Download Purulent-inflammatory diseases of bones, joints and soft tissue

Special features of diagnostics
and management of purulent
inflammation in children.
Plan:
1.
2.
3.
4.
5.
6.
Systemic Inflammatory Response Syndrome (SIRS)
,Sepsis.
Acute hematogenous osteomyelitis.
Chronic osteomyelitis.
Neonatal phlegmon
Neonatal mastitis.
Lung abscess
Overview
The problem of management of suppurative
infections is one of the longest standing in the
history of pediatric surgery. Widespread use of
anti-bacterial madication and consequent
microbial 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
Інфекція
Burnes,
Опіки,
pancreonecrosis
ssпанкреонекроз
Systemic inflammatory
Синдромsyndrome
системної
Respound
запальної
(SIRS)відповіді
(ССЗВ)
Trauma
Травма
Massive
Масивна
bleeding
крововтрата
SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS),
BACTERIAL SEPSIS
Sepsis can be simply defined as a spectrum
of clinical conditions caused by the
immune response of a patient to infection
that is characterized by systemic
inflammation and coagulation.
It includes the full range of response from
systemic inflammatory response (SIRS)
to organ dysfunction to multiple organ
failure and ultimately death
Factors contributing to the
increasing incidence of sepsis
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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, and
intravenous, umbilical and urinary catheters.
The following is the 1992 Consensus Conference's
definitions for diagnosis of SIRS to MODS
– Systemic Inflammatory Response Syndrome
–
–
–
–
(SIRS)
Sepsis
Severe Sepsis
Septic Shock
Multiple Organ Dysfunction Syndrome
(MODS)
Systemic Inflammatory Response
Syndrome (SIRS)

heart rate > 90 beats/minute
 temperature > 38°C or < 36°C
 respiration > 20/min or PaCO2 < 32mm
Hg
 leukocyte count > 12,000/mm3, <
4,000/mm3 or > 10% immature (band)
cells

Sepsis
SIRS plus a documented infection site
(documented by positive culture for organisms
from that site).
 Blood cultures do NOT need to be positive.
 Bacteremia may be transient, as is seen
commonly after injury to a mucosal surface,
primary (without an identifiable focus of
infection), or more commonly secondary, to an
intravascular or extravascular focus of
infection
Severe Sepsis
Sepsis 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 Shock
hypotension despite fluid
resuscitation
plus hypoperfusion abnormalities
Multiple Organ Dysfunction
Syndrome (MODS)
Presence of altered organ function in an
acutely ill patient such that
homeostasis cannot be maintained
without intervention
Microbial triggers of sepsis

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gram-negative bacteria: endotoxin, formyl
peptides, exotoxins, and proteases
gram-positive bacteria: exotoxins,
superantigens (toxic shock syndrome toxin
(TSST), streptococcal pyrogenic exotoxin
A (SpeA)), enterotoxins, hemolysins,
peptidoglycans, and lipotechoic acid
fungal cell wall material
Organ Dysfunctions associated with
Severe Sepsis and Septic Shock
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Lungs: early fall in arterial PO2, Acute
Respiratory Distress Syndrome (ARDS): capillaryleakage into alveoli; tachypnea, hyperpnea
Kidneys (acute renal failure): oliguria, anuria,
azotemia, proteinuria
Liver- elevated levels of serum bilirubin, alkaline
phosphatase, cholestatic jaundice
Digestive tract- nausea, vomiting, diarrhea and ileus
Heart- cardiac output is initially normal or
elevated,
Brain - confusion
Skin - ecthyma gangrenosum
THERAPY: three priorities
Immediate Stabilization of the
Patient
2. The blood must be rapidly cleared
of microorganisms
3. The original focus of infection must
be treated
1.
Immediate Stabilization of the Patient.
The immediate concern for patients with severe sepsis is reversal
of life-threatening abnormalities (ABCs: airway, breathing,
circulation). Altered mental status or depressed level of
consciousness secondary to sepsis may require immediate protection
of the patient's airway. Intubation may also be necessary to deliver
higher oxygen concentrations. Mechanical ventilation may help lower
oxygen consumption by the respiratory muscles and increase oxygen
availibility for other tissues. Circulation may be compromised and
significant decreases in blood pressure may require aggressive
combined empiric therapy with fluids (with crystalloids or colloids)
and inotropes/vasopressors (dopamine, dobutamine, phenylephrine,
epinephrine, or norepinephrine). In severe sepsis monitoring of the
circulation may be necessary. Normal CVP (central venous pressure)
is 10-15 cm of 0.9% NaCl; normal PAW (pulmonary arterial wedge
pressure) is 14-18 mm Hg; maintain adequate plasma volume with
fluid infusion.
The blood must be rapidly cleared of
microorganisms.
Certain antimicrobial agents may cause the patients to get
worse. It is believed that certain antimicobials cause more
LPS to be released cause more problems for the patient.
Antimicrobials that do NOT cause the patient to get worse
are: carbapenems, ceftriaxone, cefepime, glycopeptides,
aminoglycosides, and quinolones.
Prompt institution of empiric treatment with antimicrobials
is essential. The early institution of antimicrobials has been
shown to decrease the development of shock and to lower the
mortality rate. After the appropriate samples are obtained
from the patient a regimen of antimicrobials with broad
spectrum of activity is needed. This is because antimicrobial
therapy is almost always instituted before the organisms
causing the sepsis are identified.
The drugs used depends on the source of the
sepsis.
• Community acquired pneumonia a 2 drug regimen is usually utilized.
•
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Usually a third (ceftriaxone) or fourth (cefepime) generation cephalosporin
is given with an aminoglycoside.
Nosocomial pneumonia: Cefipime or Imipenem-cilastatin and an
aminoglycoside.
Abdominal infection: Imipenem-cilastatin or Pipercillin-tazobactam and
aminoglycoside.
Nosocomial abdominal infection: Imipenem-cilastatin and aminoglycoside
or Pipercillin-tazobactam and Amphotericin B.
Skin/soft tissue: Vancomycin and Imipenem-cilastatin or Piperacillintazobactam
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 or
Meropenem
Nosocomial CNS infection: Meropenem and Vancomycin
The original focus of infection must be
treated.
Remove foreign bodies. Drain purulent
exudate, particularly for anaerobic infections.
Remove infected organs; debride or amputate
gangrenous tissues.
Acute hematogenous
osteomyelitis
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Acute hematogenous osteomyelitis(AHO)-bacterial
infections of bones with subsequent involving of the
surrounding soft-tissue
Antacedent infections -Immunological disbalance widesread by way of bloodstream -hematogenous
abscess in the marrow cavity
The most common pathogen culture is Staphyloccus
aureus
The male: female ratio is 3:2
The most common involving long tubular bones
Hematogenous osteomyelitis

Frequency. The
overall prevalence is
1 per 5,000 children.
 Neonatal prevalence
is approximately 1
per 1,000.

50 % are preschoolaged children
Classification of AHO by clinical
pictures:
 Toxic
(adynamic) type
 Septico-pyemic type
 Local
Pathogenetic stages of AHO

Bone marrow phlegmon
 Periosteal abscess
 Soft tissue phlegmone
 Dermal fistula
Classification of AHO by
localization
•Epiphyseal
•Metaphyseal
•Diaphyseal
•Metadiaphyseal
•Pelvic
•Other localization
Bacterial causes of acute
hematogenous osteomyelitis:
– Newborns (younger than 4 mo): S aureus,
Enterobacter species, and group A and B
Streptococcus species;
– Children (aged 4 mo to 4 y): S aureus, group A
Streptococcus species, Haemophilus influenzae, and
Enterobacter species;
– Children, adolescents (aged 4 y to adult): S aureus
(80%), group A Streptococcus species, H
influenzae, and Enterobacter species;
– Adult: S aureus and occasionally Enterobacter or
Streptococcus species
Bacterial causes
of direct osteomyelitis
– Generally: S aureus, Enterobacter species,
and Pseudomonas species;
– Puncture wound through an athletic shoe:
S aureus and Pseudomonas species.
Clinical manifestations
(1st phase)
Acute hematogenous osteomyelitis is
often preceded by the signs and
symptoms of bacteremia:
fever,
 inflammation,
 malaise,
 cephalgia,
 myalgia,
 anorexia

The 2nd phase of the osteomyelitis is the
clinical onset of involvement of bone:
 restricted
motion,
 pseudoparalysis,
 soft tissue around the inflamed bone
which is, hyperemic, warm,
edematous, tender,
 bone tenderness
Findings at physical
examination
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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 extremity
is involved or pseudoparalysis of limb in
neonates)
Sinus tract drainage (usually a late finding or
one that occurs with chronic infection)
pseudoparalysis
Lab Studies

The WBC count may be elevated, but it
frequently is normal. A leftward shift is
common with increased polymorphonuclear
leukocyte counts
 The C-reactive protein level usually is
elevated and nonspecific
 The erythrocyte sedimentation rate usually
is elevated (90%)

Imaging Studies:
Radiograph
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 10-14 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.
Radiographic image depicting long-bone regions (left labels) and bony changes (right labels)
due to Staphylococcus aureus osteomyelitis occurring in the distal right humerus of a 12month-old infant.
Conrad D A Pediatrics in Review 2010;31:464-471
©2010 by American Academy of Pediatrics
osteomyelitis of
the tibia
(X-ray)
 periosteal
elevation
 medullary
lucencies
The involucrum-subperiosteal new bone
Imaging Studies (osteomyelitis)

Magnetic resonance imaging (MRI) can be
extremely helpful in unclear situations.
Sensitivity ranges from 90-100%
 An ultrasound examination can detect fluid
collections (e.g., an abscess) and surface
abnormalities of bone (e.g., periostitis)
 Computed tomographic (CT) scanning can
reveal small areas of osteolysis in cortical
bone, small foci of gas and minute foreign
bodies
Magnetic resonance image (short T1 inversion recovery pulse sequence) depicting long-bone
regions (left femur) and extensive marrow edema and significant enhancement of the periosteum
and adjacent soft tissues (right femur) due to Staphylococcus aureus osteomyelitis occurring in
the distal right femur of a 26-month-old infant.
Conrad D A Pediatrics in Review 2010;31:464-471
©2010 by American Academy of Pediatrics
Procedures

Needle aspiration: During this test, a needle is
used 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 the
infectious 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).
The diagnosis of osteomyelitis
requires 2 of the 4 following
criteria
1.
2.
3.
4.
Pus on aspiration
Positive bacterial culture from bone or
blood
Presence of classic signs and symptoms
of acute osteomyelitis
Radiographic changes typical of
osteomyelitis
Differential diagnosis

Rheumatic fever
 Monoarthritic rheumatoid arthritis
 Poliomyelitis
 Septic arthritis
 Bacterial cellulitis
 In newborns and infants in whom
osteomyelitis may present as a
pseudoparalysis, also consider nervous system
disease, cerebral hemorrhage, trauma, scurvy,
and child abuse
Features of neonatal
osteomyelitis
– S. aureus,
enteric gram-negative bacilli (eg,
Escherichia coli, Klebsiella species), and group
B streptococci are common pathogens.
– IV sites, scalp electrodes, and puncture wounds
are often predisposing factors.
– Diagnosis may be delayed because swelling and
erythema may not be evident at onset.
– Decreased movement (pseudoparalysis) of the
affected area may be the only symptom.
Features of neonatal osteomyelitis

As many as 50% of affected newborns may
have multiple bone involvement.
 Associated arthritis also is common.
 Unlike radiographic findings in older children,
plain radiographs of newborns often have a
lytic area at the time of diagnosis.
 A significant number of patients develop
permanent sequelae due to involvement of the
adjacent joint and damage to the cartilaginous
growth plate
X-ray findings of neonatal acute
hematogenous osteomyelitis
Treatment
 Medications
 Drainage
 Splinting or cast
immobilization
 Surgery
 Alternative
treatment
Initial Antibiotic Regimens for Patients with Osteomyelitis
Organism
Staphylococcus aureus or
coagulasenegative (methicillinsensitive) Staphylococci
Antibiotic(s) of first choice
Alternative antibiotics
Nafcillin (Unipen), 2 g IV every 6 hours, or First-generation cephalosporin or
clindamycin phosphate (Cleocin
vancomycin (Vancocin)
Phosphate), 900 mg IV every 8 hours
S. aureus or coagulase-negative
(methicillin-resistant) staphylococci
Vancomycin, 1 g IV every 12 hours
Various streptococci (groups A and B Penicillin G, 4 million units IV every 6
β-hemolytic organisms or penicillin- hours
sensitive Streptococcus pneumoniae)
Teicoplanin (Targocid),* trimethoprimsulfamethoxazole (Bactrim, Septra) or
minocycline (Minocin) plus rifampin
(Rifadin)
Clindamycin, erythromycin,
vancomycin or ceftriaxone (Rocephin)
Intermediate penicillin-resistant S.
pneumoniae
Cefotaxime (Claforan), 1 g IV every 6
hours, or ceftriaxone, 2 g IV once daily
Erythromycin or clindamycin
Penicillin-resistant S. pneumoniae
Enterococcus species
Vancomycin, 1 g IV every 12 hours
Ampicillin, 1 g IV every 6 hours, or
vancomycin, 1 g IV every 12 hours
Levofloxacin (Levaquin)
Ampicillin-sulbactam (Unasyn)
Enteric gram-negative rods
Fluoroquinolone (e.g., ciprofloxacin
[Cipro], 750 mg orally every 12 hours)
Third-generation cephalosporin
Serratia species or Pseudomonas
aeruginosa
Ceftazidime (Fortaz), 2 g IV every 8 hours
(with an aminoglycoside given IV once
daily or in multiple doses for at least the
first 2 weeks)
Clindamycin, 600 mg IV or orally every 6
hours
Imipenem (Primaxin I.V.), piperacillintazobactam (Zosyn) or cefepime
(Maxipime; given with an
aminoglycoside)
For gram-negative anaerobes:
amoxicillin-clavulanate (Augmentin) or
metronidazole (Flagyl)
Imipenem
Anaerobes
Mixed aerobic and anaerobic
Organisms
Amoxicillin-clavulanate, 875 mg and 125
mg, respectively, orally every 12 hours
Splinting or cast
immobilization
This may be necessary to immobilize the
affected bone and nearby joints in order to
avoid further trauma and to help the area
heal adequately and as quickly as possible.
Splinting and cast immobilization are
frequently done in children. However,
eventually early motion of joints after
initial control is important to prevent
stiffness and atrophy.
Treatment of neonatal AHO:Shade’s
reduction traction
Immobilization-wide diapering as a
prophylactic management of
acquired dislocation of the hip
Surgical Care

Immediate bone aspiration
 If signs and symptoms do not resolve within
48-72 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 procedures
during which the destroyed bone is scraped
out
Alternative treatment of
Osteomyelitis

General recommendations for the treatment
of infections include increasing vitamin
supplements, such as vitamins A and C.
 Liquid garlic extract
 Herbs such as echinacea (Echinacea spp.),
goldenseal (Hydrastis canadensis), Siberian
ginseng (Eleutherococcus senticosus), and
myrrh (Commiphora molmol)
 Juice therapists recommend drinking
combinations of carrot, celery, beet, and
cantaloupe juices
Complications
 Bone
abscess
 Sepsis
 Fracture
 Overlying soft-tissue cellulitis
 Draining soft-tissue sinus tracts
Further complication of AHO:varus
deformation and limb contraction
Symptomatology of the primary
subacute haematogenous
osteomyelitis
 insidious in onset,
 looks a systemic reaction and mimics
various benign and malignant
condition
 symptoms for 2 weeks or more,
 negative blood cultures
 positive findings on plain x-rays
CHRONIC OSTEOMYELITIS:
Clinical Features

With progressive osteonecrosis a large mass
of dead bone forms and detaches from
healthy bone as “sequestrum”
 The living bone surrounding it is known as
“involucrum”
 The sinus continues to discharge pus and
small pieces of dead bone
CHRONIC OSTEOMYELITIS
X-Ray
Treatment of Chronic
Osteomyelitis:
 removal
of all dead bone (may be
very extensive and require external
fixation and later grafting)
 and long periods of antibiotic
therapy
Serious Complications of Chronic
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
Atypical forms of osteomyelitis

Brodie’s abscess
 Albuminous osteomyelitis
 Sclerosing osteomyelitis
 “Antibiotic” osteomyelitis
Brodie's
abscesses
radiolucent
with
adjacent
sclerosis
Neonatal 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 phlegmon
Neonatal phlegmon
Neonatal phlegmon-surgical
treatment
Neonatal mastitis
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Neonatal mastitis is a local bacterial infection
during 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
Neonatal mastitis.Surgical
management
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. Passive 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.
Special features of surgical methods of
management of acute suppurative
infections in childhood

Operative aproach (wide excision of the infection site)
 Drainage
 Collection of pus for culture
 Special features of surgical management of neonatal
phlegmon (multiple cuts in the zone of the lesion including
the border with healthy tissue and frequent dressing every 6 8 hours)
 Special features of surgical management of neonatal mastitis
depending on clinical type
 Peculiarities of placement and removal of sutures
Pneumothorax
General considerations
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Air within the pleural space
Spontaneous pneumothorax is especially common in male teenagers,
caused for example by rupture of a small lung bubble without any lung
disease
Risk of recurrence is 16% after the first and 80% after the third episode
Pneumothorax may be caused by trauma (lung injured by broken ribs),
a penetrating chest wall injury (sucking chest wound), injury to the
tracheobronchial tree, a severe asthma attack, pulmonary infections
with development of an air fistula, artificial ventilation, resuscitation,
or by a congenital cystic lung disease
Induced by a valve-like mechanism, tension pneumothorax is caused
by increasing accumulation of air within the pleural cavity leading to a
mediastinal shift which develops into a dangerous situation
Signs
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-
Mild dyspnea or no signs in cases of mild
spontaneous pneumothorax
- Chest pain and shortness of breath
- Varying degrees of respiratory distress
- Reduced or absent breath sounds on the side
of the pneumothorax
- In
patients
suffering
from
tension
pneumothorax (in addition to respiratory
insufficiency) hemodynamic deterioration (neck
vein distension in normovolemic patients) occurs
Preoperative work-up

- Chest X-ray (misinterpretation of medial
margin of the scapula with the lung surface)
 - CT scan if necessary
Therapy
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Observation in cases of minimally closed stable pneumothorax. Supplemental
oxygen may be necessary
Chest tube insertion
If significant signs occur insert a chest tube [2nd or 3rd intercostal space in the
midclavicular line (classic technique) or in the midaxillary line at the level of the breast
nipples] to provide a water seal drainage (Bulau drainage)
•
Make a small skin incision with the patient under general anesthetic
•
Perforate the intercostal space slowly via the upper edge of the rib with the tip of
a clamp
•
Remove the clamp and insert the chest tube (reinforced by a trocar) through the
prepared canal
•
Remove the trocar and fix the tube with sutures (size: 3-0 to 1).
A second purse suture is placed to close the skin after the chest tube has been removed
•
Connect the chest tube to the water-sealed drainage system (Bulau system)
•
Induced by breathing movements, air bubbles should pass through the watersealed drainage system
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Operation
- Surgical therapy should be considered under the following
conditions:
•
If the air leak is persistent over a period of 1 week of watersealed drainage
•
If the CT scan shows an underlying lung disease
•
In the case of a second episode
•
If full lung expansion is not possible
Surgical methods
•
Closure of the air leak (suture or stapling with bleb resection) and/or
parietal pleurectomy (apical and anterolateral areas) via thoracotomy or
thoracoscopic surgery. Pulmonary blebs may be overlooked when using just
the thoracoscopic approach
•
In cases of multiple recurrence, intrapleural instillation of tetracycline
(for pain control instill 2% lidocaine into the chest tube 30min beforehand) to
obliterate the pleural cavity (pleurodesis) may beindicated
Postoperative care
Chest tubes may be removed if the lung is fully expanded and drainage
volumes decrease to below 20-50 ml within a 24-h period
Start respiratory exercises and physiotherapy as soon as possible