduction in the color-encoded flow lumen, imaging of a high velocity flow
region with color bar aliasing, and development of a mosaic flow pattern
in the lumen signifying turbulent flow At the site of a high-grade (>75%
diameter reduction) stenosis, real-time color Doppler flow will appear as
a whitened, color-desaturated “flow
jet” with mosaic color flow extending
for several vessel diameters
downstream corresponding to
poststenotic turbulence (Fig. 22.2).
The presence of persistence of color,

color bar aliasing, and changes in
flow lumen diameter on color Doppler
imaging is indicative of abnormal flow
patterns produced by stenosis.
The pulsed Doppler spectral

parameters of acceleration time,
pulsatility index (PI), resistive index
(RI), and maximum spectral velocity
measured at peak systole (PSV) and
end-diastole (EDV) constitute the

primary criteria used for test interpretation. The PSV measurement
is reproducible and thus the most common velocity spectral
parameter used for the interpretation of normal arterial flow and
critical limb ischemia and for the grading of arterial stenosis. The
EDV measurement is used in conjunction with PSV for evaluating high-
grade stenosis (>70% diameter reduction
The RI is calculated by subtracting EDV from PSV and then

dividing by PSV. It is used clinically to assess the renal and cerebral
circulations for abnormal peripheral

resistance. The PI is calculated by dividing the peak-to-peak
velocityspectral shift by the average (mean) velocity.
The PI of normal peripheral arteries is greater than 4.0 (femoral
artery, >6; popliteal artery, >8). PI values lower than 4 may reflect
proximal inflow or occlusive disease, and change in PI or spectral
waveform damping is diagnostic of multilevel occlusive disease.
Division of distal artery PI by proximal artery PI calculates the “damping
factor;” a normal value is 0.9 or higher, and a value of less than 0.9 is
diagnostic of occlusive disease.
Classification of peripheral arterial stenosis is based on duplex-
derived criteria, similar to carotid duplex testing (e.g., PSV, EDV, and
PSV ratio across a stenosis identified by color Doppler imaging) (Fig. 22.6)
(Table 22.3).

A doubling or step-up in PSV to more than 150 cm/s (Vr >2)
indicates 50% or greater diameter reduction stenosis. Duplex criteria for
a critical flow-limiting stenosis include loss of the triphasic
waveform, spectral broadening with an increase in velocity
(PSV >200 cm/s, EDV >0 cm/s), and Vr greater than 3 across the
stenosis. Higher degrees of stenosis (>75%) are associated with an EDV
higher than 100 cm/s and a Vr
above 4.
Color flow Doppler and pulsed

Doppler spectral waveform analysis
are used to evaluate venous flow
characteristics (Fig. 25.1). Terms for
describing Doppler waveforms have
been standardized. Venous
waveforms are described by major
key descriptors (flow direction, flow
pattern, and spontaneity).In the
arterial system, pumping action of
the heart is the primary driving force
for blood flow, but in the low-
pressure
venous system antegrade
movement of venous blood flow is
substantially affected by other
factors. Normal venous flow is
phasic with respiratory movements
(respirophasic). During inspiration, the diaphragm moves downward and
intraabdominal pressure is increased. This decreases venous return from
the lower extremities. Flow increases during expiration. In the upper
extremity veins, respiratory phasicity has a different pattern.

Intrathoracic pressure is decreased during inspiration; antegrade flow in
upper extremity veins is increased. The cardiac cycle has greater effects
on venous flow patterns in more central veins.
Direct ultrasound visualization of thrombus within a vein is the most

obvious finding associated with deep vein thrombosis (DVT). Deep veins
that are acutely occluded by thrombosis are often distended, appearing
round and larger than the adjacent artery. Thrombus echogenicity
increases as the clot organizes, making it easier to detect with B-mode
imaging over time. Acute thrombus may be adherent to the vein wall, or

it may be loosely attached and mobile, a “free floating thrombus” or
“thrombus tail.”

incompetence of venous valves is the most common etiology of
chronic venous insufficiency. Valvular incompetence can be primary
(without an underlying or antecedent disorder) or secondary, where
valvular dysfunction is the result prior venous thrombosis or injury.
Competent venous valves and muscular pumping of venous blood are

needed to move blood from the lower extremities to the central circulation
when upright.
When valves are incompetent, the musculovenous pump becomes
ineffective. Distal limb pressure is not decreased with walking as it should,
and ambulatory venous hypertension results.
A duplex scan for CVI directly evaluates for obstruction by examining the
appearance and compressibility of the vein, as well as flow patterns,
including assessment with provocative maneuvers to augment antegrade
flow or to cause retrograde flow. Indirect findings that may indicate more
central venous obstruction include asymmetry in flow velocity, lack of
respiratory flow variation, or lack of spontaneous flow.
A 4- to 7-MHz linear array transducer is commonly used, though a
lower frequency curved array probe may be useful for large or obese
patients. A higher-frequency probe is best for scanning superficial veins.
Testing for deep and superficial vein reflux is properly performed with the
patient upright, with the lower extremity externally rotated (Fig. 25.12).
The heel may be on the ground, with weight-bearing on the opposite limb,
or a step may be used to offload the examined side.
Though some venous valves may be visualized with highresolution
B-mode imaging, the functioning of the bicuspid venous valves is
determined observing the direction of blood flow. Normally, in the supine
position, venous flow is phasic with respiration. Retrograde flow may be
physiologic, as valve closure may not occur if the velocity of the
retrograde flow is less than 30cm/s, too slow to close the valve leaflets.
In the upright position, vein valves open to allow antegrade flow, then
snap shut as forward flow ceases and flow reversal commences.
Venous reflux is defined as retrograde flow of abnormal duration (Fig.
25.13). Venous reflux can be characterized as axial if there is
uninterrupted retrograde flow from the groin to the calf. Segmental reflux
involves only some segments of the venous system, while other
segments retain competent functioning valves.

ORTHOPEDI
Fracture repair can be divided into four histologic stages: inflammation,

soft callus, hard callus, and remodeling

Faktor pengaruh healing fracture
Systemic : Age, Nutrisi, Disease (DM), Defisiensi vit. ADEK, NSAID,
Hormonal
Loca l : Abnormal Bone, Degree of damage, Loss of tissue, Infeksi

Principles of Treatment
- Fractures that are nondisplaced or minimally displaced do not require

reduction and are mostly immobilized in situ by external devices (eg,
casts or splints) for comfort and protection.
- To reduce a fracture means to realign the fragments, to correct the
displacements.
- Anatomic reduction restores the position of the fragments exactly to
their preinjury condition (i.e., the exact shape of the bone is
reestablished).
- For many fractures, however, anatomic reduction is not necessary and
only certain components of the displacement need to be corrected. For
example, diaphyseal fractures of a long bone, such as the femur, do not
need anatomic reduction but do need to have approximately the correct
length, rotation, and reasonable alignment restored so that the hip and
knee have the correct relationship to each other.
- Once the fracture has been reduced adequately, some form of
stabilization is needed for comfort and to prevent re-displacement.
usually provided through a cast, splint, or brace that incorporates the
joint above and the joint below the fracture.
External fixators are used most commonly when there is damage

to the soft tissues, such as occurs with open fractures, burns, or
compartment syndromes, or in fractures that do not require internal
fixation but require greater fixation than can be obtained with a cast (eg,
certain metaphyseal fractures of the distal radius, proximal tibia, and
distal tibia)

Implants available for internal fixation include plates and screws,
intramedullary nails, pins, wires, staples, and sutures. Screws may be
used to attach bone fragments together directly, and when inserted in a
manner that compresses the fracture, they are known as lag screws.
More often, screws are used to attach a plate to the bone, which then
functions as an internal splint or a buttress
that significantly increases fracture
stabilization

Intramedullary nails are commonly used for fixation of long-bone
diaphyseal fractures, particularly in the femur, tibia, and humerus. Rods
are inserted through small incisions distant from the fracture site, thus
minimizing disruption of the fracture wound and the risk of infection.
Intramedullary rods are biomechanically favorable because of their
location near the axis of the long bone. They can be locked proximally
and distally to provide stability against rotational or longitudinal
displacement ( Figure 9-9 ).
Protection and Rehabilitation

The bone must be protected from excessive deformation during
healing. Stable fracture patterns allow part of the load to be transmitted
across the fracture, and they permit early weight bearing in a cast or after
internal fixation.
Unstable fracture patterns do not provide load sharing across the
fracture and must be protected by activity restriction or supplemental
bracing until adequate healing has occurred.
The goals of rehabilitation are to return joints to full range of motion,
maintain muscle strength and endurance, and return the patient to as
close to full prefracture activity as possible.

Joint stiffness and muscle atrophy result from immobilization after
injury, and their degree is related to the severity of the injury and the
duration of immobilization. Stable fixation facilitates early motion, and
early functional weight bearing promotes fracture healing. Early motion is
particularly desirable for intra-articular fractures.

CLINICAL FEATURES OF FRACTURES
Pain and tenderness
Loss of function
Deformity
Abnormal mobility and crepitus (avoid)
Altered neurovascular status (important to document)

- Pada pasien trauma tatalaksana sesuai ATLS :
PRIMARY SURVEY
AMPLE
SECONDARY SURVEY - Head
To Toe
LIMB STATUS -diatas dan
dibawah lesi
ADJUNCT - Imaging,
Laboratorium
- AMPLE :
Past surgery, medical illnesses,
Allergies, medications
History of Present Illness
Mechanism of injury: remember the process leading to the fracture
• Traumatic
• Pathologic - tumour, metabolic bone disease, infection,
osteopenia
• Stress - repetitive mechanical loading
- Treatment pada pasien Trauma :

- RESUSCITATION
- ANALGESIA
- SPLINT FRACTURE → 3 Sides
- IMAGING.
- GOALS : 3R (Reduksi, Retensi (Stabilisasi), Rehabilitasi).
Tercapainya union fraktur dengan alignment yang dapat
diterima.
- Prinsip imaging, Rule of 2 : 2 View : AP/Lateral
2 Joint
2 Time

2 Limb (Anggota gerak kanan - kiri)
- FRAKTUR : Open atau Closed, Complete atau Incomplete

(Torus/Greenstick), Displace atau Undisplace.
Fractures are considered displaced if the distance
between the fragments is greater than 1 cm or if angulation
of the fragments is greater than 45°.
- Site : Diafisis (Proximal, Mid, Distal), extraarticular, intraarticular.

• Extra-articular: diaphysis/metaphysis
• Intra-articular

-
Displacement : Posisi fragmen distal terhadap proximal (Shortening,

Translation, Angulasi, Rotasi).
• apposition/translation - describes what percentage of surfaces remain
in contact
• angulation - describes which way the apex is facing
• rotation - distal fragment compared to proximal fragment
• shortened - due to overlap or impaction

CLOSED REDUCTION
- PRINSIP :
- FRAKTUR DISPLACE
- MELAPISI SEMUA TONJOLAN TULANG (Padding)
- ANALGETIK ADEKUAT
- REDUKSI DENGAN TRAKSI AKSIAL DAN KEBALIKAN DARI
MEKANISME INJURY
- IMMOBILISASI SENDI PROXIMAL DAN DISTAL
- 3 POINT CONTACT

- Tujuan Traksi : Menurunkan nyeri
Minimalisir spasme otot
Immobilisasi fraktur
Kurangi deformitas
- Skin Traksi : Adhesive (Max. 15 Pounds / 6 kg) dan non adhesive
Kontraindikasi : Laserasi, Abrasi, Gangguan Sirkulasi.
■ Plaster: Cold water will maximize the molding time. Room
temperature water is preferred.
■ 6-inch width for thigh
■ 4- to 6-inch width for leg
■ 4- to 6-inch width for arm
■ 2- to 4-inch width for forearm

-

Padding → 2 layer → ekstra di tonjolan tulang
- Plaster of Paris → 6 inchi untuk paha
4-6 inchi untuk tungkai
4-6 inchi untuk arm
2-4 inchi untuk forearm

INDIKASI OPEN REDUKSI : NOCAST
- Non Union
- Open Fraktur
- Compromised Neurovaskular
- Intra Articular Fracture
- Salter Harris III,IV,V
- Trauma Multiple
- Internal Fixation : Intramedullary (Rods), Extramedullary (Plate,

Screw)
* Plate harus melewati garis fraktur, 8 hole, 4.5 mm, mulai dari
tengah ke luar.
Fracture Fixation Principles: Traditional AO Principles

Anatomical reduction of the fracture fragments
Preservation of blood supply
Stable internal fixation
Early active mobilisation

Cortical screws are intended for dense cortical bone, but cancellous
screws are for less dense cancellous bone.
Thread design
Cortical screws feature a lower thread depth and a more

aggressive pitch, allowing them to engage well in cortical bone.
Cancellous screws, on the other hand, have a deeper thread with a
more excellent pitch, providing better purchase in the porous structure
of the cancellous bone.
Self-tapping vs. pre-drilling
Cortical screws are frequently self-tapping, which means they

may drill their pilot hole while inserted. This function eliminates pre-
drilling, resulting in a more efficient technique. Cancellous screws, on
the other hand, often need pre-drilling to ensure appropriate placement
and reduce the chance of bone fractures.
Surgical applications
Cortical screws are often employed in load-bearing situations

where robust fixation is required, such as mending fractures in long
bones, due to their properties. They give good cortical bone stability and
support. Cancellous screws, with their broader thread pitch and smaller
core diameter, are ideal for use in areas with low bone density, such as
vertebral bodies or the extremities of long bones.

Common Types of Plates
Neutralisation plating : Clinical application: segmental fracture, long

bone with some comminution, short oblique fracture
Buttress plating Mostly for fractures at the metaphysis of the long bone,
where the
cancellous bone require support or buttress action besides prevention of
collapse (or loss of length) In order to work, the plate should extend from
the diaphysis to the
metaphysis; and the large surface area of coverage is essential to enable
a wide load distribution. Clinical application, e.g. tibial plateau fracture
Compression plating
Tension band plating
Condylar plates

- External Fixation : 1 plane atau 2 plane, Pin 2-2, Jauh-jauh, dekat-
dekat. 4mm pin untuk extremitas atas, 5-6mm untuk femur dan tibia.
Komplikasi :
- Infeksi
- Non Union : 6 Bulan setelah operasi
- Mal Union
- New Fracture
- Implant Failure

- Open Fraktur Gustillo Anderson :
1. Grade I : Clean, Opening <1 cm.
2. Grade 2 : Laserasi >1-10 cm.
3. Grade 3 : >10 cm disertai extensive soft tissue damage.
A. Segmental fraktur, luka dapat ditutup
B. Bone expose, kontaminasi masif
C. Vascular injury
Open Fraktur → Emergency : * Jangan di Reduksi - Kecuali gangguan

NVD.
* Pressure pada luka perdarahan aktif
Golden Hour 6 Jam * Bersihkan Debris
* Kultur dan tutup luka steril
* Vaksin Tetanus
* Start Antibiotik
* Splint

* Puasa dan persiapan operasi
→ Intra Operasi : * Irigasi 8-10 Liter sebaiknya secara
pulsatil - Occasionally, if the risk of wound
contamination is high, antimicrobial irrigating
solutions are used. Dirschl and Wilson
recommend a triple antibiotic solution of bacitracin, neomycin,
and polymyxin,
* Debridement
* Reduksi
* Stabilisasi
* Wound usually left open to drain re-
examine, with possible repeat I&D in 48
hours and closure if appropriate

- Complications of Open Fractures
Osteomyelitis
Soft tissue damage
Neurovascular injury
Blood loss
Nonunion
Rehabilitation
- Mencegah kekakuan sendi dan atrofi otot.
Isometric exercises to avoid muscle atrophy
Range of motion (ROM) for adjacent joints
Continous Passive Movement following rigid fixation of fracture
allows joint motion to prevent stiffness for intra-articular fractures
After cast/splint removed and fracture healed ––> resistive
muscle strengthening
EVALUASI
Evaluate bone healing (clinical, x-ray)
Evaluation of Healing - Tests of Union
- Clinical - No longer tender to palpation or angulation stress
- X-ray - trabeculae cross fracture site, visible callus bridging site
- Delay Union : Tidak tercapai dalam 3-6 bulan tapi masih berpotensi
sembuh, diterapi konservatif dengan exercise dan weight bearing 4-12
minggu.
- Non Union : Tidak tercapai setelah 6 bulan, tipe A bila <1 cm bone
loss, tipe B bila >1 cm bone loss.

Physical Examination
- Prinsip ATLS bila trauma

- Bila non trauma, mulai dari status generalis, status vitalis, head to toe
lalu ke status lokalis/orthopedi.
- LOOK, FEEL, MOVE, NVD.
- Look : Kulit, Bentuk, Posisi, (SEADS ; Swelling, Eritem, Atrofi,
Deformitas, Skin Change) Bandingkan kontralateral.
- Feel : Palpasi Soft tissue, Bone , Joint line. Cek nyeri tekan,
temperatur, deformitas.
- Move : ROM aktif dan pasif.
- PERIKSA SENDI DIATAS DAN DIBAWAH LESI
- Neurovaskular : Reflex, Sensation, Motorik, Pulse, CRT, Akral

dingin.
- Neurologic Examination :
A) Upper Limb : - Motorik : Flexi elbow (N. Musculocutaneus),
Abduksi Shoulder (N.Axillaris), Thumb Sign (N.Radialis), OK Sign
(N.Medianus), Abduksi-adduksi jari (N.Ulnaris)
- Sensorik :Dorsal Forearm (N. Musculocutaneus),
Badge (N.Axillaris), 1st dorsal web (N.Radialis), Ujung jari 2 (N.
Medianus), Ujung jari 5 (N.Ulnaris).
B) Lower Limb : - Motorik : Ankle Plantar Flexi - Injak Rem (N.
Tibialis), Ankle eversi (N. Sup. Peroneal), Ankle Dorsoflexi- Kasih naik
gigi (N. Deep Peroneal).
- Sensorik : Plantar (N. Tibialis), Dorsal
(N.Sup.Peroneal), 1st dorsal web (N. Deep Peroneal), Lateral kaki
(N.Sural), Medial kaki (N. Saphenous).
- Observe gait

CLAVICULA
The deformity frequently involves shortening, angulation and medial

rotation
Pathomechanics
- Falling on the point of the shoulder, direct blows rare.
- Middle third fractures are most common because it represents a
region of transition in bone curvature and cross-sectional anatomy
Fractured Clavicle Classification
Popular classification:
Group I refers to middle third fractures
Group II refers to lateral third fractures, which in turn are divided into
three types
Group III refers to medial third fractures
Classification of Lateral Third Fractures
Type 1: CC ligament intact
Type 2: CC ligament torn, with high riding fractured end of clavicle
Type 3: Intra-articular fracture, extending to involve the ACJ
Conservative Treatment: Majority of Patients

Usually involves either a figure-of-eight bandage or arm sling with ROM
exercise for 2-4 weeks and strengthening iat weeks 6th - 10th
Operative Indications
⚫ Floating shoulder
⚫ Open fractures
⚫ Associated neurovascular injury
⚫ Skin impingement
⚫ Increasing trend to fix widely displaced fractures.
⚫ The extent of the fracture displacement (e.g. shortening > 15–20
mm in the younger, high-demand patient)
⚫ Segmental fractures
Choice of Fixation
Plate and screw most popular – avoid weak plates such as one-
third tubulars (use LC-DCP) placed on the tension side (superior). Avoid
the use of k-wires, and cerclage. Also, need to avoid unnecessary
periosteal stripping, neuroma, and need to protect the neurovascular
structures during drilling. Proper plate contouring is essential.
- Fraktur : 1/3 Lateral : Open Fraktur → ORIF (Locking Plate 8 hole
3.5mm)
1/3 Middle : Ada plexus brachialis, Subclavia vessel.

SHOULDER
- Terdapat 4 Sendi : A. Glenohumeral

B. Acromioclavicular - Nyeri saat adduksi)
C. Scapulothoracic
D. Sternoclavicular
- Periksa pergerakan ke-4 sendi.
- MOVE - Active/Passive
Active ROM
• Forward flexion and abduction
• External rotation (elbows at side and flexed 90 degrees, move arms
away from midline)
• Internal rotation (hand behind the back, measure wrt. level of the
spine)
Passive ROM
• abduction – 180 degrees
• adduction – 45 degrees
• flexion – 180 degrees
• extension – 45 degrees
• internal rotation – level of T4
• external rotation – 40 - 45 degrees

- Dislokasi Shoulder
- Subluksasi : Partial loss diantara permukaan sendi

- Dislokasi : Total Loss
Dislocation of the glenohumeral joint may be anterior, posterior,

or multidirectional. Anterior is most common, accounting for
approximately 98% of the dislocations. Anterior dislocations may occur
at any age but are more common after athletic injuries in adolescents
and young adults.

Patients may present after spontaneous reduction or reduction in
the field. If the patient is not in acute pain, examination may reveal a
positive apprehension test, in which passive placement of the
shoulder in the provocative position (abduction, extension, and external
rotation) reproduces the patient’s
sense of instability and pain (Fig.
14.5)

ANTERIOR DISLOCATION
The anterior capsule and associated ligaments are stretched or

torn with subsequent anterior dislocation of the humeral head when
the arm is positioned in abduction, extension, and external rotation.
The humeral head usually rests in a subcoracoid position, but it may
be positioned inferior to the glenoid or subclavicular.
These patients experience the sudden onset of pain and an
inability to use the arm after a fall or forceful throwing movement.
Inspection typically shows the patient supporting the arm with
the other hand.
Examination reveals flattening of the deltoid prominence,

prominence of the acromion, fullness of the subcoracoid region,
and downward displacement of the axillary fold. Any attempt at
motion elicits pain.

Physical Examination
⚫ “squared off” shoulder
⚫ Humeral head can be palpated anteriorly
⚫ Arm held in slight abduction and external rotation
⚫ Loss of internal rotation with anterioinferior humeral head
⚫ Axillary nerve may be damaged, therefore check sensation and
contraction over lateral deltoid;
⚫ Musculocutaneous nerve check sensation of lateral forearm and
contraction of biceps apprehension test: for recurrent shoulder
instability
⚫ Flattening of the deltoid prominence, Prominence of the
acromion, Fullness of the subcoracoid region, and
⚫ Downward displacement of the axillary fold

X-Rays
Radiographic views of the shoulder should include

⚫ AP, trans-scapular/Scapular - Y, and axillary views (at least)
⚫ Stress views of the acromioclavicular joint where indicated look for
the Mercedes
Benz sign
⚫ In the trans-
scapular
radiograph to look
for dislocation
⚫ Humeral head
should occupy the
circle and be
overlapping
glenoid
⚫ Humeral head anterior (to Mercedes Benz sign) in trans-scapular
view
⚫ Axillary view is diagnostic
⚫ AP view may show Hill-Sachs lesion if recurrent rule out associated
humeral neck fracture

Axillary, AP, and scapular Y radiographs should be obtained
before reduction so that the type of dislocation and any associated
fractures may be documented. Radiographs may show a defect in the
posterolateral humeral head, called a Hill-Sachs lesion, resulting from
impaction of the humeral head on the anterior rim of the glenoid fossa.
Avulsion of the anteroinferior glenoid labrum, called a Bankart
lesion, also may occur. Hill-Sachs and Bankart lesions are predisposing
factors for recurrent instability.
After reduction, AP and axillary radiographs should be obtained to
confirm concentric reduction. Hill Sachs and bony Bankart lesions also
may be identified on postreduction radiographs.

-Subcoracoid : Head humerus terletak inferior dari
coracoid, medial dari glenoid.
-Subglenoid (anteroinferior) : Head humerus terletak inferior dari
glenoid.

POSTERIOR DISLOCATION
Posterior glenohumeral dislocations are uncommon, and the diagnosis

may be missed, particularly if only an AP radiograph is obtained .
Posterior dislocations occur with an internal rotation–adduction force
and are more common in patients who have a seizure disorder or
who have experienced an electric shock injury.
• Shoulder is adducted, internally rotated and flexed

the four Es which cause posterior dislocation are:
• E pileptic seizure
• E thanol intoxication
• E lectricity (ECT, Electrocution)
• Encephalitis
Examination reveals decreased fullness of the deltoid,

posterior prominence of the humeral head, and marked restriction
of abduction and external rotation. Appropriate radiographs are the
same as for an anterior dislocation. Reduction is accomplished by distal
traction
and the

application of manual pressure to the humeral head in an anterior
direction.
X-rays: in two planes (axillary and AP) are most useful
MANUVER PROCEDURE PICTURE

Traction - • 1. Countertraction using
a swathe wrapped through
Counter
the axilla to stabilize the
Traction chest
• 2. After the patient is
sedated, gentle
traction is applied for 5-10
minutes at the arm in the
line of deformity
• 3. As the traction is
increased gradually,
internal or extrernal
rotation is used to
disengage the head of
humerus over the glenoid
rim
• 4. With a gentle
manuver, the reduction
can usually be
accomplished and the
head slipped into the
socket
Stimpson Pasien pronasi, lengan

tergantung dipinggir
meja, gantung beban di
wrist (5 pound/2.2 kg
selama 15-20 menit),
sling 3 minggu.

Kocher • Affected elbow is flexed
to 90 degree
Manuver
• Wrist and point of elbow
are gently grasped by the
surgeon as the patient
relaxes.
• Arm is slowly externally
rotated up to about 80
degree where resistance
is felt
• Extrernally rotated arm is
lift upward in the sagittal
plane as far as possible
• Humerus in internally
rotated , and
the head gently pops into
the joint as
reduction is achieved
• Internally rotated arm is
then brought down against
the chest with the
shoulder reduced
Hipoccratic • Surgeon foot is placed

between the
Method
patient chest wall and
axillary folds but
not in the axilla
• Steady traction is
maintaned while the
patient gradually relaxes
• Shoulder is slowly
rotated extrernally
and adducted

• Gentle internal rotation
reduces the
humeral head
The arm is immobilized in a sling, and the patient begins

circumduction exercises at 1 week and range-of-motion exercises at 3
weeks. The abduction–external rotation position is avoided for 6 weeks.
Strengthening exercises are initiated after the patient has regained full
range of motion without apprehension.
■ In comparison to a simple sling, immobilization in a Velpeau dressing
does not
appear to alter the subsequent development of recurrent instability.
■ Therapy should be instituted following immobilization, including
increasing
degrees of shoulder external rotation, flexion, and abduction as time
progresses,
accompanied by full, active range of motion to the hand, wrist, and
elbow.
Surgical intervention rarely is needed for acute glenohumeral joint

dislocation but usually is required for a fracture-dislocation and when
the glenohumeral joint remains unreduced.

HUMERAL SHAFT
Anatomy : Memanjang dari insertio pectoralis mayor ke cekungan

supracondylar.
Vaskularisasi dari A. Brachialis
Klinis : Pain, Swelling, Shortening.
Pemfis : Look, Feel, Move, NVD (MARMU)
Xray : AP dan Lateral (termasuk shoulder dan elbow joint)
Deskripsi : - Open atau Closed
- Karakter : Transverse, Oblique, Spiral, Kominutif.
- Lokasi
- Displace atau non displaced

Treatment : NOM diindikasikan pada non displaced dan minimal
displaced, Hanging cast (shoulder to wrist)
- elbow flexi 90°- Sling 2-3 minggu - Ganti
ke functional bracing.
Nonoperative
■ Most humeral shaft fractures (>90%) will heal with nonsurgical
management.
■ Nonoperative treatment requirements are:
■ A cooperative and preferably upright and mobile patient
■ An acceptable fracture reduction
■ Intact/innervated arm musculature (e.g., intact brachial plexus)
■ Twenty degrees of anterior (sagittal) angulation, 30 degrees of varus
(coronal)

angulation, and up to 3 cm of bayonet apposition are acceptable and
will not
compromise function or appearance.
■ Hanging cast: Utilizes dependency traction by the weight of the cast

and arm to
affect fracture reduction.
■ Indications include displaced midshaft humeral fractures with
shortening,
particularly spiral or oblique patterns. Transverse or short oblique
fractures
represent relative contraindications because of the potential for
distraction and
healing complications.
■ The patient must remain upright or semiupright at all times with the
cast in adependent position for effectiveness.
■ It may be exchanged for functional bracing following early callus
formation.
■ More than 95% union is reported.

■ Coaptation splint: Utilizes dependency traction and hydrostatic
pressure to effect
fracture reduction but with greater stabilization and less distraction than
a hanging
arm cast. The forearm is suspended in a collar and cuff.
■ It is indicated for the acute treatment of humeral shaft fractures with
minimal
shortening and for short oblique or transverse fracture patterns that may
displace with a hanging arm cast.
■ Disadvantages include irritation of the patient’s axilla and the potential
for
splint slippage.
■ It is frequently exchanged for functional bracing 1 to 2 weeks after
injury.
■ Thoracobrachial immobilization (Velpeau dressing): This is used

only in elderly patients or children who are unable to tolerate other
methods of treatment and in whom comfort is the primary concern.
■ It is indicated for minimally displaced or nondisplaced fractures that
do not
require reduction.
■ Passive shoulder pendulum exercises may be performed within 1 to 2
weeks
after injury.
■ It may be exchanged for functional bracing 1 to 2 weeks after injury.

■ Functional bracing: This utilizes hydrostatic soft tissue compression
to effect and
maintain fracture alignment while allowing motion of adjacent joints.
■ It is typically applied 1 to 2 weeks after injury, after the patient has
been placed in a hanging arm cast or coaptation splint and
pain/swelling has subsided.
■ It consists of an anterior and posterior (or medial–lateral) shell held
together
with Velcro straps.
■ Success depends on an upright patient and brace tightening daily, as
well as
functioning upper arm musculature.
■ Contraindications include massive soft tissue injury, an unreliable
patient, and
an inability to obtain or maintain acceptable fracture reduction.
■ A collar and cuff may be used to support the forearm, but sling
application mayresult in varus angulation.

■ The functional brace is worn for a minimum of 8 weeks after fracture
or until radiographic evidence of union.
Surgery : Indikasi Operasi : Shortening >3 cm,

angulasi >20°,
rotasi >30°,
fraktur segmental, Displace 3-4
bagian, Open fraktur,
Dislokasi proximal humerus,
Fraktur patologis
Multiple trauma
Fraktur intraartikular
Nerve injury
Nonunion
- Plate osteosintesis , Nailing intramedullary atau external fiksasi
- Approach : Anterolateral (split brachialis), posterior (triceps
split).

Post OP : Rehabilitasi ROM : Kepal dan regangkan jari, Rotasi
shoulder, Jempol ke bahu kontralateral.
Complication : Shoulder stiffness, Radial nerve palsy - Wrist drop
(Fraktur humerus 1/3 distal)

ELBOW
CLASSIFICATION
■ Simple versus complex (associated with fracture)
■ According to the direction of displacement of the ulna relative to the
humerus
■ Posterior
■ Posterolateral
■ Posteromedial
■ Lateral
■ Medial
■ Anterior

After reduction, elbow stability is assessed with the forearm in
pronation. If ligament disruption involves the anterior band of the medial
collateral ligament, instability is noted with the elbow in extension. This
injury will need 3 to 6 weeks of protection, starting with the elbow
in pronation and 90°of flexion.
More stable injuries should be immobilized for a short time (1
to 2 weeks) to prevent the complications of elbow stiffness and loss
of extension. Other complications, such as heterotopic
ossification, brachial artery injury, ulnar nerve injury, and
compartment syndrome, are associated with high-energy injuries and
concomitant fractures.

FOREARM

FRAC CLINICAL OVERVIEW TREATMENT
TURE
Monteggia
- Fraktur Ulna + Proximal Radioulnar joint dislokasi Reposisi Fraktur Ulna
Ulna
Fraktur + Radiocapitellar joint dislokasi. terlebih dahulu (ORIF).
- Tipe dari arah dislokasi radial head (BADO) :
Tipe 1 :Anterior ORIF is recommended
open reduction of the
Tipe 2 : Posterior
ulna is usually
Tipe 3 : Lateral followed by indirect
reduction of the radius
Tipe 4 : Fr. Radius + Ulna + Dislokasi Anterior
■ Closed reduction
and casting of
Monteggia fractures
should be reserved
only for the pediatric
population.
■ Monteggia fractures
require operative
treatment, open
reduction, and internal
fixation of the ulna
shaft with a 3.5-mm
DC plate or
reconstruction plate.
Closed reduction of
the radial head with
restoration of ulnar
length is the rule.
Plate application on
the tension side
(dorsal) is
recommended
especially in Bado
type II
fracture.
■ After fixation of the

ulna, the radial head is
usually stable (>90%).
■ Postoperatively, the
patient is placed in a

posterior elbow splint
for 5 to 7 days.
With stable fixation,
physical therapy can
be started with active
flexion–extension
and supination–
pronation exercises.
Galleazzi - Fraktur Distal Radius + Disrupsi Radioulnar Joint Close Reduction →

Radius
Fraktur
- Pediatri : Immobilisasi →
Tipe 1 : Displace Apex Volar Supinasi + Casting
Tipe 2 : Displace Apex Dorsal Above Elbow 4-6
- Adult : Tipe 1: <7.5 cm distal radius minggu.
Tipe 2 : >7.5 cm distal radius ■ Open reduction
and internal fixation
comprise the
treatment of choice,
because closed
treatment is
associated with a high
failure rate.
■ Plate and screw

fixation (3.5-mm DC
plating) is the
treatment of choice.
■ An anterior Henry
approach (interval
between the flexor
carpi radialis and the
brachioradialis)
typically provides
adequate exposure of
the radius fracture,
with plate fixation on
the flat, volar surface
of the radius.

Colles Dinner Fork Deformity Reduksi tertutup
The mechanism of injury is a fall onto a →Casting posisi
hyperextended, radially deviated wrist
Plantar fleksi dan
with the forearm in pronation.
Ulnar deviasi.
Circular cast after 1-2

weeks; check cast at
1, 2, 6 weeks; cast off
after 6 weeks,
physiotherapy
(ROM, grip strength)

Smith ■ This describes a fracture with volar angulation Reduksi tertutup →
(apex dorsal) of the distal radius
Casting posisi supine
with a “garden spade” deformity or volar
displacement of the hand and distal dan dorsal flexi.
radius.
■ The mechanism of injury is a fall onto a flexed
wrist with the forearm fixed in ■ This is a notoriously
supination. unstable fracture
pattern; it often
requires open
reduction and internal

fixation because of
difficulty in maintaining
adequate closed
reduction.
Barton
■ The mechanism of injury is a fall onto a ■ Almost all fractures
dorsiflexed wrist with the forearm of this type are
fixed in pronation. unstable and require
open reduction and
internal fixation with
a buttress plate to
achieve stable,
anatomic reduction.
Median nerve dysfunction is the most common

associated injury.
Chauffeur
A transverse or oblique fracture across the radial
styloid (a chauffeur fracture) results from a direct
blow to the lateral aspect of the forearm.

COMPLICATIONS OF WRIST FRACTURES
• Compartment syndrome
• Extensor pollicis longus (EPL) tendon rupture
• Acute carpal tunnel syndrome
• Finger swelling with venous or lymphatic block late
• Malunion, radial shortening
• Painful wrist secondary to ulnar prominence
• Frozen shoulder ("shoulder hand syndrome")
• Post-traumatic arthritis
• Carpal tunnel syndrome
• Reflex sympathetic dystrophy (RSD)

COMPARTMENT SYNDROME
Diagnosis
Clinical mainly:
- Pain out of proportion, not relieved by analgetics
- Pain caused by passive stretching of the muscles in the
compartment
- The compartment usually feels hard or tense to the touch,
especially when compared with the contralateral limb; the skin is
tight and shiny and cannot be wrinkled. (Swell)
- Pallor, paresthesia, paralysis, and pulselessness are late findings
or are unreliable.
- Pressure measurement is also useful in obtunded, intubated, or

unreliable patients who have a swollen extremity but who otherwise
cannot be evaluated.
- Differential pressure (diastolic minus compartment
pressure) less than or equal of 30 mmHg
- Direct compartment pressure of 45 mmHg (Matsen)
Compartment Pressure Measurement Method
Whitesides infusion technique
The slit catheter

Highest tissue pressure is usually recorded at the level of the fracture or
within 5 cm of the fracture
Management
Remove all (tight) plaster and bandage (if any)

Emergency fasciotomy once diagnosis made
Do not elevate the involved limb
Indication for Decompression – Fasciotomy

High index of suspicion
Clinical evaluation
Supplemented by compartment pressure measurement and monitoring
Kompartemen Anatomy Fasciotomy

Arm 2 → Anterior
Posterior.
Forearm 3 → Volar, Fasciotomy pada dorsal dan
Dorsal, volar.
Mobile wad. Forearm compartments
are interrelated – volar
fasciotomy alone lowered
pressure in the dorsal
compartment significantly

Hand 10 → Thenar, Hipothenar, Muscle compartments in the
Adductor policis, Dorsal 4, volar 3 hand are isolated and require
(interossei) individual release
Adequate decompression of the
median nerve – at lacertus
fibrosus, edge of pronator
teres, proximal edge of flexor
superficialis and carpal tunnel
Carpal tunnel – raised pressure

in the forearm/hand;
compartment
syndrome, release of the carpal
tunnel, also indirectly releasing
Guyon’s canal

Thigh 3 → Anterior, Posterior, Adductor Fasciotomy pada lateral.
LEG 4 → Anterior, Lateral, Deep dan Double incision - Anterolateral,

Superficial posterior. Posteromedial
Single incision - Head fibula

sampai distal ankle (lateral)

Foot 8 , Fasciotomy dual dorsal incision.
Complications of Compartment Syndrome

Volkmann’s Ischaemic Contracture
Irreversible tissue ischaemia because of delayed or incomplete
fasciotomy → muscle necrosis and scar down → contracture
Forearm: elbow flexion, forearm pronation, wrist flexion, thumb
adduction, MCPJ extension, IPJ flexion
Volkmann’s Ischaemic Contracture: Treatment
Splinting
Physiotherapy
Surgery – muscle excision, muscle sliding, tendon transfer, free muscle
transplantation (gracilis muscle)

HIP DISLOCATION
- Simple - Tidak ada fraktur, Complex - Fraktur acetabulum atau

proximal femur.
- Posterior : Deformitas Adduksi, Internal Rotasi, Flexi dan terdapat
jejas di anterior lutut.
Approximately 90% of hip dislocations are posterior and are caused by
a high energy impact on the knee of a person sitting with the hip flexed
and adducted

- Xray : AP view, 45° Oblique view, Judet view (Jika
acetabulum fraktur)

- Treatment : Close Reduction within 6 hours - Kontraindikasi : Fr.
Femoral Neck
MANUVER PROCEDURE
Allis Supine
manuver Stabilisasi pelvis (tekan SIAS kebawah)
Flexi lutut
Traksi lalu internal rotasi + adduksi.

Stimson Pasien Prone
Manuver Dorong dari belakang
Lefkowitz Pasien Supine

Manuver Pakai lutut operator menyanggah
Bigelow • The patient is positioned supine
• The assistant stabilizes the pelvis
Manuver
• The surgeon places one arm beneath
the patient’s proximal calf and grasps the
ankle with his or her other arm
• The surgeon applies longitudinal traction
on the limb.
• The adducted and internally rotated
thigh is then flexed at least 90 degrees.
• The femoral head is then leveres into
the acetabulum by abduction, external
rotation, and extension of the hip
Baltimore
Manuver

Post-reduction radiographs are critically assessed to confirm a
congruent reduction and no evidence of osteochondral fragments
in the joint.
Komplikasi :
Early : - Sciatic nerve injury
- Vascular injury
- Fracture femoral shaft
Delay :- Avaskular nekrosis of head femur
- Osteoarthritis
- Recurrent dislocation
- Anterior : Rotasi eksterna, Abduksi, Fleksi.

Tipe I : Pubic (superior)
Tipe II : Obturator (inferior)
Anterior dislocations often occur in sporting events. A forceful

abduction and external rotation movement ruptures the stout anterior
capsule, with the femoral head typically displaced to an inferior obturator
position. Impaction fractures of the posterior femoral head may occur.
The femoral nerve and artery are vulnerable.
Treatment : Manuver - Traksi → internal dan eksternal rotasi→dorong

dari anterior

PELVIC FRACTURE
- Struktur yang beresiko : Plexus lumbosakral, Nervus sciatic,
Urogenital.
- Klasifikasi :
Young & Burgess : APC → struktur anterior terbuka (Open Book)
Tipe I : <2.5 cm
Tipe II : >2.5 cm
Tipe III : Dislokasi SI Joint
LC → Trauma dari samping
Vertical Sheer → Jatuh dari ketinggian
- Pemfis : - Hematom/jejas pada skrotum, perineum, gluteus.

- Blood pada meatus urethra
- Hematom perirectum
- Defisit neurologis
- Leg length
- Syok
- XRay : Pelvic inlet view (dari cranial miring 25°)
Pelvic outlet view (dari caudal miring 42°)

Pelvic ring injuries can be classified as stable or unstable.
⚫ Stable injuries involve only one side of the ring.

⚫ Unstable pelvic fractures include fracture and/or ligamentous
disruption in two parts of the ring.

Stable injuries involve only one side of the ring.
Examples include direct-impact fracture of the sacrum, coccyx, or iliac
wing and isolated pubic ramus fractures associated with low-energy
falls in osteoporotic elderly individuals. Stable injuries can be
treated symptomatically with crutch- or walker-assisted
ambulation.
Unstable pelvic fractures include fracture and/or ligamentous

disruption in two parts of the ring. Examples include straddle injuries
with bilateral superior and inferior pubic rami fractures, lateral
compression injuries with overlapping pelvis, open book fractures with
disruption of symphysis pubis and anteriorsacroiliac ligaments, and
vertical shear fractures with ipsilateral disruption of the anterior and
posterior ring. Some unstable pelvic fractures can be treated
nonoperatively with a period of bed rest to allow initial healing, followed
by progression to assisted ambulation. Other injuries require reduction
and internal fixation of one or both sides of the ring to avoid or minimize
the risk of pelvic deformity and associated pain and dysfunction.

- Treatment :
ABCs
assess genitourinary injury (rectal exam/vaginal exam mandatory)
Type A - bedrest and mobilization with walking aids
Type B/C - external or internal fixation
Pelvic binder, Pelvic C-Clamp
Surgery setelah 5-7 hari.

MUSCLE
Sprain:
Partial or complete tear of a ligament.
Strain:
Partial tear of a muscle, usually at the musculotendinous junction
ANATOMY AND PHYSIOLOGY OF TENDONS AND LIGAMENTS
Tendons attach muscle to bone. Ligaments and their

associated capsular tissues connect bone to bone. Tendons and
ligaments are composed of fibroblasts, collagen, proteoglycan,
glycoproteins, elastin, water, and connective tissue covering. The major
constituent of tendons and ligaments is type I collagen.
An acute ligament injury is called a sprain. The disruption

may be partial or complete. Grade I sprains are partial tears with
mild rupture or stretching of the collagen fibers and no apparent
instability of the joint when the ligament is stressed. Grade II sprains
are partial but more severe, and there is some laxity on stressing of
the joint. Grade III sprains are complete ligament ruptures with
complete instability of the ligament on stress maneuvers.

Similar to healing of other soft tissues, healing of tendons and
ligaments progresses through four stages:
inflammation, proliferation, remodeling, and maturation. And goes from
12 weeks until one year.
ACL - PCL

Examination shows a marked effusion, and most patients with an acute
knee hemarthrosis have a torn ACL.
The Lachman test is the most sensitive maneuver for detecting
ACL tears. It is performed with the knee flexed to 20°. One hand placed
laterally stabilizes the distal femur, and the other hand grasps the
proximal tibia medially. The proximal tibia is pulled forward. With an
intact ligament, minimal translation is felt and a firm end point is noted.
With a torn ligament, more translation is noted, and the end point is soft.
The anterior drawer test is easier to perform. It is performed with
the patient supine, with the hamstrings relaxed, and the knee in 90°of
flexion. The proximal tibia is grasped with both hands and pulled
forward. Displacement >5 mm compared with the uninvolved side
indicates an ACL tear.
Radiographs mostly rule out other injuries, but a lateral avulsion
fracture (Segond fracture) indicating an associated lateral capsular tear
may be present. If surgical reconstruction is planned, MRI is usually
obtained to confirm diagnosis and to delineate associated injuries.
Cruciate ligaments do not heal with nonoperative treatment.
With no treatment, the resultant recurrent instability makes return to
previous level of sports participation unlikely and predisposes the patient
to subsequent meniscal tears. Direct repair does not work. Intra-articular
midpatellar bone-tendon-bone or hamstring tendon autograft
reconstructive procedures provide the most consistent results, but
allograft or extra-articular procedures are also used in selected cases.
Possible complications include arthrofibrosis, repeat ACL tear, and
patellar symptoms

Achilles Tendon Rupture
Rupture of the Achilles tendon typically occurs in middle-aged males

who are participating in sports activities, especially basketball. The
rupture typically occurs in a relatively avascular area 4 to 6 cm proximal
to the tendon's insertion.
A typical patient reports, “I was starting to jump and felt a sudden onset
of severe pain, like a gunshot went through my calf.” However, the
severe pain resolves, the patient can walk with a limp, and the injury
may be mislabeled as a sprain. Examination shows tenderness in the
area of the rupture. A palpable
defect may be appreciated. The most sensitive and reliable sign is a
positive Thompson test

ORTHOPEDI NON TRAUMA
HISTORY
Identification
• include: occupation, hobbies, hand dominance
Chief complaint
History of Present Illness
important to obtain details regarding onset and progression of
symptoms
pain
• OPQRST ( Onset, Provoking / Alleviating factors,Quality, Radiation,
Site, Timing)
• muscular, bony, or joint pain ?
• number of joints involved and symmetry of involvement inflammatory
symptoms
• morning stiffness (> 30 min), tenderness, swelling, redness, warmth
mechanical/degenerative symptoms
• increased with activity, decreased with rest
• locking, giving way, instability weakness, deformity, stiffness, crepitus
Neoplastic and infectious symptoms
• constant pain, night pain
• fever, night sweats
• anorexia, fatigue, weakness, weight loss
• mets from Prostate, Thyroid, Breast, Lungs, Kidney
Past orthopedic history
• injuries, past non-surgical treatment, past surgery
• investigations: Xray, CT scan, MRI, etc.
Other medical history
• past surgery, medical illnesses, allergies, medications
Activities of daily living

• getting up, sitting down, using bathroom, combing hair, transferring
referred symptoms
• shoulder pain from the heart or diaphragm
• arm pain from the neck
• leg pain from back
• back pain from the kidney, aortic aneurysm, duodenal ulcer,
pancreatitis
PHYSICAL EXAMINATION
Look, Feel, Move
always examine the joint above and below
look - skin, shape, position - compare sides
• SEADS: S welling, E rythema, A trophy, Deformity,Skin changes
feel - palpate soft tissue, bone, joint line
• assess: tenderness, temperature, effusion, deformity
• active and passive range of motion (ROM), crepitus present?,
instability?
• passive ROM > active ROM suggests soft tissue inflammation or
muscle weakness
neurovascular tests
• pulse, reflexes, power (grade with MRC scale), sensation
Special tests depend on joint
Observe gait: walking, heel-to-toe, on heels, on toes
Diagnostic Imaging
plain X-rays: 2 views taken at 90º to each other
CT/myelography, MRI.
• reflects osteoblastic activity or inflammatory reaction
• positive with fractures, tumours.
• reflects hypervascularity, taken up by leukocytes
• positive with infection

Blood Tests for Painful, Swollen Joint
CBC, ESR, Rheumatoid Factor (RF), ANA, C-reactive protein (CRP)
FRACTURES - GENERAL PRINCIPLES
Primary idiopathic osteoarthritis

Describes the condition in patients when no obvious underlying cause
can
be discerned.
Secondary osteoarthritis
Degenerative joint disease that is secondary to specific conditions that
cause accelerated erosion of articular cartilage.
Common sites of OA include the distal and proximal interphalangeal
joints of the fingers, the carpometacarpal joint of the thumb, the cervical
and lumbar spine, the hip, the knee, and the the metatarsophalangeal
joint of the great toe.
In the early stages of OA, articular cartilage loses its pearly white
appearance. Progressive changes include softening, fissuring, and

flaking of the cartilage surface. When full-thickness loss of cartilage
occurs, the subchondral bone becomes eburnated. Radiographic findings
include narrowing of the joint space secondary to thinning of articular
cartilage, subchondral sclerosis representing new bone formation
and response to healing microfractures, osteophytes at the joint
margin, and subchondral cysts that typically communicate with the
joint space. As the disease progresses, the joint space may become
completely obliterated, and subchondral cysts and proliferative
osteophytes may markedly distort normal joint congruity.

Patients with OA present with local signs and symptoms that are
specific to the affected joint.
symptoms expressed by patients with arthritic disease are
generally focus toward pain, limitation of motion, and impaired
function.

Pain is initially provoked by load-bearing activity, is relieved by
rest, and then is aggravated on resumption of activity after rest.
As symptoms progress, the pain may become constant, being present
even at rest and awakening the patient at night.
Occasionally, the pain is referred to the buttocks or distal thigh.
As degeneration of the articular cartilage progresses, the duration and
the frequency of the pain intensify. Pain at rest or pain that wakens the
patient at night is associated with severe arthritis. The most sensitive
sign of early osteoarthritis of the hip is loss of internal rotation. As the
disease and joint contractures progress, decreased abduction, flexion,
and extension are observed. A coxalgic limp, with or without
Trendelenburg lurch, is often present.
The nonoperative management of OA depends on which joint is

involved, but the principles of treatment include activity modification,
intermittent rest and splints, nonforceful strengthening exercises,
external aids to reduce load-bearing stress, and non-addictive pain
medication. Nonsteroidal anti-inflammatory drugs (NSAIDs) do not
alter the natural course of OA, and in some patients, they may be no more

effective than acetaminophen; however, they offer the theoretical
advantages of reduced pain and alleviated synovitis. Selection of a
particular NSAID is determined by cost, convenience of dosing interval,
and individual tolerance of gastrointestinal, renal, and cardiac adverse
effects.
The goals of OA reconstructive procedures are to relieve or
decrease pain, to correct deformity, and to improve function. The
procedures usually fit into one of four categories:
⚫ osteotomy, to realign joint surfaces so as to redistribute load to a
relatively preserved portion of the joint,
⚫ resection arthroplasty, with or without release of contracture and/or
interposition of a biologic spacer.
⚫ arthrodesis, to fuse the end-stage joint and thus alleviate pain when
anatomic considerations do not permit effective joint replacement, or
in a young patient who has functional demands in excess of those
reasonably expected of a prosthetic arthroplasty; and
⚫ prosthetic arthroplasty (total joint replacement) for end-stage disease
in an older patient or one with moderate functional demands

RHEUMATOID ARTHRITIS
Rheumatoid arthritis (RA) is a systemic autoimmune disease of unknown

cause characterized by an inflammatory synovitis that is destructive to
articular cartilage.
The incidence of RA increases with advancing age, with peak onset

during the fourth and fifth decades. The female-to-male ratio is 2.5:1.
Female hormones appear to influence the development of RA because

there is a decreased incidence with the use of oral contraceptives, an
increased risk in nulliparous women, remission of symptoms during
pregnancy, and increased onset of the disease around the time of
menopause. Genetic factors also have a role, as suggested by family
association.
The onset of RA is characterized by the insidious development of

symptoms over a period of several weeks to months. The arthritis is
typically symmetric, with early involvement more common in the
hands, wrists, feet, and ankles.
The inflammatory nature of the patient's arthritis is suggested by

morning stiffness and stiffness with inactivity (gel phenomena).
Generalized malaise and fatigue also are noted at disease onset.
The most common ocular manifestation in RA is
keratoconjunctivitis sicca, which may cause only dry eye or may
include burning, foreign body sensation, and mucoid discharge.
Episcleritis, scleritis, and scleromalacia may also occur.

Accepted criteria for the diagnosis of RA are the presence of at least
four of
seven findings that continue for at least 6 weeks.
American Rheumatism Association 1987 Revised Criteria for the
Diagnosis of
Rheumatoid Arthritis
Radiographic characteristics of RA include osteopenia,

subchondral erosion, and uniform narrowing of the joint space.
These features may be contrasted with the sclerosis and asymmetric joint
erosion that typify OA.

Initial treatment begins with
NSAIDs, but many patients
require disease-modifying agents
such as methotrexate.
Corticosteroids provide
symptomatic relief but do not stop
progression of the disease. Their
adverse effects are multiple;
therefore, these agents are used
most often for life-threatening
vasculitis that complicates RA.
If the disease progresses despite
optimal medical management,
then surgical intervention may be
beneficial. Tenosynovectomy or
synovectomy for uncontrolled inflammation of a tendon sheath or
joint may improve function and prevent the complication of tendon
rupture.

PEDIATRIC

TREATMENT OF PEDIATRIC FRACTURES
Fracture healing is more rapid in children than in adults. For

example, a fracture of the femoral shaft in an adult requires 16 to 20
weeks of immobilization if treated in a cast. By comparison, the same
fracture needs only 2 weeks of immobilization in an infant and 4 to 6
weeks of casting in a young child.
As acorollary to rapid healing, nonunion is uncommon in children.
Closed reduction and casting is the primary

method of treating pediatric fractures. The thicker
periosteum, more rapid healing, and greater
potential for remodeling found in children are factors
that facilitate closed treatment.
Even with a displaced fracture, the thick periosteum in children
usually
remains intact on one side of the fracture. The intact periosteum,
combined with appropriate positioning and molding of the cast, helps to
maintain closed reduction.
The more rapid healing of bone in children reduces the
complications associated with prolonged immobilization. Furthermore,
complications of prolonged immobilization that are often observed in
adults, such as pneumonia and thrombophlebitis, are very uncommon in
children.
Finally, because remodeling of bone occurs to a greater extent in
children,

angulation and displacement that would necessitate open reduction in
adults may be acceptable in children without the requirement for open
reduction.

Supracondylar Fracture
- 2nd most fracture in pediatric, usia 1-7 tahun.

- Mekanisme → Hiperekstensi dan fleksi
- Tipe → Gartland
- Treatment : Close reduction dan casting → Fleksi 120°

Traksi dan kounter traksi 180° → Flexi 90° elbow
Splint 90° dan sling selama 3 minggu

CTEV - Congenital Talipes Equinus Varus
Deformitas : CAVE : Cavus - Midfoot cavus → Medial arch increased

Adduktus forefoot
Varus - Hindfoot varus → Calcaneus adduksi dan
inversi
Equinus - Heel Equinus → Ankle plantar fleksi
Pemfis : Pergerakan sendi ankle - Dorso/Plantar flexi
Periksa Head to toe - cari kelainan kongenital - Vertebra
dan oral
Treatment : Ponseti Method - Serial Casting - Mulai 2 minggu setelah
lahir
1st → metatarsal satu di eversikan untuk
mengkoreksi cavus dan membuat flat batas
media kaki, sejajar forefoot dan midfoot.
2nd → Forefoot di abduksikan
3rd → Dorsifleksi ankle joint

DVT D-Dimer
The degradation of fibrin polymers by plasmin ultimately results in the

creation of fragment E and two molecules of fragment D, which are
released as a covalently linked dimer (D-dimer). Detection of D-dimer in
the circulation is a marker for ongoing thrombus metabolism and has
been shown to accurately predict ongoing risk of recurrent VTE.


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CATATAN RESIDEN BEDAH

DIGESTIF - ONKOLOGI - ANAK - ORTHOPEDI - VASKULAR

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

- Batas atas/panjang : Batas fusi 2 taenia mesenterik dengan promontorium

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

Gangguan aliran normal usus akibat hambatan mekanik yang

PENINGKATAN TEKANAN INTRALUMEN

- Dehidrasi merangsang reabsorbsi bikarbonat pada tubulus proximal ginjal,

HAPPY HEART TEAM - Edited by MIY

ONSET : Akut, Subakut, Kronis

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

1. STATUS GENERALIS : Sakit ringan/sedang/berat, gizi cukup, sadar

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

COLON ASCENDEN COLON REKTUM

HAPPY HEART TEAM - Edited by MIY

COLON ASCENDENS JARANG OBSTRUKSI KARENA ;

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

- CT scan bila diagnosis belum definitif, Non kontras → kontras

NCCN initial workup/staging : Chest, Abdomen, Pelvic CT untuk evaluasi ekstensi

HAPPY HEART TEAM - Edited by MIY

Setelah diagnosis tegak → staging → tentukan resektabilitas & metastasis

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

HAPPY HEART TEAM - Edited by MIY

- TENTUKAN RESEKTABILITAS (STAGING)

HAPPY HEART TEAM - Edited by MIY

Pada metastase yang unresektable :

Pada metastase peritoneal :

KEMOTERAPI NEOADJUVAN → Bila metastase → Cek Oncogen / mutasi ALL RAS,

HAPPY HEART TEAM - Edited by MIY

- Anti Metabolit → Spesifik pada siklus sel → fase S

-Antibiotik antitumor→merusak sintesi DNA/RNA,untuk tumor pertumbuhan lambat

- Alkaloid → menghambat siklus mitosis ; vincristine, Taxane ( Paclitaxel, docitaxel)

HAPPY HEART TEAM - Edited by MIY

- Anti EGFR:Cetuximab →Ca.Colorectal metastatic (BRAF +)

HAPPY HEART TEAM - Edited by MIY

Cetuximab : 500 mg/m2 iv hari pertama, siklus tiap 2 minggu

FOLFOXIRI : irinotecan 180 mg/m2 IV hari pertama, siklus tiap 2 minggu.

2. PA : A. Poorly differentiated / High Grade

C. Margin tidak clear

B) Rektum → cT1N0 → Transanal local eksisi → High Risk → Kemoradiasi

HAPPY HEART TEAM - Edited by MIY

- Tis, cT1, N0, M0 → Observasi

High Risk : - MSS (Microsatellite Stability)

- Histopatologi tidak berdiferensiasi

- Lesi perforasi lokal

- Margin dekat, tidak jelas

- Nodul < 12 KGB yang diambil

- Riwayat Obstruksi usus

- T4b atau bulky node → Neoadjuvant FOLFOX/CAPEOX → Reseksi

- Ca. Colon metastatik → Cek biomarker KRAS/RAS, BRAF, HER2, MSI

- Metastasis hepar → tidak dianjurkan debulking (R1/R2), terapi operasi harus

HAPPY HEART TEAM - Edited by MIY