Problem 2

group 13
9-10-2014

Tutor

Dr.silviana & dr.niko

Anggota

Eva fauziah

Anggota

Monica

Anggota

Viorencia halim

Anggota

Ellisa

Anggota

William

Anggota

Agustisnus kristantoko

Anggota

Michael joey

Penulis

Acyuta ganakin

Anggota

Patrick gianny warouw

Anggota

Yohanna octaviany gultom

sekretaris

Rafli elzandri

Ketua

Visensius thomas

A 28 years old male was brought to the local primary

health center with scald wounds caused by an
overturned meatball cart and was treated for 6 days.
On the 7 day the patient was referred to hospital.
On physical examination, his blood pressure is 120/80
mmHg, pulse 128 beats per minute, respiratory rate
32 breath per minute, temperature was 39,4C.
There are bullae on all parts of his wound. The bullae
are seen containing pus. The skin is painful to the
touch.
On admission, lab result show a leucocyte count of
21.600/mm (normal: 4.000-10.000), and creatinine
level of 4.1 mg/dl (normal <0,6 1,2 mg/dl)
What can you learn from this problem ?

Unfamillar Term
Scald wouds : luka bakar akibat
cairan panas

Rumusan masalah
1. Kenapa pasien di rujuk pada hari ke
7?
2. Kenapa timbul bullae berisi pus pada
lesi ? Dan kenapa nyeri saat di tekan ?
3. Interpretasi pemeriksaan fisik ?
4. Interpretasi pemeriksaan lab ?

Curah pendapat
1. Kemungkinan terjadi :
Infeksi sekunder
Sepsis

2. inflamasi (nyeri tekan ) infeksi sekunder

bullae dan push
3. Nadi :128x/mnt (takikardi)
TandaRR : 32x/mnt (takipneu)
tanda syok
hipovolemik
Suhu :39.4C (febris)
Luka
bullae dan pus : infeksi
bakar
derajat 2
nyeri tekan : infeksi sudah meluas

4. Leukosit : 21.600/mm () infeksi

sistemik
kreatinine : 4,1 mg/dL () tandatanda dehidrasi ekskresi urine

Mind map

Learning Objective
1. Menjelaskan patofisiologi luka bakar

Menjelaskan
Menjelaskan
Menjelaskan
Menjelaskan
Menjelaskan
Menjelaskan

etiologi luka bakar

klasifikasi luka bakar
komplikasi luka bakar
tanda dan gejala KGD
tata laksana KGD
prognosis

2. Menjelaskan patofisiologi sepsis

Menjelaskan
Menjelaskan
Menjelaskan
Menjelaskan
Menjelaskan
Menjelaskan
Menjelaskan

definisi sepsis
etiologi sepsis
tanda dan gejala sepsis
diagnosis
diagnosis banding
terapi
prognosis

Luka bakar
LO 1

DEFINISI
Luka bakar adalah suatu bentuk
kerusakan atau kehilangan jaringan
yang disebabkan kontak dengan
sumber panas seperti api, air panas,
bahan kimia, listrik, dan radiasi.
Luka bakar merupakan suatu jenis
trauma dengan morbiditas dan
mortalitas tinggi yang memerlukan
penatalaksanaan khusus sejak awal
(fase syok) sampai fase lanjut.

ETIOLOGI
Paparan api
Flame
Benda panas
(kontak)

Scalds (air
panas)
Uap panas
Gas panas

Aliran listrik
Zat kimia
Radiasi
Sunburn

Assessment of Thermal Burns

General Signs & Symptoms
Pain
Changes in skin
condition at affected
site
Adventitious sounds
Blisters
Sloughing of skin
Hoarseness
Dysphagia
Dysphasia

Burnt hair
Edema
Paresthesia
Hemorrhage
Other soft tissue
injury
Musculoskeletal
injury
Dyspnea
Chest pain

FASE LUKA BAKAR

Fase awal, fase akut, fase syok
Gangguan pada saluran nafas akibat eskar melingkar di dada
atau trauma multipel di rongga toraks; dan gangguan
sirkulasi seperti keseimbangan cairan elektrolit, syok
hipovolemia.

Fase setelah syok berakhir, fase sub akut

Systemic Inflammatory Response Syndrome (SIRS) dan Multisystem Organ Dysfunction Syndrome (MODS) dan sepsis.

Fase lanjut
Berlangsung setelah penutupan luka sampai terjadinya
maturasi jaringan. Masalah yang dihadapi adalah penyulit
dari luka bakar seperti parut hipertrofik, kontraktur dan
deformitas lain

Klasifikasi luka bakar

Berdasarkan penyebab:
Luka bakar karena
Luka bakar karena
Luka bakar karena
dan basa kuat)
Luka bakar karena
Luka bakar karena

api
air panas
bahan kimia (asam kuat
radiasi
listrik dan petir

Berdasarkan kedalaman kerusakan

jaringan:
Luka bakar derajat I (first degree)
Luka bakar derajat II (second degree)
Luka bakar derajat III (third degree)

KLASIFIKASI TRADISIONAL

Derajat 1
Terbatas pada epidermis
Eritema (+), nyeri (+)
sunburn
Blister (-)
Sembuh dalan 5-10 hari

Derajat 2
Mengenai dermis dan
epidermis
Bullae (+)
Dermis merah dan lembab
nyeri (+) ujung saraf
sensorik teriritasi

Derajat 3
Kerusakan meliputi
seluruh ketebalan
dermis dan lapisan yg
lebihn dalam
Bullae (-)
Saraf terbakar
sensasi (-)
Kulit berwarna abuabu / pucat, kering
letaknya lebih rendah
Penyembuhan lama

Klasifikasi Berdasarkan
Kedalaman Luka Bakar Thermal

Hiperemis
Eritema
Nyeri
Sensasi
menyengat
Penyembuhan; 510 hari

Superficial
Bula pecah
serum
Nyeri bila disentuh
Edema
Basah
Penyembuhan: 10Deep
14 hr
Lepuh pecah
luka tampak putih &
kering
Penyembuhan: > 1

Kulit retak2 &

tkoagulasi
Tdk nyeri bila
disentuh atau
ditusuk

DERAJAT KEDALAM LB
PEMBEDA

LOKASI
DERMALEPIDERMAL
JUNCTION
WARNA atau
PENAMPAKAN
NYERI
TEKSTUR
APENDISES
KULIT (folikel
rambut, kel
keringat, kel
sebacea)
DURASI & EFEK
SEMBUH

Derajat 1 (10)

Derajat 2 (20)/
Partial
Thickness Burn

Derajat 2 (20)/
Superficial Partial
Thickness Bunr)

Derajat 3 (30)/
Deep Partial
Thickness Burn

Epidermis

Epidermis-1/3
dermis

Hampir seluruh
dermis

Epidermisdermis-lapisan
yg > dalam
(tulang & otot

Utuh

Rusak

Rusak

Rusak

Merah

Merah-kadang
pucatedematous &
eksudatif; lepuh

Pink putih
Putih
kekuningan
(eskar tipis)

Pucat atau >

putih OK eskar,
hitam, atau
coklat

(+)

(+)

(+)

(-)

Normal

Edema (bula)

Tebal

Leathery

Utuh

Utuh

Sebagian utuh

Rusak

10-14 hari +/jar parut

25-60 hari + jar

parut tebal

5-7 hari
tanpa jar
parut

1ST & 2ND DEGREE BURN

INJURY

Rosens Emergency Medicine 7th Ed

1st degree
Fitzpatricks Dermatology in General Medicine 7th Ed

3RD
DEGREE
BURN
INJURY

Rosens Emergency Medicine 7th Ed

patricks Dermatology in General Medicine 7th Ed

4TH DEGREE BURN INJURY

Fitzpatricks Dermatology in General Medicine 7th

 Berat-ringan luka bakar penyebab & lama

kontak
Penyebab:
Kerusakan jaringan akibat : api > air panas < koloid
Asam diskonfigurasi jaringan ggg proses
penyembuhan
Luka bakar akibat listrik, kerusakan jaringan tubuh
disebabkan:
Aliran listrik
Loncatan energi yg ditimbulkan oleh udara, berubah
menjadi api
Kerusakan pembuluh darah di bagian tubuh yg dialiri
tubuh kerusakan jaringan lambat tp pasti & tidak
dapat diperkirakan luasnya

 Lama kontak menentukan luas &

kedalaman kerusakan jaringan.
semakin lama waktu kontak, semakin
luas & dalam kerusakan jaringan yg
terjadi

Zona kerusakan jaringan

Zona koagulasi
Daerah yg langsung mengalami kerusakan nekrosis

Zona stasis
Daerah yang di luar/di sekitar koagulasi
kerusakan endotel pembuluh darah
kerusakan trombosit & leukosit
Gangguan perfusi
Perubahan permeabilitas kapiler & respon inflamasi lokal
12-24 jam

Zona hiperemi
Diluar zona stasis
Reaksi : vasodilatasi

CLASSIFICATION

1st degree epidermis

2nd degree superficial papilary dermis
2nd degree deep reticular dermis
3rd degree full thickness
4rd degree subcutaneous or deeper

Rosens Emergency Medicine 7th E

Derajat 1

Derajat
2

Superficial partial
thickness

Deep partial

Derajat 3

Burns
Percentage
(Adults)

RULE OF NINE

Lund & Browder Chart

http://www.medstudentlc.com/uploaded_images/Lund%20Browder%20Rakel.gif

Berdasarkan berat ringannya luka bakar:

a) Luka bakar ringan

Luka bakar derajat I dan II dengan luas <15% pada orang

dewasa
Luka bakar derajat I dan II dengan luas <10% pada anak-anak
Luka bakar derajat III dengan luas < 2%
Penderita cukup berobat jalan

b) Luka bakar sedang

Luka bakar derajat II dengan luas 15-25% pada orang dewasa

Luka bakar derajat II dengan luas 10-20% pada anak-anak
Luka bakar derajat III dengan luas <10%
Penderita sebaiknya dirawat

c) Luka bakar berat

Luka bakar derajat II dengan luas >25% pada orang dewasa

Luka bakar derajat II dengan luas >20% pada anak-anak
Luka bakar derajat III dengan luas >10%
Luka bakar yang mengenai tangan, wajah, mata, telinga, kaki,
genitalia, persendiaan sekitar ketiak
Semua penderita dengan inhalasi, luka bakar dengan
komplikasi trauma berat, luka bakar resiko tinggi
Penderita harus dirawat

PATOFISIOLOGI LUKA
BAKAR

Patofisiologi luka bakar fase

akut
Gangguan saluran pernafasan cedera inhalasi
Edema obstruksi saluran nafas
Hipersekresi mukosa saluran nafas
Fibrin pada alveolus gangguan difusi dan perfusi

Gangguan mekanisme bernafas

Eskar melingkar di permukaan rongga toraks
gangguan compliance paru
Fraktur tulang iga

Gangguan sirkulasi cedera termis pada

sirkulasi dan jaringan
Perubahan permeabilitas kapiler
Cairan di interstisial syok hipovolemik
gangguan perfusi

Syok hipovolemik
Gangguan sirkulasi otak: disorientasi,
gelisah, penurunan kesadaran
Vasokonstriksi perifer suhu ,
produksi urin , gangguan sistem
pencernaan (gaster, usus, dan hepar
gangguan metabolisme, SGOT dan
SGPT )
Pernapasan cepat dan dangkal
Palpitasi dan takikardi

Systemic Inflammatory Response

Syndrome Multi-system Organ
Dysfunction Syndrome
Mediator inflamasi kerusakan organ
sitokin (sampai homeostasis terjaga)
destruktif mediator inflamasi di sirkulasi
syok septik, DIC, ARDS, MODS, kematian
Infection dan injury
Inflammation
Inadequate
Blood flow
Ischemia-reperfusion injury

Tanda SIRS
Hipertermia (> 38C) atau
hipotermia (< 36C)
Takikardi (> 90/menit)
Takipnu (> 20/menit) atau PaCO <
32 mmHg
Leukositosis (> 12.000) atau
leukopenia (< 4.000)

Patogenesis
1. Syok gangguan sirkulasi berbagai
organ kulit fungsi barrier
translokasi bakteri
2. Jaringan cedera termis Lipid
Protein Complex (sangat toksik)
berkembang menjadi sistemik
3. Mediator pro-inflamasi kerusakan
jaringan organ sistemik

LUKA AKIBAT LISTRIK

 Luka bakar listrik disebabkan oleh

kontak langsung aliran listrik dengan
badan.
Luka biasanya lebih serius dari apa
yang terlihat pada permukaan
Tubuh manusia sbg penghantar
listrik, dan mengakibatkan kerusakan
jaringan akibat panas yang
ditimbulkan.

 Perbedaan kecepatan hilangnya

panas antar kulit dengan jaringan
yang lebih dalam terlihatnya
permukaan kulit tampak seakan
normal, padahal jaringan otot
didalamnya mengalami nekrosis.
Rhabdomiolisis mioglobin lepas
gagal ginjal akut.

Penanganan (segera)
Jalan nafas dan pernafasan
Pemberian cairan intravena pada
ekstremitas yang tidak terkena
EKG
Pemasangan kateter

 Urin yang berwarna gelap

menandakan hemokromogens
didalamnya segera lakukan terapi
untuk mioglobinuria tanpa harus
tunggu hasil laboratorium.
Pemberian cairan harus ditingkatkan
agar produksi urin 1 2mL/KgBB/jam (pada org dewasa)

 Bila penambahan cairan, urin tetap

belum jernih beri manitol 25g
segera dan pada tiap liter cairan
berikutnya tambahkan manitol
12,5g.
Penanganan asidosis metabolik :
Mempertahankan perfusi
Tambahkan natrium bikarbonat agar
urin alkalis dan meningkatkan kelarutan
miogloblin dalam urin

TATA LAKSANA LUKA

BAKAR

SURVEI PRIMER DAN

SEKUNDER

Survey Primer
Airway
Perhatikan apakah ada riwayat terkurung api
atau ada trauma jalan nafas
Trauma laring menyebabkan edem laring
karenanya memerlukan pembebasan nafas
segera
Biasanya edema belum terjadi pada 24 jam
pertama
Bila dokter menunggu hasil analisa gas darah,
edema akan terjadi dan susah untuk
melakukan intubasi

Survey Primer
Breathing
Penanganan bisanya didasarkan atas tanda dan
gejeala yang ada, yang timbul akibat trauma :
Trauma bakar langsung, menyebabkan edema dan
obstruksi jalan nafas atas
Inhalasi hasil pembakaran (CO) dan asap beracun
Keracunan karbonmonoksida

Pemeriksaan CO harus dilakukan karena penderita

dengan CO >20 % sangat bahaya. Bisa menimbulkan
gejala, sakit kepala mual muntah, sampai koma
bahkan kematian
Penderita dengan CO tinggi, diberikan Oksigen 100%

Survey Primer
Sirkulasi
Penilaian sirkulasi agak susah pada
pendeerita luka bakar karena biasanya
mengalami syok hemodinamik
Tekanan darah kadang sulit diukur dan
dipercaya sehingga pengukuran biasanya
menggunakan urine untuk menilai ada
tidaknya sirkulasi darah,diuresis osmotik
Pada pemberian cairan, pertahankan produksi
urin pada 1ml/kgBB pada anak dan 0,5 1,0
ml/kgBB pada dewasa

Survey Primer
Sirkulasi
Pada luka bakar 2 dan 3, pasien
memerlukan RL sebanya 2-4 ml/kgBB
Separuhnya diberikan 8 jam pertama dan
sisanya diberikan 16 jam setelahnya
Pada luka bakar 3, sebaiknya dimulai
langsung dengan RL 4 ml/kgBB
Formula ini hanyalah keperluan cairan
pada waktu terjadinya luka bakar, bukan
pada waktu dimulainya resusitasi

RESUSCITATION FORMULAS

Rosens Emergency Medicine 7th E

MANAGEMENT
Prior to ED arrival
Stop burning process, extinguish flame,
chemical injury tap water wash
Protect from additional injury
Adequacy of airway and ventilation intubation
CO poisoning 100% oxygen
Extensive burns IV fluid LR, Parkland Formula
Morphine sulfate 2-4mg IV bolus
Cover burns with clean dressing
Prevent hypotermia

Rosens Emergency Medicine 7th E

INPATIENT / OUTPATIENT

Fitzpatricks Dermatology in General Medicine 7th

MANAGEMENT
At Emergency Department (ABC!!)
Airway
Check for upper airway edema fiberoptic
laryngoscopy
Endotracheal intubation or crycothyrotomi if
needed
Escharotomies if needed
Maintain PO2 >92%
Urethral catheter monitor urine output
and eval for rhabdomiolysis and
myoglobinuria
NGT prevent gastric distention

Rosens Emergency Medicine 7th E

MANAGEMENT
Inhalation Injury

Fiberoptic laryngoscope & bronchoscopy

soot, charring, inflammation, edema,
necrosis
Injury to parenchyma xenon ventilation
(RARE)
Other : CO and cyanides
Treatment : mechanical ventilation,
aleveolar lavage, PO2 >92%, airway
pressure <35cm H2O, pH >7,25
Bronchospasm bronchodilators +
suctioning
N-acetylsistein with/without
heparin
Rosens
Emergency Medicine 7th E

Rosens Emergency Medicine 7th E

MANAGEMENT
Local Wound Care
Cleansing with soap + water, removal of
debris and necrotic tissue, TT booster
Cooling : tap water 10o-25o C up to
30mins after injury, avoid hypothermia,
ice/ice water contraindicated
Burn Blisters : Fluid confined by necrotic
skin heal faster less infection, 2nd
degree debridement + intact less
scaring, heal faster

Rosens Emergency Medicine 7th E

MANAGEMENT
Burn dressing
Open method : antimicrobial topical until
skin is re-epithelialized. Used on exudative
burn. Mostly used silver sulfadiazine and
mafenide acetate. Daily removed
Closed method : moist wound healing
environment heal faster. Mostly used :
Nanocrystalline silver.
At home : washing, apply topicals. Occlusive
should not be opened unless saturated or
malodorous go to ER. If swelling of fever
go to ER

Rosens Emergency Medicine 7th E

BURN DRESSINGS

Rosens Emergency Medicine 7th E

MANAGEMENT
Escharotomy
Releasing constriction of burn eschar
with scalpel
Eschar constriction interrupts
arterial outflow pain, loss of
sensation, delayed capilarry refill.
Indication: Doppler Signal & Pulse
oximetry <90%
Avoid to cut underlying vessels and
nerves

Rosens Emergency Medicine 7th E

MANAGEMENT
Pain Types and Management
3 phases of burn recovery
Emergency / Resuscitative Phase
Healing Phase
Rehabilitative Phase

In Emergency Phase, there are 3 kinds

of pain
Background Pain
Breakthrough Pain
Procedural Pain

Rosens Emergency Medicine 7th E

MANAGEMENT
Non pharmacologic
Cooling, tap water 10o-25oC
Moist occlusive dressing

Pharmacologic

Morphine Sulfate (0,05-0,1mg/kg) titrated

Acetaminophen (1g adults, 15mg/kg child) /4-6h
Ibuprofen (400-800mg adults, 10mg/kg child) / 6-8h
Fentanyl 0,5-1mg/kg
Lidocaine
Anxyolytics : benzodiazepin (Lorazepam)
Others : gabapentin, stimulants, B-Blockers,
antidepressants

Rosens Emergency Medicine 7th E

COMPLICATION

Fitzpatricks Dermatology in General Medicine 7th

COMPLICATION
Streptococcal Cellulitis

Fitzpatricks Dermatology in General Medicine 7th

HYPERTROPHIC SCAR
BEFORE SURGERY

AFTER SURGERY

Fitzpatricks Dermatology in General Medicine 7th

Lo2

SEPSIS

DEFINITIONS
Activated Inflammatory cascade
cause the bodyd defenses and
regulatory system become
overwhelmed leading to disruption of
hemeostasis
Systemic Inflammatory Response
Syndrome (SIRS) 2 or more :
tachycardia, tachypnea,
hyperthermia or hypothermia, high
or low WBC count, bandemia.

Rosens Emergency Medicine 7th E

DEFINITIONS

Sepsis : SIRS + infection

Severe Sepsis : Sepsis + Organ
Dysfunction
Septic Shock : Severe Sepsis +
hypotension which is not responsive
to fluid challange
Approach : PIRO (predisposition,
infection source, response of host,
organ dysfuntion)
Bacteremia is not obligatory
in
Rosens Emergency
Medicine 7th E

Etiology
Gram-negative bacteria most
common:
Escherichia coli
Pseudomonas aeruginosa
Rickettsiae
Legionella species

Etiology
Gram-positive bacteria:
Enterococcus species
Staphylococcus aureus
Streptococcus pneumoniae

Fungi (Candida species)

Viruses

Etiology
Pediatric Considerations
Children with a minor infection may
have many of the findings of SIRS.
Major causes of pediatric bacterial
sepsis
Neisseria meningitis
Streptococcal pneumoniae
Haemophilus influenzae

EPIDEMIOLOGY
In United States :
10th most common
cause of death
571.000 cases of
severe sepsis
Mortality rate 2050%
Incidence

Rosens Emergency Medicine 7th E

PATHOPHYSIOLOGY
Infection host response
neutrophil and macrophage
mobilization to injury site release
cytokines inflammatory cascade
synthesis is not well regulated
sepsis
Ongoing toxin persistent
inflammatory response mediator
activation cellular hypoxia, tissue
injury, shock, Multi-Organ Failure,

Rosens Emergency Medicine 7th E

PATHOPHYSIOLOGY
Mediators of Sepsis
Proinflammatory : IL-1, IL8, TNF
Anti-inflammatory IL-10, IL-6 TGF B,
IL-1ra
Growth promoting

Arachidonat acid pathway

peripheral dilation, vasocontriction,
leukocyte and platelet aggregation
PG fever

Rosens Emergency Medicine 7th E

PATHOPHYSIOLOGY
Vasopressin release in stress
condition, cause vasoconstriction,
osmoregulation, maintenance of
normovolemia
NO Regulating vascular tone,
platelet adhesion, insulin secretion,
neurotransmission, tissue injurt,
inflammation and cytotoxicity

Rosens Emergency Medicine 7th E

ORGAN SYSTEM DYSFUNCTION

AND DEATH

Rosens Emergency Medicine 7th E

ORGAN SYSTEM
DYSFUNCTION
Neurologic
Altered mental status and lethargy septic
encephalopathy

Cardiovascular
Myocardial depression : killed organism /
bacteria
Distributive shock : toxic mediators
Early sepsis : Cardiac output , vascular
resistance
Reversible cardiac function usually in 10 days

Rosens Emergency Medicine 7th E

ORGAN SYSTEM
DYSFUNCTION
Pulmonary
Right-to-left shunting, arterial
hypoxemia, intractable hypoxemia
Sepsis : High catabolic state + airway
resistance ARDS

Gastrointestinal
Ileus hypoperfusion. splanchnic blood
flow.
Aminotransferase + bilirubin
hepatic failure (rare)

Rosens Emergency Medicine 7th E

ORGAN SYSTEM
DYSFUNCTION
Endocrine
Adrenal insufficiency
IL-1 & IL-6 activate hypothalamicpituitary axis
TNF-A & corticostatin, depressed bloow
flow, depress pituitary function and
secretion

Hematologic

DIC, fibrin deposition, microvascular

thrombi
Associated with Protein CRosens Emergency Medicine 7th E

CLINICAL SIGNS &

SYMPTOMS
Identify systemic infection and the source
Altered conciousness intubation
Systemic Infection : tachycardia,
tachypnea, hypo/hyperthermia,
hypotension (severe)
Flushed/warm skin while in vasodilation
state
Hypoperfused mottled and cyanotic
Shock exclude other shock etiologies
Use MEDS score for risk stratification

Rosens Emergency Medicine 7th E

MEDS
SCORE

Rosens Emergency Medicine 7th E

SOURCE OF INFECTIONS
Respiratory (most common) : cough, fever,
chills, throat and ear pain, pneumonia, etc
GI (2nd most common) : abdominal pain,
Murphy sign, McBurney Sign, etc
Neurologic : meningitis
Genitourinary :Flank pain,dysuria,polyuria,
etc
Musculoskeletal
IV drug abuse, artificial heart valve,
endocarditis

Rosens Emergency Medicine 7th E

DIAGNOSTIC FEATURES
Hematology
Leukocytosis
Febrile neutropenic admission, isolation,
empirical IV antimicrobial
Bandemiarelease of immature cell from
marrow
Ht >30%, Hb >10g/dL
Acute phase platelet
Low platelet shock
Thrombocytopenia, pTT & aPTT , fibrinogen
, DIC & severe sepsis syndrome

Rosens Emergency Medicine 7th E

DIAGNOSTIC FEATURES
Chemistry
bicarbonate acidosis & inadequate
perfusion
serum creatinine ARF
Lactate inadequate perfusion, shock
Arterial blood gas detect acid base
disturbance
Metabolic acidosis inadequate perfusion
Bilirubin source from gallbladder
Amilase & Lipase pancreatitis

Rosens Emergency Medicine 7th E

DIAGNOSTIC FEATURES
Microbiology
Culture from blood, sputum, urine, CSF, tissue
Obtained before/soon after AB administration
Start with empirical therapy

Radiology
Chest pneumonia, ARDS
Bowel perforation free air aunder
diaphragm
Pneumomediastinum esophageal
perforation, mediastinitis

Rosens Emergency Medicine 7th E

DIAGNOSTIC FEATURES
Ct-Scan diverticulitis, appendicitis,
necrotizing pancreatitis,
microperforation, intra-abdominal
abscess
Head CT septic emboli
Abdominal USG Cholycystitis
Pelvic USG endometritis
Transesophageal USG --> endocaditis
MRI soft tissue

Rosens Emergency Medicine 7th E

DIAGNOSTIC FEATURES
(B) Imaging
Chest radiograph:
Determine whether pneumonia is the
infectious source.
Fluffy, bilateral infiltrates may indicate
that ARDS is already present.
Free air under the diaphragm indicates
the source of the infection in
intraperitoneal and a surgical
intervention

DIAGNOSTIC FEATURES
CT scan of the abdomen and pelvis
Suspicion of abdominal source of infection:
Diverticulitis, appendicitis, necrotizing pancreatitis,
microperforation of the stomach or bowel, or
formation of an intra-abdominal abscess

Abdominal ultrasound:
Indicated for suspected cholecystitis

Pelvic ultrasound:
Tubo-ovarian abscess or

MRI:
May be useful to identify soft tissue infections
or epidural abscess

DIAGNOSTIC FEATURES
Diagnostic Procedures/Surgery
(C) Lumbar puncture:
Indicated when meningeal signs are present or
altered mental status without a source of infection
Cerebrospinal fluid analysis:

Cell count and differential, tube 1

Total protein and glucose, tube 2
Culture and gram stain, tube 3
Cell count and differential, tube 4
Depending on the clinical situation: cytology, venereal
disease research laboratory, AFB stain/culture, fungal
stain

DIFFERENTIAL DIAGNOSIS

Rosens Emergency Medicine 7th E

MANAGEMENT
Principles
AB therapy
Maintenance of adequate tissue
perfusion

Rosens Emergency Medicine 7th E

MANAGEMENT
Respiratory Support
Airway protection, intubation,
mechanical ventilatory support if
needed

Cardiovascular support

Initial therapy 2L of isotonic

crystalloid
Normal Saline/ LR.
Maintain MAP >65mmHg, but 75mmHg
in patient ith history of severe
hypertensive patient
Rosens Emergency Medicine 7th E

MANAGEMENT
Drugs : Vasopresin, Norepinephrine,
Dopamine, Phenylephrine, Epinephrine.
Inotropic agents : Dobutamine,
Bicarbonate, AB

Novel Therapies
Activated Protein C
Steroid Therapy

Rosens Emergency Medicine 7th E

MANAGEMENT

Rosens Emergency Medicine 7th E

Rosens Emergency Medicine 7th E

Kesimpulan
Kami telah mempelajari :
1. Patofisiologi luka bakar

etiologi luka bakar

klasifikasi luka bakar
komplikasi luka bakar
tanda dan gejala KGD
tata laksana KGD
prognosis

2. patofisiologi sepsis

definisi sepsis
etiologi sepsis
tanda dan gejala sepsis
diagnosis
diagnosis banding
terapi
prognosis

Pasien mengalami
luka bakar derajat
2 superfisialis dan
kemungkinan
pasien mengalami
komplikasi Sepsi

Saran
vinsensiusthomas@yahoo.co.id
yohannaog@yahoo.com

REFERENCES
Marx JA, Hockberger RS, Walls RM,
Adams JG, editors. Rosens
Emergency Medicine Concepts and
Clinical Practice. 7th Ed. Philadelpia :
Mosby Elsevier, 2010
Wolff K, Goldsmith LA, Katz SI,
Gilchrest BA, editors. Fitzpatricks
Dermatology in General Medicine.
7th Ed. New York : McGraw-Hill, 2008