Professional Documents
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Pneumonia
- penyakit saluran nafas yg disebabkan oleh infeksi
bakteri, virus & fungi
- disertai inflamasi pd daerah terinfeksi
- fungsi paru2 tdk normal masalah berat krn
kesulitan bernafas
Ming, C.K., 2011
Pneumonia:
infeksi sal nafas akut yg berat effek spesifik pd
paru2
pd salah satu atau ke dua paru tertimbun cairan
& nanah mengganggu absorpsi oksigen susah
bernafas
Unicef-WHO, 2006
CAP in children in the United States, the focus of these guidelines, is defined
simply as the presence of signs and symptoms of pneumonia in a previously
healthy child caused by an infection that has been acquired outside of the
hospital. However, pneumonia definitions can also be designed to be very
sensitive for epidemiologic considerations (eg, fever and cough) or very specific,
as defined by government regulatory agencies for approval of antimicrobials to
treat pneumonia (eg, clinical symptoms and signs in combination with radiologic
documentation or microbiologic confirmation). Pneumonia, broadly defined asa
lower respiratory tract infection (LRTI), may also be defined in a way that is clinically oriented,
to assist practitioners with diagnosis and management.
Bradley, J.S., et al., 2011
C. KLASSIFIKASI
D. EPIDEMIOLOGI
a common disorder that is potentially life threatening, older adults and
those with comorbid disease.
File Jr, T.M 2003
Pneumonia is a very common disease among children less than 5 years old in developing nations as it
cause up to 5 million deaths among them each year.
FIGURE 4
15 COUNTRIES ACCOUNT FOR THREE QUARTERS OF CHILDHOOD
PNEUMONIA CASES WORLDWIDE
India 44 million
China 18 million
Nigeria 7 million
Pakistan 7 million
Bangladesh 6 million
Indonesia 6 million
Brazil 4 million
Ethiopia 4 million
Congo, Democratic Republic of the 3 million
Philippines 3 million
Afghanistan 2 million
Egypt 2 million
Mexico 2 million
Sudan 2 million
Viet Nam 2 million
Total 113 million
Injuries 3%
Figure 1 presents the global distribution of the primary causes of all under-
five deaths and shows that pneumonia kills more children than any other
illness accounting for 19 per cent of all under-five deaths (see the
Appendix for more detailed information on these estimates of cause-
specific mortality ).
This figure, however, does not include deaths due to pneumonia during
the first four weeks of life, the neonatal period. It has been estimated that
26 per cent of neonatal deaths, or 10 per cent of all under-five deaths, are
caused by severe infections during the neonatal period. And a significant
proportion of these infections is caused by pneumonia/sepsis (sepsis is a
serious blood-borne bacterial infection that is also treated with antibiotics).
If these deaths were included in the overall estimate, pneumonia would
account for up to 3 million, or as many as one third (29 per cent), of under-
five deaths each year
Unicef-WHO, 2006
IVACS., 2013
E. PENYEBAB
Although many pathogens have been associated with CAP, it is a small
range of key pathogens that cause most cases. The emergence of newly
recognised pathogens,
such as the novel coronavirus associated with (SARS), increases the
challenge for appropriate management of these infections.
The predominant pathogen in CAP is Streptococcus pneumoniae
(pneumococcus), which accounts for about two-thirds of all cases of
bacteraemic pneumonia.
Cigarette smoking is the strongest independent risk factor for invasive
pneumococcal disease in immunocompetent, non-elderly adults.
Other causative agents include, but are not limited to Haemophilus influenzae,
Mycoplasma pneumoniae, Chlamydophila pneumoniae (Chlamydia pneumoniae),
Legionella spp, Chlamydophila psittaci (Chlamydia psittaci), Coxiella burnetii,
enteric gram-negative bacteria (enterobacteriaceae), Pseudomonas aeruginosa,
Staphylococcus aureus, anaerobes (aspiration pneumonia), and respiratory
viruses (influenza virus, adenovirus, respiratory syncytial virus, parainfluenza
virus, coronavirus. Gram-negative cause of CAP in some patients (those who
have had previous antimicrobial treatment or who have pulmonary
comorbidities). The frequency of other causes, such as Mycobacterium
tuberculosis, C psittaci (psittacosis), C burnetii (Q fever), Francisella tularensis
(tularaemia), and endemic fungi (histoplasmosis, coccidioidomycosis,
blastomycosis) vary between epidemiological settings.
Table 118, shows the causes of CAP in adults in hospital as reported by workers
from several prospective studies in several worldwide locations who used
comprehensive diagnostic approaches. The incidence of specific pathogens
varied in accordance with the completeness of testing and specificity of
diagnostic criteria (ie, definite vs presumptive diagnosis [table 1]).
Collectively, S pneumoniae was the most frequently isolated organism, with the
highest incidence of this pathogen reported in studies that included detection by
a urinary antigen test. Relative to other pathogens, M pneumoniae, C
pneumoniae, and L pneumophila were also common. These organisms (along
with other Chlamydia spp and C burnetii) are often referred to as atypicals, a
label of contended scientific merit. Nevertheless, the term remains popular with
clinicians and is in widespread use in recent scientific reports. These atypical
pathogens are not often identified in clinical practice, however, because (with
the exception of L pneumophila) there is not a specific, rapid, or standardised
test for their detection; as such, the frequency of these pathogens is probably
underreported
The proportion of cases in recent studies with a defined cause ranged from 52 to
83%. By contrast, in an observational study that assessed the real-world
practice from several centres in the USA, only 6% of outpatients and a quarter of
inpatients with CAP had the cause of their disease defined. In a study of
consecutive patients with CAP, Ruiz-Gonzales and colleagues used
microbiological
analysis and PCR to test for respiratory pathogens in lung aspirate specimens
obtained by transthoracic needle aspiration. Their results showed that use of
these tests increased the proportion of cases of CAP for which a cause could be
established to 83%, from 50% reported when
conventional testsie, sputum and blood cultures and serological testswere
used. Their results also changed the ranking of pathogens established by
conventional testing from M pneumoniae (35%), C pneumoniae (17%), S
pneumoniae (17%) to S pneumoniae (30%), M pneumonia (22%), C pneumoniae
(13%). Importantly, S pneumonia represented one third of all causes not
documented by conventional testing.
Legionella spp are still a common cause of severe CAP. A review of nine studies
of CAP that resulted in admission to an intensive care unit (seven from Europe
and one each from USA and South Africa) noted that Legionella spp were the
second most commonly identified pathogens, with S pneumoniae being most
often detected. Aerobic gramnegative bacilli, H influenzae, and S aureus were
also identified, although few of these cases could be judged as definite (ie,
confirmed bacteraemia or isolation from pleural fluid or lung tissue). In an
international collaborative survey of 508 patients with culture-positive
legionellosis, 92% of the isolates with serogroup 1 were L pneumophila,
accounting for 84% of the total. L pneumophila serogroup 1 accounted for 88%
of isolates in America and Europe but for only 46% in Australia and New Zealand
where L longbeachae accounted for 30% of cases.
The most common pathogens identified from recent studies of mild (ie, in
ambulatory patients) CAP were S pneumoniae, M pneumoniae, Chlamydia spp,
and viruses (mostly influenza virus). Mycoplasma spp were most common in
patients younger than 50 years and without important comorbid conditions or
abnormality of vital signs, whereas S pneumoniae was the most common
pathogen for older patients or those with significant underlying disease.
An awareness of the likely cause of CAP in different settings is important to allow
the start of appropriate antimicrobial treatment. Table 2 shows the most common
pathogens associated with CAP as derived from collective results of various
studies. Severity of illness is judged by site of care (outpatient vs inpatient).
Although objective confirmation is often difficult, multiple organisms that infect a
patient concurrently or sequentially can cause CAP. For example, influenza A or
C pneumoniae infection might be followed by a secondary infection with S
pneumoniae. In one study of patients admitted with serologically diagnosed C
pneumonia pneumonia, 45% of patients were infected with other pathogens, the
most common copathogen being S pneumoniae.
The incidence of mixed infection varied from 2 to 11% (table 1). The importance
of treating multiple infecting organisms has not been established; however,
identification of one pathogen should not preclude tests for other causes when a
patient is not responding to treatment.
File Jr, T.M 2003
Many pathogens are responsible for CAP in children, most prominently viruses
and bacteria. Investigators have used a variety of laboratory tests to establish a
microbial etiology of CAP.
Furthermore, unique to pediatrics, the developing immune system and age-
related exposures result in infection caused by different bacterial and viral
pathogens, requiring that the incidence of CAP and potential pathogens be
defined separately for each age group.
Reports of epidemiologic investigations on the etiology of CAP before the
widespread use of these vaccines cited S. pneumoniae as the most common
documented bacterial pathogen, occurring in 4%44% of all children
investigated.
In some studies, viral etiologies of CAP have been documented in up to 80%of
children younger than 2 years; in contrast, investigations of older children, 1016
years, who had both clinical and radiographic evidence of pneumonia,
documented a much lower percentage of viral pathogens.
Of viral pathogens, RSV is consistently the most frequently detected,
representing up to 40%of identified pathogens in those younger than 2 years,
but rarely identified in older children with CAP. Less frequently detected are
adenoviruses, bocavirus, human metapneumovirus, influenza A and B viruses,
parainfluenza viruses, coronaviruses and rhinovirus.
Epidemiologic investigations of hospitalized children with CAP document that
2%33% are simultaneously infected by 2 or more viruses.
Epidemiologic studies that have assessed both viral and bacterial pathogens
have reported bacterial pathogens isolated in 2%50% of children with CAP;
inpatient studies that enroll more seriously ill children often document higher
rates of bacterial infection compared with outpatient studies.
Pathogens responsible for atypical pneumonia have been identified in 3%23%
of children studied, with M. pneumonia most often identified in older children and
C. pneumoniae in infants. Atypical pneumonia caused by Mycoplasma is
characteristically slowly progressing, with malaise, sore throat, low-grade fever,
and cough developing over 35 days. In contrast to adults with pneumonia,
Legionella sp. has only rarely been identified in children.
Although CAP caused by Mycobacterium tuberculosis and the nontuberculous
mycobacteria have been well-documented, the incidence of these serious
infections in the United States is far less than that of viral or bacterial CAP and is
often linked to high-risk exposures. Likewise, fungal pneumonia in normal hosts
caused by Histoplasma, Coccidioides, Blastomyces, and Cryptococcus is
uncommon, and in most epidemiologic studies, children with fungal pneumonia
are not identified. Mycobacterial and fungal pneumonia are not addressed in
these guidelines
Bradley, J.S., et al., 2011
Unicef-WHO, 2006
F. PENULARAN
Pathogens causing pneumonia may reach the childs lungs through
different routes. Although information on the pathogenesis of childhood
pneumonia is limited, it is widely believed that common bacterial
pathogens causing pneumonia are often already present in a childs nose
or throat and are then inhaled into the lungs, causing infection. Pathogens
may also be spread through contaminated air droplets or may result from
blood-borne infections. During or shortly after birth, babies are at higher
risk of developing pneumonia from coming into contact with organisms in
the birth canal or from contaminated substances contacted during
delivery.
Unicef-WHO, 2006
INESSS. 2009
G. PATOMEKANISME
Most acute respiratory infections result in mild illnesses, such as the
common cold. But in vulnerable children, infections that begin with mild
symptoms may sometimes lead to more severe illnesses, such as
pneumonia especially when they coincide with other illnesses like
diarrhoea or malaria.
A healthy child has many natural defences that protect its lungs from the
invading pathogens that cause pneumonia. However, children and infants
with compromised immune systems have weakened defences.
Undernourished children, particularly those not exclusively breastfed or
with inadequate zinc intake, are at higher risk of developing pneumonia.
Similarly, children and infants suffering from other illnesses, such as AIDS
or measles, are more likely to develop pneumonia. Environmental factors,
such as living in crowded homes and exposure to parental smoking or
indoor air pollution, may also have a role to play in increasing childrens
susceptibility to pneumonia and its severe consequences
Unicef-WHO, 2006
H. FAKTOR RESIKO
compromised immune systems
Comorbid: diarrhoea or malaria.
Environmental factors, such as living in crowded homes and exposure to
parental smoking or indoor air pollution
Undernourished children particularly those not exclusively breastfed or
with inadequate zinc intake,
children and infants suffering from other illnesses, such as AIDS or
measles,
Unicef-WHO, 2006
I. GAMBARAN KLINIK
Breathing can become very difficult, especially for young children. Other
symptoms can include intense coughing, a high fever, and chills. As
pneumonia progresses, children can experience convulsions,
unconsciousness, feeding problems, and without timely treatment, often
death.
IHME. 2014
J. DIAGNOSIS
Once caregivers have recognized the danger signs of pneumonia (cough
and fast or difficult breathing) and taken their children to appropriate
medical care, health personnel including trained community health
workers should then diagnose and treat pneumonia in children
according to the following Integrated Management of Childhood Illness
(IMCI) guidelines:
Diagnosis: Children aged 2 months to 5 years are diagnosed with
pneumonia if they exhibit a cough and fast or difficult breathing.
Thresholds for fast breathing depend on the childs age (see What is
fast breathing?,
below). Severe pneumonia in children is diagnosed if they exhibit lower
chest wall
indrawing (when the childs chest moves in or retracts during inhalation)
or stridor (a harsh noise made during inhalation). Respiratory rate timers
should be available to help health personnel count breathing rates.
Unicef-WHO, 2006
Knowing the signs and symptoms only is not enough to treat the
pneumonia. Diagnosis should be done in further to choose the right and
more effective treatment. Understanding the patients medical and
personal history is important before making a pneumonia diagnosis. It is
because pneumonia may be caused by chronic diseases such as lung
disease and the treatment will be totally different from those who have no
chronic diseases or any medical history.
Knowing the signs and symptoms only is not enough to treat the
pneumonia. Diagnosis should be done further to choose the right and
more effective treatment.
Understanding the patients medical and personal history is important
before making a pneumonia diagnosis. It is because pneumonia may be
caused by chronic diseases such as lung disease and the treatment will be
totally different from those who have no chronic diseases or any medical
history.
Diagnosis of pneumonia is typically based on chest x-ray, consideration of
pulmonary embolism and sometimes identification of patho Chest
radiography or chest x-ray is the most common way to diagnose
pneumonia. It is used to check which part of lungs is infected and it can
show the abnormal fluid collection in the lungs which leads to pneumonia.
Chest x-ray is recommended to the patients showing complicated signs and
symptoms. However, the x-ray findings may be different for different types
of pneumonia.
Besides that, tests such as laboratory tests and listening to heart and lungs
through stethoscope are also some common diagnosis for pneumonia
patients. Laboratory testing such as white blood cells count, serum
electrolytes, blood tests and creatinine testing are recommended for
hospitalized-acquired pneumonia patients to test the severity of disease.
Blood test is carried out to see whether the patients immune system is
working to fight against the pneumonia or not. The tests are conducted to
see how severe the pneumonia is.
However, for aspiration pneumonia patient, tests such as swallowing
studies or special tests of throat or esophagus might work better.
Other than that, sputum cultures can also be carried out to identify the
microorganism that causes pneumonia. It is advisable to identify a
pathogen in patients who are showing therapeutic failure or are critically ill.
Pathogen identification is important as different pathogen-causing
pneumonia needs different treatment. For example, antibiotics are
prescribed for bacterial pneumonia but not viral pneumonia. Besides the
type of pneumonia, different type of bacteria-causing pneumonia may need
different antibiotics.
Other investigations like urea and electrolytes examination and liver
function tests are also recommended for patients with non-severe
community acquired pneumonia.
Ming, C.K., 2011
Chest X-rays and laboratory tests are used to confirm the presence of
pneumonia, including the extent and location of the infection and its cause.
But in resource-poor settings without access to these technologies,
suspected cases of pneumonia are diagnosed by their clinical symptoms.
Children and infants are presumed to have pneumonia if they exhibit a
cough and fast or difficult breathing (see detailed guidelines in Box 5, page
24).
Caregivers, therefore, have an important role to play in recognizing the
symptoms of pneumonia in children and seeking appropriate medical care
as necessary.
Unicef-WHO, 2006
Recommendations
Microbiologic Testing
Blood Cultures: Outpatient
12. Blood cultures should not be routinely performed in nontoxic, fully
immunized children with CAP managed in the outpatient setting.
(strong recommendation; moderate-quality evidence)
13. Blood cultures should be obtained in children who fail to demonstrate
clinical improvement and in those who have progressive symptoms or
clinical deterioration after initiation of antibiotic therapy (strong
recommendation; moderate-quality evidence).
Acute-Phase Reactants
27. Acute-phase reactants, such as the erythrocyte sedimentation rate
(ESR), C-reactive protein (CRP) concentration, or serum procalcitonin
concentration, cannot be used as the sole determinant to distinguish
between viral and bacterial causes of CAP. (strong recommendation;
high-quality evidence)
28. Acute-phase reactants need not be routinely measured in fully
immunized children with CAP who are managed as outpatients,
although for more serious disease, acute-phase reactants may provide
useful information for clinical management. (strong recommendation;
low-quality evidence)
29. In patients with more serious disease, such as those requiring
hospitalization or those with pneumonia-associated complications,
acute-phase reactants may be used in conjunction with clinical findings
to assess response to therapy. (weak recommendation; low-quality
evidence)
Pulse Oximetry
30. Pulse oximetry should be performed in all children with pneumonia and
suspected hypoxemia. The presence of hypoxemia should guide decisions
regarding site of care and
further diagnostic testing. (strong recommendation; moderatequality
evidence)
Chest Radiography
Initial Chest Radiographs: Outpatient
31. Routine chest radiographs are not necessary for the confirmation of
suspected CAP in patients well enough to be treated in the outpatient
setting (after evaluation in the office, clinic, or emergency department
setting). (strong recommendation; high-quality evidence)
32. Chest radiographs, postero-anterior and lateral, should be obtained in
patients with suspected or documented hypoxemia or significant
respiratory distress and in those with failed initial antibiotic therapy to
verify the presence or absence of complications of pneumonia,
including parapneumonic effusions, necrotizing pneumonia, and
pneumothorax. (strong recommendation; moderate-quality evidence)
39. The clinician should obtain tracheal aspirates for Gram stain and
culture, as well as clinically and epidemiologically guided testing for
viral pathogens, including influenza virus, at the time of initial
endotracheal tube placement in children requiring mechanical
ventilation. (strong recommendation; lowquality evidence)
40. Bronchoscopic or blind protected specimen brush sampling,
bronchoalveolar lavage (BAL), percutaneous lung aspiration, or open
lung biopsy should be reserved for the immunocompetent child with
severe CAP if initial diagnostic tests are not positive. (weak
recommendation; low-quality evidence)
Bradley, J.S., et al., 2011
K. MANAGEMEN
Pathogen-directed therapy
Treatment options are obviously simplified if the causative agent is
established or strongly suspectedDiagnostic procedures that provide
identification of a specific cause within 2472 h can still be useful for
guiding continued treatment. If, for example, an appropriate culture shows
the isolation of penicillinsusceptible S pneumoniae, treatment can be
specified by selecting a narrow spectrum agent (such as penicillin or
amoxicillin), which will hopefully reduce the selective pressure for
resistance. This information is often available at the time for consideration
when the patient is switched from parenteral to oral therapy. Length and
route of antimicrobial treatment
There are no controlled trials that have specifically assessed the optimum
duration of antimicrobial treatment in CAP. The decision is usually based
on the causative pathogen, response to treatment, comorbid illness, and
complications. Until further data are available, it seems reasonable to treat
bacterial infections such as those caused by S pneumoniae until a patient
is afebrile for 72 h.
Most randomised clinical trials for the new fluoroquinolones or newer
macrolides have shown good outcomes with 710 days of treatment, and
shorter courses could even be possible with the use of these agents
(azithromycin could be used for shorter courses of treatment in
ambulatory patients because of its longer half-life in tissue).
For many pathogens, there is no clear advantage of intravenous therapy
over oral therapy; however, for most patients admitted to hospital the
common practice is to begin therapy with intravenous drugs. Changing
from intravenous to oral therapy when the patient is clinically stable or
improving and is able to ingest drug is associated with several economic,
care, and social benefits. This approach has been shown to be
appropriate, even for patients with pneumococcal bacteraemia. Most
patients can be safely discharged without inhospital observation after
switch to oral treatment. Ideally, parenteral drugs should be given in an
oral formulation with adequate bioavailability; if no oral formulation is
available, then an oral agent with a similar spectrum of activity should be
selected on the basis of in vitro or predicted susceptibility patterns of the
established or probable pathogen.
The treatments for pneumonia depend on the type of pneumonia and the
severity of the condition.
The most common type of pneumonia is community-acquired pneumonia.
Normally, people who have community-acquired pneumonia will be
treated at home provided his condition is not very serious.
Most people can be treated at home by following these steps:
Drinking plenty of fluids to help loosen secretions and bring up the
phlegm.
Resting alone.
Cough medicines may make it harder for your body to cough up the extra
sputum. Thus, do not take cough medicines without consulting the doctor
first.
Controlling fever with acetaminophen, aspirin or non-steroidal anti-
inflammatory drugs. But never give aspirin to children.
Bacterial Pneumonia
In order to cure this type of pneumonia, antibiotics will be a wise choice to
kill the bacteria.
Streptococcus pneumonia
Antibiotics including penicillin such as amoxicillin in combination with
clavulanic acid and macrolide antibiotics such as erythromycin,
azithromycin and clarithromycin are used to treat this type of pneumonia.
Macrolide is used for penicillin-resistant Streptococcus pneumonia.
oral fluoroquinolones is used in the treatment of mild to moderate
community-acquired pneumonia.
However, overuse of fluoroquinolones as a single agent may promote
quinolone resistance.
Besides that, for elderly patient, combination therapy with a beta-lactam
and macrolide may give a better outcome in hospitalised patients.
Klebsiella pneumonia
The antibiotics that can be used are second and third generation
cephalosporins, amoxicillin in combination with clavulanic acid,
fluoroquinolones (levofloxacin), oral moxifloxacin, and trimethoprim in
combination with sulfamethoxazole.
Besides that, tigecycline can be used too but its significance side effect
(empyema recurrence) should be considered first before giving the
treatment.
Mycoplasma pneumonia
Macrolides such as erythromycin, clarithromycin and azithromycin is the
first line of therapy use in the treatment of community-acquired
pneumonia that is not responsive to beta-lactam antibiotics alone.
Tetracycline and fluoroquinolone are groups of antimicrobials that can be
used to treat this disease too.
However, both tetracyclines and fluoroquinolones are not recommended for
use in children. Fluoroquinolones are not recommended for use in children
younger than 18 years of age due to their potential for damaging cartilage
whereas tetracyclines is limited to children older than 8 years due to their
liability to cause permanent dental discolouration.
Legionella pneumophila pneumonia
Macrolides and fluoroquinolones are the monotherapy in the treatment of L.
pneumophila pneumonia whereas rifampin-based combination therapy is
used for severe community-acquired Legionella pneumophila pneumonia.
However, rifampin therapy should be considered only for patients with
severe disease or significant comorbid conditions such as uncontrolled
diabetes, smoking, or obstructive lung disease, immunocompromised hosts
and those patients who are refractory to conventional monotherapy
regimens. It is due to its significant adverse drug events and drug-drug
interactions
Chlamydia pneumonia
Most Chlamydia Pneumonia infections in children and young adults are
generally quite mild and do not require hospitalization. Severe cases of
Chlamydia Pneumonia most probably will happen in elderly people with
other pre-existing health complications. Chlamydia Pneumonia treatment
includes tetracyclines (eg. doxycycline) which is usually not for pregnant
women, macrolides( eg. trythromycin) and in some cases fluoroquinolones
are used.
Staphylococcus aureus pneumonia
Vancomycin and linezolid can be used to treat this type of pneumonia.
Besides that, ?-cyclodextrin
derivative (IB201) is use to treat Staphylococcus aureus pneumonia too. It
provides a high level of protection against lethal disease caused by both
methicillin-sensitive and methicillin-resistant clinical isolates. Early
treatment with IB201 is required to prevent mortality from Staphylococcus
aureus pneumonia.
Treatment of multidrug-resistant pneumonia
A patient will usually get multidrug-resistant pneumonia from a hospital
and thus multidrug resistant pneumonia is always related to hospital-
acquired pneumonia. Several drugs can be used to treat this type of
pneumonia.
Penicillin-resistant and cephalosporin-resistant pneumococcal pneumonia
Patients with mild/moderate pneumococcal pneumonia may be treated with
oral amoxicillin whereas patient with severe pneumonia may be
successfully treated with intravenous ceftriaxone, cefotaxime, or
amoxicillin-clavulanic acid. Imipenem and vancomycin should not be widely
used for the treatment of pneumococcal pneumonia except for well-
selected patients.
Methicillin- resistant staphylococcus aureus (MRSA) pneumonia
MRSA is resistant to all classes of beta-lactam antibiotics. Vancomycin is
the only antibiotic that consistently shows activity against MRSA. Besides
that, ceftaroline, teicoplanin and linezolid are the alternative therapy to
treat MRSA. Linezolid shows a better efficacy than vancomycin because of
its better pharmacokinetics and pharmacodynamics index.
Teicoplanin is another glycopeptide antibiotic available in Europe for the
treatment of MRSA. (Linezolid is
superior treatment for drug-resistant pneumonia n.d.) Other than that,
tigecycline is useful in the salvage therapy after linezolid failure.
Macrolide-resistant pneumonia
The ketolides represent a new class of macrolide-like antibacterials that are
highly effective in vitro against macrolide-resistant pneumococci.
Alternative therapy for pediatric pneumonia including tetracyclines and
fluoroquinolones should be considered in children experiencing treatment
failure although they are currently not approved for this indication.
Fluoroquinolone (levofloxacin)-resistant pneumonia
Cephalosporins can be used with or without the co-drug to treat this
disease. Combinations of potent parenteral cephalosporins (cefepime and
ceftriaxone) and some newer fluoroquinolones (gatifloxacin, gemifloxacin,
and moxifloxacin) have the greatest initial empiric coverage. These
treatments are less effective than vancomycin or quinupristin and
dalfopristin, but these latter agents possess narrower spectrums of overall
activity and higher associated toxicity.
Trimethoprim-sulfamethoxazole (TMP-SMX) resistant pneumonia
The combination of clindamycin and primaquine is use to treat this disease.
It is likely to be more effective than intravenous pentamidine.
Viral Pneumonia
Pneumonia caused by virus can be treated with antiviral agent which
inhibits DNA synthesis and viral replication by competing for viral DNA
polymerase with deoxyguanosine triphosphate. For example amantadine,
rimantadine, zanamivir, oseltamivir, ribavirin, acyclovir, ganciclovir, and
foscarnet are used as antiviral agent.
Amantadine and Rimantadine prevent penetration of the virus into the host
by inhibiting uncoating of influenza A. However during influenza season in
2005-2006, resistance to Rimantadine has emerged. Zanamivir and
Oseltamivir inhibit a glycoprotein on the surface of the influenza virus
called neuraminidase that destroys the infected cell's receptor for viral
hemagglutinin. The release of viruses from infected cells is reduced and the
spreading of virus is controlled through the inhibition of neuraminidase.
Similarly to Rimantadine, resistant strains of seasonal influenza and H1N1
to Oseltamivir have been reported.
Ribavirin inhibits DNA and RNA synthesis and thus preventing viral
replication. It has shown in vitro antiviral properties against RSV,
parainfluenza, hantavirus, measles, and many other. Acyclovir has affinity
for viral thymidine kinase and it causes DNA chain termination when
phosporylated when acted on by DNA polymerase. Thus it has inhibitory
activity of both HSV-1 and HSV-2 when it is used within 24-48 hours of rash
onset, patients experience less pain and faster resolution of HSV or VZV
lesions.
Ganciclovir is an acyclic nucleoside analog of 2'-deoxyguanosine and is a
synthetic guanine derivative. It inhibits replication of herpesviruses both in
vitro and in vivo and is active against CMV, HSV, H H V - 6 , and H H V - 8 .
The level of ganciclovir-triphosphate could reach 100-fold greater In CMV-
infected cells than in uninfected cells, possibly due to preferential
phosphorylation of ganciclovir in virus-infected cells.
Valganciclovir is an oral prodrug of Ganciclovir that is available now. For the
treatment of CMV pneumonia, high-dose intravenous immunoglobulin has
been used successfully in conjunction with ganciclovir. Through anti-
idiotypic antibodies, immune globulin IV neutralizes circulating myelin
antibodies. It down-regulates proinflammatory cytokines; blocks Fc
receptors on macrophages suppresses inducer T cells and B cells; amplify
suppressor T cells; stops the complement cascade, encourages
remyelination, and may increase CSF IgG levels (10%).
Foscarnet is an organic analog of inorganic pyrophosphate that inhibits viral
replication at pyrophosphate-binding sites on virus-specific DNA
polymerases of known herpesviruses, including CMV, HSV-1, and HSV-2.
Viral resistance may occur and this is shown if there is poor clinical
response or persistent viral excretion during therapy.
Fungal pneumonia
Pneumonia caused by fungi is treated using antifungal agent.Against
Cryptococcus neoformans, it is recommended that a regimen for induction
therapy is Amphotericin B plus flucytosine for at least 2 weeks followed by
consolidation therapy with fluconazole (400 mg daily) for 8 weeks, and
then maintenance therapy with fluconazole (200 mg daily) for life or until
the CD4 cell count rises above 200 cells/?L for at least 6 months as a result
of antiretroviral therapy.
Amphotericin B (liposomal) is also recommended as first-line treatment for
disseminated histoplasmosis caused by Histoplasma capsulatumand,
disseminated coccidioidomycosis caused by Coccidioides immitis and
Coccidioides posadasii and for cases of diffuse pneumonia.
Patients with histoplasmosis and coccidioidomycosis should be treated with
Amphotericin B until clinical improvement (usually at least 2 weeks). This is
followed by itraconazole (200 mg three times daily for 3 days, then 200 mg
twice daily) for a total of at least 12 months. Persons with severe
disseminated histoplasmosis or CNS involvement and those who relapse
despite appropriate therapy should receive itraconazole (200 mg daily)
probably for life.
Ming, C.K., 2011
General care:
- Adequate hydration - Routine use of antitussives not
recommended
- Analgesic/antipyretic if necessary - Oxygen therapy if hypoxemia
INESSS. 2009
Recommendations
1. Children and infants who have moderate to severe CAP, as defined by
several factors, including respiratory distress and hypoxemia (sustained
saturation of peripheral oxygen [SpO2], 90 % at sea level) (Table 3)
should be hospitalized for management, including skilled pediatric
nursing care. (strong recommendation; high-quality evidence)
2. Infants less than 36 months of age with suspected bacterial CAP are
likely to benefit from hospitalization. (strong recommendation; low-
quality evidence)
3. Children and infants with suspected or documented CAP caused by a
pathogen with increased virulence, such as community-associated
methicillin-resistant Staphylococcus aureus (CA-MRSA) should be
hospitalized. (strong recommendation; lowquality evidence)
4. Children and infants for whom there is concern about careful
observation at home or who are unable to comply with therapy or unable
to be followed up should be hospitalized. (strong recommendation; low-
quality evidence).
Bradley, J.S., et al., 2011
Recommendations
5. A child should be admitted to an ICU if the child requires invasive
ventilation via nonpermanent artificial airway (eg, endotracheal tube).
(strong recommendation; high-quality evidence)
6. A child should be admitted to an ICU or a unit with continuous
cardiorespirator monitoring capabilities if the child acutely requires use
of noninvasive positive pressure ventilation (eg, continuous positive
airway pressure or bilevel positive airway pressure). (strong
recommendation; very lowquality evidence)
7. A child should be admitted to an ICU or a unit with continuous
cardiorespirator monitoring capabilities if the child has impending
respiratory failure. (strong recommendation; moderate-quality evidence)
8. A child should be admitted to an ICU or a unit with continuous
cardiorespiratory monitoring capabilities if the child has sustained
tachycardia, inadequate blood pressure, or need for pharmacologic
support of blood pressure or perfusion. (strong recommendation;
moderate-quality evidence)
9. A child should be admitted to an ICU if the pulse oximetry measurement
is ,92% on inspired oxygen of $0.50. (strong recommendation; low-
quality evidence)
10. A child should be admitted to an ICU or a unit with continuous
cardiorespiratory monitoring capabilities if the child has altered mental
status, whether due to hypercarbia or hypoxemia as a result of
pneumonia. (strong recommendation; low-quality evidence)
11. Severity of illness scores should not be used as the sole criteria for ICU
admission but should be used in the context of other clinical, laboratory,
and radiologic findings. (strong recommendation; low-quality evidence)
Bradley, J.S., et al., 2011
ANTI-INFECTIVE TREATMENT
V. Which Anti-Infective Therapy Should Be Provided to a
Child With Suspected CAP in Both Outpatient and Inpatient
Settings?
Recommendations
Outpatients
Inpatients
46. Ampicillin or penicillin G should be administered to the fully
immunized infant or school-aged child admitted to a hospital ward
with CAP when local epidemiologic data document lack of substantial
high-level penicillin resistance for invasive S. pneumoniae. Other
antimicrobial agents for empiric therapy are provided in Table 7.
(strong recommendation; moderate-quality evidence)
47. Empiric therapy with a third-generation parenteral cephalosporin
(ceftriaxone or cefotaxime) should be prescribed for hospitalized
infants and children who are not fully immunized, in regions where
local epidemiology of invasive pneumococcal strains documents
high-level penicillin resistance, or for infants and children with
lifethreatening infection, including those with empyema. Nonb-
lactam agents, such as vancomycin, have not been shown to be
more effective than third-generation cephalosporins in the
treatment of pneumococcal pneumonia for the degree of resistance
noted currently in North America. (weak recommendation;
moderate-quality evidence)
48. Empiric combination therapy with a macrolide (oral or parenteral), in
addition to a b-lactam antibiotic, should be prescribed for the
hospitalized child for whom M. pneumonia and C. pneumoniae are
significant considerations; diagnostic testing should be performed if
available in a clinically relevant time frame (weak recommendation;
moderate-quality evidence)
49. Vancomycin or clindamycin (based on local susceptibility data)
should be provided in addition to b-lactam therapy if clinical,
laboratory, or imaging characteristics are consistent with infection
caused by S. aureus (strong recommendation; low-quality evidence)
VIII. How Should the Clinician Follow the Child With CAP for the
Expected Response to Therapy?
Recommendation
56. Children on adequate therapy should demonstrate clinical and
laboratory signs of improvement within 4872 hours. For children
whose condition deteriorates after admission and initiation of
antimicrobial therapy or who show no improvement within 4872
hours, further investigation should be performed. (strong
recommendation; moderate-quality evidence)
Bradley, J.S., et al., 2011
72. Children who are not responding to initial therapy after 4872 hours
should bemanaged by one ormore of the following:
a. Clinical and laboratory assessment of the current severity of
illness and anticipated progression in order to determine whether
higher levels of care or support are required. (strong
recommendation; low-quality evidence)
b. Imaging evaluation to assess the extent and progression of the
pneumonic or parapneumonic process. (weak recommendation;
low-quality evidence)
c. Further investigation to identify whether the original pathogen
persists, the original pathogen has developed resistance to the
agent used, or there is a new secondary infecting agent. (weak
recommendation; low-quality evidence)
73. A BAL specimen should be obtained for Gram stain and culture for
the mechanically ventilated child. (strong recommendation;
moderate-quality evidence)
74. A percutaneous lung aspirate should be obtained for Gram stain and
culture in the persistently and seriously ill child for whom previous
investigations have not yielded a microbiologic diagnosis. (weak
recommendation; low-quality evidence)
75. An open lung biopsy for Gram stain and culture should be obtained
in the persistently and critically ill, mechanically ventilated child in
whom previous investigations have not yielded a microbiologic
diagnosis. (weak recommendation; low-quality evidence)
DISCHARGE CRITERIA
77. Patients are eligible for discharge when they have documented
overall clinical improvement, including level of activity, appetite, and
decreased fever for at least 1224 hours. (strong recommendation;
very low-quality evidence)
78. Patients are eligible for discharge when they demonstrate consistent
pulse oximetry measurements .90% in room air for at least 1224
hours. (strong recommendation; moderatequality evidence)
79. Patients are eligible for discharge only if they demonstrate stable
and/or baseline mental status. (strong recommendation; very low-
quality evidence)
80. Patients are not eligible for discharge if they have substantially
increased work of breathing or sustained tachypnea or tachycardia
(strong recommendation; high-quality evidence)
81. Patients should have documentation that they can tolerate their
home anti-infective regimen, whether oral or intravenous, and home
oxygen regimen, if applicable, before hospital discharge. (strong
recommendation; low-quality evidence)
82. For infants or young children requiring outpatient oral antibiotic
therapy, clinicians should demonstrate that parents are able to
administer and children are able to comply adequately with taking
those antibiotics before discharge. (weak recommendation; very low-
quality evidence)
83. For children who have had a chest tube and meet the requirements
listed above, hospital discharge is appropriate after the chest tube
has been removed for 1224 hours, either if there is no clinical
evidence of deterioration since removal or if a chest radiograph,
obtained for clinical concerns, shows no significant reaccumulation of
a parapneumonic effusion or pneumothorax. (strong
recommendation; very low-quality evidence)
84. In infants and children with barriers to care, including concern about
careful observation at home, inability to comply with therapy, or lack
of availability for follow-up, these issues should be identified and
addressed before discharge. (weak recommendation; very low-
quality evidence)
The treatment plan must be followed and all medicines must be taken as
prescribed and ongoing medical care should be seeked. The doctor may want to
have a chest x ray on the patient to make sure the pneumonia is gone thus
follow up is necessary. Fatigue can persist for up to a month or more though the
patients may start to feel better after a few days or weeks. People who are
treated in the hospital may need minimum 3 weeks before they resume normal
routines.
L. KOMPLJKASI
pneumonia may lead to other diseases such as meningitis, etc.
Ming, C.K., 2011
705 928 patients were admitted to the hospital with community acquired
pneumonia (incidence: 3.5 cases per 1000 adults per year). The in-hospital
mortality of these patients was 13.1% (92 227 persons).
Strau, R., e al, 2014.
M. PROGNOSIS
Respiratory rate is an independent risk marker for in-hospital mortality in
community acquired pneumonia. It should be measured when patients are
admitted to the hospital with pneumonia and other acute conditions..
The plot of mortality as a function of respiratory rate on admission was U-
shaped and slanted to the right, with the lowest mortality at a respiratory
rate of 20/min on admission. If patients with a respiratory rate of 12
20/min are used as a baseline for comparison, patients with a respiratory
rate of 2733/min had an odds ratio (OR) of 1.72 for in-hospital death, and
those with a respiratory rate above 33/min had an OR of 2.55. Further
independent risk factors for in-hospital death were age, admission from a
nursing home, hospital, or rehabilitation facility, chronic bedridden state,
disorientation, systolic blood pressure, and pulse pressure.
N. PENGENDALIAN
PREVENTING PNEUMONIA IS KEY
Reducing pneumonia deaths also requires implementing effective
prevention measures so that children are healthier and less likely to
develop pneumonia in the first place. The prevention measures listed
below all show at least some evidence of reducing pneumonia mortality
among under-fives.a Some research has also suggested that hand
washing and lowering indoor air pollution play a role in reducing
pneumonia deaths among children in the developing world. For HIV-
infected children, preventing pneumonia (PCP) through cotrimoxazole
prophylaxis is essential (see Box 3, page 8 ).
IMMUNIZATION
Immunizations help reduce childhood deaths from pneumonia in two
ways.
First, vaccinations help prevent children from developing infections that
directly cause pneumonia, such as Haemophilus influenzae type b (Hib).
Second, immunizations may prevent infections that can lead to
pneumonia as a complication (e.g., measles and pertussis). Three
vaccines have the potential to significantly reduce child deaths from
pneumonia. These vaccines include the measles, Hib and pneumococcal
conjugate vaccines. Their ability to reduce pneumonia deaths is detailed
in Box 8, page 27.
ADEQUATE NUTRITION
Undernourished children are at a substantially higher risk of suffering
childhood death or disability. It has been estimated that child
undernutrition contributes to more than half of all child deaths in
developing countries, and that undernutrition in children aged 0-4 years
contributes to more than 1 million pneumonia deaths each year.e
Undernutrition may place children at an increased risk of developing
pneumonia in two ways. First malnutrition weakens a childs overall
immune system, as an adequate amount of protein and energy is
needed for proper immune system functioning. Second, undernourish
children have weakened respiratory muscles, which inhibits them from
adequately clearing secretions found in their respiratory tract.
EXCLUSIVE BREASTFEEDING
It is widely recognized that children who are exclusively breastfed
develop fewer infections and have less severe illnesses than those who
are not.
Breast milk contains the nutrients, antioxidants, hormones and
antibodies needed by the child to survive and develop, and specifically
for a childs immune system to function properly. Yet only about one third
of infants in the developing world are exclusively breastfed for the first
six months of life. Infants under six months old who are not breastfed are
at five times the risk of dying from pneumonia as infants who are
exclusively breastfed for the first six months of life. Furthermore, infants
6 - 11 months old who are not breastfed are also at an increased risk of
dying from pneumonia compared to those who are breastfed.
ZINC
Children who lack sufficient amounts of specific micronutrients,
particularly zinc, face additional risks of developing and dying from
pneumonia. A growing body of research highlights the importance of zinc
to child survival and to specifically reducing deaths from pneumonia.
intake helps reduce the incidence of pneumonia and the severity of the
disease.
Specifically, research has shown that zinc intake during the acute phase
of severe pneumonia decreased the duration and severity of pneumonia
and reduced treatment failure rates when compared with a placebo
intervention. Improving the zinc status of children is currently being
considered by public health and nutrition experts
Unicef-WHO, 2006
sles vaccine).
- Smoke-free home
- Vaccination: Haemophilus influenzae type b (Pediacel) vaccine;
pneumococcal conjugate vaccine (Prevnar, Synflorix)
INESSS. 2009
PREVENTION