special features of diagnostics and management of purulent inflammation in children

8/3/2019 Special Features of Diagnostics and Management of Purulent Inflammation in Children.

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Special features of diagnosticsSpecial features of diagnosticsand management of purulentand management of purulent

inflammation in children.inflammation in children.



Plan:Plan:1. Systemic Inflammatory Response Syndrome (SIRS)

,Sepsis.

2. Acute hematogenous osteomyelitis.3. Chronic osteomyelitis.

4. Neonatal phlegmon

5. Neonatal mastitis.

6. Lung abscess



Overview

The problem of management of suppurativeinfections is one of the longest standing in the

history of pediatric surgery. Widespread use of

anti-bacterial madication and consequentmicrobial resistance to these medications has

lead to changes in the type and characteristics of

infecting microbes. Important aspects of the

study of this problem includes early diagnosis

with etiopathogenetic treatment and prevention

of these infections in childhood.



Infection

,

Burnes,pancreonecrosis

()

Systemic inflammatoryRespound syndrome

(SIRS)

Massive

bleeding

Trauma



SYSTEMIC INFLAMMATORYSYSTEMIC INFLAMMATORY

RESPONSE SYNDROME (SIRS),RESPONSE SYNDROME (SIRS),

BACTERIAL SEPSISBACTERIAL SEPSIS

Sepsis can be simply defined as a spectrumof clinical conditions caused by the

immune response of a patient to infectionthat is characterized by systemicinflammation and coagulation.

It includes the full range of response fromsystemic inflammatory response (SIR S) to organ dysfunction to multiple organfailure and ultimately death



Factors contributing to the Factors contributing to the

increasing incidence of sepsisincreasing incidence of sepsis chemotherapy and radiation therapy

corticosteroid and immunosuppressive therapies

diabetics, cancer patients, patients with major organ failure, and with granulocyopenia.

Neonates are more likely to develop sepsis (ex.group B Streptococcal infections).

surgical protheses, inhalation equipment, andintravenous, umbilical and urinary catheters.



The following is the 1992 Consensus Conference'sThe following is the 1992 Consensus Conference's

definitions for diagnosis of SIRS to MODSdefinitions for diagnosis of SIRS to MODS

± Systemic Inflammatory Response Syndrome

(SIR S)

± Sepsis

± Severe Sepsis

± Septic Shock

± Multiple Organ Dysfunction Syndrome(MODS)



Systemic Inflammator y Response Systemic Inflammator y Response

Syndrome (SIRS)Syndrome (SIRS)

heart rate > 90 beats/minute

temperature > 38°C or < 36°C respiration > 20/min or PaCO2 < 32mm

Hg

l eukocyte count > 12,000/mm3, <4,000/mm3 or > 10% immature (band)

cells



Severe SepsisSevere SepsisSepsis associated with organ dysfunction,hypoperfusion abnormalities, or

hypotension.

Hypoperfusion abnormalities include but

are not limited to:

± lactic acidosis,

± oliguria,

± or an acute alteration in mental status



Septic ShockSeptic Shock

hypotension despite fluidresuscitation

plus hypoperfusion abnormalities



THERAPY: three THERAPY: three prioritiespriorities1. Immediate Stabilization of the

Patient

2. The blood must be rapidly cleared

of microorganisms

3. The original focus of infection mustbe treated



The drugs used depends on the source of the The drugs used depends on the source of the

sepsis.sepsis.

Community acquired pneumonia a 2 drug regimen is usually utilized.Usually a third (ceftriaxone) or fourth (cefepime) generation cephalosporinis given with an aminoglycoside.

Nosocomial pneumonia: Cefipime or Imipenem-cilastatin and anaminoglycoside.

Abdominal infection: Imipenem-cilastatin or Pipercillin-tazobactam andaminoglycoside.

Nosocomial abdominal infection: Imipenem-cilastatin and aminoglycosideor Pipercillin-tazobactam and Amphotericin B.

Skin/soft tissue: Vancomycin and Imipenem-cilastatin or Piperacillin-tazobactam

Nosocomial skin/soft tissue: Vancomycin and Cefipime Urinary tract infection: Ciprofloxacin and aminoglycoside

Nosocomial urinary tract infection: Vancomycin and Cefipime

CNS infection: Vancomycin and third generation cephalosporin orMeropenem

Nosocomial CNS infection: Meropenem and Vancomycin



Hematogenous osteomyelitisHematogenous osteomyelitis

Frequency. The

overall prevalence is

1 per 5,000 children. Neonatal prevalence

is approximately 1

per 1,000.

50 % are preschool-

aged children



Bacterial causes of acute Bacterial causes of acute

hematogenous osteomyelitis: hematogenous osteomyelitis:

± Newborns (younger than 4 mo): S aureus,

Enterobacter species, and group A and B

S treptococcus species;

± Children (aged 4 mo to 4 y): S aureus, group A S treptococcus species, H aemophi l us in fl uenzae, and

Enterobacter species;

± Children, adolescents (aged 4 y to adult): S aureus

(80%), group A S treptococcus species, H

in fl uenzae, and Enterobacter species;

± Adult: S aureus and occasionally Enterobacter or

S treptococcus species



Bacterial causesBacterial causes

of direct osteomyelitisof direct osteomyelitis

± Generally: S aureus, Enterobacter species,

and Pseudomonas species;

± Puncture wound through an athletic shoe:

S aureus and Pseudomonas species.



The 2The 2ndnd phase of the osteomyelitis is the phase of the osteomyelitis is the

clinical onset of clinical onset of involvement of boneinvolvement of bone::

restricted motion,

pseudoparalysis, soft tissue around the inflamed bone

which is, hyperemic, warm,

edematous, tender,bone tenderness



Findings at physical Findings at physical

examination examination Fever (present in only 50% of neonates)

Edema

Warmth Fluctuance

Tenderness to palpation

Reduction in the use of the extremity (eg,

reluctance to ambulate, if the lower extremityis involved or pseudoparalysis of limb inneonates)

Sinus tract drainage (usually a late finding or

one that occurs with chronic infection)



pseudoparalysispseudoparalysis



Imaging Studies:Imaging Studies:

RadiographRadiograph X-ray evidence of acute osteomyelitis first is

suggested by overlying soft-tissue edema at 3-5

days after infection.

Bony changes are not evident for 14-21 days

and initially manifest as periosteal elevation

followed by cortical or medullary lucencies.

Approximately 40-50% focal bone loss is

necessary to cause detectable lucency on plain

films.



osteomyelitis of osteomyelitis of

the tibiathe tibia(X(X--ray)ray)

periosteal

elevation

medullary

lucencies



Imaging StudiesImaging Studies ((osteomyelitis)osteomyelitis)

M a g netic resonance ima g in g ( MRI) can be

extremely helpful in unclear situations.

Sensitivity ranges from 90-100%

An ul trasound examination can detect fluid

collections (e.g., an abscess) and surface

abnormalities of bone (e.g., periostitis)

C omputed tomo g raphic ( CT ) scanning can

reveal small areas of osteolysis in cortical

bone, small foci of gas and minute foreign

bodies



P roceduresP rocedures

Needle aspiration: During this test, a needle isused to remove a sample of fluid and cells

from the vertebral space or bony area. It is then

sent to the lab to be evaluated by allowing theinfectious agent to grow on media.

Biopsy: A biopsy (tissue sample) of the

infected bone may be taken and tested for

signs of an invading organism. This can be

accomplished by needle core often

accomplished under radiographic control

(fluoroscopy or CT scan).



XX--ray findings of neonatal acuteray findings of neonatal acute

hematogenous osteomyelitishematogenous osteomyelitis



TreatmentTreatment

Medications

Drainage

Splinting or castimmobilization

Surgery

Alternativetreatment



Treatment of neonatal AHO:ShadeTreatment of neonatal AHO:Shade¶¶s s

reduction traction reduction traction



S urgical CareS urgical Care

Immediate bone aspiration

If signs and symptoms do not resolve within48-72 hours of initiation of appropriate

antimicrobial treatment, consider repeat bone aspiration to drain the pus

Joint aspiration

Most well-established bone infections are

managed through open surgical proceduresduring which the destroyed bone is scrapedout



ComplicationsComplications

Bone abscess

S epsis Fracture

Over l yin g so f t-tissue cell ul itis

Drainin g so f t-tissue sinus tracts



Further complication of AHO:varusFurther complication of AHO:varus

deformation and limb contractiondeformation and limb contraction



Symptomatology of the primar ySymptomatology of the primar y

subacute haematogenous subacute haematogenous

osteomyelitisosteomyelitis

insidious in onset,

looks a systemic reaction and mimicsvarious benign and malignant

condition

symptoms for 2 weeks or more,

negative blood cultures

positive findings on plain x-rays



CHRONIC OSTE OMY ELI T I S:CHRONIC OSTE OMY ELI T I S:

Clinical FeaturesClinical Features With progressive osteonecrosis a large mass

of dead bone forms and detaches from

healthy bone as ³ seque strum´

The living bone surrounding it is known as

³involucrum´

The sinus continues to discharge pus andsmall pieces of dead bone



S erious Complications of Chronic S erious Complications of Chronic

Osteomyelitis:Osteomyelitis: Damage to epiphyseal plates results in

growth arrest and deformity

Chronic infection can lead to amyloid

disease

Skin margins can undergo malignant

change ± Squamous Cell Carcinoma( Marjolin's ulcer )

Risk of septic arthritis in nearby joints



Brodie's Brodie's

abscessesabscesses

radiolucent radiolucent

with with adjacent adjacent

sclerosissclerosis



Neonatal phlegmonNeonatal phlegmon

Neonatal phlegmon-acute soft-tissue

infections in childhood. Types: simple, toxic

and septicopyemic. Etiology: most common-Staphylococcus

epidermidis

Typical localizations: lumbar area, back,

anterior and lateral superficies of the thorax

Local symptoms: pain, local rise in

temperature, hyperemia, swelling.



Neonatal phlegmonNeonatal phlegmon



Neonatal phlegmonNeonatal phlegmon--surgical surgical

treatmenttreatment



Adyponecrosis



Er ysipelas Er ysipelas



Neonatal mastitisNeonatal mastitis

Neonatal mastitis is a local bacterial infectionduring the first mounth (first weeks) of life

Causative organisms. Staphylococcal organisms

(S.epidermidis,S.aures)

The male:female ratio is 1

:1

Physiological enlargement of mammalian glands

is a prepodisposatary factor for the development

of the disease

General symptoms

Local symptoms (tenderness, swelling,

hyperemia, local rise in temperature, fluctuation)



Neonatal mastitis.Surgical Neonatal mastitis.Surgical

managementmanagement



Special features of conservative treatment of

neonates with acute suppurative infections

1. Anti-bacterial therapy.

2. Intensive infusive therapy of hemostatic dysbalance

(IV and IM administration of drugs)3. Passsive and active immunization

4. Symptomatic treatment

5. Desensitization and hormonal therapy

6. Administration of physiotherapeutic procedures

(compresses, warm baths, ultraviolet therapy)

7. Hyperbaric oxygen therapy.



ClassificationClassification

Lung abscesses are considered acute or chronic depending on the duration of symptoms at the time of patient presentation.The arbitrary dividing time is 4-6 weeks.

Primary lung abscess are commonly observedin patients who are predisposed to aspirationor in otherwise healthy individuals, whereassecondary lung abscesses represent

complications of a preexisting local lesionsuch as a bronchogenic carcinoma or asystemic disease (eg, HIV infection) thatcompromises immune function.



Factors contributing to lung abscessFactors contributing to lung abscess



Factors contributing to lung abscessFactors contributing to lung abscess

Oral cavity disease : Periodontal disease, Gingivitis Altered consciousness : Alcoholism, Coma, Drug abuse,

Anesthesia, Seizures

Immunocompromised host : Steroid chemotherapy,

Malnutrition, Multiple trauma

Esophageal disease : Achalasia, Reflux disease,

Depressed cough and gag reflex

± Esophageal obstruction

Bronchial obstruction : Tumor, Foreign body, Stricture

Generalized sepsis



Bacteriology of lung abscessBacteriology of lung abscess



Bacteriology of lung abscessBacteriology of lung abscess

Gram-negative organisms

± Bacteroide s species ± F u sobacterium species

± Proteu s species

± Aerobacter species

± E scherichia coli

Gram-positive organisms ± Pepto streptococcu s species

± M icroaerophilic streptococcu s

± C lo stridium species

± St a phylococcu s species

± Actinomyce s species

Opportunistic organisms

± Candid a species

± Legionell a species

The diagnosis of a typical lung abscess canThe diagnosis of a typical lung abscess can



The diagnosis of a typical lung abscess can The diagnosis of a typical lung abscess can

usually be confirmed based on histor y and usually be confirmed based on histor y and

physical examination findings.physical examination findings.

Evaluation of expectorated sputum

Chest radiographs (An area of thick pneumonic

consolidation precedes the emergence of thetypical cavitary air-fluid form. The distinctivecharacteristic of lung abscess, the air-fluid level,can only be observed on a chest x-ray film takenwith the patient upright or in the lateral decubitus

position. In the presence of associated pleuralthickening, atelectasis, or pneumothorax, the air-fluid level may be obscured.



Chest CT scan images are valuable for

demonstrating cavitation within an area of

consolidation, for evaluating the thickness andregularity of the abscess wall, and for determining

the exact position of the abscess with regard to the

chest wall and bronchus. CT scan images can also

aid in evaluating the extent of bronchial

involvement proximal or distal to the abscess.



Lung abscess. XLung abscess. X--ray findingsray findings



Pleural effusion Pleural empyema



SpontaneousSpontaneous

pneumothoraxpneumothorax Pyopneumothorax

TreatmentTreatment



Antibiotics in lung abscess Anaerobic organisms

± First choice - Clindamycin (Cleocin 3) ± Alternative - Penicillin

± Oral therapy - Clindamycin, metronidazole (Flagyl), amoxicillin (Amoxil)

Gram-negative organisms ± First choices - Cephalosporins, aminoglycosides, quinolones

± Alternatives - Penicillins and cephalexin (Biocef)

± Oral therapy - Trimethoprim/sulfamethoxazole (Septra)

Pseudomonal organisms: First choices include aminoglycosides,quinolones, and cephalosporin.

Gram-positive organisms ± First choices - Oxacillin (Bactocill), clindamycin, cephalexin, nafcillin

(Nafcil), and amoxicillin ± Alternatives - Cefuroxime (Ceftin) and clindamycin

± Oral therapy - Vancomycin (Lyphocin)

Nocardial organisms: First choices includetrimethoprim/sulfamethoxazole and tetracycline (Sumycin).

DrainageDrainage



gg Most lung abscesses communicate with the tracheobronchial tree

early in the course of the infection and drain spontaneously during

the course of therapy. Dependent drainage (with appropriate positions based on the pulmonary segment) is commonlyadvocated using chest physical therapy and sometimes

bronchoscopy. Bronchoscopy can also facilitate abscess drainage by aspiration of the appropriate bronchus through the

bronchoscope. Transbronchial drainage by catheterization of theappropriate bronchus under fluoroscopy has been successful.

Generally, augmenting this passive drainage with invasive procedures is unnecessary. In fact, attempts at therapeutic bronchoscopy may sometimes produce adverse consequences.

Reports have been received of bronchoscopy-induced release of large amounts of purulent material from the involved lung segmentinto other parts of the lung, occasionally inducing acute respiratoryfailure, acute respiratory distress syndrome (ARDS), or both.





Approximately one third of lung abscesses

are complicated by empyema. This may be

observed with or without bronchopleural

fistulas. Hemoptysis is a common

complication of a lung abscess and can betreated with bronchial artery embolization.

Occasionally, the hemoptysis can be massive,

thus requiring urgent surgery. Brain abscessmay also be a complication in patients who

receive inadequate treatment.

special features of diagnostics and management of purulent inflammation in children

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