makalah selulitis

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

1

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

2

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

4

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

5

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

http://en.wikipedia.org/wiki/Erythema_chronicum_migrans

http://en.wikipedia.org/wiki/Lyme_disease

http://en.wikipedia.org/wiki/Stasis_dermatitis

http://en.wikipedia.org/wiki/Stasis_dermatitis

http://en.wikipedia.org/wiki/Medical_ultrasonography

http://en.wikipedia.org/wiki/Deep_vein_thrombosis

http://en.wikipedia.org/wiki/Deep_vein_thrombosis

http://en.wikipedia.org/wiki/Sepsis

http://en.wikipedia.org/wiki/Blood_culture

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.


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


Compress Nacl 0,9% at leg and penis abcess

Diet MB 1560 kcal with 46 gr protein

Laboratory result : 27 October 2009

16

Complete blood count :

o WBC 17,3 k/ul

o NEU 11,8 68,4 %N

o LYM 3,13 18,1%L

o MONO 1,07 6,19%M

o EOS 1.10 6,34%E

o BASO ,164 ,948%B

o RBC 4,72 M/ul

o HGB 13,4 g/dl

o HCT 40,0%

o MCV 84,7 fl

o MCH 28,4 pg

o MCHC 33,6 g/dl

o RDW 16,7%

o PLT 470 k/ul

o MPV 6,88 fl

o PCT ,323 %

o PDW 16,0 10(GSD)

Manual Differential :

o Neu 67

o Band 3

o Lymph 18

o Mono 6

o Eosin 6

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 Glucose -

o Billirubin -

o Ketone -

o GS 1,025

o pH 5,0

o Protein -

o Urobilinogen -

o Nitrit -

o Blood -

Urine Sediment

o Erythrocyte 0-1

o Leukocyte 1-3

o Epithel cell 1-3

o Casts -

o Crystal -

Feces Analysis

17

o Macroscopic

Color brown

Consistency solid

Blood -

Mucosa -

o Microscopic

Worm eggs -

Amoeba -

Erythrocyte -

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





(-), RR : 20 - 30 bpm, regular, ronchi (-)




18



ulcus at left patella. TC = 43cm, LC = 11cm

A : dd/ cellulitis, filariasis + hypoalbuminemia

P :


Inj Cefotaxime 1gr / 8 hours / IV


Nacl 0,9% compress at leg and penis abcess


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




19








ulcus at left patella. TC = 42.5cm, LC = 10.5cm

A : Cellulitis on the left inferior extremity + Orchitis + hypoalbuminemia

P :


Cefotaxime inj 1gr / 8 hours / IV (D7) stop

IVFD metronidazole 200mg / 8 hours, should finish in half an hour (80 micro drops/

min)




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

Laboratory Result : 4 November 2009

20

Complete blood count :

o WBC 21.49 + k/ul

o NEU 17.04* 79.3 %N

o LYM 1.80 8.4 %L

o MONO 2.16 + 10.1 %M

o EOS 0.44 * 2.0 %E

o BASO 0.05 * 0.2 %B

o RBC 4,48 M/ul

o HGB 13.0 g/dl

o HCT 38,6 %

o MCV 86,2 fl

o MCH 29.0 pg

o MCHC 33,7 g/dl

o RDW-SD 47.2 fl

o RDW-CV 15.2 + %

o PLT 506 + k/ul

o MPV 9.2 fl

o PCT 0.47 + %

o PDW 10,3 fl

o P-LCR 18.9 %

o LED 35 mm/hour

Manual Differential :

o Neu 79

o Band 0

o Lymph 9

o Mono 10

o Eosin 2

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













P :

21



min)




Amoxiclav 3 x 500 mg stop

Meropenem inj 500mg / 8h / IV


S : Swelling at left leg (+) ↓, fever (-)

O: Sens : CM T: 36.50C – 37.20C BB : 22kg













P :



min)



MB diet 1560 kcal with 60 gr protein

Meropenem inj 500mg / 8jam / IV

12 – 13 November 2009 Follow up

22


O: Sens : CM T: 36.80C – 37.80C BB : 22kg








Genital : male, scrotum edem (+) ↓, hyperemi (+), pain (+)





P :


IVFD metronidazole 200mg / 8 hours, should finish in half an hour (80 micro

drops / min)stop



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)



O: Sens : CM T: 36.80C – 37.80C BB : 22kg






23



Genital : male, scrotum edem (+) ↓, hyperemi (+), pain (+)





P :


Meropenem inj 500mg / 8 h / IV



HCHP diet 1560 kcal with 60 gr protein

Dexametaxone injection 1 amp / 8 h / IV

CHAPTER 4

SUMMARY

24

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

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

25

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

26

http://emedicine.medscape.com/article/781412-diagnosis

http://emedicine.medscape.com/article/214222-overview

http://www.mdconsult.com/das/citation/body/173053825-%202/jorg=journal&source=MI&sp=16100254&sid=0/N/16100254/1.html?issn=

http://www.mdconsult.com/das/citation/body/173053825-%202/jorg=journal&source=MI&sp=16100254&sid=0/N/16100254/1.html?issn=

http://www.medicinenet.com/cellulitis/page3.htm

http://en.wikipedia.org/wiki/Cellulitis

http://www.uptodate.com/patients/content/topic.do?Topickey=~28011/ummi_fni3

http://www.uptodate.com/patients/content/topic.do?Topickey=~28011/ummi_fni3

makalah selulitis

Documents