Subject: Pneumonia in Children Section: Pediatrics Hours: 4 hours. Individual preparation for classes: 2 hours.

Transcription

1 Subject: Pneumonia in Children Section: Pediatrics Hours: 4 hours. Individual preparation for classes: 2 hours. 1. ACTUALITY Pneumonia in children - nonspecific pneumonia based on the infectious toxicosis, respiratory failure, fluid and electrolyte and other metabolic disorders with abnormal changes in all organs and systems of a child's body. Despite the great advances in diagnosis and treatment of respiratory diseases, the condition at the beginning of. Continues grow. Extremely important are pneumonia, which is often noted in the therapeutic practice. Thanks conducted randomized controlled trial (RCT) is review the effectiveness of antibiotic therapy for pneumonia. Every year there improvement of methods and tactics for treatment of pneumonia. 2. THE AIM Learn how to identify the etiologic factors and pathogenic mechanisms of pneumonia children, classify and analyze the typical clinical presentation, diagnose and clinical diagnosis and prescribe appropriate treatment, to forecast and provide preventive recommendations for this disease. 3. EDUCATIONAL OBJECTIVES The student should know: - Pneumonia etiological structure according to age and children pathogenetic factors; - Classification of pneumonia in children; - Clinical signs of respiratory distress in children; - Diagnosis of pneumonia in children, the use of laboratory and instrumental research methods; - The treatment of pneumonia in children; - Prevention and prognosis of pneumonia in children; - Complications of pneumonia in children; - Diagnosis and emergency care for acute respiratory failure in children. The student should be able to: - Collect medical history and physical examination of the patient; - Evaluate the results of paraclinical investigations; - To put and to formulate a diagnosis according to modern classification; - Evaluate the results of X-ray; - Assigned treatment regimen, taking into account the patient's age; - Prescription; - Develop creativity in the laboratory, clinical examination of the child, - Theoretical research on problems of the subject; - Demonstrate the moral and ethical principles of medical specialist and principles of professional subordination;

2 4. INTEGRATION Anatomy Biochemiostry Patholopgic Anatomy Pathoilogic Physiology Microbiology Propedevtics Therapy Radiology Intensive care Anatomical and physiological features of the respiratory system children of different age groups biochemical parameters blood tests. The main pathological changes the respiratory system in children. Mechanisms of inflammation process The methods of sampling and seeding sputum, blood, pleural exudate. Determine microbiological spectrum infectious factors respiratory diseases. Methodology and research semiotics of diseases respiratory system. Methodology of spirometric research. Clinical and medical history laboratory and instrumental complex signs of pneumonia Indications and methods of radiation diagnosis of diseases respiratory tract Signs of respiratory failure varying degrees, causes it development and principles first aid Use knowledge to adequately assess clinical parameters Rate biochemical blood tests Know the stages and dates inflammatory changes for timely and adequate therapy Identify signs of frustration Rate microbiological research To conduct an objective review patient (inspection, palpation, percussion, auscultation) evaluate the results spirometry Identify features pneumonia, forecast further complications Rate radiographs Identify respiratory failure to assess ii the extent to emergency help

3 5. MATERIALS Acute pneumonia - an acute inflammatory disease of the lungs characterized infiltrative changes in lung tissue and respiratory failure. Acute pneumonia is an acute non-specific inflammation of lung tissue, based which is infectious toxicosis, respiratory failure, fluid and electrolyte and other metabolic disorders with abnormal shifts in all organs and systems of children body. According to other views, in pneumonia should be understood as a group of different etiology, pathogenesis and morphological characterization of focal acute infectious and inflammatory lung disease with the obligatory presence of inflammatory vnutrishnoalveolyarnoyi exudation. Over the etiology of acute pneumonia may be bacterial, viral (MS-virus, flu etc.), viral, bacterial, fungal and caused by intracellular pathogens atypical pneumonia (mycoplasma, chlamydia, herpes, cytomegalovirus), protozoa agents. Classification: 1. By location acquired o 1.1 Community-acquired o 1.2 Hospital-acquired 2. By cause o 2.1 Bronchiolitis obliterans organizing pneumonia o 2.2 Chemical pneumonia o 2.3 Aspiration pneumonia o 2.4 Dust pneumonia o 2.5 Necrotizing pneumonia o 2.6 Opportunistic pneumonia o 2.7 Double pneumonia (bilateral pneumonia) o 2.8 Severe acute respiratory syndrome 3. By area of lung affected 4. Clinical Severity - I, II, III, IV, V degree. I level - <50 points, the risk of mortality - 0.1, outpatient treatment; II level points, the risk of mortality - 0.6, outpatient treatment; III level points, the risk of mortality - 2.8, hospitalization; IV degree points, the risk of mortality - 8.2, hospitalization; V level -> 130 points, the risk of mortality , hospitalization; Scores are calculated by the index of severity: Age: <6 months - (25); > 6 months -3 years - (15); 3-15 years - (10). Concomitant diseases: - Congenital heart defects - (+30); - Wasting - (+10); - Immunodeficiency condition - (+10); - Violation of consciousness - (+20); - Shortness of breath - (+20); - Cyanosis - (+15);

4 - Pain in the chest - (+20); - Toxic Encephalopathy - (+30); - Body temperature less than 39 or 36 - (15). Laboratory features: - Leukocytosis - (+20); - Leukopenia - (+10); - Anaemia - (+10); - PH <7,35 - (+30); - BUN> 11 mg / dl - (+20); - Hct <30% - (10); - SaO2 <90% - (20); - Equipment - (20); - Multylobarna infiltration on X-ray - (+15); - Infectious shock -toksychnyy - (40); - Pleural fluid - (+30); - Destruction - (+50). Etiology A specific aetiological agent cannot be identified in 40% to 60% of cases6,7. Viral pneumonia cannot be distinguished from bacterial pneumonia based on a combination of clinical findings. The majority of lower respiratory tract infections that present for medical attention in young children are viral in origin such as respiratory syncytial virus, influenza, adenovirus and parainfluenza virus. Pathogens causing pneumonia Newborns: Group B streptococcus, Escherichia coli, Klebsiella species, Enterobacteriaceae. 1-3 months: Chlamydia trachomatis. Preschool: Streptococcus pneumoniae, Haemophilus influenzae type b, Staphylococcal aureus, Less common: group A streptococcus, Moraxella catarrhalis, Pseudomonas aeruginosa. School: Mycoplasma pneumoniae, Chlamydia pneumoniae. Pathogenesis Pneumonia is characterized by inflammation of the alveoli and terminal airspaces in response to invasion by an infectious agent introduced into the lungs through hematogenous spread or inhalation. The inflammatory cascade triggers the leakage of plasma and the loss of surfactant, resulting in air loss and consolidation. The activated inflammatory response often results in targeted migration of phagocytes, with the release of toxic substances from granules and other microbicidal packages and the initiation of poorly regulated cascades (eg, complement, coagulation, cytokines). These cascades may directly injure host tissues and adversely alter endothelial and epithelial integrity, vasomotor tone, intravascular hemostasis, and the activation state of fixed and migratory phagocytes at the inflammatory focus. The role of apoptosis (noninflammatory programmed cell death) in pneumonia is poorly understood. Pulmonary injuries are caused directly and/or indirectly by invading microorganisms or foreign material and by poorly targeted or inappropriate responses by the host

5 defense system that may damage healthy host tissues as badly as or worse than the invading agent. Direct injury by the invading agent usually results from synthesis and secretion of microbial enzymes, proteins, toxic lipids, and toxins that disrupt host cell membranes, metabolic machinery, and the extracellular matrix that usually inhibits microbial migration. Indirect injury is mediated by structural or secreted molecules, such as endotoxin, leukocidin, and toxic shock syndrome toxin-1 (TSST-1), which may alter local vasomotor tone and integrity, change the characteristics of the tissue perfusate, and generally interfere with the delivery of oxygen and nutrients and removal of waste products from local tissues. On a macroscopic level, the invading agents and the host defenses both tend to increase airway smooth muscle tone and resistance, mucus secretion, and the presence of inflammatory cells and debris in these secretions. These materials may further increase airway resistance and obstruct the airways, partially or totally, causing airtrapping, atelectasis, and ventilatory dead space. In addition, disruption of endothelial and alveolar epithelial integrity may allow surfactant to be inactivated by proteinaceous exudate, a process that may be exacerbated further by the direct effects of meconium or pathogenic microorganisms. In the end, conducting airways offer much more resistance and may become obstructed, alveoli may be atelectatic or hyperexpanded, alveolar perfusion may be markedly altered, and multiple tissues and cell populations in the lung and elsewhere sustain injury that increases the basal requirements for oxygen uptake and excretory gas removal at a time when the lungs are less able to accomplish these tasks. Alveolar diffusion barriers may increase, intrapulmonary shunts may worsen, and ventilation/perfusion (V/Q) mismatch may further impair gas exchange despite endogenous homeostatic attempts to improve matching by regional airway and vascular constriction or dilatation. Because the myocardium has to work harder to overcome the alterations in pulmonary vascular resistance that accompany the above changes of pneumonia, the lungs may be less able to add oxygen and remove carbon dioxide from mixed venous blood for delivery to end organs. The spread of infection or inflammatory response, either systemically or to other focal sites, further exacerbates the situation. Viral infections are characterized by the accumulation of mononuclear cells in the submucosa and perivascular space, resulting in partial obstruction of the airway. Patients with these infections present with wheezing and crackles. Disease progresses when the alveolar type II cells lose their structural integrity and surfactant production is diminished, a hyaline membrane forms, and pulmonary edema develops. In bacterial infections, the alveoli fill with proteinaceous fluid, which triggers a brisk influx of red blood cells (RBCs) and polymorphonuclear (PMN) cells (red hepatization) followed by the deposition of fibrin and the degradation of inflammatory cells (gray hepatization). During resolution, intra-alveolar debris is ingested and removed by the alveolar macrophages. This consolidation leads to decreased air entry and dullness to percussion; inflammation in the small airways leads to crackles. Four stages of lobar pneumonia have been described. In the first stage, which occurs within 24 hours of infection, the lung is characterized microscopically by vascular congestion and alveolar edema. Many bacteria and few neutrophils are present. The

6 stage of red hepatization (2-3 d), so called because of its similarity to the consistency of liver, is characterized by the presence of many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin within the alveoli. In the stage of gray hepatization (2-3 d), the lung is gray-brown to yellow because of fibrinopurulent exudate, disintegration of RBCs, and hemosiderin. The final stage of resolution is characterized by resorption and restoration of the pulmonary architecture. Fibrinous inflammation may lead to resolution or to organization and pleural adhesions. Bronchopneumonia, a patchy consolidation involving one or more lobes, usually involves the dependent lung zones, a pattern attributable to aspiration of oropharyngeal contents. The neutrophilic exudate is centered in bronchi and bronchioles, with centrifugal spread to the adjacent alveoli. In interstitial pneumonia, patchy or diffuse inflammation involving the interstitium is characterized by infiltration of lymphocytes and macrophages. The alveoli do not contain a significant exudate, but protein-rich hyaline membranes similar to those found in adult respiratory distress syndrome (ARDS) may line the alveolar spaces. Bacterial superinfection of viral pneumonia can also produce a mixed pattern of interstitial and alveolar airspace inflammation. Miliary pneumonia is a term applied to multiple, discrete lesions resulting from the spread of the pathogen to the lungs via the bloodstream. The varying degrees of immunocompromise in miliary tuberculosis (TB), histoplasmosis, and coccidioidomycosis may manifest as granulomas with caseous necrosis to foci of necrosis. Miliary herpesvirus, cytomegalovirus (CMV), or varicella-zoster virus infection in severely immunocompromised patients results in numerous acute necrotizing hemorrhagic lesions. Clinical features The clinical diagnosis of pneumonia has traditionally been made using auscultatory findings such as bronchial breath sounds and crepitations in children with cough. However, the sensitivity of auscultation has been shown to be poor and varies between 33 %- 60% with an average of 50 % in children. Tachypnoea is the best single predictor in children of all ages.10 Measurement of tachypnoea is better compared with observations of retractions or auscultatory findings. It is nonetheless important to measure respiratory rate accurately. Respiratory rate should be counted by inspection for 60 seconds. However in the young infants, pneumonia may present with irregular breathing and hypopnea. Investigations Children with bacterial pneumonia cannot be reliably distinguished from those with viral disease on the basis of any single parameter; clinical, laboratory or chest radiograph findings. 1. Chest radiograph Chest radiograph is indicated when clinical criteria suggests pneumonia. It will not identify the aetiological agent. However the chest radiograph is not always necessary if facilities are not available or the pneumonia is mild. 2. Complete white blood cell and differential count This test may be helpful as an increased white blood count with predominance of

7 polymorphonuclear cells may suggest bacterial cause. However, leucopenia can either suggest a viral cause or severe overwhelming infection. 3. Blood culture Blood culture remains the non-invasive gold standard for determining the precise aetiology of pneumonia. However the sensitivity of this test is very low. Positive blood cultures are found only in 10% to 30% of patients with pneumonia15. Even in 44% of patients with radiographic findings consistent with pneumonia, only 2.7% were positive for pathogenic bacteria.16 Blood culture should be performed in severe pneumonia or when there is poor response to the first line antibiotics. 4. Culture from respiratory secretions It should be noted that bacteria isolates from throat swabs and upper respiratory tract secretions are not representative of pathogens present in the lower respiratory tract. Samples from the nasopharynx and throat have no predictive values. This investigation should not be routinely done. 5. Other tests Bronchoalveolar lavage is usually necessary for the diagnosis of Pneumocystis carini infections primarily in immunosuppressed children. It is only to be done when facilities and expertise are available. If there is significant pleural effusion diagnostic, pleural tap will be helpful. Mycoplasma pneumoniae, Chlamydia, Legio nella and Moxarella catarrhalis are difficult organisms to culture, and thus serological studies should be performed in children with suspected atypical pneumonia. An acute phase serum titre of more than 1:160 or paired samples taken 2-4 weeks apart showing four fold rise is a good indicator of Mycoplasma pneumoniae infection. This test should be considered for children aged five years or older with pneumonia. Management I Assessment of severity of pneumonia II Assessment of oxygenation The best objective measurement of hypoxia is by pulse oximetry which avoids the need for arterial blood gases. It is a good indicator of the severity of pneumonia III Criteria for hospitalization Community acquired pneumonia can be treated at home. It is crucial to identify indicators of severity in children who may need admission as failure to do so may result in death. The following indicators can be used as a guide for admission. IV Antibiotic therapy When treating pneumonia clinical, laboratory and radiographic findings should be considered. The age of the child, local epidemiology of respiratory pathogens and sensitivity of these pathogens to particular microbial agents and the emergence of antimicrobial resistance also determine the choice of antibiotic therapy. The severity of the pneumonia and drug costs have also a great impact on the selection of therapy. The majority of childhood infections are caused by viruses and do not require any antibiotic. However, it is also very important to remember that we should be vigilant to choose appropriate antibiotics especially in the initial treatment to reduce further mortality and morbidity. For inpatient management of children with severe pneumonia, the following antibiotic therapy is recommended.

8 1st line drugs: lactams drugs: Benzlypenicillin, Amoxycillin, Ampicillin, Amoxycillin-Clavulanate 2nd line: Cephalosporins : Cefotaxime, Cefuroxime, Ceftazidime, 3rd line: Carbapenem: Imepenam Others Aminoglycosides: Gentamicin, Amikacin If there are no signs of recovery; especially if the patient remains toxic and ill with spiking temperature for hours, a 2nd of 3rd line antibiotic therapy need to be considered. If Mycoplasma or Chlamydia species are the causative agents, a macrolideis the appropriate choice. A child admitted to hospital with severe community acquired pneumonia must receivenparenteral antibiotics. As a rule, in severe cases of pneumonia, combination therapy using a second or third generation cephalasporins and macrolide should be given. Staphylococcal infections and infection caused by Gram negative organisms such as Klebsiella sp are more frequently reported in malnourished children. 8. Respiratory failure Classification of respiratory failure: respiratory failur-1 degree - shortness of breath occurs during usual physical activity; respiratory failur-2 degree -weezing with little physical exertion; respiratory failure-3 level - a significant dyspnea in rest. Acute respiratory failure with pneumonia refers to the diffusion-restrictive type respiratory failure. Classification NAM for young children 1st degree - shortness of breath, tachycardia during exercise (physical Baby load - breastfeeding, scream, excitement) partial pressure of oxygen arterial blood mm Hg. 2nd degree - shortness of breath, tachycardia alone, much of the gain in physical load. Slight cyanosis of the lips, akrotsianoz. Fanning wings of the nose, involvement intercostal spaces during breathing. Lifeless child irritable. The partial pressure of oxygen arterial blood mm 3rd degree - shortness of breath to breaths per minute at rest. Total cyanosis of the skin, mucous. In the act of breathing ancillary muscles involved. Can develop hypoxic encephalopathy (disturbance of consciousness, convulsions). The partial pressure of oxygen - below 50 mmhg General principles of treatment of respiratory failure. Treatment of acute respiratory failure with pneumonia combines the following actions: 1. infants and children with impaired immune status or patients in hospital pneumonia should be prescribed broad-spectrum antibiotics, ampicillin and oxacillin (Kloksatsylin) or cephalosporins. Often shown additional appointment aminoglycosides. In other cases prescribed amoxicillin or erythromycin (for suspected mycoplasma PA etiology of pneumonia). Antibiotics administered parenterally way. 2. Bed rest, nutrition patient through a tube or the PA administration 3. humidified oxygen (40%) when cyanosis, severe respiratory failure or anxiety. 4. Dilution sputum by introducing a sufficient amount of fluid humidifying inhaled air and purpose bromhexine. 5. gammaglobuline for suspected immunodeficiency in a child.

9 6. In the event of severe disease with concomitant acute respiratory failure showing endotracheal intubation and mechanical ventilation. A special place in the restrictive type of acute respiratory failure ranks a condition which can rapidly lead to adverse consequences - a syndrome intrathoracic strain (hard cyst lung pnevmomediastynum, pneumothorax) due to bacterial degradation of lung and diaphragmatic hernia. In a tense pneumothorax occur such paradoxical clinical features: 1. On the inhale lung on the affected side is not increased, but decreased in volume, due to increased intra-pleural pressure and compression of the lungs. 2. inhaling air from damaged lungs due to its compression comes in healthy lung. 3. On the exhale air from the lungs enters the healthy lung damaged, resulting in it increases in volume. The movement of air during inhalation victim with a healthy lung, and under a healthy exhalation of the lung affected is described in the literature as pendulous. 4. The shift of the mediastinum relatively healthy spine toward the lungs, which leads to reduce its surface for gas exchange. Because of the displacement of the mediastinum can happen bend large vessels, leading to cessation of circulation. Treatment involves removal of intrathoracic tension by puncture and (Or) drainage of pleural cavity. Mandatory inhalation of oxygen. Place puncture pleural cavity - the second intercostal gap along the midclavicular line with hydrothorax or hidropnevmotorax - along the middle or posterior axillary at the level of the nipple. Most authors prefer passive pleural decompression oral, citing the fact that the lungs of a child, regardless of the nature of decompression, (Passive or active) finishes for hours, meaning development Board of the normalization of lung ventilation nerfuziynoho ratio. While active thoracostomy has many disadvantages such as the need special adaptations, the relative immobilization of the child, increasing the risk of bleeding in postoperative period. 9. MATERIALS 6.1 Quiz 1. etiological and pathogenetic factors of pneumonia in children. 2. Classification of acute pneumonia in children. 3. Clinical manifestations of respiratory failure in children. 4. Differential diagnosis of pneumonia in children. 5. Clinical management of patients with different clinical variants of pneumonia. 6. Preventing pneumonia complications in her children. 7. Clinical management of patients with different clinical variants of complications of pneumonia in children. 8. Diagnosis of acute pneumonia in children, and use of laboratory instrumental methods; 9. Treatment of acute pneumonia in children. 10. The prevention and prognosis of acute pneumonia in children. 11. Complications of acute pneumonia in children. 12. Diagnostics and emergency treatment of acute respiratory failure in children.

10 6.2 MCQ 6 years old child suffers 2nd week febrilna body temperature, dry cough, there pain in the right side, shortness of breath. An objective examination, obliteration in the lower right chest; percussion - blunting pulmonary tone in the lower case; auscultation - a place blunting breath sharply weakened. Install preliminary diagnosis. A) Pneumothorax B) Bronchitis B) pulmonary atelectasis D) Pleurisy case D) lung tumors 6.3 Case The boy 3 months. there is restlessness, frequent shallow breathing, cough. Objectively: t body - 38,40S, cyanosis nasolabial triangle involving shallow breathing ancillary muscles, BH-60 for 1 min., over lungs- moist rales, heart rate for 1 min., Heart sounds are muffled. Blood: white blood cells g / l; ESR, 22 mm / h. X-ray of the lungs, both lungs focal shadow on the background of intensified bronchopulmonary picture, roots are infiltrated. 1. State the previous diagnosis 2. Plan survey 3. Treatment