03. Purulent-inflammatory diseases of lungs, pleura, bones, joints and soft tissue

June 29, 2024
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LECTURE№3

THEME: Purulent-inflammatory diseases of lungs and pleura, bones, joints AND soft tissue.

 

Plan:

1        Purulent-inflammatory diseases of lungs and pleura:

1.1           Bullous Lung Disease.

1.2           Lung Abscess.

1.3           Pneumothorax.

1.4           Pyopneumothorax.

1.5           Empyema.

2        Purulent-inflammatory disease of bones and joints:

2.2  Acute and chronic osteomyelitis.

3        Purulent-inflammatory disease of soft tissue:

3.1           Neonatal phlegmon.

3.2           Neonatal omphalitis.

3.3           Mastitis.

3.4            Perianal and Perirectal Abscess.

 

1. Purulent-inflammatory diseases of lungs and pleura:

1.1. Bullous Lung Disease.

Bullae or blebs are saccular areas of subpleural air within the lung that are believed to result from an air leak from an adjacent alveolus. Generally, the term bleb refers to a smaller air collection and bulla to a larger one. although there are no specific numeric thresholds to distinguish between the use of the two terms. The important functional distinction is that the grossly apparent lesions (bullae) are associated with the loss of adjacent lung parenchyma, whereas this is not true of blebs. Blebs and bullae are not associated with normal alveoli or capillaries; hence, no gas exchange occurs within them, although they do communicate with the tracheobronchial tree (53).

Bullae and blebs are either congenital or acquired. Acquired lesions are usually a consequence of chronic infection related to a problem such as CF, 0±,-antitrypsin deficiency, or another

similar condition. Bullous emphysema is a common form of acquired chronic obstructive pulmonary disease in adults, but this is rarely seen in children. Congenital bullae and blebs apparently result from disordered development of alveoli and terminal airways during organogenesis. The discussion that follows deals principally with blebs and bullae rather than the underlying pulmonary diseases.

The clinical symptoms of blebs and bullae are generally the result of either spontaneous pneumothorax from rupture into the pleural space or exercise intolerance because of diminished lung volumes and inadequate respiratory reserve. The latter problem is generally associated with underlying diffuse lung disease. Plain chest radiographs and CT are usually adequate for definitive imaging. Apical disease is most common, and bilateral disease is frequent. 0±.-Antitrypsin deficiency is unique in its propensity to form basal blebs (54).

The management of blebs and bullae is dependent on the degree of symptomatology and the underlying lung problem. Treatment of smaller lesions is usually limited to problems that result from air leak, specifically pneumothorax. Generally, tube thoracostomy is the appropriate treatment for the first spontaneous pneumothorax. Recurrent pneumothorax occurs in 20% to 50% of patients with congenital bullous disease, and this incidence increases significantly with each additional pneumothorax (55). It is therefore appropriate to consider definitive operative treatment after a first recurrent pneumothorax associated with congenital bullous disease.

The principles for operative management of lung bullae are to remove the area of involvement, to conserve all possible normal lung tissue, and to obtain a secure, airtight closure of the lung. The resections, therefore, generally are not segmental or lobar, but rather nonanatomic in nature (55,56). Resection of bullae with or without pleurodesis is highly effective. Closure of the bleb margin can present problems, but modern stapling devices confer more security and efficiency to this procedure than do traditional suture closure techniques. Therefore, stapled resections are considered routine for this problem. Resection of bullae can be done through either a thoracoscopic approach or an open thoracotomy, with limited morbidity and mortality (55,56,57). The thoracoscopic approach appears to be highly effective, rapid, and less morbid than open thoracotomy. Potential problems with air leak are best prevented by concurrent pleurodesis or pleurectomy.

The outcome after bleb resection is dependent on the amount of remaining lung and the extent of underlying disease. For congenital blebs with a large portion of the normal lung retained, the outcome is predictably excellent. For extensive local disease or for blebs acquired as a consequence of systemic disease, this is more problematic. Specifically, if preoperative evaluation shows that the bullae occupy more than one-third of the ipsilateral thorax, if ventilationBTb’perfusion scan shows little or no function in the area of the bullae, and if pulmonary function studies indicate tolerance for thoracotomy and lung resection, the outcome is much more favorable (55).

 

1.2. Lung Abscess.

Generally, a lung abscess develops when at least one of two fundamental problems exist: (1) a primary failure of host defenses is present, or (2) repeated aspiration of oral or intestinal bacteria into the tracheobronchial tree occurs.. A chronic lung abscess develops with varying degrees of circumferential fibrosis and may involve substantial destruction of parenchyma, usually in a lobar distribution. Typically, the abscess cavity communicates with the normal tracheobronchial tree, and this relation has important diagnostic and treatment implications.

Lung abscesses are typically polymicrobial, with both anaerobic and aerobic bacteria. Since the 1970s, when anaerobic cultures became routine, oral anaerobic organisms have predominated in epidemiologic reviews of causative organisms. Bacteroides sp. group B Ol-hemolytic streptococci. Streptococcus pneumoniae, Escherichia coli, Pseudomonas sp. Proteus sp. and Aerobacter aerogenes ate all important and relatively frequent pathogens in this setting (37,38). This is in contrast to Staphylococcus aureus and Klebsiella pneumoniae, which were the most common and important causes of lung abscesses in Western countries in the 1980s. It remains important, however, to recognize that the latter organisms are both associated with substantial parenchymal lung destruction and are still important pathogens. Both require long-term and aggressive antibiotic treatment.

Secondary and even primary pulmonary infection with a variety of fungal and other organisms may also lead to the development of a lung abscess. Aspergillus, Actinomyces, and Nocardia spp are among these pathogenic organisms. Cavitary tuberculosis was once an important risk factor for the development of secondary pyogenic lung abscesses in adults. Given the worldwide resurgence of tuberculosis, including among children in the United States, it may be worthwhile to recall this experience in coming years.

The clinical presentation of a patient with a lung abscess commonly includes systemic complaints, such as fever, chills, night sweats, anorexia, and weight loss. Nonspecific respiratory symptoms, such as coughing and wheezing, are also frequent. More specific and alarming symptoms, such as a productive cough, fetid sputum, or hemoptysis, are later events associated with suppurative disease and cavitation. These latter findings in particular should lead to a prompt laboratory and imaging evaluation because the physical examination generally yields only nonspecific signs of pulmonary consolidation. The most important examination is generally a plain chest radiograph. A single cavity in a dependent location with an aireTb^fluid level is classic (Fig. 61-13). Predictably, lung abscesses occur in areas of the lung that are dependent. Two-thirds are found in the right lung; the superior segment of the lower lobe and the posterior segment of the upper lobe are most common (37,38). An ambulatory patient is more likely to have involvement of basal segments of the lower lobes because these are dependent on the upright position. Areas of surrounding consolidation, pneumonia, and a thick fibrous wall are all typical, but variable in appearance. It may be impossible to differentiate a lung abscess from an infected cystic lung lesion on radiographs obtained at a single point in time. Generally, sequential films demonstrate resolution of pneumonia or an abscess, whereas congenital cystic lesions remain and become conspicuous. A pneumatocele may develop after treatment of necrotizing pneumonia or a lung abscess and may have a residual cystic appearance; however, these airB”B*filled cavities typically do not have airB”b”fluid levels. In addition, patients generally improve clinically or have no symptoms after treatment when the typical air-filled cavity becomes apparent. CT and MR imaging are both excellent techniques for evaluating intrathoracic mass lesions such as a lung abscess; however, their routine use is not required, and their expense can be substantial.

Endoscopic drainage of a lung abscess into the tracheobronchial tree can be achieved with a variety of needles, catheters, or other instruments passed through rigid or flexible instruments. If possible, this is preferred to other methods of surgical drainage. Intraoperative control of the airway is essential when endoscopic drainage of a lung abscess is performed because the decompression of purulent material into an adjacent bronchus or the contralateral lung may be life threatening if the abscess is sizable. The contralateral lung is best protected either by positioning the involved lung dependently or by selective intubation and balloon exclusion of the normal mainstem bronchus. A flexible endoscope has the advantage of better access to the peripheral airways, whereas a rigid bronchoscope allows the use of larger instruments and provides better visualization and control of the trachea and primary bronchi. The choice is best individualized. Most infants and children require general anesthesia for the initial endobronchial drainage procedure because of the absolute need for control of the airway. Fluoroscopy or ultrasound may provide valuable guidance in localizing the lesion intraoperatively, if necessary. Subsequent drainage or aspiration procedures may be needed, depending on the clinical response.

Transpleural diagnostic aspiration and both open and closed external drainage are all described and appropriate for selected patients. The risks of pleural contamination, empyema, and bronchopleural fistula, however, make these approaches desirable only in circumstances in which the abscess is peripheral in location and chronic enough that the visceral and parietal pleura are adherent. These approaches are best reserved for specific indications in complex abscesses after failure of initial drainage and antibiotics. Regardless of the drainage technique selected, the abscess contents require microbiologic evaluation to identify the organisms involved and to direct subsequent antibiotic therapy. Empiric initial therapy should cover anaerobic organisms, as well as gram-negative organisms and S. aureus. Clindamycin rather than penicillin G is recommended because increasing numbers of resistant oral anaerobes and resistant S. aureus organisms make penicillin therapy prone to failure. Antibiotic therapy is generally required for 6 to 12 weeks, although this depends on the patient’s response and the rate at which the chest radiograph clears (37.38). Most patients with lung abscesses are successfully treated with drainage and antibiotics alone. Patients with underlying immunodeficiencies that can be corrected or modified should have this done. Modulation of immunosuppression drugs in transplant recipients, delay in chemotherapy for oncology patients, treatment with granulocyte colony-stimulating factor, and other similar approaches are appropriate when possible.

Operative management of a lung abscess is reserved for patients with specific related complications. Failure to control the initial infection or recurrent infection, massive or recurrent hemoptysis, bronchopleural fistula, and a persistent cavitary lesion are indications for operative resection of the affected lung. Immunosuppressed patients are at particular risk for these complications. Although a trial of medical therapy is appropriate in immunosuppressed patients, failure is much more probable, and prompt parenchymal resection is often required. The surgical principle that governs management of the complicated lung abscess is that resection of the involved parenchyma is required. This generally takes the form of a formal lobectomy; if done in the face of acute inflammation, this can be a formidable technical challenge. In this circumstance, the bronchial stump closure requires particular care to avoid an air leak and a bronchopleural fistula.

 

1.3. Pneumothorax.

A pneumothorax is an accumulation of air within the pleural space. It may occur spontaneously or as the result of trauma, surgery, or a therapeutic intervention. If the air accumulates under pressure, a tension pneumothorax ensues. A pneumothorax decreases pulmonary volume, compliance, and diffusing capacity. If the pneumothorax is greater than 50% of chest volume, hypoxia may result secondary to ventilation perfusion mismatch. A normal lung can often compensate this for. Spontaneous pneumothorax may occur in children with no known underlying disease or may result from or. in fact, reveal an underlying condition, such as a congenital bleb, pneumonia with pneumatocele or abscess, tuberculosis, or cystic adenomatoid malformation. Traumatic pneumothorax may result from a tear in the pleura, esophagus, trachea, or bronchi. Iatrogenic causes include mechanical ventilation, thoracentesis or central venous catheter insertion, bronchoscopy, or cardiopulmonary resuscitation

The most common presenting symptoms of pneumothorax are ipsilateral chest pain and dyspnea (60.64). Severe dyspnea should alert the surgeon to the presence of a tension pneumothorax. Physical examination may reveal diminished breath sounds on one side of the chest or a shift of the trachea from the suprasternal notch. A pneumothorax is usually detectable on a chest radiograph and is enhanced if the radiograph is taken at end expiration. It is common practice for the size of a pneumothorax to be described as a proportion of the chest field on an upright radiograph. The actual volume loss of the lung is greater than such a description because pulmonary volume is lost in three dimensions. The following formula is used to more accurately estimate this loss:

Symptomatic or large pneumothoraces usually require intervention. Options for treatment of a small pneumothorax include thoracentesis, placement of a unidirectional (Heimlich-type) valve, or placement of a small pigtail catheter .However, if air is continuously aspirated or if the pneumothorax recurs, a standard chest tube should be inserted. A tension pneumothorax poses a surgical emergency and a chest tube should be placed immediately. If a chest tube is not immediately available or if the patient’s condition deteriorates during preparation for placement, a large-bore (14-gauge) needle should be placed in the second intercostal space anteriorly to relieve the tension. If the pneumothorax recurs after tube thoracostomy, or if the air leak persists, further intervention is necessary.

Pleurodesis can be undertaken by instilling chemical agents into the pleural space through a chest tube, by thoracoscopy, or by thoracotomy. Traditionally, thoracotomy has been used for more aggressive interventions such as mechanical pleurodesis. pleurectomy. or resection of lung blebs or cysts. However, thoracoscopy has emerged as a preferred technique by many for all these interventions (80.81.82.83). It allows excellent visualization of the entire pleural space with a low surgical morbidity. It also allows use of a wider range of anesthetic techniques because older children can often undergo thoracoscopic pleurodesis under sedation with intercostal nerve block. The results of thoracoscopic pleurodesis for pneumothorax have been excellent, and complications of the technique are very uncommon.

 

1.4. Pyopneumothorax.

Background: Pleural effusion is defined as the collection of at least 10-20 mL of fluid in the pleural space. Pleural effusion develops because of excessive filtration or defective absorption of accumulated fluid. The presence of pleural effusion may be a primary manifestation or a secondary complication of many disorders.

History: The clinical picture and presenting symptoms depend on the underlying disease and size of the effusion.

  • Often, in parapneumonic effusion or empyema, history of a recent upper respiratory tract infection, bronchitis, or pneumonia exists.

  • Commonly, an initial improvement associated with antibiotics occurs, and then fever and onset of chest pain recurs.

  • Pleurisy causes chest pain, tightness, and shortness of breath. Pain can be referred to the shoulder.

  • Subpulmonic fluid collection can be associated with vomiting, abdominal pain, or abdominal distension caused by partial paralytic ileus.

  • Parapneumonic effusion and empyema usually present with chills, fever, anorexia, tachypnea, and sweating.

  • Accumulation of a small amount of fluid may be asymptomatic.

  • A large collection of fluid leads to dyspnea, respiratory distress, dull pain, and coughing, which may vary with alteration in body position.

  • Malignancy-related effusion often occurs after the diagnosis is established and can be associated with significant and rapid weight loss.

  • Although effusion occurs in association with systemic lupus erythematosus, it is rarely the initial manifestation. Inquiry should be made into exposure to tuberculosis (TB), recent trauma, surgery, and central line placement.

Physical:

  • The patient may look tachypneic and anxious because of pain, discomfort, or hypoxemia.

  • A pleural rub may be the only initial manifestation during the early stage of pleurisy. The rub disappears as more fluid accumulates between the 2 pleural surfaces.

  • Dullness to percussion, decreased air entry, decreased tactile and vocal fremitus, and voice egophony over the effusion all may be present, although difficult to detect in younger children.

  • Large fluid collection causes fullness of the intercostal spaces and diminished chest excursion on the affected side.

  • Excessive unilateral fluid accumulation shifts the mediastinum and displaces the trachea and cardiac apex to the contralateral side.

Causes: In children, infection is the most common cause of pleural effusion. Congenital heart disease (CHD) constitutes the second most common etiology, followed by malignancy.

  • In 1968, Wolf reported 60 cases of empyema in 98 cases of pleural effusion. Of the remaining 38 children in the same series, 34% had nonempyemic parapneumonic effusion, 26% had malignant effusion, and 16% had effusion caused by TB.

  • In a recent Canadian study of 127 children with pleural effusion, Alkrinawi reported the frequency of several types of effusions. Fifty percent of effusions were parapneumonic, 17% were caused by CHD, 10% by malignancy, 9% by renal disease, 7% by trauma, and 6% were associated with other causes.

  • In another North American report of 210 children admitted with pleural effusion, Hardie showed that 68% of the effusions were parapneumonic (50 out of 143 had empyema), 11% were caused by CHD, 5% were caused by malignancy, and 3% were associated with other causes.

  • The types of bacteria causing pleural effusions and their sensitivities to different antibiotics have changed over the years.

    • In Freij’s 1984 review of 227 cases of pediatric parapneumonic effusion and empyema, 76% had positive cultures; S aureus accounted for 29% of cases, S pneumoniae accounted for 22% of cases, and Haemophilus accounted for 18% of cases. Most of the cases of Haemophilus were type B.

    • In Brook’s 1990 series of 72 patients with gross pus and positive cultures from empyema, careful anaerobic cultures were included. A total of 93 organisms were isolated—60 aerobic and 33 anaerobic. H influenzae, S pneumoniae, and S aureus were the predominant aerobic organisms found in association with pneumonia. Anaerobes, including Bacteroides and Fusobacterium, were found frequently, particularly in empyema associated with aspiration pneumonia. Anaerobes also were found in empyema associated with intraoral and subdiaphragmatic abscesses.

    • In Hardie’s more recent 1998 series of 64 children with complicated parapneumonic effusions, 26 had positive cultures (88% were S pneumoniae). It was found that 26% of the S pneumoniae were penicillin-resistant. The decrease in complicated parapneumonic effusion caused by H influenzae is attributed to immunization. The authors speculate that the availability of broad-spectrum antibiotics effective against S aureus may account for the decrease in complicated parapneumonic effusion caused by this organism.

  • Pleural effusion occurs in 8-22% of pulmonary tuberculosis in children. Tuberculous pleural effusion usually is unilateral and associated with an underlying parenchymal disease in almost 60% of the cases.

  • Malignancy-related effusion is associated more often with lymphoblastic lymphoma than with Hodgkin disease.

  • Congenital effusions, including chylothorax, occur in 1 per 10,000-15,000 births.

    • Congenital effusion can be associated with Down syndrome, diaphragmatic hernia, hydrops fetalis, polyhydramnios, and pulmonary hypoplasia.

    • Chylothorax may be congenital or acquired.

      • Acquired chylothorax usually follows surgical trauma to the thoracic duct.

      • Obstruction, thrombosis, or high pressure in the superior vena cava caused by cardiac malformation or Fontan repair of various cardiac anomalies also can cause chylothorax.

  • Unusual intrapleural fluid collections include fluids given via a central venous catheter, which inadvertently has been placed or migrated to an intrathoracic location, and inadequate absorption of cerebrospinal fluid from a ventriculopleural shunt.

  • Other rare causes of pediatric pleural effusion are rupture of a pulmonary hydatid cyst into the pleural space, in association with Lemierre syndrome (postpharyngitis anaerobic sepsis with internal jugular vein thrombophlebitis).

  • Hemothorax can occur as a result of trauma, malignancy, pulmonary infarction, and postpericardiotomy syndrome. Hemothorax has been reported from puncture of the pleura by a costal exostosis. Hemothorax should be suspected if pleural fluid hematocrit is more than 50% of peripheral blood hematocrit.

Lab Studies:

  • Obtain a complete blood count, differential white count, and blood culture initially in a patient suspected of having a pleural effusion.

  • Although nonspecific, the erythrocyte sedimentation rate often is very elevated in children with empyema and may be useful for comparison in the follow-up period.

  • Studies helpful in interpretation of pleural fluid analysis include serum glucose, lactate dehydrogenase (LDH), protein, triglycerides, and electrolytes or pH.

  • Serologic studies may be helpful if specific organisms, such as Mycoplasma, Legionella, or adenovirus, are suspected.

  • Pleural fluid analysis

Imaging Studies:

  • Chest x-ray

  • Ultrasound

  • CT scan

Other Tests:

  • A purified protein derivative (PPD) test should be performed, particularly if risk factors for TB are present. A recent study by Merino reported a sensitivity of 97.4% for more than 5-mm PPD skin test induration in 39 children with tuberculous pleural effusion.

Procedures:

  • Thoracentesis

    • Thoracentesis is recommended for diagnosis of most pleural effusions of sufficient size; however, prospective studies in children are lacking.

    • Thoracentesis often is not performed if the diagnosis is thought to be certain, and the likelihood of empyema or malignancy is low. Such circumstances include small bilateral infiltrates in congestive heart failure or nephrosis or a small parapneumonic effusion in an afebrile child recovering from pneumonia.

    • Thoracentesis should be performed when pleural effusion compromises respiratory status, with empyema or malignancy, or in newborns.

  • Pleural biopsy may be needed in cases of unexplained inflammatory effusion, suspected tuberculosis, or malignancy.

Histologic Findings: N/A

Medical Care: Treatment of the underlying disorder generally is all that is required for effusions caused by renal, cardiac, or rheumatologic diseases.

  • Parapneumonic effusion usually progresses through 3 stages (exudative, fibrinopurulent, organizational). The exudative stage is associated with capillary leak during the first 3 days, the fibrinopurulent stage is associated with bacterial invasion of the pleura from 3-7 days, and the organizational stage is characterized by fibroblast growth occurring from 2-3 weeks if the effusion is not treated properly.

  • Parapneumonic effusion and empyema are treated initially with empiric antibiotics based on the patient’s age and the organisms and sensitivities commonly present in the community. As stated above, the most common cause is S pneumoniae.

    • Antibiotics can be changed if a positive culture is obtained.

    • In a hospitalized patient with complicated parapneumonic effusion, antibiotics are administered intravenously while a thoracostomy tube is present until the patient is afebrile and clearly improving clinically. Oral antibiotics frequently are continued for weeks following these procedures.

Surgical Care: Prospective studies in pediatric parapneumonic effusion and empyema are lacking; much of practice is based on studies in adults and retrospective analysis of series of children. Technologic and pharmacologic advances have provided options and changes in approach. In the early exudative stage, thoracentesis and antibiotics may be effective.

  • Chest tube placement is necessary to drain fluid causing respiratory distress.

    • Some clinicians believe that unorganized parapneumonic effusion or empyema can be treated with antibiotics alone, without the need for chest tube placement.

    • In the late 1960s, Walter et al reviewed their experience of treating 38 children with pleural effusion and 60 with empyema over a period of 15 years. All the patients who had nonempyemic effusions did not require chest tube drainage, and 13 of the 60 patients with empyema needed thoracentesis only, without placement of a chest tube.

    • Murphy et al described 9 children with empyema secondary to S pneumoniae, and 3 of these patients had thoracentesis but did not require chest tubes.

    • Redding et al treated 8 of 15 children with empyema without chest tube drainage. The 7 patients who had chest tube drainage had longer hospital stays and longer durations of parental antibiotics therapy than those who did not have the chest tube.

    • Ginsburg et al reported that 49 of 65 children with H influenza pneumonia had pleural effusion; only 20 of these 49 children required chest tube placement, one required open chest drainage, and the rest did not need chest tube drainage.

    • Recently, Chan et al reviewed their experience of treating 47 children with empyema over 26 years in a Canadian institution. The empyema was divided into acute, fibropurulent, and chronic effusions. Of the patients who had acute empyema, 3 out of 7 did well without chest tube placement. Most of the 39 children with fibropurulent effusions were treated successfully with chest tube, and only 7 of them required decortication for persistent loculation.

    • Criteria for chest tube placement based on pleural fluid characteristics derive mainly from experience in adults and include the following:

      • Frank pus on thoracentesis

      • Organisms seen on Gram stain

      • Pleural fluid pH less than 7 or glucose less than 40

    • As the effusion becomes fibrinopurulent and subsequently organizes, chest tubes often become ineffective because fibrinous strands and loculations divide the pleural space into compartments. Chest ultrasound and CT scan may demonstrate this process. To avoid or treat this condition, fibrinolytic agents have been instilled via the thoracostomy tube. Although streptokinase and urokinase have been used safely in children, concerns about these agents (allergy, in the case of streptokinase, and the possibility of transmission of viral agents from the humaeonatal kidney cells used to produce urokinase) have dampened the enthusiasm for the use of these drugs. Recombinant tissue plasminogen activator may prove useful, but studies are lacking.

  • Open thoracotomy with lysis of adhesions generally has been reserved for cases in which fevers and illness have failed to respond to antibiotics and chest tube drainage, or if drainage of loculated fluid by thoracostomy tubes has not been successful.

  • The advent of video-assisted thoracoscopic surgery (VATS), which allows visualization of the pleural space but is less invasive than open thoracotomy, has made early surgical intervention more attractive. A recent retrospective analysis of early VATS in children compared with the previous practice of thoracentesis, fibrinolytic therapy, and treatment failures (either thoracotomy or VATS) showed that early VATS decreased the number of procedures and hospital days when compared to earlier approaches.

  • Pleural biopsy may be needed in cases of unexplained inflammatory effusion, suspected tuberculosis, or malignancy.

1.5. Empyema.

Empyema refers to the accumulation of infected fluid in the pleural space. In children, this is usually the result of severe pneumonia (97). However, empyema may also result from infection of the retropharyngeal, mediastinal, or paravertebral spaces, thoracic trauma, or an immunocompromised state (97,98). In 1962. the American Thoracic Society described what are now the three classic stages of empyema (99). The first stage, or the exudative stage, is characterized by an accumulation of thin pleural fluid with few cells. The pleura and lung are mobile, and the fluid is amenable to drainage by thoracentesis. This stage may last only 24 to 72 hours. The second stage is the fibrinopurulent stage. Consolidation of infected pleural fluid results in an accumulation of fibrinous material, formation of loculations. and loss of lung mobility. This stage lasts 7 to 10 days. The third stage is the organizing stage. A pleural peel forms secondary to fibroblast proliferation and resorption of fibrin. The lung becomes entrapped, and capillary proliferation extends from the fibrinous peel into the visceral pleura itself. This usually occurs 2 to 4 weeks after the initial development of the empyema.

Before the widespread use of antibiotics, empyema was caused principally by infections of Streptococcus pneumoniae, Streptococcus pyogenes. Staphylococcus aureus, and Haemophilus influenzae. The introduction of sulfapyridine and penicillin decreased the overall incidence of empyema, but S. aureus emerged as the primary offending pathogen. Since the mid-1980s, effective therapy for S. aureus has allowed the emergence of a variety of bacterial organisms, including anaerobic bacteria, as common causes of empyema in children (100):

Contemporary series report a preponderance of H. influenza and Streptococcal species in children . However, some series still report S. aureus as the most common pathogen. Interestingly, a number of these latter series are from developing countries. Children with empyema generally present with fever, cough, respiratory insufficiency, and chest pain. Physical signs may include dullness on chest percussion, tactile and vocal fremitus, decreased breath sounds, rales, and a pleural friction rub. A chest radiograph reveals a thickened pleura in addition to the primary pneumonic process and pleural fluid. Transthoracic ultrasound or chest CT scan are beneficial in assessing the degree of pleural thickening, fluid loculation, and lung consolidation. The diagnosis of empyema is confirmed by thoracentesis. The fluid is characteristically turbid and may be thick during the later stages of the infection. Laboratory analysis reveals a specific gravity greater than 1.016. protein greater than 3 g per dL, lactate dehydrogenase (LDH) greater than 200 U per L. pleural fluid protein/serum protein ratio greater than 0.5, pleural fluid LDH/serum LDH ratio greater than 0.6. and white blood cell count higher than 15.000 per mm3. Fibrin clots may also be present. Once the diagnosis of empyema is made, appropriate antibiotics should be administered based on Gram’s stain and culture of the pleural fluid or sputum. Frequently, however, antibiotics have already been started prior to drainage and the fluid is unrevealing. Complete drainage of the empyema should be accomplished either by thoracentesis or tube thoracostomy. Some children present with such advanced disease that the pleural involvement has passed the exudative stage. In these patients, thoracentesis or even tube drainage may not be adequate to obtain a clinical response. In general, the longer the prehospital or pretreatment illness has persisted, the more likely further interventions will be needed .

In the event that a lung abscess develops, treatment may require pneumonostomy. wedge resection, or lobar resection. Radiographic findings often lag behind clinical response; therefore, they should not be used alone as indications for further intervention. With prompt and adequate treatment, the overall outcome for children with empyema is excellent. Pulmonary function after recovery is usually clinically normal, although some investigators have found mild restrictive or obstructive disease on follow-up spirometry.

2. Purulent-inflammatory disease of bones and joints:

2.1. Acute chronic osteomyelitis.

 

Osteomyelitis, or inflammation of the bone, usually is caused by bacterial infection. Bone infections in children are primarily of hematogenous origin, although cases secondary to penetrating trauma, surgery, or infection in a contiguous site also are seen.

Classification.

    Toxic (adynamic) type

    Septico-pyemic type

    Local

Classification of AHO by localization

    Epiphyseal

    Metaphyseal

    Diaphyseal

    Metadiaphyseal

    Pelvic

    Other localization

Clinical manifestations. Acute hematogenous osteomyelitis is often preceded by the signs and symptoms of bacteremia: fever, inflammation, malaise, cephalgia, myalgia, anorexia. This phase of the illness may last for several days.

The second phase of the disease is the clinical onset of involvement of bone. This gives rise to: restricted motion, pseudoparalysis, soft tissue around the inflamed bone which is, hyperemic, warm, edematous, tender, bone tenderness .

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; it may be more useful than the erythrocyte sedimentation rate.

The erythrocyte sedimentation rate usually is elevated (90%); this finding is clinically nonspecific.

Imaging Studies.

Radiograph.

Magnetic resonance imaging (MRI)

Ultrasonography and computed tomographic (CT)

Histopathologic and microbiologic examination of bone.

Treatment.

Medical care. Osteomyelitis rarely requires emergent stabilization or resuscitation. The primary treatment for osteomyelitis is parenteral antibiotics that penetrate bone and joint cavities.

Optimal antibiotic selection, adequate dose regimen, and a sufficiently prolonged antibiotic course are essential. Initiate antibiotic treatment promptly, preferably after obtaining blood and bone aspirates for culture. Initially, select one or more antimicrobial agents that provide adequate coverage for common pathogens.

Even though Haemophilus influenzae type b (Hib) disease has virtually disappeared from the Hib-immune population, third-generation cephalosporins (eg, cefotaxime, ceftriaxone) are used, in addition to nafcillin or clindamycin. This additional treatment is used commonly in children younger than 3 years. Do not use third-generation cephalosporins alone to treat osteomyelitis, as they are not optimal for treating serious S aureus infections.

Cefuroxime, a second-generation cephalosporin, can be used as a single agent against both S aureus and Hib.

Increasing incidence of penicillin-resistant S pneumoniae warrants the use of a clindamycin and cefotaxime/ceftriaxone combination in infants and children.

When treating neonatal osteomyelitis, consider nafcillin and tobramycin or nafcillin and cefotaxime combinations to provide coverage of bacteria from Enterobacteriaceae family, in addition to group B streptococci and S aureus.

Consider vancomycin as an alternative to clindamycin for empiric therapy in patients living in communities where there is a higher incidence of penicillin resistant S pneumoniae or community-acquired methicillin-resistant S aureus.

Surgical Care. Bone aspiration may be necessary to identify the pathogen. Consider bone biopsy if other diagnoses are possible (eg, tumors). The patient may require repeat aspiration of the bone if fever, pain, and swelling fail to respond promptly, or if radiographs demonstrate significant periosteal elevation or periosteal abscess. Joint aspiration is recommended if signs and symptoms point toward pathology near shoulder or hip joints. This is critical, as arthrotomy is indicated if evidence of hip or shoulder arthritis is present. 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.

Drainage: If there is an open wound or abscess, it may be drained through a procedure called needle aspiration. In this procedure, a needle is inserted into the infected area and the fluid is withdrawn. Deep aspirations or biopsy is much preferred in contrast to often-unreliable surface swabs.

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.

 Complications:

·          Bone abscess

·          Bacteremia

·          Fracture

·          Overlying soft-tissue cellulitis

·          Draining soft-tissue sinus tracts

Prognosis. Despite adequate treatment and appropriate surgical intervention, 5-10% of patients may experience recurrence. Recurrences may lead to chronic osteomyelitis with discharging sinuses and other systemic sequelae.

 

3. Purulent-inflammatory disease of soft tissue:

2.1. Neonatal phlegmon.

Necrotizing fasciitis (NF) is a group of infections that present in any age group as an abrupt, rapidly advancing soft-tissue infection with systemic toxicity and high mortality (1). It is characterized by microbial spread along the fascial planes into deep tissue, which results iecrosis of the superficial tissue.

NF falls under the general category of necrotizing soft tissue infection (NSTI). There are three types of NSTI: 1) NF, 2) necrotizing cellulitis, and 3) myonecrosis

NF is regularly confused with cellulitis because its early clinical presentation is also pain, erythema, and edema. However, cellulitis extends only to the subcutaneous tissue and is poorly demarcated.

Pain in an extremity is usually the presenting symptom. It is extreme and often out of proportion with the physical findings. NF has a propensity for the extremities, but can occur anywhere there is deep fascia (16). In the first 24-48 hours, it is associated with edema, erythema, and warmth of the skin overlying the necrotizing tissue. After that point, the skin will become dusky and discolored. It will develop blisters and bulla over the next seven to ten days. During that time, the discoloration will become sharply demarcated. Its tenderness will also disappear as the superficial nerves experience ischemia (17). This progression is both faster and more severe than that seen in cellulitis or erysipelas (18). If not addressed, NF can quickly progress to multi-organ failure, acute respiratory distress syndrome, renal impairment, coagulopathy, liver abnormalities, and generalized erythroderma (19).

Although the diagnosis of NF is primarily clinical, laboratory workup and imaging may be helpful. Surgical probing and frozen section biopsy are used for diagnosis of NF, but they are invasive and take time to complete. There must be a high index of suspicion for NF to move straight to surgery. Therefore, the most important first steps of medical management are probably the gram stain and cultures of both the blood and the wound, if one is present. This will help guide antibiotic therapy over the course of the disease. In addition, routine blood work such as a CBC and chemistry panels may be helpful.

The mainstays of treatment for NF are intravenous antibiotics and surgical debridement. Surgical debridement is recommended every day until the patient is stable and without signs of infection or sepsis. Debridement should cover the infected area as well as a margin of healthy tissue to prevent reoccurrence of infection. As a result, the patient may need extensive skin grafting to cover the debridement area. During recovery, frequent dressing changes are necessary. Unfortunately, scarring and disfigurement are very common after NF debridement and grafting. In addition, physical therapy and rehabilitation will be needed for those with extensive skin grafts (20).

3.2. Neonatal omphalitis.

Omphalitis is an infection of the umbilical stump. Omphalitis typically presents as a superficial cellulitis that may progress to necrotizing fasciitis, myonecrosis, or systemic disease. The introduction of aseptic umbilical cord care has greatly reduced the occurrence of omphalitis iewborn infants. Omphalitis is predominantly a disease of the neonate, although several cases have been reported in adult patients.

Approximately 85% of cases are polymicrobial in origin. Aerobic bacteria are present in approximately 85% of infections, predominated by Staphylococcus aureus, group A Streptococcus, Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis.

Clinical manifestations

History. A detailed review of the pregnancy, labor, delivery, and the neonatal course is important

Physical. Local disease: Physical signs vary with the extent of disease. Signs of localized infection include the following:

       Purulent or malodorous discharge from the umbilical stump

       Periumbilical erythema

       Edema

       Tenderness

Extensive local disease: The following signs indicate more extensive local disease, such as fasciitis or myonecrosis. These signs also may suggest infection by both aerobic and anaerobic organisms and include the following:

   Periumbilical ecchymoses

   Crepitus

   Bullae

   Progression of cellulitis despite antimicrobial therapy

Systemic disease: Signs of sepsis or other systemic disease are nonspecific and include disturbances of thermoregulation or evidence of dysfunction of multiple organ systems.

Treatment

Treatment of omphalitis (periumbilical edema, erythema, and tenderness) in the newborn includes antimicrobial therapy and supportive care.

Antimicrobial therapy

Include parenteral antimicrobial coverage for gram-positive and gram-negative organisms.

supportive care is essential to survival. These measures include the following:

Provide ventilatory assistance and supplementary oxygen for hypoxemia or apnea unresponsive to stimulation. Administer fluid, vasoactive agents, or both for hypotension. Administration of platelets, fresh frozen plasma, or cryoprecipitate for DIC and clinical bleeding is suggested.

Surgical Care.

Management of necrotizing fasciitis and myonecrosis involves early and complete surgical debridement of the affected tissue and muscle. excision of preperitoneal tissue (including the umbilicus, umbilical vessels, and urachal remnant) is critically important in the eradication of the infection.

Complications

The sequelae of omphalitis may be associated with significant morbidity and mortality. These include necrotizing fasciitis, myonecrosis, endocarditis, portal vein thrombosis, sepsis, septic embolization, and death.

 

3.3. Mastitis.

Inflammation or infection of breast tissue may occur in the neonatal period, this condition referred to as mastitis neonatorum. It typically presents as a subareolar abscess in the second or third week of life manifested by erythema, swelling, tenderness, and occasionally discharge at the location of the breast bud, accompanied by fever and agitation. The responsible microorganism is usually Staphylococcus aureus (6).

The preferred management of mastitis neonatorum includes antibiotics and needle aspiration of any abscesses

Infection and abscess in the postpartum lactating breast is a well-described entity (8). Presentation typically includes local pain, tenderness, erythema, and occasionally purulent discharge. Ultrasound examination can sometimes be helpful to identify abscesses. Treatment employs adequate surgical drainage for abscess formation and antibiotics for cellulitis.

3.4. Perianal and Perirectal Abscess.

Infants are commonly affected with infections and abscesses in the perianal area. Infected diaper rash is the most common cause of superficial abscesses. Staphylococ­cal or gram negative enteric organisms are the most common organisms involved. Deeper abscesses of the anal canal or perirectal tissues arise from crypt infections. These infections are usually caused by enteric and anaerobic organisms.

Clinical Presentation

perianal mass and sitting intolerance. tender, erythematous mass lateral to the anus. fever and malaise

Treatment

Superficial perianal abscesses can be treated with Sitz baths. Typically antibiotics are not required. If the area becomes fluctuant, incision and drainage may be offered. Deeper infections require immediate drainage under general anesthesia along with intravenous antibiotics.

 

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