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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

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 .SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS).

. umbilical and urinary catheters.Factors contributing to the increasing incidence of sepsis      chemotherapy and radiation therapy corticosteroid and immunosuppressive therapies diabetics. and intravenous. inhalation equipment. Neonates are more likely to develop sepsis (ex. cancer patients. group B Streptococcal infections). and with granulocyopenia. patients with major organ failure. surgical protheses.

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) .

000/mm3 or > 10% immature (band) cells . < 4.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.

SIRS plus a documented infection site (documented by positive culture for organisms from that site). as is seen commonly after injury to a mucosal surface. or more commonly secondary. to an intravascular or extravascular focus of infection  Sepsis . primary (without an identifiable focus of infection).  Bacteremia may be transient.  Blood cultures do NOT need to be positive.

Sepsis associated with organ dysfunction. Hypoperfusion abnormalities include but are not limited to: ± lactic acidosis. hypoperfusion abnormalities. or hypotension. ± 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 .

and lipotechoic acid fungal cell wall material . and proteases gram-positive bacteria: exotoxins. hemolysins. exotoxins. superantigens (toxic shock syndrome toxin (TSST). streptococcal pyrogenic exotoxin A (SpeA)). peptidoglycans.Microbial triggers of sepsis    gram-negative bacteria: endotoxin. formyl peptides. enterotoxins.

LPS Lysed bacterial protein cells LPS binding LPS-LPS binding Protein complex .

IL-12. IFNgamma Prostaglandins leukotriens Activation of complement cascade Activation of Coagulation cascade DIC MOD Endothelian cell damage . IL-1.macrophage Respiratory Dystress Syndrome TNF. L-6.

cholestatic jaundice Digestive tract. proteinuria Liver. Acute Respiratory Distress Syndrome (ARDS): capillaryleakage into alveoli.Organ Dysfunctions associated with Severe Sepsis and Septic Shock       Lungs: early fall in arterial PO2. hyperpnea Kidneys (acute renal failure): oliguria. anuria. azotemia. tachypnea.nausea.cardiac output is initially normal or elevated. alkaline phosphatase.confusion .elevated levels of serum bilirubin. vomiting. rain . diarrhea and ileus Heart.

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ecthyma gangrenosum .Skin .

2. Immediate Stabilization of the Patient The blood must be rapidly cleared of microorganisms The original focus of infection must be treated .THERAPY: three priorities 1. 3.

circulation). Intubation may also be necessary to deliver higher oxygen concentrations. . epinephrine. breathing. Normal CVP (central venous pressure) is 10-15 cm of 0. The immediate concern for patients with severe sepsis is reversal of life-threatening abnormalities (ABCs: airway. dobutamine. or norepinephrine).Immediate Stabilization of the Patient. In severe sepsis monitoring of the circulation may be necessary. phenylephrine. maintain adequate plasma volume with fluid infusion.9% NaCl. 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. normal PAW (pulmonary arterial wedge pressure) is 14-18 mm Hg. Altered mental status or depressed level of consciousness secondary to sepsis may require immediate protection of the patient's airway.

glycopeptides. aminoglycosides. Antimicrobials that do NOT cause the patient to get worse are: carbapenems. After the appropriate samples are obtained from the patient a regimen of antimicrobials with broad spectrum of activity is needed. ceftriaxone. The early institution of antimicrobials has been shown to decrease the development of shock and to lower the mortality rate. 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. cefepime. Prompt institution of empiric treatment with antimicrobials is essential. .The blood must be rapidly cleared of microorganisms. This is because antimicrobial therapy is almost always instituted before the organisms causing the sepsis are identified. and quinolones.

‡ Community acquired pneumonia a 2 drug regimen is usually utilized. Nosocomial abdominal infection: Imipenem-cilastatin and aminoglycoside or Pipercillin-tazobactam and Amphotericin B. Nosocomial pneumonia: Cefipime or Imipenem-cilastatin and an aminoglycoside. ‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ Usually a third (ceftriaxone) or fourth (cefepime) generation cephalosporin is given with an aminoglycoside. Abdominal infection: Imipenem-cilastatin or Pipercillin-tazobactam and aminoglycoside.The drugs used depends on the source of the sepsis. 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 .

treated.The original focus of infection must be treated. Remove foreign bodies. debride or amputate gangrenous tissues. Remove infected organs. Drain purulent exudate. . particularly for anaerobic infections.

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 .

000 children. The overall prevalence is 1 per 5. Neonatal prevalence is approximately 1 per 1.Hematogenous osteomyelitis   Frequency.  50 % are preschoolaged children .000.

.

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 .

and Enterobacter species. H influenzae. ± Children (aged 4 mo to 4 y): S aureus. adolescents (aged 4 y to adult): S aureus (80%).Bacterial causes of acute hematogenous osteomyelitis: ± Newborns (younger than 4 mo): S aureus. and Enterobacter species. Haemophilus influenzae. ± Children. Enterobacter species. ± Adult: S aureus and occasionally Enterobacter or Streptococcus species . and group A and B Streptococcus species. group A Streptococcus species. group A Streptococcus species.

and Pseudomonas species.Bacterial causes of direct osteomyelitis ± Generally: S aureus. . ± Puncture wound through an athletic shoe: S aureus and Pseudomonas species. Enterobacter species.

 malaise.  myalgia.  inflammation.  anorexia  .Clinical manifestations (1st phase) Acute hematogenous osteomyelitis is often preceded by the signs and symptoms of bacteremia: fever.  cephalgia.

hyperemic.The 2nd phase of the osteomyelitis is the bone: clinical onset of involvement of bone:  restricted motion.  bone tenderness . edematous.  pseudoparalysis. warm. tender.  soft tissue around the inflamed bone which is.

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) .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.

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-

periostitis)  Computed tomographic (CT) scanning can reveal small areas of osteolysis in cortical bone. small foci of gas and minute foreign bodies  . an abscess) and surface abnormalities of bone (e.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.g..

 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). .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.

3.The diagnosis of osteomyelitis requires 2 of the 4 following criteria 1. 4. 2. Pus on aspiration Positive bacterial culture from bone or blood Presence of classic signs and symptoms of acute osteomyelitis Radiographic changes typical of osteomyelitis .

and child abuse .Differential diagnosis  Rheumatic fever  Monoarthritic rheumatoid arthritis  Poliomyelitis  Septic arthritis  Bacterial cellulitis  In newborns and infants in whom osteomyelitis may present as a pseudoparalysis. trauma. cerebral hemorrhage. also consider nervous system disease. scurvy.

± Diagnosis may be delayed because swelling and erythema may not be evident at onset. scalp electrodes. ± Decreased movement (pseudoparalysis) of the affected area may be the only symptom. ± IV sites. Escherichia coli.Features of neonatal osteomyelitis enteric gram-negative bacilli (eg. aureus. and puncture wounds are often predisposing factors. Klebsiella species). . ± S. and group B streptococci are common pathogens.

 Associated arthritis also is common. plain radiographs of newborns often have a lytic area at the time of diagnosis.Features of neonatal osteomyelitis As many as 50% of affected newborns may have multiple bone involvement.  Unlike radiographic findings in older children.  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 .

 clindamycin.  ceftriaxone or ceftazidime  .  vancomycin.Medications The primary treatment for osteomyelitis is parenteral antibiotics that penetrate bone and joint cavities  The usual choice is an antistaphylococcal antibiotic:  nafcillin.

Splinting and cast immobilization are frequently done in children. However.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. . eventually early motion of joints after initial control is important to prevent stiffness and atrophy.

Treatment of neonatal AHO:Shade¶s 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. celery. and cantaloupe juices  . and myrrh (Commiphora molmol)  Juice therapists recommend drinking combinations of carrot.  Liquid garlic extract  Herbs such as echinacea (Echinacea spp. goldenseal (Hydrastis canadensis). Siberian ginseng (Eleutherococcus senticosus).). beet.

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.  negative blood cultures  positive findings on plain x-rays .  looks a systemic reaction and mimics various benign and malignant condition  symptoms for 2 weeks or more.

CHRONIC OSTEOMYELITIS: Clinical Features With progressive osteonecrosis a large mass of dead bone forms and detaches from healthy bone as ³sequestrum´  The living bone surrounding it is known as ³involucrum´  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 ³Antibiotic´ osteomyelitis .

Brodie's abscesses radiolucent with adjacent sclerosis .

anterior and lateral superficies of the thorax Local symptoms: pain. swelling. hyperemia. Etiology: most common-Staphylococcus epidermidis Typical localizations: lumbar area.Neonatal phlegmon     Neonatal phlegmon-acute soft-tissue infections in childhood. . back. toxic and septicopyemic. Types: simple. local rise in temperature.

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.epidermidis. swelling. Staphylococcal organisms (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. local rise in temperature. hyperemia.S. fluctuation) .

Neonatal mastitis .

Neonatal mastitis.Surgical management .

ultraviolet therapy) 7. Passsive and active immunization 4. Desensitization and hormonal therapy 6. Hyperbaric oxygen therapy. Administration of physiotherapeutic procedures (compresses. . warm baths. Symptomatic treatment 5. Intensive infusive therapy of hemostatic dysbalance (IV and IM administration of drugs) 3.Special features of conservative treatment of neonates with acute suppurative infections 1. Anti-bacterial therapy. 2.

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. often with an air-fluid level. Because the development of a cavity requires some amount of prior tissue damage and necrosis. lung abscesses usually begin as a localized pneumonia. chest radiographs reveal one or more cavities. presumably. . Further.

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.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.

Etiology Lung abscesses have numerous infectious causes. lung cavities may not always be due to an underlying infection. 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. Anaerobic bacteria continue to be accountable for most cases.

Factors contributing to lung abscess  Oral cavity disease : Periodontal disease. Drug abuse. Stricture  Generalized sepsis . Multiple trauma  Esophageal disease : Achalasia. Foreign body. Coma. Reflux disease. Malnutrition. Gingivitis  Altered consciousness : Alcoholism. Depressed cough and gag reflex ± Esophageal obstruction  Bronchial obstruction : Tumor. Seizures  Immunocompromised host : Steroid chemotherapy. Anesthesia.

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

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 .

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

CT scan images can also aid in evaluating the extent of bronchial involvement proximal or distal to the abscess. for evaluating the thickness and regularity of the abscess wall. . Chest CT scan images are valuable for demonstrating cavitation within an area of consolidation. and for determining the exact position of the abscess with regard to the chest wall and bronchus.

Lung abscess. X-ray findings X- .

 Pleural effusion  Pleural empyema .

Spontaneous pneumothorax Pyopneumothorax .

quinolones ± Alternatives . aminoglycosides.Penicillin ± Oral therapy . quinolones.Clindamycin. clindamycin.  Gram-positive organisms  ± First choices . amoxicillin (Amoxil)  Gram-negative organisms ± First choices .Vancomycin (Lyphocin)  Nocardial organisms: First choices include trimethoprim/sulfamethoxazole and tetracycline (Sumycin).Trimethoprim/sulfamethoxazole (Septra) Pseudomonal organisms: First choices include aminoglycosides.Clindamycin (Cleocin 3) ± Alternative .Oxacillin (Bactocill).Treatment Antibiotics in lung abscess  Anaerobic organisms ± First choice .Cefuroxime (Ceftin) and clindamycin ± Oral therapy .Penicillins and cephalexin (Biocef) ± Oral therapy .Cephalosporins. metronidazole (Flagyl). nafcillin (Nafcil). . and cephalosporin. and amoxicillin ± Alternatives . cephalexin.

occasionally inducing acute respiratory failure. acute respiratory distress syndrome (ARDS). Dependent drainage (with appropriate positions based on the pulmonary segment) is commonly advocated using chest physical therapy and sometimes bronchoscopy.Drainage  Most lung abscesses communicate with the tracheobronchial tree early in the course of the infection and drain spontaneously during the course of therapy. or both. 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. . Bronchoscopy can also facilitate abscess drainage by aspiration of the appropriate bronchus through the bronchoscope. attempts at therapeutic bronchoscopy may sometimes produce adverse consequences. In fact. Transbronchial drainage by catheterization of the appropriate bronchus under fluoroscopy has been successful. augmenting this passive drainage with invasive procedures is unnecessary.  Generally.

This may be observed with or without bronchopleural fistulas. Brain abscess may also be a complication in patients who receive inadequate treatment. Occasionally.Complications Approximately one third of lung abscesses are complicated by empyema. . Hemoptysis is a common complication of a lung abscess and can be treated with bronchial artery embolization. thus requiring urgent surgery. the hemoptysis can be massive.