Pneumonia berat

Tatalaksana

 Anak dirawat di rumah sakit

Terapi Antibiotik

 Beri ampisilin/amoksisilin (25-50 mg/kgBB/kali IV atau IM setiap 6 jam), yang harus

dipantau dalam 24 jam selama 72 jam pertama. Bila anak memberi respons yang baik
maka diberikan selama 5 hari. Selanjutnya terapi dilanjutkan di rumah atau di rumah
sakit dengan amoksisilin oral (15 mg/ kgBB/kali tiga kali sehari) untuk 5 hari berikutnya.
 Bila keadaan klinis memburuk sebelum 48 jam, atau terdapat keadaan yang berat (tidak
dapat menyusu atau minum/makan, atau memuntahkan semuanya, kejang, letargis
atau tidak sadar, sianosis, distres pernapasan berat) maka ditambahkan kloramfenikol
(25 mg/kgBB/kali IM atau IV setiap 8 jam).
 Bila pasien datang dalam keadaan klinis berat, segera berikan oksigen dan pengobatan
kombinasi ampilisin-kloramfenikol atau ampisilin-gentamisin.
 Sebagai alternatif, beri seftriakson (80-100 mg/kgBB IM atau IV sekali sehari).
 Bila anak tidak membaik dalam 48 jam, maka bila memungkinkan buat foto dada.
 Apabila diduga pneumonia stafilokokal (dijelaskan di bawah untuk pneumonia
stafilokokal), ganti antibiotik dengan gentamisin (7.5 mg/kgBB IM sekali sehari) dan
kloksasilin (50 mg/kgBB IM atau IV setiap 6 jam) atau klindamisin (15 mg/kgBB/hari –3
kali pemberian). Bila keadaan anak membaik, lanjutkan kloksasilin (atau dikloksasilin)
secara oral 4 kali sehari sampai secara keseluruhan mencapai 3 minggu, atau
klindamisin secara oral selama 2 minggu.

Pneunomia ringan
Tatalaksana

 Anak di rawat jalan

 Beri antibiotik: Kotrimoksasol (4 mg TMP/kg BB/kali) 2 kali sehari selama 3 hari atau
Amoksisilin (25 mg/kg BB/kali) 2 kali sehari selama 3 hari. Untuk pasien HIV diberikan
selama 5 hari.

Tindak lanjut
Anjurkan ibu untuk memberi makan anak. Nasihati ibu untuk membawa kembali anaknya
setelah 2 hari, atau lebih cepat kalau keadaan anak memburuk atau tidak bisa minum atau
menyusu.
Ketika anak kembali:

 Jika pernapasannya membaik (melambat), demam berkurang, nafsu makan membaik,

lanjutkan pengobatan sampai seluruhnya 3 hari.
 Jika frekuensi pernapasan, demam dan nafsu makan tidak ada perubahan, ganti ke
antibiotik lini kedua dan nasihati ibu untuk kembali 2 hari lagi.
 Jika ada tanda pneumonia berat, rawat anak di rumah sakit dan tangani sesuai
pedoman di bawah ini.
Antibiotic Therapy
The initial antibiotic treatment of CAP is empiric because the pathogen is rarely known at the
time of diagnosis (Tables 3 and 4).7,25,26 Empiric antibiotic choices should be based on the
patient’s age and severity of illness, and local resistance patterns of common
pathogens.7,25,26 Few large randomized controlled trials have compared antibiotics in the
treatment of childhood CAP, but several organizations have published treatment
guidelines.7,25,26 Oral administration of antibiotics is preferred except when the patient cannot
tolerate oral therapy or has severe CAP.26

Enlarge Print
Table 3.
Recommended Empiric Outpatient Treatment of Childhood Community-Acquired
Pneumonia
AGE ALBERTA GUIDELINE 25 CINCINNATI GUIDELINE 7

60 days to 5 Preferred regimens

years*

Amoxicillin† Amoxicillin

40 mg per kg per day for 7 to 10 days 80 to 90 mg per kg per day, in two

divided doses, for 7 to 10 days

or

90 mg per kg per day, in three divided

doses, for 7 to 10 days

Alternative regimens for patients allergic to penicillin or beta-lactam antibiotics

Azithromycin (Zithromax) Azithromycin

Day 1: 10 mg per kg Day 1: 10 mg per kg

Days 2 through 5: 5 mg per kg per day Days 2 through 5: 5 mg per kg per day

Clarithromycin (Biaxin) Clarithromycin

15 mg per kg per day, in two divided 15 mg per kg per day, in two divided
doses, for 7 to 10 days doses, for 7 to 10 days

Erythromycin Cefprozil (Cefzil)

 AGE ALBERTA GUIDELINE 25 CINCINNATI GUIDELINE 7

40 mg per kg per day, in four divided 30 mg per kg per day, in two divided
doses, for 7 to 10 days doses, for 7 to 10 days

Cefuroxime (Ceftin)

30 mg per kg per day, in two divided

doses, for 7 to 10 days

Ceftriaxone (Rocephin)‡

Single dose of 50 mg per kg,

administered intramuscularly

5 to 16 years Azithromycin§ Azithromycin∥

Day 1: 10 mg per kg Day 1: 10 mg per kg

Days 2 through 5: 5 mg per kg per day Days 2 through 5: 5 mg per kg per day

*—Age range in Alberta guideline is three months to five years.

†—Higher dose for patients who attend child care or who received antibiotics in the previous three months.

‡—Clarithromycin or erythromycin may be used as an alternative for seven to 10 days. Doxycycline (4 mg

per kg per day orally every 12 hours) may be used in children older than eight years who are allergic to
macrolides.

§—Follow with oral antibiotic therapy.

∥—Clarithromycin may also be used for seven to 10 days.

Information from references 7, 25, and 26.

Enlarge Print
Table 4.
Recommended Empiric Inpatient Treatment of Childhood Community-Acquired
Pneumonia
CINCINNATI
AGE ALBERTA GUIDELINE 25 GUIDELINE 7

Cefuroxime (Zinacef) See Table 3

 CINCINNATI
AGE ALBERTA GUIDELINE 25 GUIDELINE 7

150 mg per kg per day IV, in divided doses, given every 8

hours for 10 to 14 days

In critically ill patients: Not applicable

Cefuroxime

150 mg per kg per day IV, in divided doses, given every 8

hours for 10 to 14 days

plus

Erythromycin

60 days to 5 40 mg per kg per day IV or orally, in divided doses, given

years* every 6 hours for 10 to 14 days

or

Cefotaxime (Claforan)

200 mg per kg per day IV, in divided doses, given every 8

hours for 10 to 14 days

plus

Cloxacillin (no longer available in the United States)

150 to 200 mg per kg per day IV, in divided doses, given

every 6 hours for 10 to 14 days

5 to 16 years Cefuroxime See Table 3

150 mg per kg per day IV, in divided doses, given every 8

hours for 10 to 14 days

plus
 CINCINNATI
AGE ALBERTA GUIDELINE 25 GUIDELINE 7

Erythromycin

40 mg per kg per day IV or orally, in divided doses, given

every 6 hours for 10 to 14 days

or

Azithromycin (Zithromax)

Day 1: 10 mg per kg IV or orally

Days 2 through 5: 5 to 10 mg per kg per day IV or orally

IV = intravenously.

*—Age range in Alberta guideline is three months to five years.

Information from references 7, 25, and 26.

A 2007 study showed that oral amoxicillin and intravenous penicillin G were equally effective in
the treatment of hospitalized children with nonsevere CAP.27 A subsequent study showed that
oral amoxicillin was more cost-effective for most hospitalized children with CAP.28 Patients
receiving parenteral therapy may be switched to oral treatment once they are afebrile and
improving clinically, can tolerate oral intake, and have no complications.25 Amoxicillin is the drug
of choice for patients 60 days to five years of age because of its activity against S. pneumoniae.
Macrolides or cephalosporins can be used in patients with penicillin allergy. Macrolides are the
treatment of choice for children five to 16 years of age because of their activity against M.
pneumoniae and C. pneumoniae.

For patients with more severe disease, amoxicillin (or another beta-lactam antibiotic) may be
combined with a macrolide.5 If MRSA infection is suspected, empiric therapy with vancomycin
should be started (15 mg per kg intravenously every six hours). Clindamycin (10 to 13 mg per kg
orally or intravenously every six to eight hours) may be used if the patient is stable without
bacteremia, and if the local resistance rate to clindamycin is less than 10 percent. Linezolid
(Zyvox) is another alternative (10 mg per kg orally or intravenously every eight hours in children
younger than 12 years, or 600 mg orally or intravenously twice per day in children 12 years and
older).2

Supportive Care
Children with pneumonia are usually febrile. They may have localized chest pain, referred pain to
the abdomen, headache, or arthralgia. Pleural pain and abdominal pain may interfere with
effective cough. These symptoms may be controlled with weight-appropriate doses of
antipyretics and analgesics, such as acetaminophen or ibuprofen. Aspirin is not recommended
for children because of the risk of Reye syndrome

How are pseudomonas infections treated?

Pseudomonas infections are treated with antibiotics. Unfortunately, many pseudomonas infections are becoming more
difficult to treat. These bacteria have developed the ability to adapt and overcome antibiotics in their environment. This is
called antibiotic resistance. The increase in antibiotic resistance has made treating infections much more challenging.
Pseudomonas infections can often develop resistance to multiple types of antibiotics. It can even sometimes develop
resistance during the course of treatment. It is important that your doctor selects an effective antibiotic. A doctor may
send a specimen from a patient to a laboratory first for testing in order to be more certain. The laboratory will test the
specimen to determine which antibiotic will work best.

Treatment may involve one or more of the following types of antibiotics:

 ceftazidime

 ciprofloxacin or levofloxacin

 gentamicin

 cefepime

 aztreonam

 carbapenems

 ticarcillin

 ureidopenicillins

Cystic Fibrosis

 Cystic fibrosis atau fibrosis kistik adalah penyakit genetika yang menyebabkan lendir-lendir di
dalam tubuh menjadi kental dan lengket, sehingga menyumbatberbagai saluran, terutama
saluran pernapasan dan pencernaan.
 Dalam keadaan normal, lendir di dalam tubuh bersifat cair, licin, dan berperan sebagai
pelumas. Sedangkan pada penderita fibrosis kistik, terdapat kelainan pada gen yang
menyebabkan lendir menjadi lengket dan menghambat sejumlah saluran, termasuk saluran
yang terdapat pada paru-paru dan pankreas. Kondisi ini mengakibatkan gangguan
pernapasan dan pencernaan bagi penderitanya sejak usia dini.

Gejala Cystic Fibrosis

Gejala fibrosis kistik dapat berbeda-beda tergantung pada tingkat keparahan penyakit tersebut.
Gejala dapat muncul setelah kelahiran atau baru muncul saat seseorang telah beranjak dewasa.
Penyumbatan saluran udara bisa terjadi pada penderita fibrosis kistik. Hal ini akan menimbulkan
beberapa gejala seperti

 Batuk berkepanjangan
 Napas pendek.
  Diare.
 Muntah
 Sesak napas atau sulit bernapas
 Mengi (bengek).
 Saluran udara melebar akibat peradangan (bronkiektasis).

Selain gejala-gejala di atas, infeksi paru-paru juga rentan dialami oleh penderita fibrosis kistik karena
lendir menjadi tempat yang sesuai untuk perkembangbiakan bakteri.
Kondisi yang sama juga dapat terjadi dalam sistem pencernaan, di mana saluran pankreas dapat
tersumbat oleh lendir yang lengket. Akibatnya, enzim pencernaan yang dihasilkan oleh pankreas
tidak dapat mencapai usus halus, untuk membantu mencerna makanan. Kondisi ini kerap
menimbulkan gejala berupa:

 Penurunan berat badan atau bahkan pertumbuhan yang terhambat akibat makanan yang
tidak tercerna dengan baik sehingga penderita kekurangan nutrisi atau malnutrisi.
 Tekstur tinja yang menggumpal, berminyak, dan berbau tajam.
 Sembelit yang parah.
 Gangguan proses pembuangan kotoran awal (mekonium) pada hari pertama atau kedua
setelah lahir, karena adanya penyumbatan. Kondisi ini disebut ileum mekonium.
 Warna kulit bayi menjadi kuning (jaundice).

Etiology
CF is a genetic disease caused by mutations in the cystic fibrosis transmembrane conductance
regulator (CFTR), an anion channel found in the apical membrane of epithelial cells. Patients
may be either homozygous or heterozygous with respect to CFTR mutations. Carriers of one
CFTR mutation and one normal CFTR allele do not demonstrate disease in most cases.

Etiology
CF is carried as an autosomal recessive trait by about 3% of the white population. The
responsible gene has been localized on the long arm of chromosome 7. It encodes a membrane-
associated protein called the cystic fibrosis transmembrane conductance regulator (CFTR). The
most common gene mutation, F508del, occurs in about 86% of CF alleles; > 1900 less common
CFTR mutations have been identified.

CFTR is a cAMP-regulated chloride channel, regulating chloride and sodium transport across
epithelial membranes. A number of additional functions are considered likely. Disease manifests
only in homozygotes. Heterozygotes may show subtle abnormalities of epithelial electrolyte
transport but are clinically unaffected.

The CFTR mutations have been divided into five classes based on how the mutation affects the
function or processing of the CFTR protein. Patients with class I, II, or III mutations are
considered to have a more severe genotype that results in little or no CFTR function, whereas
patients with 1 or 2 class IV or V mutations are considered to have a milder genotype that results
in residual CFTR function. However, there is no strict relationship between specific mutations
and disease manifestation, so clinical testing (ie, of organ function) rather than genotyping is a
better guide to prognosis.

What Are the Risk Factors?

The only risk factor for getting CF is having two parents who carry abnormal CF genes and pass the

abnormal gene to their child. However, there are factors that impact how severe the CF is.
  Genes: CF gene mutations are divided into classes based on how damaged the CFTR protein

function is. Classes I, II, and III are generally more severe causing "classic CF." Classes IV

and V are usually milder. Also, other genes called modifier genes can affect a person’s

symptoms and outcome.

 Environment and lifestyle: People with CF need to consume a very large number of calories to

maintain weight and grow, which can be difficult to achieve. Physical activity is also important

to help keep lungs healthy. People with CF should not smoke or be exposed to secondhand

smoke, as it will worsen lung disease. You should also be careful with alcohol intake, and

avoid it altogether if you have liver disease.

 Age: CF worsens with age. If you have CF, you usually experience a small decline in lung

function each year.

Doctors diagnose cystic fibrosis (CF) based on the results from various tests.

Newborn Screening

All States screen newborns for CF using a genetic test or a blood test. The genetic test shows
whether a newborn has faulty CFTR genes. The blood test shows whether a newborn's pancreas is
working properly.

Sweat Test

If a genetic test or blood test suggests CF, a doctor will confirm the diagnosis using a sweat test.
This test is the most useful test for diagnosing CF. A sweat test measures the amount of salt in
sweat.

For this test, the doctor triggers sweating on a small patch of skin on an arm or leg. He or she
rubs the skin with a sweat-producing chemical and then uses an electrode to provide a mild
electrical current. This may cause a tingling or warm feeling.

Sweat is collected on a pad or paper and then analyzed. The sweat test usually is done twice. High
salt levels confirm a diagnosis of CF.

Other Tests

If you or your child has CF, your doctor may recommend other tests, such as:

 Genetic tests to find out what type of CFTR defect is causing your CF.
 A chest x ray. This test creates pictures of the structures in your chest, such as your heart, lungs,
and blood vessels. A chest x ray can show whether your lungs are inflamed or scarred, or whether
they trap air.
 A sinus x ray. This test may show signs of sinusitis, a complication of CF.
 Lung function tests. These tests measure how much air you can breathe in and out, how fast you
can breathe air out, and how well your lungs deliver oxygen to your blood.
 A sputum culture. For this test, your doctor will take a sample of your sputum (spit) to see
whether bacteria are growing in it. If you have bacteria called mucoid Pseudomonas, you may
have more advanced CF that needs aggressive treatment.

Prenatal Screening

If you're pregnant, prenatal genetic tests can show whether your fetus has CF. These tests include
amniocentesis (AM-ne-o-sen-TE-sis) and chorionic villus (ko-re-ON-ik VIL-us) sampling (CVS).

In amniocentesis, your doctor inserts a hollow needle through your abdominal wall into your
uterus. He or she removes a small amount of fluid from the sac around the baby. The fluid is
tested to see whether both of the baby's CFTR genes are normal.

In CVS, your doctor threads a thin tube through the vagina and cervix to the placenta. The doctor
removes a tissue sample from the placenta using gentle suction. The sample is tested to see
whether the baby has CF.

Cystic Fibrosis Carrier Testing

People who have one normal CFTR gene and one faulty CFTR gene are CF carriers. CF carriers
usually have no symptoms of CF and live normal lives. However, carriers can pass faulty CFTR
genes on to their children.

If you have a family history of CF or a partner who has CF (or a family history of it) and you're
planning a pregnancy, you may want to find out whether you're a CF carrier.

A genetics counselor can test a blood or saliva sample to find out whether you have a faulty CF
gene. This type of testing can detect faulty CF genes in 9 out of 10 cases.

How Is Cystic Fibrosis Treated?

Although there’s no cure for cystic fibrosis, there are various treatments available that may help relieve symptoms and

reduce the risk of complications.

Medications

 Antibiotics may be prescribed to get rid of a lung infection and to prevent another infection from occurring in the future.

They’re usually given as liquids, tablets, or capsules. In more severe cases, injections or infusions of antibiotics can be

given intravenously, or through a vein.

 Mucus-thinning medications make the mucus thinner and less sticky. They also help you to cough up the mucus so it

leaves the lungs. This significantly improves lung function.

 Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and indomethacin, may help reduce any pain and

fever associated with cystic fibrosis.

 Bronchodilators relax the muscles around the tubes that carry air to the lungs, which helps increase airflow. You can

take this medication through an inhaler or a nebulizer.

 Bowel surgery is an emergency surgery that involves the removal of a section of the bowel. It may be performed to

relieve a blockage in the bowels.

 Cystic fibrosis may interfere with digestion and prevent the absorption of nutrients from food. A feeding tube to supply

nutrition can be passed through the nose or surgically inserted directly into the stomach.

 A lung transplant involves removing a damaged lung and replacing it with a healthy one, usually from a deceased donor.

The surgery may be necessary when someone with cystic fibrosis has severe breathing problems. In some cases, both

lungs may need to be replaced. This can potentially lead to serious complications after surgery, including pneumonia.

Surgical Procedures

Chest Physical Therapy

Chest therapy helps loosen the thick mucus in the lungs, making it easier to cough it up. It’s typically performed one to four

times per day. A common technique involves placing the head over the edge of a bed and clapping with cupped hands along

the sides of the chest. Mechanical devices may also be used to clear mucus. These include:

 a chest clapper, which imitates the effects of clapping with cupped hands along the sides of the chest

 an inflatable vest, which vibrates at a high frequency to help remove chest mucus

Home Care

Cystic fibrosis can prevent the intestines from absorbing necessary nutrients from food. If you have cystic fibrosis, you

might need up to 50 percent more calories per day than people who don’t the disease. You may also need to take pancreatic

enzyme capsules with every meal. Your doctor may also recommend antacids, multivitamins, and a diet high in fiber and

salt.

If you have cystic fibrosis, you should do the following:

 Drink plenty of fluids because they can help thin the mucus in the lungs.

 Exercise regularly to help loosen mucus in the airways. Walking, biking, and swimming are great options.

 Avoid smoke, pollen, and mold whenever possible. These irritants can make symptoms worse.

 Get influenza and pneumonia vaccinations regularly.

The Cellular Mechanism

To begin to understand cystic fibrosis it is important to understand the root cause that leads to the clinical
manifestations of the disease. The development of CF results from a misfolded or improperly functioning
protein known as the cystic fibrosis conductance regulator (CFTR). The protein works in the apical
membrane of epithelial cells in organs throughout the body as a chloride ion channel, which, as its name
suggests, allows for the passage of chloride ions out of the cell. This movement attracts sodium ions across
the cell membrane followed by a subsequent flow of water to the cell’s exterior. The passage of water is
key because it hydrates and thins mucous so it can be properly cleared from organ passages, specifically in
the lungs.
In CF, the absence, or dysfunction of this CFTR channel inhibits the flow of water and leaves mucous
dehydrated and thickened, making it difficult to move with normal ciliary clearance. The immobilized, or
stuck mucous then creates a nice, little niche for bacteria to grow, which gives rise to the classic
manifestations of the disease including, chronic pulmonary infections, inflammation and decay of lung
function. However, it should be noted that the thickened mucous plays a role in creating complications not
only in the lung but other parts of the body, such as the sinuses, liver, pancreas, intestine and male
reproductive tract.





The
bronchus in the lungs are lined with hair-like projections called cilia that move microbes and
debris up and out of the airways. Scattered throughout the cilia are goblet cells that secrete
mucus which helps protect the lining of the bronchus and trap microorganisms.

Metabolisme Kalsium dalam tubuh

Untuk bisa diserap oleh tubuh, kalsium harus berbentuk cair.
Tetapi biasanya kita mengkonsumsi kalsium dalam bentuk padat. Adanya
asam pada lambung akan mengubah bentuk kalsium padat menjadi cair.
Setelah itu, barulah perjalanan kalsium di tubuh dimulai. Dari lambung,
kalsium akan diserap oleh usus. Setelah itu, apabila kalsium tersedia di
dalam jumlah yang banyak, kalsium akan langsung diedarkan ke pembuluh
darah melalui proses difusi. Namun, apabila jumlah kalsium yang tersedia
hanya sedikit maka metabolisme kalsium akan dilakukan melalui proses
transport aktif. Di dalam proses transport aktif, kalsium harus dibantu oleh
vitamin D. Itulah mengapa kita memerlukan vitamin D untuk kesehatan
tulang. Melalui aliran cairan tubuh termasuk aliran darah, kalsium akan
dibawa untuk disimpan di tulang. Tetapi, perjalanan ini belum berakhir
karena kalsium masih dapat terlepas lagi dari tulang. Proses ini sebenarnya
terjadi secara alami, namun proses ini juga perlu diantisipasi agar kalsium
yang tersusun harus seimbang dengan kalsium yang terlepas dari tulang
karena bila yang tersusun lebih sedikit dari yang terlepas, maka tulang akan
dapat mengalami kerapuhan, mudah patah, dan tingkat yang lebih parah lagi
yakni osteoporosis.
 Absorpsi dan Metabolisme Natrium
 Natrium diabsorpsi di usus halus secara aktif (membutuhkan energi), lalu dibawa oleh
aliran darah ke ginjal untuk disaring kemudian dikembalikan ke aliran darah dalam
jumlah cukup untuk mempertahankan taraf natrium dalam darah. Kelebihan natrium
akan dikeluarkan melalui urin yang diatur oleh hormon aldosteron yang dikeluarkan
oleh kelenjar adrenal jika kadar natrium darah menurun.
Ekskresi Natrium
Ekskresi natrium terutama dilakukan oleh ginjal. Pengaturan eksresi ini dilakukan
untuk mempertahankan homeostasis natrium, yang sangat diperlukan untuk
mempertahankan volume cairan tubuh. Pengeluaran natrium juga terjadi lewat
pengeluaran keringat dan tinja dalam jumlah kecil. Kekuran natrium dari rute-rute ini
dapat mengakibatkan kematian pada kasus berkeringat dan diare yang berlebihan.
Ingesti natrium dipengaruhi oleh rasa dan dorongan homeostatis (selera terhadap
garam) untuk mempertahankan keseimbangan natrium. Hewan mempunyai
dorongan untuk memakan garam yang di picu oleh natrium plasma yang rendah
(Sectiono, 2004).