CHAPTER II
LITERATURE REVIEW
2.1. Definition
Bronchopneumonia is a condition that child with respiratory distress;
any of: rapid, noisy, or difficult breathing; respiratory rate >60/min;
chest retractions; cough; grunting; who has a positive blood culture or
predisposing factors. Bronchopneumonia
which is a febrile illness with cough, respiratory distress with evidence of
localised or generalised patchy infiltrates on chest x-ray.1
In bronchopneumonia, the focus of infection
and the inflammatory response is in the bronchi and surrounding parenchyma.
Consolidation is segmental in distribution, and involvement is patchy;
segmental involvement may become confluent to produce a more homogeneous
pattern. Bronchopneumonic patterns
are commonly observed in pulmonary infections due to S. aureus or
nonencapsulated H. influenzae. With S. aureus infections,
macro- and microabscess formation may occur rapidly. Also, pneumatoceles occur
during the first week of lung involvement in about half the children with S.
aureus pneumonia. These cystic spaces are believed to be the consequence of
a check valve opening between a peribronchial abscess and an adjacent bronchus.
A bronchopneumonic pattern of consolidation
is commonly observed when pneumonia is engrafted on underlying bronchiectasis
or chronic bronchitis. In such predisposing circumstances, S. pneumoniae infection
may produce a bronchopneumonic pattern rather than its usual lobar
consolidation. In
the presence of underlying emphysema, the radiographic pattern of pneumococcal
pneumonia may also be altered from its usual homogeneous pattern to one that
contains multiple radiolucencies (representing unconsolidated emphysematous
areas) that may be misinterpreted as abscesses.
Segmental bronchopneumonia is the
radiographic picture in pneumonia due to C. pneumoniae or M.
pneumoniae, and in many viral pneumonias. Any of the bacterial species that
cause nosocomial pneumonia can produce a radiographic pattern of
bronchopneumonic consolidation.
Like lobar pneumonia, centrilobular and
peribronchiolar opacity pneumonia (bronchopneumonia), a characteristic imaging
category of pneumonia that is commonly encountered in all patient groups. It is
an especially common imaging category in CAP that follows viral infection. It
is also called bronchopneumonia because it is associated with acute infection
of the walls of bronchioles that spreads into the peribronchiolar alveoli, and
often involves the lung in a patchy multifocal distribution.
I.
Predisposing factors
of bronchopneumonia;
a. Maternal fever (≥ 38˚C)
b. Foul smelling liquor
c. Prolonged rupture of membranes
(>24 hours)
II.
Clinical picture of
sepsis
a. Poor feeding
b. Lethargy
c. Poor reflexes
d. Hypothermia or hyperthermia
e. Abdominal distension
III.
Radiograph suggestive
of pneumonia
a. nodular or coarse patchy infiltrate
b. diffuse haziness or granularity
c. air bronchogram
d. lobar or segmental consolidation
e. radiological changes not resolved within 48 hours
IV.
Positive sepsis
screen (any of the following):
a. Bands ≥ 20% of leucocytes
b. Leucocyte count out of reference range
c. Raised C reactive protein
d. Raised erythrocyte sedimentation rate
2.2. Etiology
Many patients with bronchopneumonia have mild
and self-limited disease attributable to respiratory viruses, including epidemic
influenza, adenovirus, rhinovirus, and respiratory syncytial viruses (RSV).
Some of these viruses can produce more serious primary pneumonia, as well as
set the stage for bacterial or other etiology superinfection pneumonia,
especially when there are co-morbid conditions. Severe acute respiratory
syndrome, a newly identified
coronavirus infection, can produce severe viral pneumonia with a broad spectrum
of imaging findings, including bronchopneumonia.
Other organisms that commonly cause
bronchopneumonia include Mycoplasma pneumoniae, Chlamydia pneumon;iae, Haemophilus
influenzae, and Neisseria catarrhalis (Moraxella catarrhalis).Klebsiella
pneumoniae, Escherichia coli, and Pseudomonas aeruginosa are
also common causes of nosocomial (and ventilator-associated) bronchopneumonia,
and of community-acquired bronchopneumonia in patients with co-morbid
conditions. These latter pneumonias are associated with necrosis, abscess
formation and pleural effusion.
The role of Staphylococcus aureus in
the etiology of bronchopneumonia in the ventilator-associated milieu pneumonia
(VAP) is controversial because airway recovery of the organism is not usually
associated with the characteristic imaging signs of CAP caused by that organism
in patients without
co-morbid conditions, i.e., rapid development and necrosis. The organisms that
cause peripheral airspace consolidation pneumonia are not restricted from also
causing bronchopneumonia when bronchioles are already inflamed by recent
infection.
Non-infectious simulators and etiologies of
centrilobular and peri-bronchial
opacities include aspiration pneumonia, itself a frequent non-infectious
cause of bronchopneumonia, as
well
as a facilitator of superinfection. Other causes include bronchiolo-alveolar cell
carcinoma, non-infectious granulomasdue to pneumoconiosis, sarcoidosis,
respiratory bronchiolitis, hypersensitivity
pneumonitis, bronchiolitis obliterans organizing
pneumonia, asthma, autoimmune disease, and
bronchiolitis obliterans. They can also be found in patients with small mucous
airway plugs and other endobronchial disease.
Etiology of
Bronchopneumonia for neonates; infant; and child;
Age
|
Common Etiology
|
Less Etiology
|
Birth-20days
|
Bacteria
|
Anaerob Bacteria
|
E. colli
|
Streptococcus group D
|
|
Streptococcus group B
|
Haemophillus influenza
|
|
Listeria monocytogenes
|
Streptococcus pneumonia
|
|
Ureaplasma urealyticum
|
||
Virus
|
||
Citomegalovirus
|
||
Herpes Simplex Virus
|
||
3weeks-3months
|
Bacteria
|
Bacteria
|
Chlamydia trechomatis
|
Bordetella pertusis
|
|
Streptococcus pneumonia
|
Haemophillus influenza type B
|
|
Virus
|
Moraxella catharalis
|
|
Adenovirus
|
Staphylococcus aureus
|
|
Influenza Virus
|
Ureaplasma urealyticum
|
|
Parainfluenza Virus 1,2,3
|
Virus
|
|
Respiratory syncytial virus
|
Cytomegalo Virus
|
|
4 months - 5 years
|
Bacteria
|
Bacteria
|
Chlamydia pneumonia
|
Haemophillus influenza type B
|
|
Mycoplasma pneumonia
|
Moraxella catharalis
|
|
Streptococcus pneumonia
|
Staphylococcus aureus
|
|
Virus
|
Neisseria meningitidia
|
|
Adenovirus
|
Virus
|
|
Influenza virus
|
Varicella-Zoster Virus
|
|
Parainfluenza virus
|
||
Rhinovirus
|
||
Respiratory Syncytial Virus
|
||
>5 years
|
Bacteria
|
Bacteria
|
Chlamydia pneumonia
|
Haemophillus influenza
|
|
Mycoplasma pneumonia
|
Legionella sp
|
|
Streptococcus pneumonia
|
Staphylococcus aureus
|
|
Virus
|
||
Adenovirus
|
||
Influenza virus
|
||
Parainfluenza virus
|
||
Rhinovirus
|
||
Respiratory Syncytial Virus
|
||
Epstein-bar virus
|
||
Varicella-zoster virus
|
2.3. Epidemiology
Bronchopneumonia is estimated
that 3.9 million of the 10.8 million deaths in children annually world wide
occur in the first 28 days of life. More than 96% of all child deaths occur in
developing countries, and pneumonia accounts for a substantial proportion of
these. Intrauterine and early onset pneumonia was found at autopsy in 10–38% of
stillborn and 20–63% of liveborn babies who subsequently died (with all but one
of six studies in the range of 20–32%). In a separate series of 1044 autopsies
on neonatal deaths in the first 48 hours of life, 20–38% had pneumonia, with
the highest incidence in poorer socioeconomic groups. There are therefore
likely to be between 750 000 and 1.2 million neonatal deaths annually where
pneumonia is involved, and neonatal pneumonia accounts for 10% of global child
mortality.
Throughout childhood, the
greatest risk of death from pneumonia is in the neonatal period. In a field
trial of community based management of childhood pneumonia in India, more than
half of all child deaths from pneumonia occurred among neonates. Pneumonia
mortality risk is strongly dependent on birth weight and age of onset. Case
fatality rates are much higher for intrauterine or early onset pneumonia than
for late onset neonatal pneumonia, and higher among low birthweight newborns.
The proportion of neonatal respiratory distress that is caused by pneumonia
will depend on where the source population is from (tertiary hospital, district
hospital, or community), the stage in the perinatal period, the gestational age
of the babies and the availability of intensive care, and the definition of
pneumonia. Of 150 neonates with respiratory distress presenting to a referral
hospital in India, 103 (68.7%) were diagnosed to have pneumonia. Using a
different case definition in a teaching hospital in Brazil, of 318 infants
presenting with respiratory distress within the first 4 days of life, bacterial
infection was proven on culture in 31 (9.7%), and another 62 (19.5%) had
radiographic signs of pneumonia.
2.4. Pathophysiology
Commonly some microorganism has inhaled to
peripheral lung by respiratory track. Swelling caused by tissue reaction that
may easily proliferating and diffusing microorganism to the other tissues.
Infected lung area may there consolidation; there were PMN cell, fibrin,
eritrosit, swelling fluid, and microorganism founded at alveoli. This stage
called red hepatisation stage. And then increasingly fibrin deposite, there is
fibrin and PMN cell founded at alveoli, then degeration cell, thining fibrin,
microorganism and loss debrisment. This is called resolution. Broncopulmonary
system for uninfected lung area will be normal.
Antibiotics should given as soon as possible for
cutting previous illness, so those stage that explained were not founded. Some
bacteria could more pathological than others bacteria. Streptococcus pneumonia
would manifestate as diffuse consolidation entire all lung area
(bronchopneumonia); and for children would manifestate localized consolidation
at one lobus (pneumonia lobaris). Pneumococcell and little absesses commonly
caused by staphylococcus aureus for neonates and infants. As staphylococcus
aureus could release some toxin and enzyme like hemolysin, lekosydine,
staphylokinase, and Coagulase. Coagulase could interacted with plasma factor
and release active agent that converting fibrinogen to fibrin; so there is
fibrinopurulent eksudate. There is correlation between coagulase product and
microorganism virulence. Some staphylococcus couldn’t release coagulase less made seriously
disease. Penumotoccell would stay at infected lung for many months; but not
needed the next management.
2.5. Diagnostic
Etiologic diagnostic according to microbiologic test and/or serologic is
the base of optimal theraphy. But, etiologic finding of bacteria is not easy
because adequate laboratorium is required. Because of that, bronchopneumonia in
infant commonly diagnosed according to symptoms which can be seen from
respiratory system, and radiologic findings. The most predictor of pneumonia is
fever, cyanotic, and more than one respiratory symptoms consist of : tachypnea, cough, nostril breathing, retraction, ronchi, and
decreased breath sound.2
Because the high rate of morbidity and mortality of infant pneumonia, in
case for the treatment, WHO develops diagnosis guidelines and simple treatment.
The guidelines is mostly given to primary heath care service, and as health
education to community in developing countries. The goal is to simplify
diagnostic criteria according to clinical manifestations that can be detected
directly; to determine disease classification, and determining antibotic used.
Simple clinical manifestation include tachypnea, dyspnoe, and some emergency sign so infant can be referred quickly to
health care service. Tachypnea can be
assessed from counting breath frequency along one minute when the infant at
calm condition. Dyspnoe can be assessed by looking chest retraction at the lower chest region when the infant
inhaled (epigastrium retraction).
Emergency sign in infant at 2 months – 5 years old is cannot be able to drink,
seizures, decreased consciousness,
stridor, and malnutrition, emergency sign for infant at age under 2 months
years old is poor feeding, seizures, decreased alertness, stridor, wheezing,
and fever.2
How to diagnose bronchopneumonia; once caregivers have recognized the
danger (signs of brochopneumonia (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 bronchopneumonia
in children according to the following Integrated Management of Childhood
Illness (IMCI) guidelines.5
Children aged 2 months to 5 years are diagnosed with bronchopneumonia if
they exhibit a cough and fast or difficult breathing. Thresholds for fast
breathing depend on the child’s age. Severe bronchopneumonia in children is diagnosed
if they exhibit lower chest wall indrawing when the child’s 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.5
The clinical diagnosis of bronchopneumonia
has traditionally been made using auscultatory findings such as bronchial
breath sounds and crepitations in children with cough. However, the sensitivity
of auscultation has been shown to be poor and varies between 33 %- 60% with an
average of 50 % in children. Tachypnea is the best single predictor in children
of all ages. Measurement of tachypnea is better compared with observations of
retractions or auscultatory findings. It is nonetheless important to measure
respiratory rate accurately. Respiratory rate should be counted by inspection
for 60 seconds. However in the young infants, bronchopneumonia may present with
irregular breathing and hypopnea.1
Bronchopneumonia is an
infection in the lungs; a germ such as bacteria, virus, fungus or parasite can
cause it. When a child gets bronchopneumonia, tiny air sacs in the lungs can
fill with fluid. This fluid blocks the air sacs and oxygen cannot get to the
body from the lungs. Signs of bronchopneumonia;
Chills, Fever, Chest Pain, Cough with yellow or green mucus, Feeling
very tired, Trouble breathing or fast breathing, Poor appetite or poor breast
or bottle feeding.4
Hospitalization indication for child with bronchopneumonia is; chest pain when he or she breathes; long coughing
spells; trouble breathing or fast breathing; nausea and vomiting; a high fever
that comes on quickly or a fever that lasts more than 1 to 2 days; confusion.4
Chest X-rays
and laboratory tests are used to confirm the presence of bronchopneumonia,
including the extent and location of the infection and its cause. But in
resource-poor settings without access to these technologies, suspected cases of
bronchopneumonia are diagnosed by their clinical symptoms. Children and infants
are presumed to have bronchopneumonia if they exhibit a cough and fast or
difficult breathing. Caregivers, therefore, have an important role to play in
recognizing the symptoms of bronchopneumonia in children and seeking
appropriate medical care as necessary.5
Children with bacterial bronchopneumonia cannot be
reliably distinguished from those with viral disease on the basis of any single
parameter; clinical, laboratory or chest radiograph findings.1
1. Chest radiograph
Chest radiograph is indicated when clinical criteria
suggests bronchopneumonia. It will not identify the aetiological agent. However
the chest radiograph is not always necessary if facilities are not available or
the bronchopneumonia is mild.
2. Complete white blood cell and differential count
This test may be helpful as an increased white blood
count with predominance of polymorphonuclear cells may suggest bacterial cause.
However, leucopenia can either suggest a viral cause or severe overwhelming
infection.
3. Blood culture
Blood culture
remains the non-invasive gold standard for determining the precise aetiology of
bronchopneumonia. However the sensitivity of this test is very low. Positive
blood cultures are found only in 10% to 30% of patients with bronchopneumonia.
Even in 44% of patients with radiographic findings consistent with bronchopneumonia,
only 2.7% were positive for pathogenic bacteria. Blood culture should be
performed in severe bronchopneumonia or when there is poor response to the
first line antibiotics.
4. Culture from respiratory secretions
It should be
noted that bacteria isolates from throat swabs and upper respiratory tract
secretions are not representative of pathogens present in the lower respiratory
tract. Samples from the nasopharynx and throat have no predictive values. This
investigation should not be routinely done.
5. Other tests
Bronchoalveolar
lavage is usually necessary for the diagnosis of pneumocystis carini infections
primarily in immunosuppressed children. It is only to be done when
facilities and expertise are available. If there is significant pleural
effusion diagnostic, pleural tap will be helpful. Mycoplasma pneumoniae,
Chlamydia, Legio nella and Moxarella catarrhalis are difficult organisms to
culture, and thus serological studies should be performed in children with
suspected atypical pneumonia. An acute phase serum titre of more than 1:160 or
paired samples taken 2-4 weeks apart showing four fold rise is a good indicator
of Mycoplasma pneumoniae infection. This test should be considered for
children aged five years or older with pneumonia.1
Differential
Diagnosis
Condition
|
Differentiating signs/symptoms
|
Differentiating tests
|
Bronchitis
|
Patient with
bronchitis often have a lower grade fever than in patient with pneumonia, and
may appear less ill, and no rales on lung examination
|
The chest
radiograph may interpretated by normal
|
Bronchiolitis
|
Infants
with pneumonia generally have higher fever (≥40°C) than with bronchiolitis.
Wheezing
is not a common finding in pneumonia. While in bronchiolitis is more common.
|
An FBC may demonstrate
leukocytosis and neutrophilia in pneumonia than in patient with bronchiolitis
The presence of a focal
infiltrate on chest x-ray would increase the suspicion of pneumonia.
|
Bronchiectasis
|
Patients
with pneumonia describe symptoms of short duration (7 to 10 days), as opposed
to years in bronchiectasis.
Auscultation
findings (rhonchi, wheezing, crackles) may be similar in bronchiectasis and
pneumonia, especially multi-lobar pneumonia. Bronchial breath sounds, which
are characteristic of pneumonia, are not present in bronchiectasis.
|
CXR and
chest CT results in pneumonia are quite variable and often depend on
aetiology.
In
bronchiectasis, there is characteristic dilation of bronchi with or without
airway thickening.
Consolidation,
which is seen in pneumonia, is not seen in bronchiectasis.
|
Patients with asthma have
bilateral wheezing; In asthma, bronchospasm is recurrent and progressive.
|
PFT may be useful to diagnose
asthma in patients who have residual obstructive findings.
|
|
Dyspnoea and
tachypnoea are common before intubation. If ARDS is secondary to an
infection, a fever will be present. Furthermore, fever is a feature of
fibroproliferative ARDS.
|
The ratio of
FiO2 to PaO2 <200 supports ARDS in the context of a diffuse opacity.
Patients are
typically intubated and sedated and therefore a common method of diagnosis is
generalised pulmonary opacity seen on CXR.
|
|
A viral infection of the
upper airways, often caused by parainfluenza viruses.
Characterised by fever,
inspiratory stridor, and a barking cough.
Symptoms often worsen at
night.
|
Diagnosis is usually
clinical.
Sub-glottic narrowing may be
seen on an AP neck radiograph; however, this investigation is rarely
indicated.
|
|
A history of
immunosuppression or prolonged course that is not responding to antibacterial
therapy suggests tuberculosis.
|
Sputum
cultures and acid fast bacilli stains positive. A cavity on the CXR may be
observed.
|
|
Atelectasis
|
Usually not hypoxic or
febrile, although a low-grade fever may be present.
|
Leukocytosis and sputum
production may or may not be present.
Opacities on a CXR tend to be
more linear than lobar shaped.
|
2.6. Management
Assessment of severity of pneumonia
The predictive value of
respiratory rate fo r the diagnosis of pneumonia is age specific (Table 7)
Age Respiratory
Rate
Less than 2 months
> 60 /min
2- 12 months >
50 /min
12 months – 5 years > 40/ min
|
Assessment of severity is essential for optimal
management of pneumonia. Pneumonia may be categorized according to mild,
severe, very severe based on the respiratory signs and symptoms (Table 8 and
Table 9)5
Table 8: Assessment of severity of pneumonia in
infants below two months old.
Severe pneumonia Severe chest indrawing or fast
breathing
Very severe pneumonia Not
feeding
Convulsions
Abnormally sleepy or difficult to wake
Fever/ low body temperature
Hypopnea with slow irregular breathing
|
Table 9: Assessment of severity of pneumonia in children age 2 months to
5 years old
Mild Pneumonia Fast
breathing
Severe pneumonia Chest
indrawing
Very severe pneumonia Not able to drink
Convulsions
Drowsiness
Malnutrition
|
II Assessment of oxygenation
The best objective
measurement of hypoxia is by pulse oximetry which avoids the need for arterial
blood gases. It is a good indicator of the severity of pneumonia.
III Criteria for hospitalization
Community acquired pneumonia
can be treated at home. It is crucial to identify indicators of severity in
children who may need admission as failure to do so may result in death. The
following indicators can be used as a guide for admission.
1. Children aged <3 months whatever the severity of
pneumonia.
2. Fever (>38.50 C), refusal to feed and vomiting
3. Rapid breathing with or without cyanosis
4. Systemic manifestation
5. Failure of previous antibiotic therapy
6. Recurrent pneumonia
7. Severe underlying disorders ( i.e.
immunodeficiency, chronic lung disease )
IV Antibiotic therapy
When treating pneumonia
clinical, laboratory and radiographic findings should be considered. The age of
the child, local epidemiology of respiratory pathogens and sensitivity of these
pathogens to particular microbial agents and the emergence of antimicrobial
resistance also determine the choice of antibiotic therapy (Table 10 and Table
11) The severity of the pneumonia and drug costs have also a great impact on
the selection of therapy.1
The majority of childhood
infections are caused by viruses and do not require any antibiotic. However, it
is also very important to remember that we should be vigilant to choose
appropriate antibiotics especially in the initial treatment to reduce further mortality
and morbidity.1
Table 10: Susceptibility (%) pattern of Streptococcus
pneumoniae found in Malaysia.
Antibiotic Susceptible
Intermediate Resistance
Azithromycin 98.1
1.9
Cefuroxime 99.6
0.4
Chloramphenicol 95.1
1.5 3.4
Chlindamycin 9.2 0.4 0.4
Cotrimoxazole 86.4
3.9 9.7
Erythromycin 98.4
0.4 1.1
Penicillin 93.0
7.0
Tetracycline 78.2
0.8 21.0
|
Pathogens Antimicrobial
agent
Beta- lactam susceptible
Streptococcus pneumonia Penicillin, Cephalosporins
Haemophilus influenzae type b Ampicillin,Chloramphenicol,
Cephalosporins
Staphylococcus aureus Cloxacillin
Group A Sreptococcus Penicillin,Cephalosporin
Mycoplasma pneumoniae Macrolides
such as erythromycin and
Azithromycin
Chlamydia pneumoniae Macrolides such as erythromycin and
Azithromycin
Bordetella pertussis Macrolides such as erythromycin and
Azithromycin
|
Table 12: Commonly used antibiotics and their dosages
Intravenous Antibiotics Dosages
Amoxycillin-Clavulanate Acid 10-25mg/kg/dose
8 hrly
Ampicillin -sulbactam 10-25 mg/kg/dose
8 hrly
Ampicillin 100mg/kg/day
6 hrly
C. Penicillin 25,000-50,000U/kg/dose
6 hourly
Cefuroxime 10-25
mg/kg/dose 8 hrly
Cefotaxime 25-50mg/kg/dose
8 hrly
Cloxacillin 25-50mg/kg/dose
6hrly
Co-trimoxazole (trimethoprim ) 4
mg/kg/dose 12 hrly
Erythromycin 7.5mg
kg/dose 6 hrly
|
Oral Antibiotis Dosages
Azithromycin 10-15
mg/kg/day daily dose
Augmentin 114
mg 12 hourly (less than 2 years)
228 mg 12 hourly (more than 2 years)
Cefuroxime 125
mg 12 hourly (less than 2 years)
250 mg 12 hourly (more than 2 years)
Cotrimoxazole 4
mg/kg/dose 12 hourly
Cloxacillin 50mg/kg
/dose 6 hourly
Erythromycin Estolate 7.5
mg/kg/dose 12 hour ly
Penicillin V 7.5
- 15 mg/kg/dose 6 hourly
|
INPATIENT MANAGEMENT
Antibiotic therapy
1st line β
lactams drugs: Benzlypenicillin, Amoxycillin, Ampicillin,
Amoxycillin-Clavulanate
2nd line Cephalosporins
: Cefotaxime, Cefuroxime, Ceftazidime,
3rd line Carbapenem:
Imepenam
Others Aminoglycosides:
Gentamicin, Amikacin
|
If there are no signs of
recovery; especially if the patient remains toxic and ill with spiking
temperature for 48-72 hours, a 2nd of 3rd line antibiotic therapy need to be considered.
If Mycoplasma or Chlamydia species are the causative agents, a
macrolide is the appropriate choice.1
A child admitted to hospital
with severe community acquired pneumonia must receive parenteral antibiotics.
As a rule, in severe cases of pneumonia, combination therapy using a second or
third generation cephalasporins and macrolide should be given. Staphylococcal
infections and infection caused by Gram negative organisms such as Klebsiella
sp are more frequently reported in malnourished children.1
Staphyloccoccal infection
Staphylococcus
aureus is responsible for a small
proportion of acute respiratory infections in children. Nevertheless a high
index of suspicion is required because of the potential for rapid deterioration.
It is chiefly a disease of infants with a significant mortality rate.
Radiological features suggestive of Staphylococcal pneumonia include the
presence of multilobar consolidation, cavitation, pneumatocoeles, spontaneous pneumothorax,
empyema and pleural effusion. Treatment with high dose intravenous cloxacillin
(200mg/kg.day) for a longer duration and drainage of empyema will result in
good outcome in the majority of cases.1
II Supportive treatment
1. Fluid therapy
Oral intake should cease
when a child is in severe respiratory distress. In severe pneumonia,
inappropriate secretion of anti-diuretic hormone is increased, dehydration is
therefore uncommon. It is important that the child should not be overhydrated.
2. Oxygen therapy
Oxygen reduces mortality
associated with severe pneumonia. It should be given especially to children who
are restless, tachypnoea with severe chest indrawing, cyanosed or not
tolerating feeds. The SpO2 should be maintained above 95%.
3. Anti-tussive remedies
It is not recommended as it
causes suppression of cough and may interfere with airway clearance. Adverse
effects and overdosa ge have been reported.
4. Chest physiotherapy
The function of chest
physiotherapy is to assist in the removal of tracheobronchial secretions
resulting in an increase gas exchange and reduction in the work of breathing. However,
trials have found no clinically discernible benefit or impact of chest physiotherapy
on the course of illness in bronchiectasis, cystic fibrosis, pneumonia, bronchiolitis,
asthma, acute atelectasis, inhaled foreign body and post extubation babies.
There is no evidence to suggest that chest physiotherapy should be routinely performed
in pneumonia1
OUTPATIENT MANAGEMENT
In children with mild
pneumonia, their breathing is fast but there is no chest indrawing. Oral
antibiotics at an appropriate dose for an adequate duration is effective for
treatment. The mother is advised to return in two days for reassessment or
earlier if the child appears to deteriorate.
Children aged 2 months to 5 years with severe pneumonia should be
referred to the nearest health facility immediately. Those diagnosed with
pneumonia may be treated at home with a full course of effective antibiotics.
Cotrimoxazole
and amoxicillin are effective drugs against bacterial pathogens and are often
used to treat children with pneumonia in developing countries. Infants under
two months with signs of pneumonia/sepsis are at risk of suffering severe
illness and death more quickly than older children, and should be immediately
referred to a hospital or clinic for treatment. Treatment regimens will need to
be chosen based on their efficacy in local settings. Some areas may have high
levels of resistance to certain antibiotics, rendering those drugs less
effective for treating pneumonia.Other areas may have large numbers of
high-risk groups, such as undernourished or HIV-positive children, and may need
to adapt their treatment strategies accordingly.5
Infants less than 2 months old with signs of pneumonia should be
referred promptly to the nearest health facility because they are at high risk
of suffering severe illnessor death.5
Sign
|
Classify As
|
Treatment
|
·
Fast breathing (see below)
·
Lower chest wall indrawing
·
Stridor in calm child
|
Severe pneumonia
|
·
Refer urgently to hospital for injectable
·
antibiotics and oxygen if needed
·
Give first dose of appropriate antibiotic
|
Fast breathing
The child has fast
breathing if you count;
·
2 months to 12 months old 50 breaths or more per
minute
·
12 months to 5 years old 40 breaths or more per
minute
|
Non-severe pneumonia
|
·
Prescribe appropriate antibiotic
·
Advise mother on other supportive measures and when
to return for a follow-up visit
|
No fast breathing
|
Other respiratory illness
|
Advise mother on
other supportive measures and when to return; if symptoms persist or get
worse
|
2.7. Prevention
There are several reasons why interventions that can only be delivered in
hospitals will make little impact on deaths from bronchopneumonia. In many societies, infant are not taken outside the home, even if they are sick, so referral to a
hospital is impossible. Often there is a preference for traditional village
remedies. In addition, because the signs of severe illness can be very subtle
in infants, parents may not recognise that their infant is
sick until it is too late, and geographical and financial constraints make
referral to hospital very difficult for much of the world’s population. On the
other hand, interventions solely at community level will not fully address the
often fatal complications of hypoxaemia and apnoea. Improving supportive care
and the safety and accessibility of hospitals for seriously ill newborn babies
is a high priority globally. A comprehensive approach to prevention and
treatment of neonatal pneumonia would therefore involve interventions at
community level, in primary health facilities, and in district and tertiary
hospitals.
a.
Teach children
to wash their hands before eating and after using the toilet.
b.
Keep children
away from people who are smoking.
c.
Make sure
children get all of their vaccines or shots:
i.
All children 2
years and younger should get the PCV vaccine to protect against pneumonia.
Children older than 2 years may need a different type of vaccine.
ii.
To limit your children’s risk of pneumonia,
have them get a flu shot every fall. You can get pneumonia from the flu.
d. Make sure children are eating a healthy diet that
includes fruits, vegetables and whole grain foods.
e. Make sure children are getting plenty of sleep.4
2.8. Complication
Complication of bronchopneumonia in infant
include thoracic empiema, purulent pericarditis, pneumothorax, or
extrapulmonary infection such as purulent meningitis. Thoracic empiema is the
most commonly complication in bacterial pneumonia.2
Ilten F et all, reported
miocarditis complication (systolic pressure of right ventricel is increased, increased
kinase creatinine, and heart failure) is enough high in pneumonia cases at 2-24
months years old. Because of that miocarditis is a fatal condition, and advises
to do detection by noninvasive technique such as ECG, Echocardiography, and
enzime test.2
2.9. Prognostic
Overall, the prognosis is good. Most
cases of viral pneumonia resolve without treatment; common bacterial pathogens
and atypical organisms respond to antimicrobial therapy. Long-term alteration
of pulmonary function is rare, even in children with pneumonia that has been
complicated by empyema or lung abscess.
Patients placed on a protocol-driven
pneumonia clinical pathway are more likely to have favorable outcomes. The
prognosis for varicella pneumonia is somewhat more guarded. Staphylococcal
pneumonia, although rare, can be very serious despite treatment.
Morbidity
Although viral pneumonias are common
in school-aged children and adolescents and are usually mild and self-limited,
these pneumonias are occasionally severe and can rapidly progress to respiratory
failure, either as a primary manifestation of viral infection or as a
consequence of subsequent bacterial infection.
Morbidity and mortality from RSV and
other viral infections is higher among premature infants and infants with
underlying lung disease. Significant sequelae occur with adenoviral disease,
including bronchiolitis obliterans and necrotizing bronchiolitis. With neonatal
pneumonia, even if the infection is eradicated, many hosts develop long-lasting
or permanent pulmonary changes that affect lung function, the quality of life,
and susceptibility to later infections.
Infants and postpubertal adolescents
with TB pneumonia are at increased risk of disease progression. If TB is not
treated during the early stages of infection, approximately 25% of children
younger than 15 years develop extrapulmonary disease.
Bronchopneumonia occurs in 0.8-2% of
all pertussis cases and 16-20% of hospitalized cases; the survival rate of
these patients is much lower than in those with pneumonia that is attributed to
other causes.
Immunocompromised children, those
with underlying lung disease, and neonates are at high risk for severe
sequelae, and they are also susceptible to various comorbidities. Cryptococcosis may occur
in as many as 5-10% of patients with AIDS, and acute chest syndrome occurs in
15-43% of patients with sickle cell disease. Individuals with sickle cell disease
not only have problems with their complement system, but they also have
functional asplenia, which predisposes them to infection with encapsulated
organisms such as S pneumoniae and H influenzae type B.
Mortality
The United Nations Children's Fund
(UNICEF) estimates that 3 million children die worldwide from pneumonia each
year; these deaths almost exclusively occur in children with underlying
conditions, such as chronic lung disease of prematurity, congenital heart
disease, and immunosuppression. Although most fatalities occur in developing
countries, pneumonia remains a significant cause of morbidity in industrialized
nations.
According to the WHO’s Global Burden
of Disease 2000 Project, lower respiratory infections were the second leading
cause of death in children younger than 5 years (about 2.1 million [19.6%]).
Most children are treated as outpatients and fully recover. However, in
young infants and immunocompromised individuals, mortality is much higher. In
studies of adults with pneumonia, a higher mortality rate is associated with
abnormal vital signs, immunodeficiency, and certain pathogens.
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