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

Burnes, , pancreonecrosis ss

Systemic inflammatory Respound syndrome

(SIRS) ( )

Massive bleeding

Trauma

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

    

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 > 38C or < 36C respiration > 20/min or PaCO2 < 32mm Hg leukocyte count > 12,000/mm3, < 4,000/mm3 or > 10% immature (band) cells

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


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

Severe Sepsis

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

 

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

LPS

Lysed bacterial protein cells

LPS binding

LPS-LPS binding Protein complex

macrophage

Respiratory Dystress Syndrome

TNF, IL-1, IL-12, L-6, IFNgamma

Prostaglandins leukotriens Activation of complement cascade

Activation of Coagulation cascade

DIC MOD
Endothelian cell damage

Organ Dysfunctions associated with Severe Sepsis and Septic Shock



    

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, rain - confusion

Skin - ecthyma gangrenosum

THERAPY: three priorities

1.

2. 3.

Immediate Stabilization of the Patient The blood must be rapidly cleared of microorganisms The original focus of infection must be treated

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.

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. treated.

Remove foreign bodies. Drain purulent exudate, particularly for anaerobic infections. Remove infected organs; debride or amputate gangrenous tissues.

Acute hematogenous osteomyelitis



  

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 bone: 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

     

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%)


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.


Imaging Studies: Radiograph

osteomyelitis of the tibia (X(X-ray)

 periosteal

elevation  medullary lucencies

The involucrum-subperiosteal new bone involucrum-

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


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

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.
S. aureus,

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

Medications
The primary treatment for osteomyelitis is parenteral antibiotics that penetrate bone and joint cavities  The usual choice is an antistaphylococcal antibiotic:


nafcillin,  vancomycin,  clindamycin,  ceftriaxone or ceftazidime



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:Shades AHO:Shade reduction traction

ImmobilizationImmobilization-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

   

Brodies 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 phlegmontreatment

Adyponecrosis

Erysipelas

Neonatal mastitis
   

 

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. 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.

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 phlegmont (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

Lung abscess
A lung abscess is a subacute infection that destroys lung parenchyma. Further, chest radiographs reveal one or more cavities, often with an air-fluid level. Because the development of a cavity requires some amount of prior tissue damage and necrosis, presumably, lung abscesses usually begin as a localized pneumonia.

Classification
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 observed in patients who are predisposed to aspiration or in otherwise healthy individuals, whereas secondary lung abscesses represent complications of a preexisting local lesion such as a bronchogenic carcinoma or a systemic disease (eg, HIV infection) that compromises immune function.

Etiology
Lung abscesses have numerous infectious causes. Anaerobic bacteria continue to be accountable for most cases. These bacteria predominate in the upper respiratory tract and are heavily concentrated in areas of oralgingival disease. Other bacteria involved in lung abscesses are gram-positive and gramnegative organisms. However, lung cavities may not always be due to an underlying infection.

Factors 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

Pathology
Abscesses generally develop in the right lung and involve the posterior segment of the right upper lobe, the superior segment of the lower lobe, or both. This is due to gravitation of the infectious material from the oropharynx into these dependent areas. Initially, the aspirated material settles in the distal bronchial system and develops into a localized pneumonitis. Within 24-48 hours, a large area of inflammation results, consisting of exudate, blood, and necrotic lung tissue. The abscess frequently connects with a bronchus and partially empties.  After pyogenic pneumonitis develops in response to the aspirated infected material, liquefactive necrosis can occur secondary to bacterial proliferation and an inflammatory reaction to produce an acute abscess. As the liquefied necrotic material empties through the draining bronchus, a necrotic cavity containing an air-fluid level is created. The infection may extend into the pleural space and produce an empyema without rupture of the abscess cavity. The infectious process can also extend to the hilar and mediastinal lymph nodes, and these too may become purulent.


Bacteriology of lung abscess

 Gram-negative organisms Bacteroides species Fusobacterium species Proteus species Aerobacter species Escherichia coli  Gram-positive organisms Peptostreptococcus species Microaerophilic streptococcus Clostridium species Staphylococcus species Actinomyces species  Opportunistic organisms Candida species Legionella species

The diagnosis of a typical lung abscess can usually be confirmed based on history and physical examination findings.
 

Evaluation of expectorated sputum Chest radiographs (An area of thick pneumonic consolidation precedes the emergence of the typical cavitary air-fluid form. The distinctive characteristic of lung abscess, the air-fluid level, can only be observed on a chest x-ray film taken with the patient upright or in the lateral decubitus position. In the presence of associated pleural thickening, atelectasis, or pneumothorax, the airfluid level may be obscured.

Chest CT scan images are valuable for demonstrating cavitation within an area of consolidation, for evaluating the thickness and regularity 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. X-ray findings X-

 Pleural effusion

 Pleural empyema

Spontaneous pneumothorax

Pyopneumothorax

Treatment
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 include trimethoprim/sulfamethoxazole and tetracycline (Sumycin).

Drainage


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 commonly advocated 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 the appropriate 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 segment into other parts of the lung, occasionally inducing acute respiratory failure, acute respiratory distress syndrome (ARDS), or both.

Complications
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 be treated with bronchial artery embolization. Occasionally, the hemoptysis can be massive, thus requiring urgent surgery. Brain abscess may also be a complication in patients who receive inadequate treatment.