INFEKSI JARINGAN LUNAK

Selulitis, Abses, Necrotizing

Fasciitis,and Gas Gangrene
KELOMPOK
AIDIL RAHMAN NOVESAR
CAROLINE DEWI
FAKHRIEL HAMDANI
NOVAN ARDIANSYAH
PUTRA HAQIQIE A. LUBIS
RAKA ADITYA
SELULITIS
Definisi

 Infeksi pada kulit dan jaringan lunak di bawah kulit

(dermis dan jaringan subcutaneous)
 Tanpa abses, purulen, atau ulcerasi.
 Invasi bakteri pada kulit yg rusak atau normal dan
mulai menyebar dibawah kulit dan kedalam jaringan
lunak dan menyebabkan infeksi dan peradangan
Faktor Risiko
 Diabetes
 Peredaran darah kurang lancar
 Aliran balik vena dan drainase limfatik yg terhambat seperti pada
varises
 Gangguan sistim imun (HIV/AIDS,post terapi kemoterapi)

Epidemiologi
 Usia > 45 tahun
 3% kasus emergensi pada rumah sakit di Inggris
Etiologi
• Staphylococcus dan Streptococcus (paling sering)
• Staphyloccoccus: biasanya pada infeksi kulit tanpa drainase, trauma
tembus, eskar, abses.
• Straptococcus: biasanya berwarna violet dan ada bula, dengan infeksi
sitemik yang lebih serius.
• Gangguan kulit seperti eksim, psoriasis, dan penyakit menular yang
menyebabkan lesi kulit seperti cacar air atau jerawat yang parah
• Infeksi tulang di bawah kulit
Lokasi
 Selulitis dapat terjadi di seluruh bagian tubuh terutama kedua kaki
 Berikutnya di kedua lengan dan di ikuti daerah kepala dan leher
Selulitis pada Extremitas Atas
Selulitis pada Extremitas Bawah
Gejala dan Tanda Selulitis
• Kemerahan pada kulit yg dapat menjadi luas (eritema)
• Pembengkakan (edema)
• Hangat pada perabaan pada kulit yg terlibat (warmth)
• Nyeri (pain)
• Tidak ada area pus
• Demam jika infeksi menyebar ke tubuh melalui darah
• Throbbing
Pemeriksaan Penunjang
 Cek laboratorium: hanya jika ada gangguan sistemik.
 Jika selulitis terlokalisi, nyeri minimal, tidak ada gangguan sistemik, tidak ada factor risiko
penyakit penyerta tidak perlu cek lab
 Cek lab: darah lengkap, hitung jenis, Cr, CRP, kultur darah
 Kultur darah dilakukan jika:
 Selulitis moderate-severe
 Area special (wajah, mata)
 On chemotherapy / immunocompromized
 Gigitan binatang
 X-ray jika ada kecurigaan benda asing dalam kulit sebagai penyebab atau untuk
mengetahui apakah tulang di bawahnya telah terinfeksi
 USG : for abses
 CT scan: for necrotizing fasciitis
 Cek kultur bakteri dan uji resistensi dari pus
Tatalaksana
Non-surgikal:
 Elevasi
 Imobilisasi
 Terapi analgetik (paracetamol atau ibuprofen)
 Terapi antibiotik (dicloxacillin atau nafcillin)
 Terapi anti jamur ( jika penyebab nya dicurigai dari tinea)

Surgikal: biopsi eksisi untuk mengetahui penyebab pada selulitis

dengan penyebab noninfeksius.

*Abses atau infeksi tertutup mungkin terjadi dan harus di

drainase jika bengkak akibat inflamasi tidak membaik setelah
48-72jam pengobatan antibiotic.
ABSES
 Definisi
 Abses adalah infeksi
jaringan lokal yang
ditandai oleh kumpulan
pus mengelilingi
jaringan inflamasi
 Dapat ditemukan di area
tubuh manapun, tetapi
paling sering di
ekstremitas, bokong,
payudara, perianal area,
atau dasar folikel rambut
 Etiologi
 Umumnya disebabkan oleh streptokokus, stafilokokus,
bakteri enterik, dan organisme gram negatif

Abses
Pus
selulitis
Tatalaksana Abses
Tatalaksana Abses (1)
Tatalaksana Abses (2)
GAS
GANGRENE
 Epidemiology
 Pasien berisiko:
Diabetes Mellitus, Penyakit
pembuluh darah, and kanker
kolon
 Kontak dengan kain
terkontaminasi dan benda
asing lain
 Trauma atau luka operasi
Overview

 Infeksi anaerobic, biasa nya disebabkan oleh

clostridium perfringens
 Kasus jarang
 Di Amerika 1000 – 3000 kasus / tahun
Causative agent
 Clostridium species – spore forming, Gram +ve
 anaerobic, gram-positive, spore-forming bacillus
of the genus Clostridium

Penyebab Gas Gangren

- Trauma
- Operasi
- Spontan
- Traumatik gas gangrene dan gas gangrene
spontan ( hematology malignancy / colorectal
adenocarcinoma)
 vegetative
cells multiply
Spores Carbohydrates
germinate Fermentation

Anaerobic
PATHOGENESIS Gas production
In tissues
environment Incubation period is
1-7 days

Distension of
Toxemia and tissues
death Interfering
Blood supply
Ischemia/
gangrene
 Pathogenesis
Examples of
- The toxins
enzyme:
(lecithinase
colagenases,
) and
proteases and
- Bacteria enzyme
lipases
enters the are
broken skin produced - These enzymes
or wound - Thebacteria will kill other host
cell and extend
are grow and the anaerobic
- Spores
are ferment the environment
produced muscle
carbohydrate - Produce gases
(nitrogen, hydrogen
- The bacteria the sulphide and carbon
present in anaerobic dioxide)
circulation tissue - Crepitant tissue
system present ( destroyed tissue)
Differential Diagnosis

 Noma is a gangrene of the face.

 Necrotizing fasciitis is attacking the

deeper layers of the skin.
(Group A streptococcus infection)

 Fournier gangrene usually affects

the male genitals.
 Symptoms
• A sudden onset of pain is usually the first
symptom of gas gangrene. The pain
gradually worsens but spreads only as the
underlying infection spreads.
• High fever
• Shock
• Massive tissue destruction
• Blackening of skin
• Severe pain around a skin of wound
• Blisters with gas bubbles form near the
infected area, hemorrhagic bullae
• crepitus
• the heartbeat and breathing become
rapid.

Late signs of gas gangrene include hypotension,

renal failure, and a paradoxical heightening
of mental acuity; metabolic acidosis.
 Presentation
Crepitation in tissues,
sickly sweet odor discharge,
rapidly progressing necrosis,
fever, hemolysis, toxemia,
shock,
renal failure, and death
Lab. Investigations

Culture and sensitivity

Lecithinase test
Pemeriksaan Penunjang

 Rapidly developing hemolytic anemia with an

increased lactate dehydrogenase (LDH) level is
common in patients with gas gangrene
 CT scanners reported 100% sensitivity to detect
necrotizing soft tissue infections
 USG : detect gas and localization in cadaver
 PCR

protein synthesis inhibitors (eg, clindamycin,

chloramphenicol, rifampin, tetracycline) may be
more effective because they inhibit the synthesis of
clostridial exotoxins and lessen the local and
systemic toxic effects of these proteins
GAS IN SOFT TISSUE
 Management

1. Surgery

2. Antibiotics and Analgesics

3. Hyperbaric Oxygen Therapy

 SURGERY

 An emergency surgery to explore or remove dead tissue

 The dead tissue is removed or limbs are amputated

 Amputating the affected body part (Limb)

 Repeated operations to remove dead tissue (debridement)

 An operation to improve blood supply to the area

 AMPUTATION
Amputate under a tourniquet
Close the stump by delayed
primary suture
Myonecrosis of left foot
 ANTIBIOTICS AND
ANALGESICS
Antibiotics should include
 Agent for gram-positive (penicillin or
cephalosporin),
 Agent for gram-negative (aminoglycoside,
third-generation cephalosporin, or
ciprofloxacin),
 Agent anaerobic coverage (clindamycin or
metronidazole)
 High doses of antibiotic : Penicillin
ANTIBIOTICS AND ANALGESICS (Contd..)

Analgesic

 Pain control is essential to quality patient care.

 Analgesics ensure patient comfort have sedating

properties, which are beneficial for patients who have
sustained trauma or have sustained injuries.
10 megaunits of benzyl penicillin daily for 5
days as four 6 hourly doses.

Or
Tetracycline 0.5 g intravenously
or 1 g orally every 6 hours.

Clostridia not sensitive to metronidazole,

some other anaerobic bacteria are, so give
it.
Hyperbaric Oxygen Therapy
 Use is controversial but can be used to supplement surgical
debridement and antibiotics. This modality may be particularly
helpful in areas where complete surgical resection of necrotic
tissue is difficult such as the paraspinal muscles or abdominal wall

 Potential benefits include improved neutrophil-mediated killing

of bacteria, direct bactericidal effect on anaerobes, improved
activity of some antibiotics, and enhanced wound healing
Pencegahan
 Cleaning the wound
 Avoid the contaminated material
 improve circulation in
patients with poor circulation
 antitoxin

Prevention
(1) Do a thorough wound toilet.
(2) In high risk wounds give the patient
penicillin 1.5 megaunits 4 hourly,
or tetracycline
FASCIITIS NEKROTICANS
Overview

 Severe inflammation of the muscle sheath that

leads to necrosis of the subcutaneous tissue and
adjacent fascia
 Often grouped alongside other severe soft tissue
infections such as myositis and myonecrosis (gas
gangrene)
 When the bacteria in a cellulitis or abscess start
spreading quickly between the fat layer and the
muscle underneath it is termed necrotizing fasciitis
 Necrotizing means turning living flesh to dead
flesh
 Fasciitis means the infection is spreading along
the space between the fat and the muscle
underneath
 The infection cuts off the blood supply to the
tissue above it and the tissue dies
 The bacteria also enter the bloodstream and
cause severe systemic illness called “sepsis”
 0.24 – 0.4 per 100 000 adults
 diabetes mellitus, alcohol abuse, and intravenous
drug abuse
Etiology

 Bacteria arising from a localized skin infection (or

contaminated wound)
 Variable progression depends on:
 Bacteria: organism, inoculum
 Infection location: local tissue hypoxia in postsurgical /
postradiation wound, extensive scars in drug abusers
 Host factors: underlying medical problems such as diabetes
mellitus, drug user, liver disease, alcoholism, chronic illness, or
other immuno-compromised condition
 Microbiology
Necrotizing Fasciitis Classification

Type Organism Characteristics

Type 1 Polymicrobial
Typical 4-5 aerobic and
anaerobic species cultured:
• non-Group A Strep
• anaerobes including Clostridia
• facultative anaerobes
• enterobacteria
• Synergistic virulence between
organisms
Type 2 Monomicrobial
• Group A β-
hemolytic Streptococci is most
common organism isolated
Type 3 Marine Vibrio vulnificus
(gram negative rods)
Type 4 MRSA
• Most common (80-90%)
• Very rapid progression in
group A streptococcal
infection, dark red bullae
formation (+)
• Seen in immunosuppressed
(diabetics and cancer
patients)
• Postop abdominal and
perineal infections
• 5% of cases
• Seen in healthy patients
• Extremities
• Marine exposure
Clinical presentation
 classic signs and symptoms are erythema, advanc- ing
cellulitis, pain, crepitance, high fever, and other systemic
signs of sepsis
 Skin bullae and necrosis are signs of a later stage of the
disease
 Early: pain, mild swelling, redness
 Fail to respond to antibiotics for cellulitis
 Severe pain, hyperpirexia, chills, tachycardia,
hypotension, or hypotherm: “critically ill”
 Acidosis, leucocytosis
LRINEC
 Laboratory Risk Indicator for Necrotizing
Fasciitis
 To distinguish Necrotizing fasciitis from other
soft tissue infections
 Score > 6 has 92% positive predictive values
of having NF:
0 1 2 4
CRP (mg/L) < 150 ≥ 150
WBC count (x103/mm3) < 15 15-25 > 25
Hemoglobi (g/dL) > 13,5 11- < 11
n 13,5
Sodium (mmol/L) ≥ 135 < 135
Creatinine (mg/dL) ≤ 1,6 > 1,6
Glucose (mg/dL) ≤ 10 > 10
Differential diagnosis
 Insect bite
 Cellulites
 Abscess
 Clostridial myonecrosis
 higher mortality rate
Imaging
 X-ray: presence of subcutaneous air is a characteristic of more
aggressive necrotizing soft tissue infections.
 Aerobic infection can produce subcutaneous air esp. in patients
with diabetic or severe peripheral vascular disease
 Anaerobic infection should be suspected
 CT
 MRI: increased T2 signal in fascia
Imaging is not required for diagnosis or treatment
A. AP radiograph of upper extremity shows extensive subcutaneous air in patient with necrotizing fasciitis
B. Oblique view radiograph
A. T1-weighted of left and
right thigh
B. T2-weighted of
necrotizing fasciitis in
3yo girl after an insect
bite to her
posterolateral right thigh
shows hiperintense
signal intensity in the
superficial and deep
fascia of the right thigh
Laboratory
 Complete blood cell count
 Serum albumin
 Serum electrolyte
 Kidney function test
 Liver function test
Infection
 Prothrombin time status
 Partial thromboplastin time
Biopsy
 To confirm diagnosis in early emergency case
 Frozen section technique
 1x1x1 cm tissue sample
 Once confirmed, early surgical intervention should not be
delayed
 Allow early surgical debridement in average of 21 hours after
presentation; compared in average of 6 days without frozen-
section biopsy
Histopathology finding
 Necrosis of the superficial fascia with blood vessel
thrombosis and suppuration
 Necrosis of superficial fat and dermis
 Vasculitis
 Local hemorrage
 Presence of inflammatory cells
 (distinguish NF from clostridial myonecrosis)
Treatment
 radical débridement is mandatory and must be extended until healthy
muscle and fascia are observed. Serial débridement is warranted
every 12 to 24 hours until the infection is suppressed. Early surgical
intervention is the key to successful treat- ment of necrotizing fasciitis
 A combination of intra- venous broad-spectrum antibiotics is
recommended, such as a cephalosporin (staphylococci and strepto-
cocci), penicillin (anaerobes), and gentamicin (gram- negative
organisms)
 Emergency surgical debridement for all involved tissue: fascial tissues
beyond the apparent superficial borders of infection.
 Findings:
 Liquefied subcutaneous fat
 Dish water pus
 Muscle necrosis
 Venous thrombosis
Treatment

 Fluid resuscitation and hemodynamic monitoring

 IV antibiotics only to reduce systemic bacterial
load and decrease organ failure incidence
 Initial empiric: Clindamycin, Metronidazole, and an
Aminoglycoside (Gentamycin/ Amikasin)
 Penicillin G for strep/ clostridium
 Meropenem for polymicrobial
 Vancomycin for MRSA suspected
 Hyperbaric oxygen chamber if anaerobic
organism is identified