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The 2022 Adama hospital study identifies family size, education, income, cooking fuel, malnutrition, and recent illness history as risk factors for pneumonia in children. It emphasizes the importance of preventive measures over treatment and highlights pneumonia as a leading cause of death in children under five, particularly in low-income countries. The document discusses pneumonia's etiology, pathogenesis, clinical manifestations, and diagnostic approaches, noting the role of both viral and bacterial pathogens in its development.

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0% found this document useful (0 votes)
20 views95 pages

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The 2022 Adama hospital study identifies family size, education, income, cooking fuel, malnutrition, and recent illness history as risk factors for pneumonia in children. It emphasizes the importance of preventive measures over treatment and highlights pneumonia as a leading cause of death in children under five, particularly in low-income countries. The document discusses pneumonia's etiology, pathogenesis, clinical manifestations, and diagnostic approaches, noting the role of both viral and bacterial pathogens in its development.

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brnard
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Adama hospital study 2022


• Family size, education status of the father, household monthly
income, mostly used fuel for cooking, malnutrition, and history of
diarrhea, and URTI in the past two weeks was found to be the risk
factors for pneumonia. Relatively simple interventions such as cooking
with electricity, and other interventions like prevention, early
detection and treatment of malnutrition, diarrhea, and URTI, and
promotion of family planning are important. Prevention of the risk
factors should get priority over treatment of cases, and health care
facilities should work with other stakeholders to reverse these risk
factors.
• Pneumonia, defined as inflammation of the lung parenchyma, is the
leading infectious cause of death globally among children younger
than 5 years.
• Pneumonia mortality is closely linked to poverty; more than 99% of
child pneumonia deaths are in low- and middle-income countries
• Effective vaccines against measles and pertussis contributed to the
decline in child pneumonia mortality during the 20th century.
• The introduction of pneumococcal conjugate vaccines (PCVs has been
an important contributor to the further reductions in pneumonia
mortality achieved over the past 2 decades. Epidemics (influenza,
severe acute respiratory system coronavirus, Middle East respiratory
syndrome, respiratory syncytial virus [RSV]) and pandemics (COVID19)
contribute to the incidence, morbidity, and mortality in pediatric
patients with pneumonia. In addition, unexpected global increases in
group A streptococcus (GAS) infections have contributed to both
morbidity and mortality in children with pneumonia.
• ETIOLOGY
• 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 .
• The cause of pneumonia in an individual patient is often difficult to
determine because direct sampling of lung tissue is invasive and rarely
performed. Bacterial cultures of sputum or upper respiratory tract
samples typically do not accurately reflect the cause of lower
respiratory tract infection in children.
• Streptococcus pneumoniae (pneumococcus) is the most common
bacterial pathogen in children 3 weeks to 5 years of age, whereas
Mycoplasma pneumoniae and Chlamydophila pneumoniae are the
most frequent bacterial pathogens in children 5 years and older. In
addition to pneumococcus, other bacterial causes of pneumonia in
previously healthy children in the United States include GAS
(Streptococcus pyogenes; and Staphylococcus aureus
• S. pneumoniae or S. aureus pneumonia often complicates an illness
caused by influenza viruses.
• S. pneumoniae, H. influenzae, GAS, 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 261),
nontuberculous mycobacteria (see Chapter 263), Salmonella (see
Chapter 244), Escherichia coli (see Chapter 246), Pneumocystis
jirovecii (see Chapter 290), and cytomegalovirus (see Chapter 302)
should also be considered. The incidence of pneumonia caused by H.
influenzae or S. pneumoniae has been significantly reduced in areas
where routine immunization has been implemented.
• Viral pathogens are the most common causes of lower respiratory
tract infections in infants and children older than 1 month but
younger than 5 years of age. Viruses can be detected in 40–80% of
children with pneumonia using molecular diagnostic methods (e.g.,
polymerase chain reaction [PCR]), with more than one respiratory
virus identified in up to 20% of cases. Of the respiratory viruses, RSV
and rhinoviruses are the most commonly identified pathogens,
especially in children younger than 2 years of age.
• However, the role of rhinoviruses in severe lower respiratory tract
infection remains unclear, as these viruses are frequently detected
with co-infecting pathogens and among asymptomatic children. Other
common viruses causing pneumonia include influenza viruses, human
metapneumovirus, parainfluenza viruses, adenoviruses,
enteroviruses, and coronaviruses, including severe acute respiratory
syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus
disease 2019 .
• 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 viruses that occur
each year. The typical pattern of these epidemics usually begins in the
fall, when parainfluenza virus infections appear and most often
manifest as croup. Later in winter, RSV, human metapneumovirus, and
influenza viruses cause widespread infection, including upper
respiratory tract infections, bronchiolitis, and pneumonia.
• RSV is particularly severe among infants and young children, whereas
influenza viruses cause disease and excess hospitalization in all age
groups. Knowledge of the prevailing viruses circulating in the
community may lead to a presumptive initial diagnosis for children
with acute respiratory illnesses. Immunization status is relevant
because children fully immunized against H. influenzae type b and S.
pneumoniae are less likely to have pneumonia caused by these
pathogens. Children who are immunocompromised or who have
certain medical comorbidities may be at risk for specific pathogens,
such as Pseudomonas spp. in patients with cystic fibrosis.
• PATHOGENESIS
• The lower respiratory tract possesses a number of defense mechanisms against
infection, including mucociliary clearance, macrophages and secretory
immunoglobulin A, and clearing of the airways by coughing. Previously, it was
believed that the lower respiratory tract was—in the absence of infection—kept
sterile by these mechanisms, supported primarily by culture-based studies.
However, recent use of culture independent techniques, including high-
throughput sequencing methods, suggests that the lower respiratory tract
contains diverse microbial communities. These data have challenged the
traditional model of pneumonia pathogenesis that maintained that pneumonia
was the result of invasion of the sterile lower respiratory tract by a single
pathogen. More recent conceptual models postulate that pneumonia results from
disruption of a complex lower respiratory ecosystem that is the
site of dynamic interactions between potential pneumonia pathogens,
resident microbial communities, and host immune defenses. 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.
• The small caliber of airways in young infants makes such patients particularly
susceptible to severe infection. Atelectasis, interstitial edema, and
hypoxemia from ventilation-perfusion mismatch often accompany airway
obstruction. Viral infection of the respiratory tract can also predispose to
secondary bacterial infection by disturbing normal host defense
mechanisms, altering secretions, and disrupting the microbial communities
that reside in the respiratory tract
• Bacterial pneumonia most often occurs when respiratory tract organisms
colonize the upper respiratory tract and subsequently gain access to the lungs,
but pneumonia may also result from direct seeding of lung tissue in the setting
of bacteremia. When bacterial infection is established in the lung parenchyma,
the pathologic process varies according to the invading organism. M.
pneumoniae attaches to the respiratory epithelium, inhibits ciliary action, and
leads to cellular destruction and an inflammatory response in the submucosa.
• When the infection progresses, sloughed cellular debris, inflammatory cells, and
mucus cause airway obstruction, with spread of infection occurring along the
bronchial tree, as is seen in viral pneumonia. S. pneumoniae produces local
edema that aids in the proliferation of organisms and their spread into adjacent
portions of the lung, often resulting in the characteristic lobar consolidation.
• Lower respiratory tract infection caused by GAS typically results in more diffuse
lung involvement with interstitial pneumonia. 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 with frequent pleural involvement. S. aureus pneumonia
manifests as confluent bronchopneumonia, which is often bilateral and
characterized by the presence of extensive areas of hemorrhagic necrosis and
irregular areas of cavitation of the lung parenchyma, resulting in pneumatoceles,
empyema, and, at times, bronchopulmonary fistulas.
• Recurrent pneumonia is defined as two or more episodes in a single year or
three or more episodes ever, with radiographic clearing between occurrences.
An underlying disorder should be considered if a child experiences recurrent
pneumonia
• CLINICAL MANIFESTATIONS Pneumonia is frequently preceded by several days of
symptoms of an upper respiratory tract infection, typically rhinitis and cough. In viral
pneumonia, fever is usually present but temperatures are generally lower than in
bacterial pneumonia. Tachypnea is the most consistent clinical manifestation of
pneumonia. Increased work of breathing manifested by intercostal, subcostal, and
suprasternal retractions; nasal flaring; and use of accessory muscles is also common.
• Severe infection may be accompanied by cyanosis and lethargy, especially in infants.
Auscultation of the chest may reveal crackles and wheezing, but it is often difficult
to localize the source of these adventitious sounds in young children with
hyperresonant chests. It is often not possible to distinguish viral pneumonia
clinically from disease caused by Mycoplasma and other bacterial pathogens.
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. 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.
Lower lobe pneumonia may cause abdominal pain (but no
tenderness), or the pain may be referred to the ipsilateral shoulder.
• Physical findings depend on the stage of pneumonia. Early in the
course of illness, diminished breath sounds, scattered crackles, and
rhonchi are commonly heard over the affected lung field. 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. A lag in
respiratory excursion often occurs on the affected side. Abdominal
distention may be prominent because of gastric dilation from
swallowed air or ileus. The liver may seem enlarged because of
downward displacement of the diaphragm secondary to
hyperinflation of the lungs or superimposed congestive heart failure.
• 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.
• In infants, there may be a prodrome of upper respiratory tract
infection and poor feeding, leading to the abrupt onset of fever,
restlessness, apprehension, and respiratory distress. These infants
typically 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.
• Auscultation may be misleading, particularly in young infants, with
meager findings disproportionate to the degree of tachypnea. Some
infants with bacterial pneumonia may have associated gastrointestinal
disturbances characterized by vomiting, anorexia, diarrhea, and
abdominal distention secondary to a paralytic ileus.
• Rapid progression of symptoms is characteristic in the most severe
cases of bacterial pneumonia. Cyanosis often predicts multilobular
involvement.
• Risk factors for severe pneumonia include temperature >38.5°C,
tachypnea, retractions, nasal flaring, grunting, capillary refill >2
seconds, cyanosis, tachycardia, and poor feeding.
• DIAGNOSIS In 2011, the Pediatric Infectious Diseases Society (PIDS) and the Infectious
Diseases Society of America (IDSA) published clinical practice guidelines for community-
acquired pneumonia in children older than 3 months of age. These evidence-based
guidelines provide recommendations for diagnostic testing and treatment of previously
healthy children with pneumonia in both outpatient and inpatient settings. With the
advent of advanced technologies and changing epidemiologic pathogens, these
guidelines have required modifications.
• An infiltrate on chest radiograph (posteroanterior and lateral views) supports the
diagnosis of pneumonia; images may also identify a complication such as a pleural
effusion or empyema.
• Viral pneumonia is usually characterized by hyperinflation with bilateral interstitial
infiltrates and peribronchial cuffing . Confluent lobar consolidation is typically seen with
pneumococcal pneumonia . The radiographic appearance alone does not accurately
identify
• pneumonia etiology, and other clinical features of the illness must be
considered. Repeat chest radiographs are not required for proof of
cure for patients with uncomplicated pneumonia. Moreover, current
PIDS-IDSA guidelines do not recommend that a chest radiograph be
performed for children with suspected pneumonia (tachypnea, cough,
fever, localized crackles, or decreased breath sounds) who are well
enough to be managed as outpatients because imaging in this context
only rarely changes management.
• 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.
• However, the reliability of this imaging modality for pneumonia
diagnosis is highly user-dependent, which has limited its widespread
use. The peripheral white blood cell (WBC) count can be useful in
differentiating viral from bacterial pneumonia. In viral pneumonia, the
WBC count can be normal or elevated but is usually not higher than
20,000/mm3, with a lymphocyte predominance. Bacterial pneumonia
is often associated with an elevated WBC count, in the range of
15,000- 40,000/mm3, and a predominance of polymorphonuclear
leukocytes.
• A large pleural effusion, lobar consolidation, and a high fever at the
onset of the illness are also suggestive of a bacterial etiology. Atypical
pneumonia caused by C. pneumoniae or M. pneumoniae is difficult to
distinguish from pneumococcal pneumonia on the basis of
radiographic and laboratory findings; although pneumococcal
pneumonia is associated with a higher WBC count, erythrocyte
sedimentation rate, procalcitonin, and C-reactive protein level, there
is considerable overlap.
• The definitive diagnosis of a viral infection rests on the detection of the
viral genome or antigen in respiratory tract secretions. Reliable PCR
assays are widely available for the rapid detection of many respiratory
viruses, including RSV, parainfluenza, influenza, human
metapneumovirus, adenovirus, enterovirus, rhinovirus, and SARS-CoV-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 virus. This diagnostic
technique is laborious, slow, and not generally clinically useful because
the infection usually has resolved by the time it is confirmed serologically.
• Serologic testing may be valuable as an epidemiologic tool to define
the incidence and prevalence of various respiratory viral pathogens.
• The definitive diagnosis of a typical bacterial infection requires
isolation of an organism from the blood, pleural fluid, or lung.
Culture of sputum is of little value in the diagnosis of pneumonia in
young children, and percutaneous lung aspiration is invasive and not
routinely performed. Blood culture is positive in only 10% of children
with pneumococcal pneumonia (bacteremia is more common in GAS
and H. influenzae pneumonias) and is not recommended for
nontoxic-appearing children treated as outpatients.
• Blood cultures are recommended for children who fail to improve or
have clinical deterioration, have complicated pneumonia (Table 449.5),
or require hospitalization. Pertussis infection can be diagnosed by PCR
or culture of a nasopharyngeal specimen; although culture is
considered the gold standard for pertussis diagnosis, it is less sensitive
than the available PCR assays. Acute infection caused by M.
pneumoniae can be diagnosed on the basis of a PCR test result from a
respiratory specimen or seroconversion in an immunoglobulin G assay.
Cold agglutinins at titers >1:64 are also found in the blood of roughly half
of patients with M. pneumoniae infections; however, cold agglutinins are
nonspecific because other pathogens such as influenza viruses may also
cause increases.
• Serologic evidence, such as antistreptolysin O and anti-DNase B titers, may also be
useful in the diagnosis of GAS pneumonia. Noninvasive diagnostic tests may help
differentiate children with bacterial versus viral causes of pneumonia. Various
biomarkers, including C-reactive protein, procalcitonin, and ESR, have been
evaluated for their ability to differentiate these pneumonia etiologies.
• For many of these biomarkers, values differ in children with bacterial compared
with viral causes of pneumonia (except adenovirus and influenza), but the
reliability of these tests is not sufficiently high to justify routine clinical use. Cell-
free next-generation sequencing of plasma or blood has been helpful in identifying
pathogens in patients suspected of having bacterial pneumonia; identified
pathogens include S. pneumoniae, S. aureus, and Fusobacterium nucleatum
(blood cultures were negative in most of these patients). In addition, culture and
PCR analysis of pleural fluid may also yield an organism.
• TREATMENT
• Treatment of suspected bacterial pneumonia is based on the
presumptive cause and the age and clinical appearance of the child.
• For mildly ill children who do not require hospitalization, amoxicillin is
recommended. With the emergence of penicillin-resistant
pneumococci, high doses of amoxicillin (90 mg/kg/day orally divided
twice daily) should be prescribed unless local data indicate a low
prevalence of resistance.
• Therapeutic alternatives include cefuroxime( 2nd gen.) and
amoxicillin/clavulanate. For school-age children and adolescents or when
infection with M. pneumoniae or C. pneumoniae is suspected, a macrolide
antibiotic is an appropriate choice for outpatient management.
• Azithromycin is generally preferred, but clarithromycin or doxycycline (for
children 8 years or older) are alternatives. For adolescents, a respiratory
fluoroquinolone (levofloxacin, moxifloxacin) may also be considered as an
alternative if there are contraindications to other agents. The empiric
treatment of suspected bacterial pneumonia in a hospitalized child requires
an approach based on local epidemiology, the immunization status of the
child, and the clinical manifestations at the time of presentation.
• In areas without substantial high-level penicillin resistance among S.
pneumoniae, children who are fully immunized against H. influenzae type b and
S. pneumoniae and are not severely ill should receive ampicillin or penicillin G.
• For children who do not meet these criteria, ceftriaxone or cefotaxime may be
used. If infection with M. pneumoniae or C. pneumoniae is suspected, a
macrolide antibiotic should be included in the treatment regimen. If clinical
features suggest staphylococcal pneumonia (pneumatoceles, empyema), initial
antimicrobial therapy should also include vancomycin or clindamycin.
• For children with respiratory failure in the setting of influenza–methicillin-
resistant S. aureus (MRSA) co-infection, data from a multicenter study support
combination therapy with vancomycin and a second antibiotic with MRSA
activity (e.g., clindamycin).
• If viral pneumonia is suspected, it is reasonable to withhold antibiotic
therapy, especially for preschool-age 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 influenza viruses, may have coexisting bacterial
pathogens. 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.
• Hospitalized children should receive supportive care and may require
intravenous fluids; respiratory support, including supplemental
oxygen, continuous positive airway pressure (CPAP), or mechanical
ventilation; or vasoactive medications for hypotension or sepsis
physiology. The optimal duration of antibiotic treatment for
pneumonia has not been well-established in controlled studies.
• However, antibiotics should generally be continued until the patient
has been afebrile for 72 hours. Several studies suggest that shorter
courses (5-7 days) may also be effective, particularly for children
managed on an outpatient basis. Available data do not support
prolonged courses of treatment for uncomplicated pneumonia.
• Some studies suggest that a reduction of previously elevated serum procalcitonin
levels to an absolute level (0.1- 0.25 μg/L) may help determine when to stop
treatment. Despite substantial gains over the past 15 years, less than two thirds of
children with symptoms of pneumonia are taken to an appropriate caregiver in low-
and middle-income countries, and fewer than half receive antibiotics.
• The World Health Organization and other international groups have developed
systems to train mothers and local healthcare providers in the recognition and
appropriate antibiotic treatment of pneumonia. In addition to antibiotics, oral zinc
(10 mg/ day for < 12 months, 20 mg/day for greater or equal to 12 months given for
7 days) may reduce mortality among children in low- and middle-income countries
with clinically defined severe pneumonia. Bubble CPAP improves mortality from
pneumonia with hypoxemia compared with standard oxygen therapy in settings
without access to ventilator-derived CPAP or mechanical ventilation.
• COMPLICATIONS
• Complications of pneumonia (see Table 449.5) are usually the result
of direct spread of bacterial infection within the thoracic cavity
(pleural effusion, empyema, and pericarditis) or bacteremia and
hematologic spread (Figs. 449.5-449.7). Meningitis, endocarditis,
suppurative arthritis, and osteomyelitis are rare complications of
hematologic spread of pneumococcal or H. influenzae type b
infection. S. aureus, S. pneumoniae, and S. pyogenes (GAS) are the
most common causes of parapneumonic effusions and empyema.
• Nonetheless many effusions that complicate bacterial pneumonia are
sterile. Analysis of pleural fluid parameters, including pH, glucose,
protein, and lactate dehydrogenase, can differentiate transudative
from exudative effusions (Table 449.6). However, current PIDS-IDSA
guidelines do not recommend that these tests be performed because
this distinction rarely changes management. Pleural fluid should be
sent for Gram stain and bacterial culture, as this may identify the
bacterial cause of pneumonia. Molecular methods, including bacterial
species–specific PCR
• assays, detect pathogens and can often determine the bacterial
etiology of the effusion if the culture is negative, particularly if the
pleural fluid sample was obtained after initiation of antibiotics. A
pleural fluid WBC count with differential may be helpful if there is
suspicion for pulmonary tuberculosis or a noninfectious etiology for
the pleural effusion, such as malignancy.
• Small ( < 1 cm on lateral decubitus radiograph), free-flowing parapneumonic
effusions often do not require drainage but respond to appropriate
antibiotic therapy. Larger effusions should typically be drained, particularly if
the effusion is purulent or associated with respiratory distress. Chest
ultrasound, or alternatively CT, may be helpful in determining whether
loculations are present. The mainstays of therapy include antibiotic therapy
and drainage by tube thoracostomy with the instillation of fibrinolytic
agents (tissue plasminogen activator). Videoassisted thoracoscopy is a less
often employed alternative that enables debridement or lysis of adhesions
and drainage of loculated areas of pus. Early diagnosis and intervention,
particularly with fibrinolysis or, less often, video-assisted thoracoscopy, may
obviate the need for thoracotomy and open debridement.

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