Pneumonia (handout) Edit.docx

Pneumonia & Community – Acquired Pneumonia Source: 1) Nelson’s Essentials of Pediatrics 8 : Chapter 110 – Pneumonia 2) Nelson’s Textbook of Pediatrics 20 : Chapter 400 – Community-Acquired Pneumonia 3) Lange Current Diagnosis & Treatment : Pediatrics, 23rd Edition, 2016 4) Panduan Diagnosis dan Terapi Edisi 5 IKA Unpad 5) WHO Pocket Book for Hospital Care of Children 2013 6) Revised WHO classification and treatment of childhood pneumonia, 2012 7) Nelson’s Pediatric Antimicrobial Therapy, 2018 (for table of Antimicrobials in bottom of page) INTRODUCTION

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Pneumonia is an infection of the lower respiratory tract that involves the airways and parenchyma, with consolidation of the alveolar spaces. [1] Pneumonia, is defined as inflammation of the lung parenchyma,[2] The term lower respiratory tract infection is often used to encompass bronchitis, bronchiolitis (see Chapter 109), pneumonia, or any combination of the three.[1] o Pneumonitis is a general term for lung inflammation that may or may not be associated with consolidation. [1] o Lobar pneumonia describes pneumonia localized to one or more lobes of the lung.[1] o Atypical pneumonia describes patterns typically more diffuse or interstitial than lobar pneumonia.[1] o Bronchopneumonia refers to inflammation of the lung that is centered in the bronchioles and leads to the production of a mucopurulent exudate that obstructs some of these small airways and causes patchy consolidation of the adjacent lobules.[1] o Interstitial pneumonitis refers to inflammation of the interstitium, which is composed of the walls of the alveoli, the alveolar sacs and ducts, and the bronchioles. [1]Interstitial pneumonitis is characteristic of acute viral infections but may also be a chronic inflammatory or fibrosing process.[1] Lower respiratory tract infections are a major cause of high mortality in disadvantaged areas of the world.[3] The infectious etiologies vary widely by geographical region and by the age of the child.[3] In developed countries the majority of pneumonias are caused by viral agents and bacterial pneumonia is a less common cause.[3] Discrimination between viral and bacterial pneumonia is challenging as neither the white blood cell count nor differential nor the chest radiograph are strong predictors.[3] In areas where the technology is readily available, chest radiography is recommended to establish with certainty the presence of pneumonia.[3]

EPIDEMIOLOGY  Penyebab utama morbiditas dan mortalitas pada anak usia <5 th di seluruh dunia, terutama di negara berkembang.[4]  Pneumonia is the leading cause of death globally among children younger than age 5 yr, accounting for an estimated 1.2 million (18% total) deaths annually (Fig. 400-1).[1] The incidence of pneumonia is more than 10-fold higher (0.29 episodes vs 0.03 episodes),

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and the number of childhood-related deaths from pneumonia ≈2,000 fold higher, in developing than in developed countries (Table 400-1). [2] Fifteen countries account for more than three-fourths of all pediatric deaths from pneumonia.[2] Immunizations have markedly reduced the incidence of pneumonia caused by pertussis, diphtheria, measles, Haemophilus inflenzae type b, and S. pneumoniae.[1]

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Where used, bacilli Calmette-Guérin (BCG) immunization for tuberculosis has also had some impact.[2] Pneumonia is the single largest contributor of childhood mortality worldwide, killing an estimated 1 million children under 5 years of age annually.[1] Risk factors for lower respiratory tract infections include gastroesophageal reflux, neurological impairment (aspiration), immunocompromised states, anatomical abnormalities of the respiratory tract, residence in residential care facilities, and hospitalization, especially in an intensive care unit.[1] Defects in host defenses increase the risk of pneumonia.[1] Di negara industri, epidemi RSV dan atau influenza koinsidensi dengan epidemi S. pneumoniae.[4] Di negara berkembang, infeksi virus sering disertai infeksi sekunder.[4] Usia merupakan prediktor yang baik untuk memperkirakan patogen penyebab pneumonia.[4]  Virus → penyebab utama pneumonia pada anak usia lebih muda (<2 th).[4]  Bakteri → penyebab sebagian besar pneumonia pada anak besar.[4]  Tabel 222 menunjukkan bakteri dan virus yang umum menyebabkan pneumonia pada anak berdasarkan usia.[4]

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Faktor risiko pneumonia pada anak meliputi malnutrisi, berat badan lahir rendah (BBLR), tidak mendapat ASI eksklusif, tidak mendapat imunisasi campak, polusi udara dalam rumah, dan kepadatan hunian.[4]

ETIOLOGY 1. Based on age group Infectious agents that commonly cause community-acquired pneumonia vary by age (Table 110.1). [1]

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Streptococcus pneumonia is the most common bacterial cause of pneumonia (particularly lobar pneumonia) and occurs in children of any age outside the neonatal period. Other common causes include respiratory syncytial virus (RSV) in infants (see Chapter 109), other respiratory viruses (parainfluenza viruses, influenza viruses, human metapneumovirus, adenoviruses) in children younger than 5 years old, and

Mycoplasma pneumoniae in children older than age 5 years.[1]

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M. pneumoniae and Chlamydophila pneumonia are principal causes of atypical pneumonia.[1]

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Chlamydia trachomatis and less commonly Mycoplasma hominis, Ureaplasma urealyticum, and cytomegalovirus (CMV) cause a similar respiratory syndrome in infants 2 weeks to 3 months of age, with subacute onset of an afebrile pneumonia; cough and hyperinflation are the predominant signs.[1]

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These infections are difficult to diagnose and distinguish from each other.[1] In adults these organisms are carried primarily as part of the genital mucosal flora.[1] Women who harbor these agents may transmit them perinatally to newborns.[1] Additional agents occasionally cause pneumonia.[1]  Severe acute respiratory syndrome (SARS) is due to SARS-associated coronavirus (SARS-CoV).[1]  Avian inflenza (bird flu) is a highly contagious viral disease of poultry and other birds caused by influenza A (H5N1). [1] There were outbreaks among humans in Southeast Asia in 1997 and 2003-2004, with high mortality rates.[1] A novel influenza A (H1N1) of swine origin began circulating in 2009.[1] Other etiological agents to consider, based on specific exposure history, include

Staphylococcus aureus and Streptococcus pyogenes (especially after influenza infection), Mycobacterium tuberculosis, Francisella tularensis, Brucella spp.,

Coxiella burnetii, Chlamydophila psittaci, Legionella pneumophila, hantavirus, Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis, and oral flora or gram-negative bacilli (after aspiration).[1]

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Causes of pneumonia in immunocompromised persons include gram-negative enteric bacteria, mycobacteria (M. avium complex), fungi (aspergillosis), viruses (CMV), and

Pneumocystis jirovecii (formerly carinii). [1]Pneumonia in patients with cystic fibrosis is usually caused by S. s aureus in infancy and Pseudomonas aeruginosa or

Burkholderia cepacia in older patients.[1] 2. Based on types and characteristics of agents a) Infectious Bakteri, virus, mikobakterium, dan jamur.[4] Pneumonia is caused by viruses or bacteria.[5] Infectious agents that commonly cause community-acquired pneumonia vary by age (Table 110.1).[2] (1) Bacterial  Bakteri adalah penyebab utama di negara berkembang, yaitu: o Streptococcus pneumoniae (30−50%), o Haemophilus influenzae type b (Hib), o Staphylococcus aureus, o Klebsiella pneumonia.[4]  The most common cause of bacterial pneumonia in children of all ages is S. pneumoniae.[3] 

Streptococcus pneumoniae (pneumococcus) is the most common bacterial pathogen in children 3 wk to 4 yr of age, whereas Mycoplasma pneumonia and Chlamydophila

pneumoniae are the most frequent bacterial pathogens in children age 5 yr and older.[1] In addition to pneumococcus, other bacterial causes of pneumonia in previously healthy children in the United States include group A streptococcus

(Streptococcus pyogenes) and Staphylococcus aureus (see Chapter 181.1 and Table 400-2).[1] 

S. aureus pneumonia often complicates an illness caused by influenza viruses.[1]

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S. pneumoniae, H. influenzae, and S. aureus are the major causes of hospitalization and death from bacterial pneumonia among children in developing countries, although in children with HIV infection, Mycobacterium tuberculosis (see Chapter 215), atypical mycobacteria, Salmonella (see Chapter 198), Escherichia coli (see Chapter 200), and

Pneumocystis jiroveci (see Chapter 244) must be considered.[1]   

The incidence of pneumonia caused by H. influenzae or S. pneumoniae has been significantly reduced in areas where routine immunization has been implemented.[1] Bacterial pneumonia usually follows a viral lower respiratory tract infection.[3] Children at high risk for bacterial pneumonia are those with compromised pulmonary defense systems.[3] For example, children with abnormal mucocilliary clearance, immunocompromised children, children who aspirate their own secretions or while eating, and malnourished children are at increased risk for bacterial pneumonia.[3]

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Immunization status is relevant because children fully immunized against H. influenzae type b and S. pneumoniae are less likely to be infected with these pathogens.[2] Children who are immunosuppressed or who have an underlying illness may be at risk for specific pathogens, such as Pseudomonas spp. in patients with cystic fibrosis (see Chapter 403).[2]

(2) Viral  Viral infection is a common cause of community-acquired pneumonia in children.[3]  Viral pathogens are a prominent cause of lower respiratory tract infections in infants and children older than 1 mo but younger than 5 yr of age.[2]  Viral pneumonia is most common in children younger than 2 years.[3]  Viruses can be detected in 40-80% of children with pneumonia using molecular diagnostic methods.[2]  Virus merupakan penyebab utama di negara maju, yaitu:  RSV → 15–40%,  Virus Influenza A dan B,  Parainfluenza,  Human metapneumovirus,  Adenovirus.[4]  Of the respiratory viruses, respiratory syncytial virus (RSV) (see Chapter 260) and rhinoviruses are the most commonly identified pathogens, especially in children younger than 2 yr of age. [2]  RSV, parainfluenza (1, 2, and 3) viruses, influenza (A an B) viruses, an human metapneumovirus are responsible for the large majority of cases.[3]  However, the role of rhinoviruses in severe lower respiratory tract infection remains poorly defined as these viruses are frequently detected in infections with 2 or more pathogens and among asymptomatic children.[2] Other common viruses causing pneumonia include influenza virus (see Chapter 258), parainfluenza viruses, adenoviruses, enteroviruses, and human metapneumovirus.[2]  Infection with more than 1 respiratory virus occurs in up to 20% of cases.[2] The age of the patient may help identify possible pathogens (Table 400-3).[2]  Lower respiratory tract viral infections are much more common in the fall and winter in both the northern and southern hemispheres in relation to the seasonal epidemics of respiratory viral infection that occur each year. [2]  The typical pattern of these epidemics usually begins in the fall, when parainfluenza infections appear and most often manifest as croup.[2]  Later in winter, RSV, human metapneumovirus, and influenza viruses cause widespread infection, including upper respiratory tract infections, bronchiolitis, and pneumonia.[2]  RSV is particularly severe among infants and young children, whereas influenza virus causes disease and excess hospitalization for acute respiratory illness in all age groups.[2]  Knowledge of the prevailing viral epidemic may lead to a presumptive initial diagnosis.[2]

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Severity of disease, severity of fever, radiographic findings, and the characteristics of cough or lung sounds do not reliably differentiate viral from bacterial pneumonias.[3] Furthermore, viral infections may predispose to bacterial pneumonia.[3] However, substantial pleural effusions, pneumatoceles, abscesses, lobar consolidation with lobar volume expansion, and “round ” pneumonias are generally inconsistent with viral disease.[3]

b) Non-infectious Although most cases of pneumonia are caused by microorganisms, noninfectious causes include aspiration (of food or gastric acid, foreign bodies, hydrocarbons, and lipoid substances), hypersensitivity reactions, and drug- or radiation-induced pneumonitis.[1] The cause of pneumonia in an individual patient is often difficult to determine because direct culture of lung tissue is invasive and rarely performed.[1] Cultures performed on specimens in children obtained from the upper respiratory tract or sputum typically do not accurately reflect the cause of lower respiratory tract infection.[1] With the use of molecular diagnostic testing, a bacterial or viral cause of pneumonia can be identified in 40-80% of children with communityacquired pneumonia.[1] PATHOGENESIS  

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Trauma, anesthesia, and aspiration increase the risk of pulmonary infection.[2] Viral pneumonia usually results from spread of infection along the airways, accompanied by direct injury of the respiratory epithelium, which results in airway obstruction from swelling, abnormal secretions, and cellular debris.[2] The small caliber of airways in young infants makes such patients particularly susceptible to severe infection.[2] Atelectasis, interstitial edema, and ventilation–perfusion mismatch causing significant hypoxemia often accompany airway obstruction.[2] Viral infection of the respiratory tract can also predispose to secondary bacterial infection by disturbing normal host defense mechanisms, altering secretions, and modifying the bacterial flora.[2] Bacterial pneumonia most often occurs when respiratory tract organisms colonize the trachea and subsequently gain access to the lungs, but pneumonia may also result from direct seeding of lung tissue after bacteremia.[2] When bacterial infection is established in the lung parenchyma, the pathologic process varies according to the invading organism.[2] o

M. pneumoniae (see Chapter 223) attaches to the respiratory epithelium, inhibits ciliary action, and leads to cellular destruction and an inflammatory response in the submucosa.[2] As the infection progresses, sloughed cellular debris, inflammatory cells, and mucus cause airway obstruction, with spread of infection occurring along the bronchial tree, as it does in viral pneumonia.[2]

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S. pneumoniae produces local edema that aids in the proliferation of organisms and their spread into adjacent portions of lung, often resulting in the characteristic focal lobar involvement.[2] Group A streptococcus infection of the lower respiratory tract results in more diffuse infection with interstitial pneumonia.[2] The pathology includes necrosis of tracheobronchial mucosa; formation of large amounts of exudate, edema, and local hemorrhage, with extension into the interalveolar septa; and involvement of lymphatic vessels and the increased likelihood of pleural involvement.[2]

S. aureus pneumonia manifests in confluent bronchopneumonia, which is often unilateral and

characterized by the presence of extensive areas of hemorrhagic necrosis and irregular areas of cavitation of the lung parenchyma, resulting in pneumatoceles, empyema, or, at times, bronchopulmonary fistulas.[2] Recurrent pneumonia is defined as 2 or more episodes in a single year or 3 or more episodes ever, with radiographic clearing between occurrences. An underlying disorder should be considered if a child experiences recurrent pneumonia (Table 400-4).[2]

CLINICAL MANIFESTATIONS & FINDINGS  Age is a determinant in the clinical manifestations of pneumonia.[1] o Neonates may have fever or hypoxia only, with subtle or absent physical examination o o

findings (see Chapter 65).[1] With a young infant, apnea may be the first sign of pneumonia.[1] Fever, chills, tachypnea, cough, malaise, pleuritic chest pain, retractions, and apprehension— because of difficulty breathing or shortness of breath—are common in older infants and children.[1]

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Physical examination findings cannot reliably distinguish viral and bacterial pneumonias, but complete physical examination may help identify other foci of disease or associated findings to suggest an etiology.[1]

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Pneumonia is frequently preceded by several days of symptoms of an upper respiratory tract infection, typically rhinitis and cough.[2]

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In viral pneumonia, fever is usually present but temperatures are generally lower than in bacterial pneumonia.[2]

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Tachypnea is the most consistent clinical manifestation of pneumonia.[2]

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Increased work of breathing accompanied by intercostal, subcostal, and suprasternal retractions, nasal flaring, and use of accessory muscles is common.[2]

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Severe infection may be accompanied by cyanosis and lethargy, especially in infants.[2]

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It is often not possible to distinguish viral pneumonia clinically from disease caused by Mycoplasma and other bacterial pathogens.[2]

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Viral pneumonias are generally associated more often with cough, wheezing, or stridor; fever is less prominent than with bacterial pneumonia.[1] Mucosal congestion and upper airway inflammation suggest a viral infection.[1]

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Bacterial pneumonias are typically associated with higher fever, chills, cough, dyspnea, and auscultatory findings of lung consolidation.[1]

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Atypical pneumonia in young infants is characterized by tachypnea, cough, and crackles on auscultation.

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Concomitant conjunctivitis may be present in infants with chlamydial pneumonia.[1] Other signs of respiratory distress include nasal flaring, intercostal and subcostal retractions, and grunting.[1] Asymmetry or shallow breathing may be due to splinting from pain. [1]

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Hyperexpansion, common in asthma but also frequently accompanying viral lower respiratory infections, may cause a low diaphragm seen on a chest x-ray.[1]

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Poor diaphragmatic excursion may indicate hyperexpanded lungs or an inability for expansion due to a large consolidation or effusion. Dullness to percussion may be due to lobar or segmental infiltrates or pleural fluid. [1]

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Auscultation may be normal in early or very focal pneumonia, but the presence of localized crackles, rhonchi, and wheezes may help one detect and locate pneumonia.[1] Distant breath sounds may indicate a large, poorly ventilated area of consolidation or pleural fluid.[1]

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Bacterial pneumonia in adults and older children typically begins suddenly with high fever, cough, and chest pain. Other symptoms that may be seen include drowsiness with intermittent periods of restlessness; rapid respirations; anxiety; and, occasionally, delirium.[2]

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In many children, splinting on the affected side to minimize pleuritic pain and improve ventilation is noted; such children may lie on one side with the knees drawn up to the chest.[2]

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Physical findings depend on the stage of pneumonia. [2] Early in the course of illness, diminished breath sounds, scattered crackles, and rhonchi are commonly heard over the affected lung field. [2] With the development of increasing consolidation or complications of pneumonia such as pleural effusion or empyema, dullness on percussion is noted and breath sounds may be diminished.[2] A lag in respiratory excursion often occurs on the affected side. [2] Abdominal distention may be prominent because of gastric dilation from swallowed air or ileus.[2]

Auscultation of the chest may reveal crackles and wheezing, but it is often difficult to localize the source of these adventitious sounds in very young children with hyperresonant chests.[2]

Abdominal pain is common in lower-lobe pneumonia. The liver may seem enlarged because of downward displacement of the diaphragm secondary to hyperinflation of the lungs or superimposed congestive heart failure.[2]

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Symptoms described in adults with pneumococcal pneumonia may be noted in older children but are rarely observed in infants and young children, in whom the clinical pattern is considerably more variable.

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In infants, there may be a prodrome of upper respiratory tract infection and diminished appetite, leading to the abrupt onset of fever, restlessness, apprehension, and respiratory distress.[1] These infants appear ill, with respiratory distress manifested as grunting; nasal flaring; retractions of the supraclavicular, intercostal, and subcostal areas; tachypnea; tachycardia; air hunger; and often cyanosis.[2]

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Results of physical examination may be misleading, particularly in young infants, with meager findings disproportionate to the degree of tachypnea.[2]

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Some infants with bacterial pneumonia may have associated gastrointestinal disturbances characterized by vomiting, anorexia, diarrhea, and abdominal distention secondary to a paralytic ileus.[2] Rapid progression of symptoms is characteristic in the most severe cases of bacterial pneumonia.[2]

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Sebagian besar pneumonia pada anak menunjukkan gambaran klinis yang ringan sampai sedang sehingga dapat berobat jalan saja.[4] Hanya sebagian kecil anak mengalami pneumonia berat yang mengancam kehidupan dan mungkin terdapat komplikasi, sehingga memerlukan perawatan di rumah sakit/[4] Gambaran klinis pneumonia pada bayi dan anak bergantung pada berat ringan infeksi.[4]  Gejala infeksi umum: demam, sakit kepala, gelisah, malaise, nafsu makan ↓, keluhan gastrointestinal seperti mual, muntah atau diare; kadang-kadang ditemukan gejala ekstraparu.[4]  Pada anak dengan malnutrisi berat, demam jarang terjadi.[4]  Gejala gangguan respiratori: batuk, sesak napas, retraksi dinding dada, takipnea, napas cuping hidung, air hunger, merintih, dan sianosis.[4]  Gambaran klinis pneumonia pada anak malnutrisi berat kurang spesifik dan dapat tumpang tindih dengan sepsis.[4]  Penelitian mengenai validasi tanda klinis WHO menunjukkan bahwa tanda klinis yang direkomendasikan oleh WHO kurang sensitif sebagai prediktor pneumonia dibandingkan dengan gambaran radiologis pada anak malnutrisi berat.[4] Pneumonia bakterial harus dipertimbangkan pada anak usia <3 th yang mengalami panas badan >38,5 °C disertai retraksi dinding dada dan frekuensi napas ≥50×/mnt.[4] o Pneumonia yang disebabkan Pneumoccocus spp. biasanya diawali dengan demam dan napas cepat.[4] Gejala lain yang umum ditemukan adalah kesukaran bernapas, retraksi dinding dada, dan anak tampak tidak sehat (unwell appearance).[4] o Pneumonia yang disebabkan Staphylococcus spp. mempunyai gejala yang sama dengan pneumonia yang disebabkan pneumoccocus, sering ditemukan pada bayi, tetapi dapat ditemukan pada anak yang lebih besar sebagai komplikasi dari influenza.[4] o Pneumonia yang disebabkan Mycoplasma spp. harus dicurigai pada anak usia sekolah yang menunjukkan gejala demam, nyeri sendi, sakit kepala, batuk.[4] o Meskipun penyebab pneumonia sulit ditentukan, tetapi ada beberapa gejala dan tanda yang dapat dikenali secara klinis, yaitu:  Staphylococcus aureus: - Progresivitas penyakit sangat cepat dengan gejala respiratori sangat berat: grunting, sianosis, takipnea, dan gambaran radiologis necrotizing pneumonia, pneumonia dengan komplikasi (efusi pleura, empiema, piopneumotoraks), perburukan klinis dan radiologis yang sangat cepat, atau pada keadaan pascainfeksi campak (saat ini atau 4 mgg sebelumnya).[4] - Pada kulit penderita dapat dijumpai bisul atau abses.[4]  Streptococcus grup A: - Penyebab tersering faringitis, tonsilitis dengan limfadenitis koli, demam, malaise, sakit kepala, dan gejala pada abdomen.[4] - Sering merupakan komplikasi infeksi kulit pada anak dengan varisela.[4] - Penyakit memburuk dalam 24 jam.[4] - Sering diikuti dengan syok septik, empiema, dan pneumatokel yang terjadi

dalam beberapa hr sampai 1 mgg sesudah pengobatan.[4] DIAGNOSIS 1) Anamnesis o Demam tinggi, batuk, gelisah, rewel, dan sesak napas.[4] o Pada bayi, gejala tidak khas, sering kali tanpa demam dan batuk.[4] o Anak besar kadang mengeluh nyeri kepala, nyeri abdomen, disertai muntah.[4] 2) Pemeriksaan Fisis o Manifestasi klinis yang terjadi akan berbeda-beda berdasarkan kelompok usia tertentu.[4] o Neonatus: sering dijumpai takipnea, grunting, pernapasan cuping hidung, retraksi dinding dada, sianosis, dan malas menetek.[4] o Bayi yang lebih besar: jarang ditemukan grunting.[4] Gejala lain yang sering terlihat adalah batuk, panas, dan iritabel.[4] o Anak prasekolah, selain gejala di atas, dapat ditemukan batuk produktif/nonproduktif, dan dispnea Anak sekolah dan remaja, gejala lainnya yang dapat dijumpai yaitu nyeri dada, nyeri kepala, dehidrasi, dan letargi o Takipnea berdasarkan WHO: - Usia <2 bl → ≥60×/mnt, - Usia 2–<12 bl → ≥50×/mnt, - Usia 1–5 th → ≥40×/mnt.[4] o Takipnea terbukti memiliki sensitivitas dan spesifisitas yang tinggi dalam mendiagnosis pneumonia.[4] o Menurut WHO derajat berat pneumonia pada anak usia 2 bl–5 th seperti Tabel 223 di bawah ini :[4]

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Auskultasi → fine crackles (ronki basah halus) yang khas pada anak besar, mungkin tidak ditemukan pada bayi.[4] Iritasi pleura akan menyebabkan nyeri dada; bila berat gerakan dada tertinggal waktu inspirasi, anak berbaring ke arah yang sakit dengan kaki fleksi.[4] Rasa nyeri dapat menjalar ke leher, bahu, dan perut.[4]

3) Pemeriksaan Penunjang : Laboratories & Imaging Studies a) Radiology o Frontal and lateral radiographs are required to localize disease and adequately visualize retrocardiac infiltrates; they are recommended for diagnosis among hospitalized children but are not necessary to confirm the diagnosis in well-appearing outpatients.[1]

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Foto Rontgen toraks proyeksi posterior-anterior (PA) merupakan dasar diagnosis utama pneumonia.[4] Foto lateral dibuat bila diperlukan informasi tambahan (tidak rutin dilakukan).[4] Untuk negara berkembang foto Rontgen toraks secara rutin tidak direkomendasikan terutama pneumonia yang tidak memerlukan perawatan di rumah sakit.[4] Indikasi spesifik foto Rontgen toraks adalah pneumonia sangat berat, dugaan komplikasi pneumonia (misal efusi pleura), atau tidak berespons terhadap terapi yang diberikan, dan kecurigaan LTBI.[4] Indikasi tambahan lainnya adalah gejala atipikal dan pemantauan pada anak dengan kolaps lobar atau gejala yang berlanjut.[4] An infiltrate on chest radiograph (posteroanterior and lateral views) supports the diagnosis of pneumonia; the film may also indicate a complication such as a pleural effusion or empyema.[2]

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Viral pneumonia is usually characterized by hyperinflation with bilateral interstitial infiltrates and peribronchial cuffing (Fig. 400-2).[2]  Confluent lobar consolidation is typically seen with pneumococcal pneumonia (Fig. 400-3).[2] The radiographic appearance alone is not diagnostic, and other clinical features must be considered.[2] Repeat chest radiographs are not required for proof of cure for patients with uncomplicated pneumonia.[2]

Pemeriksaan foto Rontgen toraks ulang hanya dilakukan bila pada foto sebelumnya didapatkan lobar collapse, gambaran round pneumonia, atau bila gejala menetap atau memburuk[4] Pada bayi dan anak yang kecil, gambaran radiologis sering tidak sesuai dengan gambaran klinis.[4]

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Some experts suggest that a chest radiograph may not be necessary for older children with suspected pneumonia (cough, fever, localized crackles, or decreased breath sounds) who are well enough to be managed as outpatients.[2]

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Although there are characteristic radiographic findings of pneumonia, radiography alone cannot provide a definitive microbiologic diagnosis.[1]  Bacterial pneumonia characteristically shows lobar consolidation or a round pneumonia, with pleural effsion in 10-30% of cases (Fig. 110.1).[1]  Viral pneumonia characteristically shows diffuse, streaky infiltrates of bronchopneumonia (Fig. 110.2) and hyperinflation.[1]

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Atypical pneumonia, as with M. pneumoniae and C. pneumoniae, shows increased interstitial markings or bronchopneumonia.[1]

Foto Rontgen toraks tidak dapat membedakan antara pneumonia bakteri dan pneumonia virus.[4] Gambaran radiologis yang klasik dapat berupa:

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Konsolidasi lobar atau segmental disertai air bronchogram, biasanya disebabkan infeksi Pneumoccocus spp. atau bakteri lain.[4] Pneumonia interstisial, biasanya karena virus atau mikoplasma; gambaran berupa corakan bronkovaskular bertambah, peribronchial cuffing, dan overaeration; bila berat terjadi patchy consolidation karena atelektasis.[4] Gambaran difus bilateral, corakan peribronkial bertambah, dan 14nfiltrate halus sampai ke perifer.[4] Gambaran pneumonia karena S. aureus biasanya menunjukkan pneumatokel.[4]

Chest radiographs may be normal in early pneumonia, with infiltrates appearing during treatment as hydration is restored.[1] Hilar lymphadenopathy is uncommon with bacterial pneumonia but may be a sign of tuberculosis, endemic mycoses, autoimmune conditions, or an underlying malignant neoplasm.[1] Decubitus views or ultrasound should be used to assess the size of pleural effusions and whether they are freely mobile.[1] Computed tomography (CT) is used to evaluate serious disease, lung abscesses, bronchiectasis, and effsion characteristics.[1] Unusual etiologies or recurrent pneumonias require special considerations (Table 110.2).[1] Lung abscesses, pneumatoceles, and empyema may require surgical management.[1]

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Point-of-care use of portable or handheld ultrasonography is highly sensitive and specific in diagnosing pneumonia in children by determining lung consolidations and air bronchograms or effusions.[2]

b) Laboratory Studies (Laboratorium)  Bacterial flora of the upper respiratory tract do not accurately reflect flora present in lower respiratory tract infections, and high-quality sputum is rarely obtainable from children. [1]

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In otherwise healthy children without life-threatening disease, invasive procedures to obtain lower respiratory tissue or secretions are seldom indicated.[1]

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Serological tests are not useful for the most common causes of bacterial pneumonia. The white blood cell (WBC) count with viral pneumonias is often normal or mildly elevated, with a predominance of lymphocytes, whereas with bacterial pneumonias the WBC count is elevated ( >15-20,000/mm3), with a predominance of neutrophils. Mild eosinophilia is characteristic of infant C.

trachomatis pneumonia. [1]

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Blood cultures should be performed on ill, hospitalized children to attempt to diagnose a bacterial cause of pneumonia. Blood cultures identify a bacterial respiratory pathogen in 5-10% of children hospitalized for pneumonia (and 10-20% of those with pneumonia with empyema or large effsion). Urinary antigen tests are especially useful for L. pneumophila (Legionnaires disease).[1]

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The peripheral white blood cell (WBC) count can be useful in differentiating viral from bacterial pneumonia.[2] o In viral pneumonia, the WBC count can be normal or elevated but is usually not higher than 20,000/mm3, with a lymphocyte predominance.[2] o Bacterial pneumonia is often associated with an elevated WBC count, in the range of 15,00040,000/mm3, and a predominance of granulocytes. A large pleural effsion, lobar consolidation, and a high fever at the onset of the illness are also suggestive of a bacterial etiology. [2]

o

Jumlah leukosit >15.000/µL dengan dominasi neutrofil sering didapatkan pada pneumonia bakteri, tetapi dapat pula karena pneumonia nonbakteri.[4]

o

Atypical pneumonia caused by C. pneumoniae or M. pneumoniae is difficult to distinguish from pneumococcal pneumonia on the basis of radiographic and laboratory findings, and although pneumococcal pneumonia is associated with a higher WBC count, erythrocyte sedimentation rate, procalcitonin, and C-reactive protein level, there is considerable overlap, particularly with adenoviruses and enteroviruses.[2]

Viral respiratory pathogens can be diagnosed using polymerase chain reaction (PCR) or rapid viral antigen detection, but neither can rule out concomitant bacterial pneumonia.[1]

M. pneumoniae can be confimed by Mycoplasma PCR. CMV pneumonitis can be diagnosed with

PCR from bronchoalveolar lavage fluid. The diagnosis of M. tuberculosis is established by the tuberculin skin test, serum interferon-gamma release assay or analysis of sputum or gastric aspirates by culture, antigen detection, or PCR.[1]



The need to establish an etiological diagnosis of pneumonia is greater in immunocompromised patients, patients with recurrent pneumonia, or those with pneumonia unresponsive to empirical therapy. For these patients, bronchoscopy with bronchoalveolar lavage and brush mucosal biopsy, needle aspiration of the lung, and open lung biopsy are methods of obtaining material for microbiologic diagnosis.[1]



The definitive diagnosis of a viral infection rests on the isolation of a virus or detection of the viral genome or antigen in respiratory tract secretions.[2] Reliable DNA or RNA tests for the rapid detection of many respiratory pathogens, such as mycoplasma, pertussis, and viruses, including RSV, parainfluenza, influenza, and adenoviruses, are available and accurate.[2] Serologic techniques can also be used to diagnose a recent respiratory viral infection but generally require testing of acute and convalescent serum samples for a rise in antibodies to a specific viral agent.[2] This diagnostic technique is laborious, slow, and not generally clinically useful because the infection usually resolves by the time it is confirmed serologically.[2] Serologic testing may be valuable as an epidemiologic tool to define the incidence and prevalence of the various respiratory viral pathogens.[2] Patient peripheral cell gene expression patterns determined by microarray reverse transcription polymerase chain reaction is an emerging technology that may help differentiate viral from bacterial causes of pneumonia.[2]



When there is a pleural effusion or empyema, a thoracentesis to obtain pleural flid can be diagnostic and therapeutic.[1] Evaluation diffrentiates between empyema and a sterile parapneumonic effsion caused by irritation of the pleura contiguous with the pneumonia.[1] Gram stain, bacterial culture, or broad-range bacterial PCR may lead to microbiologic diagnosis.[1] The pleural fluid can also be cultured for mycobacteria and fungi.[1] Removal of grossly purulent pleural fluid reduces the patient’s toxicity and associated discomfort and may facilitate more rapid recovery.[1] Drainage of large pleural accumulations also improves pulmonary mechanics and gas exchange by increasing the ability of the lung to expand.[1]



The definitive diagnosis of a bacterial infection requires isolation of an organism from the blood, pleural fluid, or lung.[2]



Diagnosis pasti pneumonia bakterial yaitu dengan isolasi mikroorganisme dari paru, cairan pleura, atau darah.[4]



Culture of sputum is of little value in the diagnosis of pneumonia in young children, while percutaneous lung aspiration is invasive and not routinely performed.[2]



Pengambilan spesimen dari paru sangat invasif dan tidak rutin diindikasikan dan dilakukan.[4]



Cold agglutinins at titers >1 : 64 are found in the blood in ≈50% of patients with M. pneumoniae infections. [2]Cold agglutinin findings are nonspecific because other pathogens such as influenza viruses may also cause increases.[2]



Acute infection caused by M. pneumonia can be diagnosed on the basis of a positive polymerase chain reaction test result or seroconversion in an IgG assay.[2] Serologic evidence, such as the antistreptolysin O titer, may be useful in the diagnosis of group A streptococcal pneumonia.[2]



Pemeriksaan C-reactive protein perlu dipertimbangkan pada pneumonia dengan komplikasi dan dapat bermanfaat untuk melihat respons antibiotic.[4] Tidak dapat membedakan pneumonia akibat virus atau bakteri.[4]



c) Pemeriksaan mikrobiologis o Pemeriksaan biakan darah harus dilakukan pada semua anak yang dicurigai menderita pneumonia bakteri, pneumonia berat, pneumonia dengan komplikasi.[4]

  

Hasil (+) hanya didapatkan pada 10–30% kasus.[4] Kultur darah hanya (+) pada 10−30% kasus.[4] Blood culture results are positive in only 10% of children with pneumococcal pneumonia and are not recommended for nontoxic appearing children treated as an outpatient.[2] Blood cultures are recommended for those who fail to improve or have clinical deterioration, in those with complicated pneumonia (Table 400-5) and those requiring hospitalization.[2]

d) Pemeriksaan sputum o Walaupun kurang berguna, tetapi jika anak memungkinkan untuk mengeluarkan sputum, periksa preparat gram.[4] o Rapid test untuk deteksi antigen bakteri mempunyai spesifisitas dan sensitivitas rendah. Saat ini di RSHS tidak tersedia dan tidak dilakukan.[4] e) Pulse oxymetri o Pengukuran saturasi O2 merupakan pemeriksaan noninvasive yang dapat memperkirakan oksigenasi arteri.[4] o Semua anak yang dirawat inap karena pneumonia seharusnya diperiksa pulse oxymetri.[4] o Pemeriksaan ini sangat dianjurkan untuk negara berkembang dengan keterbatasan sarana untuk mendeteksi hipoksemia.[4] DIFFERENTIAL DIAGNOSIS  Pneumonia must be differentiated from other acute pulmonary diseases, including allergic pneumonitis, asthma, and cystic fbirosis; cardiac diseases, such as pulmonary edema caused by heart failure; and autoimmune diseases, such as certain vasculitides and systemic lupus erythematosus.[1]



Radiographically pneumonia must be differentiated from lung trauma and contusion, hemorrhage, foreign body aspiration, and sympathetic effusion due to subdiaphragmatic inflammation.[1]

MANAGEMENT & TREATMENT  Therapy for pneumonia includes supportive and specific treatment and depends on the degree of illness, complications, and knowledge of the infectious agent likely causing the pneumonia.[1] Most cases of pneumonia in healthy children can be managed on an outpatient basis.[2]



However, children with hypoxemia, inability to maintain adequate hydration, or moderate to severe respiratory distress should be hospitalized.[1]



Table 400-5 notes the indications for admission to a hospital. [2]



Hospitalization should be considered in infants under 6 months with suspected bacterial pneumonia, those in whom there is a concern for a pathogen with increased virulence (e.g., methicillin-resistant S. aureus), or when concern exists about a family’s ability to care for the child and to assess symptom progression.[1]



Because viruses cause many community-acquired pneumonias in young children, not all children require empiric antibiotic treatment for pneumonia. [1]



Recommended therapies in those without recent antibiotic exposure are listed in Table 110.1.[1] Exceptional situations include lack of response to empiric therapy, unusually severe presentations, nosocomial pneumonia, and immunocompromised children susceptible to infections with opportunistic pathogens (Table 110.3).[1]



Presumed pneumococcal pneumonia can be treated with high-dose ampicillin therapy even with high-level penicillin resistance.[1]



Ceftriaxone and/or vancomycin can be used if the isolate shows high-level resistance and the patient is severely ill.[1]



For infants 2-18 weeks old with afebrile pneumonia most likely caused by C. trachomatis, a macrolide is the recommended treatment.[1]



Oseltamivir or zanamivir should be used if influenza is identified or suspected, ideally within 48 hours of symptom onset.[1]



Treatment of suspected bacterial pneumonia is based on the presumptive cause and the age and clinical appearance of the child.[2]



For mildly ill children who do not require hospitalization, amoxicillin is recommended. With the emergence of penicillin-resistant pneumococci, high doses of amoxicillin (80-90 mg/kg/24 hr) should be prescribed unless local data indicate a low prevalence of resistance.[2]

 

Therapeutic alternatives include cefuroxime axetil and amoxicillin/clavulanate.[2]



In adolescents, a respiratory floroquinolone (levoflxacin, moxiflxacin) may be considered as an alternative.[2]



Despite substantial gains over the past decade, in developing countries only ≈60% of children with symptoms of pneumonia ( ≈50% in sub-Saharan Africa) are taken to an appropriate caregiver, and less than one-third receive antibiotics. [2]

For school-age children and in children in whom infection with M. pneumoniae or C. pneumoniae is suggested, a macrolide antibiotic such as azithromycin is an appropriate choice.[2]



The World Health Organization and other international groups have developed systems to train mothers and local healthcare providers in the recognition and treatment of pneumonia.[2]



The empiric treatment of suspected bacterial pneumonia in a hospitalized child requires an approach based on the clinical manifestations at the time of presentation.[2] In areas without substantial high-level penicillin resistance among S. pneumoniae, children who are fully immunized against H. inflenzae type b and S. pneumoniae and are not severely ill should receive ampicillin or penicillin G.[2] For children who do not meet these criteria, ceftiaxone or cefotaxime should be used.[2]



If clinical features suggest staphylococcal pneumonia (pneumatoceles, empyema), initial antimicrobial therapy should also include vancomycin or clindamycin.[2]



If viral pneumonia is suspected, it is reasonable to withhold antibiotic therapy, especially for those patients who are mildly ill, have clinical evidence suggesting viral infection, and are in no respiratory distress. However, up to 30% of patients with known viral infection, particularly inflenza viruses, may have coexisting bacterial pathogens.[2] Therefore, if the decision is made to withhold antibiotic therapy on the basis of presumptive diagnosis of a viral infection, deterioration in clinical status should signal the possibility of superimposed bacterial infection, and antibiotic therapy should be initiated.[2]



The optimal duration of antibiotic treatment for pneumonia has not been well-established in controlled studies.[2] However, antibiotics should generally be continued until the patient has been afebrile for 72 hr, and the total duration should not be less than 10 days (or 5 days if azithromycin is used).[2] Shorter courses (5-7 days) may also be effctive, particularly for children managed on an outpatient basis, but further study is needed.[2]



Available data do not support prolonged courses of treatment for uncomplicated pneumonia. In developing countries, oral zinc (10 mg/day for <12 mo, 20 mg/day for ≥12 mo) reduces mortality among children with clinically defied severe pneumonia.[2]



Tatalaksana Pneumonia Berat o Rawat di rumah sakit o Pemberian oksigen bila saturasi O2 <90% o Tatalaksana patensi jalan napas o Pemberian antibiotic o Terapi demam



Perawatan Umum di Rumah Sakit o Terapi oksigen 

Bayi dan anak yang mengalami hipoksia mungkin tidak tampak sianosis



Agitasi mungkin menjadi indikasi hipoksia



Oksigen diberikan pada penderita dengan saturasi oksigen <90% pada udara kamar untuk mempertahankan saturasi oksigen ≥90%, dan pada penderita dengan distres napas

o Analgetik antipiretik Anak yang terkena infeksi saluran respiratori bagian bawah akut

umumnya mengalami pireksia dan dapat merasakan nyeri seperti nyeri kepala, nyeri dada, nyeri sendi, nyeri perut, dan nyeri telinga. o Terapi Cairan 

Anak yang tidak mampu mempertahankan asupan cairan akibat sesak atau kelelahan memerlukan terapi cairan



Pipa nasogastrik dapat memengaruhi pernapasan dan karena itu harus dihindari pada anak yang sakit berat, terutama bayi dengan lubang hidung yang kecil.



Penderita yang muntah-muntah atau sakit berat memerlukan cairan i.v.



Bila diperlukan, cairan i.v. diberikan 80% dari kebutuhan basal dan perlu dipantau elektrolit serum.

o Pemberian antibiotik 

Antibiotik empiris diberikan berdasarkan usia penderita dan derajat penyakit.



Antibiotik yang sesuai harus diberikan segera sesudah penderita masuk rumah sakit.



Untuk pneumonia atau bukan pneumonia berat dapat diberikan kotrimoksazol (8 mg/kgBB/dosis trimetoprim dalam 2 dosis p.o.) atau amoksisilin 25 mg/kgBB/dosis diberikan tiap 12 jam p.o. (penelitian menunjukkan amoksisilin dua dosis sehari memiliki konsentrasi dalam darah yang sama dengan amoksisilin 3 dosis/hr) selama 3–5 hr.



Efikasi kedua obat sama, kecuali di daerah yang mengalami resistensi pada salah satu obat.



Antibiotik parenteral harus diberikan pada anak dengan pneumonia berat.



Pilihan pemberian antibiotik inisial pada pneumonia anak Ampisilin 50 mg/kgBB/dosis i.v. atau i.m. setiap 6 jam yang harus dipantau dalam 24 jam selama 48–72 jam pertama.



Bila keadaan klinis berat, pengobatan inisial berupa kombinasi ampisilin-gentamisin.



Bayi usia <2 bl atau pneumonia sangat berat, ampisilin dosis di atas ditambah gentamisin 7,5 mg/kgBB i.v. atau i.m. sekali sehari.



Pada keadaan dicurigai meningitis (malas menetek, letargis, kejang, menangis lemah, fontanel menojol) dan septikemia, maka obat pilihan pertama adalah sefotaksim atau seftriakson i.v.



Sesudah 48 jam pengobatan pneumonia sangat berat tidak tampak perbaikan, antibiotik diubah menjadi sefalosporin generasi ketiga, seperti seftriakson dan sefotaksim

o Pneumonia pada anak HIV 

Pada anak bukan pneumonia berat, terapi inisial dengan amoksisilin oral (25–30 mg/kgBB/dosis, 2×/hr selama 5 hr).



Penderita memerlukan pemantauan kondisi klinis.



Pneumonia berat harus dirawat di rumah sakit karena risiko tinggi cepat perburukan dan kegagalan terapi.



Pemberian antibiotik inisial harus memerhatikan pemberian antibiotik sebelumnya dan prevalensi resistensi antibiotik di daerah tersebut



Ampisilin dan gentamisin dapat diberikan selama 10 hr. Bila tidak ada respons, antibiotik dapat diganti dengan seftriakson atau sefotaksim



Jika diduga infeksi S. aureus dapat diberikan kloksasilin dan gentamisin



Pada anak usia <1 th dengan pneumonia berat dapat diterapi secara empiris dengan kotrimoksazol i.v. (15–20 mg/kgBB/hr komponen trimetoprim) dalam tiga atau empat dosis terbagi diinfus dalam 1 jam selama 21 hr.



Terapi kotrimoksazol oral diberikan pada penyakit yang ringan atau sedang atau bila sudah terjadi perbaikan.



Perbaikan klinis biasanya lambat, membutuhkan 5–7 hr



Kortikosteroid sudah terbukti menurunkan ketergantungan O2 dan mortalitas penderita HIV dewasa bila diberikan dalam 72 jam pemberian terapi kotrimoksazol.



Hal ini belum dapat dibuktikan pada anak, tetapi mungkin efektif pada dosis 1 mg/kgBB/hr selama 7 hr dan kemudian ditappering selama 7 hr berikutnya.

o Pneumonia pada anak malnutrisi berat Ampisilin dan gentamisin merupakan antibiotik inisial Terapi suportif seperti mempertahankan suhu, pencegahan hipoglikemia, dan pemberian nutrisi yang tepat sangat penting untuk memperoleh hasil terapi yang baik o Pemantauan 

Sesudah pemberian antibiotik inisial, pantau dalam 24 jam selama 48–72 jam pertama.



Apabila kondisi klinis membaik; tidak didapatkan tanda sepsis, empiema, necrotizing pneumonia, dan abses paru; tanda vital stabil selama min. 48 jam; biakan darah tidak menunjukkan pertumbuhan kuman; dan dapat makan/minum p.o. maka:



Antibiotik i.v dapat diganti dengan antibiotik oral. Umumnya peralihan ke antibiotik oral dilakukan sesudah 2–4 hr pemberian antibiotik i.v.



Selanjutnya, terapi dilanjutkan di rumah dengan amoksisilin p.o. (15 mg/kgBB/kali 3×/hr).



Pemberian antibiotik pada pneumonia berat dilanjutkan sampai 5–7 hr atau kepustakaan lain menyatakan 7−10 hr, dan pada pneumonia sangat berat diberikan selama 7–10 hr atau kepustakaan lain menyatakan 10–14 hr.

o Apabila: 

Demam atau manifestasi klinis lainnya menetap sesudah 48 jam pemberian antibiotik, atau keadaan klinis memburuk sebelum 48 jam, atau terdapat keadaan yang berat (tidak dapat menyusu atau minum/makan, atau memuntahkan semuanya, kejang, letargis atau

tidak sadar, sianosis, distress pernapasan berat) maka terapi harus dievaluasi kembali dan dipertimbangkan foto Rontgen toraks ulang. 

Tambahkan kloramfenikol 25 mg/kgBB/kali i.m. atau i.v. setiap 8 jam atau gentamisin 7,5 mg/kgBB i.v. atau i.m. 1×/hr.



Apabila terjadi kegagalan terapi pada penderita yang diberi kotrimoksazol, diganti dengan amoksisilin



Jika obat pertama yang diberikan adalah amoksisilin, maka bila terjadi kegagalan terapi dapat ditambahkan gentamisin atau diganti dengan amoksisilin-asam klavulanat (80−90 mg/kgBB/hr amoksisilin dalam dosis terbagi dengan maks. 6,4 mg/kgBB/hr asam klavulanat) untuk meningkatkan aktivitas terhadap Haemophilus influenzae penghasil βlaktamase dan S. pneumoniae yang resisten



Bila terjadi kegagalan terapi berikutnya, sefalosporin generasi ke-2 (sefuroksim) atau generasi ke-3 (seftriakson, sefopodoksim) dapat digunakan untuk memperluas cakupan terhadap organisme penghasil β-laktamase.



Apabila diduga pneumonia stafilokokal, ganti antibiotic dengan gentamisin (7,5 mg/kgBB i.m. 1×/hr) dan kloksasilin (50 mg/kgBB i.m. atau i.v. setiap 6 jam). Bila keadaan anak membaik, lanjutkan kloksasilin (atau dikloksasilin) secara oral 4×/hr sampai mencapai 3 mgg, atau klindamisin secara oral selama 2 mgg.



Pilihan antibiotik selanjutnya berdasarkan hasil pemeriksaan pola kepekaan antibiotic.

o Indikasi Penderita Dipulangkan 

Perbaikan secara klinis, nafsu makan membaik, bebas demam 12–24 jam,



stabil,



saturasi O2 >92% dalam udara ruangan selama 12–24 jam (tanpa O2),



orangtua sudah mengerti untuk melanjutkan pemberian antibiotik oral

Pencegahan



Vaksinasi dengan vaksin pertusis (DTP), campak, pneumokokus, dan H. influenza



Vaksin influenza untuk bayi >6 bl dan usia remaja



Untuk orangtua atau pengasuh bayi <6 bl disarankan untuk diberikan vaksin influenza dan pertusis



Makan bergizi



Jaga kebersihan

Revised WHO Recommendation of Treatment Oral amoxicillin is preferable to oral cotrimoxazole for the treatment of “fast breathing pneumonia” and is equivalent to injectable penicillin/ampicillin in cases of “chest indrawing pneumonia”. Hence, in a programmatic context, the distinction between previously defined “pneumonia” (fast breathing) and “severe pneumonia” (chest indrawing) loses its significance. The new classification is therefore simplified to include only two categories of pneumonia; “pneumonia” with fast breathing and/or chest indrawing, which requires home therapy with oral amoxicillin, and “severe pneumonia”, pneumonia with any general danger sign, which requires referral and injectable therapy. Dosages for pneumonia treatment at health facilities have been revised to reflect three age bands: 2 months up to 12 months (4–<10 kg); 12 months up to 3 years (10–<14 kg); 3 years up to 5 years (14–19 kg). Dosages and age bands for treatment of fast breathing pneumonia by community health workers (CHWs) have not changed. Recommendation 1 Children with fast breathing pneumonia with no chest indrawing or general danger sign should be treated with oral amoxicillin: at least 40mg/kg/dose twice daily (80mg/kg/day) for five days. In areas with low HIV prevalence, give amoxicillin for three days. Children with fast-breathing pneumonia who fail on fist-line treatment with amoxicillin should have the option of referral to a facility where there is appropriate second-line treatment.

Recommendation 2 Children age 2–59 months with chest indrawing pneumonia should be treated with oral amoxicillin: at least 40mg/kg/dose twice daily for five days.

Recommendation 3 Children aged 2–59 months with severe pneumonia should be treated with parenteral ampicillin (or penicillin) and gentamicin as a first-line treatment. — Ampicillin: 50 mg/kg, or benzyl penicillin: 50 000 units per kg IM/IV every 6 hours for at least

five days — Gentamicin: 7.5 mg/kg IM/IV once a day for at least five days Ceftriaxone should be used as a second-line treatment in children with severe pneumonia having failed on the first-line treatment.

Recommendation 4 Ampicillin (or penicillin when ampicillin is not available) plus gentamicin or ceftriaxone are recommended as a fist-line antibiotic regimen for HIV-infected and -exposed infants and for children under 5 years of age with chest indrawing pneumonia or severe pneumonia. For HIV-infected and -exposed infants and for children with chest indrawing pneumonia or severe pneumonia, who do not respond to treatment with ampicillin or penicillin plus gentamicin, ceftriaxone alone is recommended for use as second-line treatment.

Recommendation 5 Empiric cotrimoxazole treatment for suspected Pneumocystis jirovecii (previously Pneumocystis carinii) pneumonia (PCP) is recommended as an additional treatment for HIV-infected and -exposed infants aged from 2 months up to 1 year with chest indrawing or severe pneumonia. Empirical cotrimoxazole treatment for Pneumocystis jirovecii pneumonia (PCP) is not recommended for HIVinfected and -exposed children over 1 year of age with chest indrawing or severe pneumonia.