CHAPTER 1

INTRODUCTION

1.1 Overview

Soft-tissue infections (STIs), are characterized by findings that include an acute,

diffuse, tender, spreading, edematous, suppurative inflammation of the dermis,
subcutaneous or muscular tissues, often associated with systemic symptoms of malaise,
fever, chills, and local pain. Nonnecrotizing STIs are treated with antibiotics, drainage
of abscesses, and supportive measures. Necrotizing STIs are often life-threatening and
require, in addition, extensive surgical débridement.1

In competent hosts these infections are usually caused by beta-hemolytic

streptococci (primarily Group A), Staphylococcus aureus, and, in deep fascia and
muscle, by mixed anaerobic and facultative gram-positive and gram-negative
organisms, including histotoxic Clostridia. There is less predictability in compromised
hosts. Organisms may include a range of traditional and rare pathogens, usual
commensals, yeast, fungi, and parasites. Adding to the importance of determining an
etiologic diagnosis is the observation that traditional patterns of symptoms and physical
findings may be lacking or nonspecific in immunocompromised patients. In both
immunocompetent and compromised hosts bullae, necrosis, or gas-forming bacterial
infections can lead to alarming physical findings, and signal urgency, as well as the
location, in defining the cause.1

Risk factors for cellulitis include:

 Cracks or peeling skin between the toes

 History of peripheral vascular disease
 Injury or trauma with a break in the skin (skin wounds)
 Insect bites and stings, animal bites, or human bites
 Ulcers from diabetes or a blockage in the blood supply (ischemia)
 Use of corticosteroid medications or medications that suppress the immune system
 Wound from a recent surgery

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1.2 Epidemiology

Cellulitis incidence rate is about 24.6/1000 person-years, with a higher incidence

among males and individuals aged 45-64 years. The most common site of infection was
the lower extremity (39.9%). The majority of patients were seen in an outpatient setting
(73.8%), and most (82.0%) had only one episode of cellulitis during the 5-year period
studied. There was a very low incidence of cellulitis complications, including
necrotizing fasciitis. Cellulitis is fairly common, usually treated in outpatient settings,
and is infrequently complicated by erysipelas, lymphadenitis, lymphangitis, or
necrotizing fasciitis.5

1.3 Mortality / Morbidity

The vast majority of cellulitis and soft-tissue infections can be treated on an

outpatient basis with oral antibiotics and do not result in lasting sequelae. However, just
as the incidence of cellulitis is increasing, so is the severity. Although the exact reason
for this is unknown, certain host and pathogen factors play a role in increasing the risk
of severe infection. Perhaps the most important contribution to the increasing severity
of cellulitis is the emergence of community-acquired methicillin-resistant
Staphylococcus aureus (CA-MRSA), specifically the USA 300 clone, as a leading
pathogen in cellulitis and soft-tissue infections associated with purulence.2 Infections
caused by CA-MRSA tend to be more severe and are resistant to many of the antibiotics
commonly used to treat cellulitis.6

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 CHAPTER 2

CONTENTS

2.1 Definition

Cellulitis is an infection of the skin and soft tissue of the skin. Cellulitis involves
more of the soft tissues, extending deeper into the dermis and subcutaneous tissue. S.
aureus and group A streptococci are by far the most common etiologic agents, but
occasionally other bacteria are identified (e.g., group B streptococci in the newborn,
pneumococci, gram-negative bacilli, and in immunocompromised individuals, a variety
of other microorganisms, including yeasts and molds).1 The infection develops when
there is a break in the skin, such as a wound or injury, which may be minor. This allows
bacteria to enter the skin and grow, causing infection and swelling. Most cases of
cellulitis are mild and heal completely with antibiotic treatment. However, the infection
can become severe and cause a bodywide infection if left untreated. It is important to
seek medical care promptly if you could have a skin infection. 2 Gangrenous cellulitis,
characterized by necrosis of the epidermis and deeper soft tissue structures including
muscle, is classified as necrotizing fasciitis, clostridial STI, progressive bacterial
synergistic gangrene and synergistic necrotizing cellulitis.1

2.2 Etiology

SPECIFIC BACTERIAL SPECIES ASSOCIATED WITH STI

Person-to-Person Spread

Staphylococcus aureus and groups a, b, c, and g beta-hemolytic streptococci

enterobacteriaceae, haemophilus influenzae, neisseria meningitidis, and pseudomonas
aeruginosa streptococcus pneumoniae.

S. pneumoniae is a rare cause of cellulitis and necrotizing fasciitis, perhaps occurring

more frequently in recent years and behaving like group A streptococcal STI.
Predisposing or associated conditions include chronic alcoholism, drug abuse, HIV,
connective-tissue disorders, glucocorticosteroids, and the use of NSAIDs. Bacteremia is
an underlying mechanism in about half of the cases described but relative or absolute
penicillin resistance does not appear to be a factor.

3
Specific Bacterial Species Associated with Aqueous Environments

Aeromonas spp. and Vibrio spp.

Specific Bacterial Species Associated with Soil Exposure

Clostridium species (primarily, excluding endogenous C. perfringens, the most

frequently isolated pathogen) was discussed earlier in this chapter.

Specific Bacterial Species Associated with Animal Exposure

Streptococcus iniae, Erysipelothrix rhusiopathiae, Bacillus anthracis, and Pasteurella

multocida are associated with animal exposure.

2.3 Pathogenesis

Normal intact skin plays a critical role in the defense against a wide range of pathogens.
The details of the host–pathogen interaction are poorly understood, but appear to
involve barrier function, bacterial factors, and host factors.1

2.4 Clinical Symptoms

In some cases, there is a history of an antecedent lesion (dermatitis, stasis ulcer,

puncture wound, percutaneous catheter, or trauma). With onset of infection, patients
often experience local pain and tenderness along with variable degrees of erythema and
systemic symptoms (fever, chills, and malaise). Erythema, at first minimal at the site of
infection, may rapidly intensify and spread. Local pain is often severe and in the
absence of erythema should raise suspicions of early deeper seated infection. In some
individuals, systemic symptoms may antedate localizing complaints and signs of STIs.
In a study of 50 patients with cellulitis, only 26 percent had fever >38°C (>100.4°F). A
potential portal of entry was identified in 66 percent of patients: 50 percent of those
with upper extremity and 67 percent of those with lower extremity cellulitis. Patients
with early gangrenous cellulitis may experience severe pain out of proportion to the
appearance of the local area.1

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Objective clinical findings in soft-tissue infections

1. Erysipelas
2. Acute Cellulitis
3. Surgical Wound Infection
4. Cellulitis complicating a pressure ulcer
5. Cellulitis arising at site of animal bites
6. Gangrenous cellulitis, infectious gangrene, and crepitant soft-tissue wounds
a. Streptococcal angrene including type II necrotizing fasciitis
b. Type I necrotizing fasciitis
c. Fournier's gangrene
d. Synergistic necrotizing cellulitis
e. Progressive bacterial synergistic gangrene (meleney's gangrene)
f. Gangrenous cellulitis in the immunocompromised individual
g. Nonclostridial crepitant cellulitis
h. Clostridial soft-tissue infections
i. Anaerobic cellulitis
j. Anaerobic myonecrosis (gas gangrene)
k. Spontaneous, nontraumatic anaerobic myonecrosis

ERYSIPELAS

In the absence of underlying edema or other skin abnormalities, erysipelas usually

begins on the face or on a lower extremity, heralded by pain, superficial erythema, and
plaquelike edema with a sharply defined margin to normal tissue ( Fig. 196-2 and Fig.
196-3). In the presence of antecedent edema or other anatomic abnormalities, the
margin between normal and diseased soft tissue may be obscure, much like in primary
cellulitis. There may not be an obvious portal of entry, and skipped areas may confuse
the nature of the process. Facial erysipelas is less frequent than lower extremity disease,
begins unilaterally but may spread by contiguity over the nasal prominence to involve
the face symmetrically

ACUTE CELLULITIS

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This has many of the features of erysipelas (erythema, tenderness, pain) but extends
deeper into the subcutaneous tissues. Cellulitis can be differentiated from erysipelas by
the lack of distinct margins between affected and normal skin, a deeper, firmer form of
tender induration, fluctuance, and occasionally the presence of crepitus on palpation. In
a study of 50 children with cellulitis, 16 percent of cases had facial infection with the
remainder occurring on an extremity, the leg being affected three times as often as the
arm. In some cases of cellulitis, the overlying epidermis undergoes bulla formation or
necrosis, resulting in extensive areas of epidermal sloughing and superficial erosion.
Alternatively, with or without antibiotic therapy, infection may localize in the soft
tissue, with dermal and subcutaneous abscess formation or fasciitis. Regional
lymphadenopathy may be associated with cellulitis on an extremity. In older
individuals, thrombophlebitis may complicate lower leg cellulitis. Most cases of
spontaneous cellulitis or those secondary to skin lesions or trauma are due to S. aureus.
Group A and other streptococci (especially groups B, C, and G), as well as Escherichia
coli and other Enterobacteriaceae and anaerobes, are involved in cellulitis, especially in
association with extremes of age, prolonged hospitalization, percutaneous intravascular
lines, diabetes, immunocompromised states and glucocorticoids.

SURGICAL WOUND INFECTIONS

These are classified as incisional (superficial) or deep. 8 Incisional wound infections

involve the skin, subcutaneous tissue, and/or muscle. Deep infections involve structures
adjacent to the surgical wound that were entered or exposed during the procedure, such
as subfascial layers, viscera, and/or spaces within the peritoneum, thorax, or joints. Up
to 80 percent of wound infections are incisional. A wound is considered to be infected if
there is drainage of purulent material and evidence of inflammation. Incisional
infections present with erythema, pain, tenderness, and local swelling ( Fig. 196-4B),
and often with low-grade fever. Purulent drainage reveals neutrophils and cultures most
often grow S. aureus.

CELLULITIS COMPLICATING A PRESSURE ULCER

Pressure ulcers, particularly those located in the sacrum in elderly, frail, malnourished
individuals pose significant problems for the patient and the physician. In addition to
reflecting poor skin nutrition, the location causes the site to be contaminated by a
variety of facultative and anaerobic microorganisms from the skin and the bowel,

6
including S. aureus, enterococci, Pseudomonas aeruginosa, and Bacteroides fragilis. In
addition to pain and cellulitis, the ulcer can be undermined and may eventually be
complicated by bacteremia, often polymicrobial, or the underlying bone can become
infected. Like other open wounds, the identity of the active pathogen(s) may be difficult
to determine.

CELLULITIS ARISING AT SITES OF ANIMAL BITES

Domestic dog and cat bites are frequent and can give rise to painful and necrotizing
cellulitis caused by Pasteurella multocida, Capnocytophaga canimorsus (especially in
asplenic individuals) and a host of other aerobes and anaerobes from the animals' mouth
or the skin of the infected individual. Dog bites are often accompanied by a crush injury
that devitalizes tissues. The bite of cats can inject organisms (via sharp incisors) deep
into tissues, including joint spaces, tendon sheaths, or below the periosteum of bone.
Human bites have a higher incidence of infection than do animal bites because of the
mix of oral bacteria (aerobes and anaerobes), as well as the crush injury imparted along
with the bite. Organisms include various streptococci, S. aureus, and the anaerobic
peptostreptococci and peptococci.

GANGRENOUS CELLULITIS, INFECTIOUS GANGRENE, AND CREPITANT

SOFT-TISSUE WOUNDS

These soft-tissue infections are characteristically rapidly developing, progressive, and

accompanied by constitutional symptoms, severe pain, and tenderness, with changes in
overlying skin that progress to bulla formation and frank necrosis. The process can be
in the superficial or deep fascia with secondary changes in the overlying soft tissues.

STREPTOCOCCAL GANGRENE INCLUDING TYPE II NECROTIZING

FASCIITIS

The pathogen is almost always a group A streptococcus, although groups C and G

isolates, as well as other microorganisms, are rarely identified. Occasionally, especially
in newborns, but also in patients early postpartum, group B streptococci have been
recovered. The location of the necrotizing lesion is most often an extremity, rarely the
face. Pain, erythema, and edema with rapid formation of bullae, constitutional
symptoms with high fever, and toxicity are characteristic of early progression. There is
bacteremia in approximately two-thirds of patients and evolution of necrosis of the

7
overlying skin can be rapid and dramatic with appearance of deeper structures including
tendon sheaths and muscle. Streptococcal toxic shocklike syndrome often accompanies
this infection, referred to in the lay press as a “flesh-eating” bacterial process. The terms
streptococcal gangrene and streptococcal necrotizing fasciitis should be considered as a
single disease continuum.

TYPE I NECROTIZING FASCIITIS

This infection is caused by a mix of facultative and anaerobic microbes, often delivered
into the subcutaneous tissues following surgery, bowel perforation secondary to
neoplasm or diverticulitis, trauma, or parenteral drug abuse via skin-popping, and often
occurs in patients compromised by diabetes or malnutrition. Organisms include
nongroupable streptococci, enterococci, anaerobic streptococci and staphylococci,
Bacteroides spp., and Enterobacteriaceae including E. coli, as well as various aquatic
bacteria. Type I necrotizing fasciitis most commonly occurs on an extremity, abdominal
wall, perineum, or about operative wounds.

FOURNIER'S GANGRENE

This is a localized variant of necrotizing fasciitis involving the scrotum and penis. It is
usually caused by the same mix of facultative and anaerobic organisms that are
associated with type I necrotizing fasciitis.

SYNERGISTIC NECROTIZING CELLULITIS

This variant of necrotizing fasciitis is unique in that all soft-tissue structures, including
muscle, can be involved in a painful, progressive, polymicrobial infection that is highly
lethal. Extensive gangrene of the superficial tissues and fat can be visualized by direct
inspection through skin open areas or with skin incisions. Gas can be palpated in the
tissues in approximately a quarter of patients. Organisms frequently isolated included
anaerobes (streptococci and/or bacteroides) and facultative bacteria, especially
Enterobacteriaceae ( E. coli, Proteus, Klebsiella, etc.). The most common site of
involvement in approximately half the cases is the perineum.

PROGRESSIVE BACTERIAL SYNERGISTIC GANGRENE

This infection typically occurs in association with wire stay sutures in a drain site
following an abdominal operation (ileostomy, colostomy), in an incision in the chest

8
wall following abdominal or thoracic infection (empyema), at the exit site of a fistulous
tract, or in a chronic ulcer. This rare infection usually is associated with a
microaerophilic or anaerobic streptococcus at the advancing margin and S. aureus (or,
rarely, an enteric gram-negative bacillus) in the central, shaggy, ulcerated area. 17 The
process usually starts with local redness, tenderness, and swelling that subsequently
develops into a painful, superficial enlarging shaggy-based ulcer.

GANGRENOUS CELLULITIS IN THE IMMUNOCOMPROMISED INDIVIDUAL

The microorganisms associated with necrotizing cutaneous infections in the normal host
are joined by a variety of other traditionally pathogenic and nonpathogenic bacteria, as
well as fungi in compromised patients. In the presence of thermal burns bacteremic
Pseudomonas aeruginosa may colonize normal skin, producing ecthyma gangrenosum,
or may home to burn areas, leading to extensive bacteremic Pseudomonas gangrenous
cellulitis.

NONCLOSTRIDIAL CREPITANT CELLULITIS

The presence of a cellulitis with palpable gas raises the specter of a histotoxic
Clostridium infection. The patient may have experienced a traumatic or surgical injury
that was inadequately débrided or had an underlying local infection, a poorly performed
needle stick or illicit drugs via skin popping.

CLOSTRIDIAL SOFT-TISSUE INFECTIONS

The histotoxic clostridia are responsible for a variety of infections that involve the
subcutaneous and muscular tissues, with changes in the overlying skin that can be
abrupt and dramatic. The histotoxic clostridia primarily involved in these infections
include the human gut commensal Clostridium perfringens and the environmentally
resident Clostridium septicum. C. perfringens is present in approximately 90 percent of
normal colons but C. septicum is rarely found, perhaps in 5 percent of asymptomatic
individuals.

ANAEROBIC CELLULITIS

This is an infection of devitalized tissue, usually caused by C. perfringens with or

without other bacteria, occurring in a dirty or inadequately débrided wound several days
after injury or following a needle stick or surgery.

9
ANAEROBIC MYONECROSIS (GAS GANGRENE)

This is a rapidly progressing, toxemic, potentially lethal infection involving muscle but
with secondary changes in the overlying skin. The infection may develop as a
complication of muscle injury, a traumatic dirty wound with extensive muscle and soft-
tissue damage, or following surgery on the bowel or gallbladder. C. perfringens is the
most common pathogen and also part of the normal flora but rarely associated with
spontaneous gas gangrene.

SPONTANEOUS, NONTRAUMATIC ANAEROBIC MYONECROSIS

In the absence of an external wound, septicemic gas gangrene may occur

spontaneously, usually caused by C. septicum and often associated with hematologic
malignancies or occult colon cancer, especially in the cecal area.

2.5 Differential diagnosis 7

1. Angioedema
2. Erythema Multiforme
3. Burns, Chemical
4. Gas Gangrene
5. Dermatitis, Atopic
6. Impetigo
7. Dermatitis, Contact
8. Plant Poisoning, Toxicodendron
9. Dermatitis, Exfoliative
10. Stevens-Johnson Syndrome
11. Erysipelas
12. Toxic Epidermal Necrolysis

2.6 Diagnosis

First, it is crucial for the doctor to distinguish whether or not the inflammation is due to
an infection. The history and physical exam can provide clues in this regard, as can
sometimes an elevated white blood cell count. A culture for bacteria may also be of

10
value, but in many cases of cellulitis, the concentration of bacteria may be low and
cultures fail to demonstrate the causative organism.4

When it is difficult or impossible to distinguish whether or not the inflammation is due

to an infection, doctors sometimes treat with antibiotics just to be sure. If the condition
does not respond, it may need to be addressed by different methods dealing with types
of inflammation that are not infected.4

Cellulitis is most often a clinical diagnosis, and local cultures do not always identify the
causative organism. Blood cultures usually are positive only if the patient develops
generalized sepsis. Conditions that may resemble cellulitis include deep vein
thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis
dermatitis, which is inflammation of the skin from poor blood flow.3

There have been many cases where Lyme disease has been misdiagnosed as staph- or
strep-induced cellulitis. Because the characteristic bullseye rash does not always appear
in patients infected with Lyme disease, the similar set of symptoms may be
misdiagnosed as cellulitis. Standard treatments for cellulitis are not sufficient for curing
Lyme disease. The only way to rule out Lyme disease is with a blood test, which is
recommended during warm months in areas where the disease is endemic.3

2.7 Treatment

Mild cases of early erysipelas can be treated on an outpatient basis with either
intramuscular procaine penicillin (600,000 units twice daily) or with oral penicillin V,
500 mg every 6 h. Erythromycin and clindamycin are also effective in penicillin-
allergic individuals.1

Individuals with more extensive streptococcal infections and with underlying

medical problems such as diabetes mellitus should be hospitalized and treated with
intravenous aqueous penicillin G (1 to 2 million units every 4 to 6 h). In severe
streptococcal skin infections (e.g., extensive erysipelas, cellulitis, or streptococcal
gangrene), parenteral aqueous penicillin G should be administered in higher doses. In
the ill patient in whom a staphylococcal etiology is identified, a penicillinase-resistant
semisynthetic penicillin (e.g., nafcillin) should be employed and/or vancomycin
substituted in the penicillin allergic individual. In the patient with a questionable

11
penicillin allergy, cefazolin (1.0 g intravenously every 8 h) may be chosen.
Vancomycin is the drug of choice in patients that have a methicillin-resistant organism
or have a prior history of an immediate type reaction (IgE mediated) to a penicillin or a
cephalosporin.1

Local Measures

Care of the local lesions of erysipelas and cellulitis includes bed rest with
immobilization and elevation of the involved area to reduce local edema. Cool, sterile
saline dressings decrease the local pain and are particularly indicated in the presence of
bullous lesions. The application of moist heat may aid in the localization of an abscess
in association with cellulitis, but it should not be used in a patient with arterial
insufficiency of the involved extremity.1

Surgical Intervention

Treatment of necrotizing STIs requires early and complete surgical débridement

of necrotic tissue in combination with appropriate drainage and high-dose antibiotics.
Inspection of the deep fascia can confirm the presence of fat necrosis, preservation of
the deep aponeurosis overlying muscle and provide material for bacterial and
pathologic study. 28 Reexploration and débridement should be performed as necessary
to ensure that all necrotic tissue has been removed and pockets of pus are drained.1

Other Therapies

Other adjunctive considerations in treatment of STI include the use of

intravenous gamma globulin for type II necrotizing fasciitis caused by group A
streptococci and recombinant human activated protein C in severe sepsis related to
these soft-tissue infections. Patients with poor granulocyte production may be helped by
granulocyte colony-stimulating factor. There is some evidence from the recent literature
and from speculative observation that NSAIDs should be avoided in patients suspected
of incubating or expressing early bacterial infections. Masking of fever and inhibition
of granulocyte migration and function are arguments that deserve continued evaluation.1

12
2.8 Prognosis

In assessing prognosis, the wide ranges described for these infections depends
upon many variables. The underlying health and immune status of the patients clearly
are factors predisposing to all of these entities. In like manner, early recognition and
definition of etiologic agents guides appropriate antibiotic usage, as well as surgical
decisions. Many of these infections are life-threatening and therefore urgent evaluation
and therapy are capable of improving prognosis.1

13
 CHAPTER 3

CASE REPORT

MR : 40.85.49
Name :T
Date of birth : January, 9th 2000
Age : 9 years old
Sex : Male
Race : Aceh
Religion : Moslem
Address : DS Pucuk Lembang Kluet Timur, South of Aceh
BW : 23 KG
Stature : 130 cm
EID index : 85%
Source of referral : RSU dr. H Yiliddin Anay
Date of Admission : October, 26th 2009

History Taking

The patient was well until 2 weeks ago when he suddenly started to have swelling on
his left leg. The swelling started from patella region and spread to the upper and lower
leg. Otherwise, he also had wound that contain pus (+) but no smell.
Subsequently, he also had fever (+) since 2 days ago. It was an on and off high grade
fever.
There was no cough and vomiting. There was no trauma history of falling down. There
was no history contact of elephantiasis patient. Bowel output and passing urine was
normal.

Past medical history : this patient was referred from RSU dr H Yiliddin Anay with
differential diagnosis : elephantiasis and cellulitis

Drug history : Ceftriaxone, ranitidine, paracetamol

14
Physical Examination

In physical examination shown a boy, the body weight was 23 kg, body length was 130
cm, and EID index was 85% nutritional status was mild underweight. body temperature
was 36,70C. the consciousness of this patient was compose mentis, anemia (-), ikterus
(-), cyanosis (-), oedema (+), dyspnoe (-).

Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva : pale
(-). Nose and mouth were normal.
Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 120 bpm, regular, murmur (-),
RR : 24 bpm, regular, ronchi (-).
Abdomen : soepel, peristaltic (+) normal, Hepar and lien were not palpable.
Genitalia : male, scrotum edema (+), hyperemi (+), pus (+)
Extremities : pulse rate 120 bpm, regular, pressure/volume was enough.
Left extremity : oedem (+), hyperemi (+), pus (+), crepitation (+)

Working diagnosis :
 Suspect cellulitis

Differential diagnosis :
1. Suspect cellulitis
2. Osteomyelitis
3. Filariasis

Therapy :
 IVFD D5% Nacl 0,45% 30 micro drops/ minute
 Cefotaxime inj 1gr / 8 hours / IV
 Paracetamol 3x250 mg
 Nacl 0,9% compress at leg and penis abcess
 MB diet 1560 kkal with 46 gr protein

15
Planning Examination :
 Complete blood count
 Routine urine and feces analysis
 Blood and pus culture
 Urine culture
 Blood glucose
 Albumin concentration
 Renal function test
 Surgery consultation
 Pediatric Infection consultation

26 – 28 October 2009 Follow Up

S : Swelling at left leg (+), fever (-)
O : sens : CM T: 36.90C BB : 23kg
Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva:
pale (-). Nose and mouth were normal.
Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 80 - 120 bpm, regular, murmur
(-), RR : 20 - 28 bpm, regular, ronchi (-).
Abdomen : Soepel, peristaltic (+) normal, hepar was not palpable, lien was difficult
to palpate, pain on palpation (+)
Genital : male, scrotum edem (+), hyperemi (+), pain (+)
Extremity : pulse rate 80 - 120 bpm, regular, pressure/volume was normal. Left
inferior extremity : oedem (+), hyperemi (+), pus (+), parasthesia (+), there were
ulcus at left patella.
A : dd/ cellulitis, osteomyelitis, filariasis + hypoalbuminemia
P:
 IVFD D5% Nacl 0,45% 30 micro drops / minute
 Inj Cefotaxime 1gr / 8 hours / IV
 Paracetamol 3x250 mg
 Compress Nacl 0,9% at leg and penis abcess
 Diet MB 1560 kcal with 46 gr protein

16
Laboratory result : 27 October 2009
 Complete blood count :
o WBC 17,3 k/ul o MCV 84,7 fl
o NEU 11,8 68,4 %N o MCH 28,4 pg
o LYM 3,13 18,1%L o MCHC 33,6 g/dl
o MONO 1,07 6,19%M o RDW 16,7%
o EOS 1.10 6,34%E o PLT 470 k/ul
o BASO ,164 ,948%B o MPV 6,88 fl
o RBC 4,72 M/ul o PCT ,323 %
o HGB 13,4 g/dl o PDW 16,0 10(GSD)
o HCT 40,0%
Manual Differential :
o Neu 67 o Mono 6
o Band 3 o Eosin 6
o Lymph 18 o Baso 0
Comment : Leukocytosis

 Albumin 2,86 g/dl (low)

 Ureum 18,2 mg/dl
 Creatinine 0,49 mg/dl (low)
 Uric Acid 4,1 mg/dl
 Glucose Ad Random 76,8 mg/dl
 Urine profile
o Color yellow o pH 5,0
o Glucose - o Protein -
o Billirubin - o Urobilinogen -
o Ketone - o Nitrit -
o GS 1,025 o Blood -
 Urine Sediment
o Erythrocyte 0-1 o Casts -
o Leukocyte 1-3 o Crystal -
o Epithel cell 1-3

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 Feces Analysis
o Macroscopic o Microscopic
 Color brown  Worm eggs -
 Consistency solid  Amoeba -
 Blood -  Erythrocyte -
 Mucosa -  Leukocyte -

Consult Radiology result : 27 October 2009

 Thorax : there were no cardiac and lung abnormality
 Right Femur anterior/lateral : shape and structure of os femur and cruris were good,
obstruction was not found, conclusion : there were no involvement of femur and
cruris

Consult Pediatric Tropic Infection Sub Division result : 27 October 2009

 The Patient was diagnosed with Cellulitis on the extremity inferior sinistra and
recommendation for blood culture.

Hypoalbumin correction
Albumin needed = (3,5 – 2,86) x 0,8 x 23 = 11,776
Plasma Albumin 20% = 58,88 cc = 60 cc

29 – 01 November 2009 Follow up

S : Swelling at left leg (+), fever (-)
O: sens : CM T: 36.50C – 37.60C BB : 23kg
Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva:
pale (-). Nose and mouth were normal.
Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 84 - 112 bpm, regular, murmur
(-), RR : 20 - 30 bpm, regular, ronchi (-)
Abdomen : Soepel, peristaltic (+) normal, hepar was not palpable, lien was difficult
to palpate, pain on palpation (+)
Genital : male, scrotum edem (+), hyperemi (+), pain (+)

18
 Extremity : pulse rate 84 - 112 bpm, regular, pressure/volume was normal. Left
inferior extremity : oedem (+), hyperemi (+), pus (+), parasthesia (+), there were
ulcus at left patella. TC = 43cm, LC = 11cm
A : dd/ cellulitis, filariasis + hypoalbuminemia
P:
 IVFD D5% Nacl 0,45% 4 micro drops / minute
 Inj Cefotaxime 1gr / 8 hours / IV
 Paracetamol 3x250 mg
 Nacl 0,9% compress at leg and penis abcess
 Diet MB 1560 kcal with 46 gr protein
 IVFD metronidazole 350mg (loading dose 70cc in 140 micro drops / min) then
200mg / 8 hours (should finish in half an hour) 80 micro drops / min

Laboratory result : 30 October 2009

 Ureum 19.0 mg/dl
 Creatinine 0,45 mg/dl (low)
 Uric Acid 3,0 mg/dl
 Bilirubin direct 0.127 mg/dl
 SGOT 293.8 U/L
 SGPT 69.8 U/L
 Alkaline Phosphatase 84 U/L
 Natrium 131 mEq/L
 Kalium 4.4 mEq/L
 Chloride 107 mEq/L
Consult vascular surgery result : 29 October 2009
 Vascular disturbance of this patient was not found

2 – 5 November 2009 Follow Up

S : Swelling at left leg (+), fever (+)
O: Sens : CM T: 36.50C – 39.30C BB : 33kg
Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva:
pale (-). Nose and mouth were normal.

19
 Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 96 - 104 bpm, regular, murmur
(-), RR : 22 - 32 bpm, regular, ronchi (-)
Abdomen : Soepel, peristaltic (+) normal, hepar was not palpable, lien was difficult
to palpate, pain on palpation (+)
Genital : male, scrotum edem (+), hyperemi (+), pain (+)
Extremity : pulse rate 96 - 104 bpm, regular, pressure/volume was normal. Left
inferior extremity : oedem (+), hyperemi (+), pus (+), parasthesia (+), there were
ulcus at left patella. TC = 42.5cm, LC = 10.5cm
A : Cellulitis on the left inferior extremity + Orchitis + hypoalbuminemia
P:
 IVFD D5% Nacl 0,45% 4 micro drops / minute
 Cefotaxime inj 1gr / 8 hours / IV (D7)  stop
 IVFD metronidazole 200mg / 8 hours, should finish in half an hour (80 micro drops/
min)
 Paracetamol 3x250 mg
 Compress Nacl 0,9% at leg and penis abcess
 Diet MB 1560 kcal with 46 gr protein
 Amoxiclav 3 x 500 mg

Blood Culture Result : 2 November 2009

 Gram negative bacilli bacteria (Enterobacter Aerogenes bacteria) were found.
Sensitivity Test Result : 2 November 2009
 Amoxiclav, Meropenem were sensitive
 Amikacin, Gentamicin, Sulfamethoxazole, Tetracycline were less sensitive
 Ampicillin, Ciprofoxacin, Cefoperazone, Cefotaxime, Erythromycin, Penicillin
were resistance.
Dipstick Urine Result : 4 November 2009
 Glucose : normal
 Protein : negative
 Billirubin : negative
 Blood : negative
 Nitrit : +1
20
Laboratory Result : 4 November 2009
 Complete blood count :
o WBC 21.49 + k/ul o MCH 29.0 pg
o NEU 17.04* 79.3 %N o MCHC 33,7 g/dl
o LYM 1.80 8.4 %L o RDW-SD 47.2 fl
o MONO 2.16 + 10.1 %M o RDW-CV 15.2 + %
o EOS 0.44 * 2.0 %E o PLT 506 + k/ul
o BASO 0.05 * 0.2 %B o MPV 9.2 fl
o RBC 4,48 M/ul o PCT 0.47 + %
o HGB 13.0 g/dl o PDW 10,3 fl
o HCT 38,6 % o P-LCR 18.9 %
o MCV 86,2 fl o LED 35 mm/hour
Manual Differential :
o Neu 79 o Mono 10
o Band 0 o Eosin 2
o Lymph 9 o Baso 0
Comment : Leukocytosis + Monocytosis + Thrombocytosis

6 - 8 November 2009 Follow Up

S : Swelling at left leg (+), fever (+)
O: Sens : CM T: 36.00C – 38.00C BB : 33kg
Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva:
pale (-). Nose and mouth were normal.
Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 96 - 108 bpm, regular, murmur
(-), RR : 22 - 32 bpm, regular, ronchi (-)
Abdomen : Soepel, peristaltic (+) normal, hepar was not palpable, lien was difficult
to palpate, pain on palpation (+)
Genital : male, scrotum edem (+), hyperemi (+), pain (+)
Extremity : pulse rate 96 - 108 bpm, regular, pressure/volume was normal. Left
inferior extremity : oedem (+), hyperemi (+), pus (+), parasthesia (+), there were
ulcus at left patella. TC = 40.5cm, LC = 9.5cm
21
A : Cellulitis on the left inferior extremity + Orchitis + hypoalbuminemia
P:
 IVFD D5% Nacl 0,45% 4 micro drops / minute
 IVFD metronidazole 200mg / 8 hours, should finish in half an hour (80 micro drops/
min)
 Paracetamol 3x250 mg
 Compress Nacl 0,9% at leg and penis abcess
 Diet MB 1560 kcal with 46 gr protein
 Amoxiclav 3 x 500 mg  stop
 Meropenem inj 500mg / 8h / IV

9 – 11 November 2009 Follow Up

S : Swelling at left leg (+) ↓, fever (-)
O: Sens : CM T: 36.50C – 37.20C BB : 22kg
Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva:
pale (-). Nose and mouth were normal.
Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 96 - 102 bpm, regular, murmur
(-), RR : 24 - 36 bpm, regular, ronchi (-)
Abdomen : Soepel, peristaltic (+) normal, hepar was not palpable, lien was difficult
to palpate, pain on palpation (+)
Genital : male, scrotum edem (+), hyperemi (+), pain (+)
Extremity : pulse rate 96 - 102 bpm, regular, pressure/volume was normal. Left
inferior extremity : oedem (+), hyperemi (+), pus (+), parasthesia (+), there were
ulcus at left patella. TC = 40.5cm, LC = 9.5cm
A : Cellulitis on the left inferior extremity + Orchitis + hypoalbuminemia
P:
 IVFD D5% Nacl 0,45% 4 micro drops / minute
 IVFD metronidazole 200mg / 8 hours, should finish in half an hour (80 micro drops/
min)
 Paracetamol 3x250 mg
 Compress Nacl 0,9% at leg and penis abcess
 MB diet 1560 kcal with 60 gr protein

22
 Meropenem inj 500mg / 8jam / IV

12 – 13 November 2009 Follow up

S : Swelling at left leg (+) ↓, fever (-)
O: Sens : CM T: 36.80C – 37.80C BB : 22kg
Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva:
pale (-). Nose and mouth were normal.
Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 96 - 114 bpm, regular, murmur
(-), RR : 24 - 30 bpm, regular, ronchi (-)
Abdomen : Soepel, peristaltic (+) normal, hepar was not palpable, lien was difficult
to palpate, pain on palpation (+)
Genital : male, scrotum edem (+) ↓, hyperemi (+), pain (+)
Extremity : pulse rate 96 - 114 bpm, regular, pressure/volume was normal. Left
inferior extremity : oedem (+), hyperemi (+), pus (+), parasthesia (+), there were
ulcus at left patella.
A : Cellulitis on the left inferior extremity + Orchitis + hypoalbuminemia
P:
 IVFD D5% Nacl 0,45% 4 micro drops / minute
 IVFD metronidazole 200mg / 8 hours, should finish in half an hour (80 micro
drops / min)stop
 Paracetamol 3x250 mg
 Compress Nacl 0,9% at leg and penis abcess
 MB diet 1560 kcal with 60 gr protein
 Meropenem inj 500mg / 8 h / IV

Laboratory result : 12 November 2009

 Albumin 2.2 g/dl (low)

14 – 16 November 2009 Follow Up

S : Swelling at left leg (+) ↓, fever (-)
O: Sens : CM T: 36.80C – 37.80C BB : 22kg

23
 Head : eye : light reflex +/+, pupils were isochoric, inferior palpebra conjunctiva:
pale (-). Nose and mouth were normal.
Neck : lymph node enlargement (-)
Thorax : symmetrical fusiformis, retraction (-), HR : 96 - 114 bpm, regular, murmur
(-), RR : 24 - 30 bpm, regular, ronchi (-)
Abdomen : Soepel, peristaltic (+) normal, hepar was not palpable, lien was difficult
to palpate, pain on palpation (+)
Genital : male, scrotum edem (+) ↓, hyperemi (+), pain (+)
Extremity : pulse rate 96 - 114 bpm, regular, pressure/volume was normal. Left
inferior extremity : oedem (+), hyperemi (+), pus (+), parasthesia (+), there were
ulcus at left patella.
A : Cellulitis on the left inferior extremity + Orchitis + hypoalbuminemia
P:
 IVFD D5% Nacl 0,45% 4 micro drops / minute
 Meropenem inj 500mg / 8 h / IV
 Paracetamol 3x250 mg
 Compress Nacl 0,9% at leg and penis abcess
 HCHP diet 1560 kcal with 60 gr protein
 Dexametaxone injection 1 amp / 8 h / IV

24
 CHAPTER 4

SUMMARY

The patient started to have swelling on his left leg. The swelling started from
patella region and spread to the upper and lower leg. Otherwise, he also had wound that
contain pus (+) without smell. Subsequently, he also had fever (+) since 2 days ago. It
was an on and off high grade fever. There was no trauma history of falling down. There
was no history contact of elephantiasis patient. Bowel output and passing urine was
normal. This patient was referred from RSU dr H Yiliddin Anay with differential
diagnosis elephantiasis and cellulitis.
Based on physical examination, the body weight was 23 kg, body length was
130 cm, and EID index was 85% nutritional status was mild underweight. Body
temperature was 36,70C. The consciousness of this patient was compose mentis. Oedem
was found on his left leg. Head, neck, thorax and abdomen were normal. At genital,
scrotum edema (+), hyperemi (+), pus (+). At left extremity, edema(+), hyperemi (+),
pus (+)
Based on laboratory result, leucocytosis was found, feces and urine profile were
normal, SGOT (293U/L), SGPT( 69.8U/L), Albumin (28.3g/dl), Creatinine
(0.45mg/dl), Uric acid (3mg/dl).

The patient initially received IVFD D5% Nacl 0,45% 30 micro drops / minute,
Inj Cefotaxime 1gr / 8 hours / IV, Paracetamol 3x250 mg, Nacl 0,9% compress at his
leg and penis abcess, MB diet 1560 kkal with 46 gr protein

The patient remained hospitalized for the past 22 days with well controlled
medication, he was given Nacl 0.9% compress at his leg and penis abcess daily,
metronidazole inj 200mg/8 hours for 13 days, meropenem injection 500mg / 8 hours for
the last 10 days, dexametaxone inj 1amp/8 hours for the last 3 days, albumin correction
was done, but the albumin level is still 2.2g/dl according to the laboratory result on
November 12nd 2009. The Patients condition became better after the treatment. Left leg

25
circumscribe and scrotum edema were decrease. November 16th 2009, the patient was
discharged from RSUP HAM on his parents will and was advised to consult the
pediatric clinic regularly.

REFERENCES

1. Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA et al. Soft-Tissue
Infections: Erysipelas, Cellulitis, Gangrenous Cellulitis, and Myonecrosis in
Fitzpatrick's Dermatology In General Medicine. USA; The McGraw-Hill
Companies. 2003(6).
2. Baddour LM, Sexton DJ, Moynihan LK. Skin and soft tissue infection (cellulitis).
Available from http://www.uptodate.com/patients/content/topic.do?
Topickey=~28011/ummi_fni3. Last Updated May 2009.
3. Cellulitis. Available from http://en.wikipedia.org/wiki/Cellulitis. Last Updated
November 2009
4. Humphrey, Isaac P, Halsey, Eric S. Cellulitis. Available From
http://www.medicinenet.com/cellulitis/page3.htm. Last updated September 2009
5. Simonsen E. Cellulitis incidence in a defined population. Available from
http://www.mdconsult.com/das/citation/body/173053825-
2/jorg=journal&source=MI&sp=16100254&sid=0/N/16100254/1.html?issn= Last
Updated April 2006
6. Humphrey IP, Halsey ES. Cellulitis – Overview. Available from
http://emedicine.medscape.com/article/214222-overview Last Updated September
2009
7. Curtis DL. Cellulitis: Differential Diagnoses & Workup. Available from
http://emedicine.medscape.com/article/781412-diagnosis Last Updated July 2009

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