A. Definition of Pneumonia

 
Pneumonia is an inflammation or inflammation of the lung parenchyma is generally caused by infectious agents.
B. Pneumonia Etiology
Pneumonia can be caused by various etiologies such as:
• Bacteria: stapilokokus, streplokokus, aeruginosa, eneterobacter
• Virus: Influenza virus, adenovirus
• Micoplasma pneumonia
• Fungi: Candida albicans
• Aspiration: stomach
C. Pathophysiology of Pneumonia
Mostly obtained through aspiration pneumonia infectious particles. There is some mechanism that normally protects the lungs from infection. Infectious particles are filtered in the nose, or trapped and cleared by the ciliated epithelium and mucus in the airways. If the particles can reach the lungs, these particles will face alveoler macrophages, as well as the systemic immune mechanisms and humoral. Infants in the first months of life has also acquired maternal antibodies that can passively protect against pneumococcal and other infectious organisms.
Changes to this protective mechanism can cause a child susceptible to pneumonia anatomical abnormalities eg congenital, acquired or congenital immune deficiency, or a neurological disorder that allows the child has aspirations and changes in the quality of mucus secretion or airway epithelium. In children with no predisposing factors, the infectious particles can reach the lungs through the changes on defense anatomical and physiological normal. This is most often caused by viral upper respiratory tract. The virus can spread to the lower respiratory tract and cause pneumonia virus.
Alternatively, the virus caused damage to the normal defense mechanisms may lead to bacterial pathogens infect the lower respiratory tract. This bacterium is an organism which can normally colonizes in the upper airway or the bacteria are transmitted from person to person through droplets spread through the air. Sometimes bacterial and viral pneumonia (eg varisella, measles, rubella, CMV, Epstein-Barr virus, herpes simplex virus) can occur through either haematogenous spread from localized sources or bacteremia / viremia generalized.
After reaching the lung parenchyma, the bacteria causing acute inflammatory response that includes fluid exudation, fibrin deposits, and polymorphonuclear leukocyte infiltration in the alveoli, followed infitrasi macrophages. Exudative fluid in the alveoli causing lobaris typical consolidation on chest X-ray. Virus, mycoplasma and chlamydia causes inflammation with mononuclear infiltrates dominated the submucosal and interstitial structure. This causes the release of epithelial cells into the airway, as occurs in bronchiolitis.
The mechanism of resistance lower respiratory tract very efficiently to prevent infection and consists of
a. Anatomic arrangement of the nasal cavity
b. Lymphoid tissue in the naso-oro-pharyngeal
c. Vibrating fur covering most of the respiratory tract epithelium and sec ¬ ret fiat issued by the epithelium sets.
d. Cough reflex
e. Epiglottis reflex that prevents aspiration of infected secretions.
f. Drainage function of the lymphatic system and regional lymph nodes filter.
g. Phagocytosis, enzymatic action and immuno-humoral response, especially from imu ¬ noglobulin A (IgA).
Children with impaired endurance will suffer recurrent pneumonia or unable to cope with the disease completely. Other factors that influence the onset of pneumonia mem ¬ durability loss is decreased, eg his ¬ protein energy malnutrition (MEP), chronic disease, factors such as trauma to the lung iatrogen, anesthesia, aspiration, treatment with antibiotics is not perfect.
D. Classification
Division no satisfactory pneumonia. In general, the division held on the basis of anatomical and etiological.
Anatomical division: (1) pneumonia lobaris, (2) pneumonia lobularis (bron ¬ kopneumonia) and (3) interstitial pneumonia (bronchiolitis).
Etiological division: (1) bacteria: Diplococcus pneumoniae, Pneumococcus, Streptococcus hemolyticus, Streptococcus aureus. Hemophilus influenzae, Ba ¬ cillus Friedlander, Mycobacterium tuberculosis. (2) virus: Respiratory syncytial virus, influenza virus, adenovirus, a virus sitomegalik. (3) Mycoplasma pneumo-'niae (4) mushrooms: Histoplasma capsulatum, Cryptococcus neoformans, ¬ ces Blastomy dermatitides, Coccidioides immitis, Aspergillus species, Candida albicans. (5) aspiration: food, kerosene (gasoline, kerosene), amniotic fluid, a foreign object. (6) hypostatic pneumonia. (7) Loeffler's syndrome. Clinically normal, it is difficult to distinguish the various etiologies. For the treatment of te-pat, knowledge about the causes of pneumonia essential, so reforming ¬ gian aetiological more rational than the anatomical division.
1. Pneumococcal pneumonia.
a. Epidemiology,
Pneumococcus is a major cause of pneumonia. Pneumococcus with serotypes 1 through 8 causes pneumonia in adults more than 80%, while the child was found Type 14, 1, 6 and 9. Highest incidence rate was found in less than 4 years of age and repeated ¬ rang with increasing age. Pneumonia lobaris almost always caused by Pneumococcus, is found in adults and big kids, while bronchopneumonia more often found in young children and infants.
b. Pathogenesis of Pneumonia
Pneumococcus into the lungs via the respiratory perci ¬ ('droplet'). Pneumonia inflammatory process can be divided into four stadia, namely: (1) Stadium congestion: kepiler widened and congestion as well as in the alveolar exudate are clear, the bacteria in large quantities, some neutrophils and macrophages. (2) red hepatization Stadium: lobes and lobules are exposed to solid and contains no air, the color to red and the palpability as he par ¬. In alveolar fibrin obtained, neutrophil leukocytes, exudate and more se ¬ times erythrocytes and bacteria. This stage is short-lived. (3) Stadium hepatization gray: lobe remains solid and the color red to pale kela ¬ bu. Pleural surface grim as covered by fibrin. Alveoli filled with fibrin and leukocyte phagocytosis occurs where Pneumococcus. No longer capillary failure. (4) Stage resolution: reduced exudate. Increase in alveolar macrophages and leukocytes undergo necrosis and fatty degeneration. Fibrin diresorbsi and disappeared. In bronchopneumonia anatomic pathology is different from Pneu ¬ tpaonia lobaris in localization as patches with irregular distribution. With antibiotic treatment stadiumn typical sequence is not terli ¬ hat.
c. The clinical features of pneumonia
Bronchopneumonia is usually preceded by an upper respiratory infection for several days. Temperature can rise so suddenly to 39-40 ° C and may be accompanied by seizures due to high fever. Children are very nervous, nu ¬ disp. Breathing fast and shallow breathing nostrils with cyano ¬ sis and around the nose and mouth. Sometimes accompanied by vomiting and diarrhea. Cough is usually not found at the beginning of the disease, there may be coughing se ¬ have a few days, at first dry and then be productive. At the beginning of the sta ¬ dium diagnosis is made difficult by physical examination, but with the rapid and shallow breathing, nostril breathing and cyanosis around the mouth and nose, to think about the possibility of pneumonia. In bronkop-neumonia, the results depend tisis than the area affected. On percussion thoracic abnormalities are often not found. On auscultation may just sound tinny wet crackles fine or medium. When the nest bronkop ¬ neumonia into one (kontluens) on percussion may sound overcast condition and breathing on auscultation audible voice hardened. At this stage the resolu ¬, crackles heard again. Without healing treatment usually occur after 2-3 weeks.
2. Pneumonia lobaris
Usually the symptoms came suddenly, but sometimes preceded by upper respiratory tract infection. In older children may be accompanied by chills and in infants with seizures. Temperature rises rapidly to 39-40 ° C and the temperature usually indicates the type of febrile continua. Breath becomes congested, tai ¬ diser nostril breath and cyanosis around the nose and mouth and pain in ¬ da da. Kids prefer to lie on the right breast exposed. Cough dry at first, then becomes productive. On physical examination, the typical symptoms appear after 1-2 days. At the beginning of weakened respiratory sound on percussion while no obvious abnormalities. Following is congested, moist crackles loud sound that will soon disappear after the consolidation. Then on percussion clearly audible overcast condition with sub-bronchial breath sounds to bronchial. In the resolution stage crackles heard more clearly. On inspection and palpation of the affected thoracic looked shift decreases. Without ¬ healers healing crisis can occur after 5-9 days.
a. Chest X-ray Inspection
This examination may show abnormalities before this can be discovered ¬ examination. In bronchopneumonia patches infiltrates in ¬ get on one or more lobes. In lobaris pneumonia seen a consolidation in one or more lobes. X-ray may also appoint ¬ complications such as pleurisy, atelectasis, lung abscess, pneumatokel, pneumothorax, pneumomediastinum or pericarditis.
b. Laboratory tests
Blood picture showed leukocytosis, usually 15,000 - 40.000/mm3 with pergesaran to the left. Germs can cause dibiak from usa pan ¬ throat and 30% of the blood. Urine is usually dark colored, might there ¬ kin mild albuminuria due to temperature rise and less piston hia ¬ lin.
c. Differential diagnosis
Pneumococcal pneumonia is indistinguishable from that in ¬ pneumonia caused by other bacteria or viruses, without microbiological examination. ¬ circumstances resembling pneumonia are: bronchiolitis, heart failure, foreign body aspiration, atelectasis, lung abscess, tuberculosis.
d. Complication
With the use of antibiotics, complications almost never encountered. Complications that can be found are: empyema, acute otitis media. Other complications such as meningitis, pericarditis, osteomyelitis, peritonitis dili ¬ less hat.
e. Prognosis
With appropriate antibiotic treatment and adequate, mortality may in ¬ down to less than 1%. Children in the state of protein energy malnutrition and a late show higher mortality.
f. Treatment and management
Treatment should be based on etiology and resistance tests, te ¬ but since this is not always feasible and time-consuming it is in practice given treatment polifragmasi. Given penicillin 50,000 U / kg / day and coupled with kloramfeniko150 - 75 mg / kg / day or in ¬ provide broad-spectrum antibiotics such as ampicillin have. Pengoba ¬ tan continues until the free heat for 4-5 days. Children are very se ¬ sak breathing require intravenous fluids and oxygen. Type of fluid used is a mixture of glucose 5% danNaC10, 9% in the ratio of 3:1 plus KC110 solution mEq/500 ml infusion bottles. The amount of fluid in ¬ needed should be calculated using the formula Darrow. Because it turns out, most people who fall into the metabolic acidosis and hypoxia due to lack of food, can be corrected by calculation to base as many flaws ¬ - 5 mEq.
3. Staphylococcal Pneumonia
Staphylococcal Pneumonia caused by Staphylococcus aureus, classified as severe pneumonia quickly become progressive and resistant to pen ¬ gobatan. In general, the baby suffered pneumonia, which is 30% below the age of 3 months and 70% before 1 year. It often happens lung abscess (multiple abscesses), pneumatokel, 'tension pneumothorax' or empyema. Treatment is given based on resistance testing, but given the rapid course of the disease, should be given broad-spectrum antibiotics that would have not been ten ¬ resistors. For Staphylococcus infection that made penicillinase, can be given cloxacillin or linkomisin. Treatment continued until there is clinical improvement and in my experience the average of 3 weeks.
4. Streptococcal pneumonia
Group A Streptococcus hemolyticus usually causes upper respiratory tract infections, but sometimes it can also cause Pneu ¬ monia. Pneumonia often is a complication of streptococcal viral diseases such as influenza, measles, chicken pox and other bacterial infections such as pertussis, pneumococcal Pneu ¬ mania. Treatment is with penicillin.
5. Gram-negative bacterial pneumonia
Gram-negative bacteria that cause pneumonia are usually Hemo ¬ philus influenzae, Friedlander bacillus (Klebsiella pneumoniae), and Pseudomonas aeruginosa. The incidence of pneumonia was very low (less than 1%), but began to rise over the past few years due to the use of antibioti ¬ ka very broad and contamination of hospital equipment such as 'humidifier', oxygen equipment, and so on. Clinically, it is difficult to distinguish pneumonia from pneumonia caused by other bacteria and can only be determined with de ¬ culture. Pneumonia due to Hemophilus influenzae in infants and young children is a severe disease and often cause complications ¬ cation such as bacteremia, empyema, pericarditis, cellulitis, and meningitis. The selected drug is ampicillin at a dose of 150 mg / kg / day with kloramfeni ¬ cabbage.
6. Pneumonia klebsiela
Usually found in the elderly and in patients with diabetes mellitus, bronchiectasis and tuberculosis. Babies can suffer this disease because Konta ¬ dominance of hospital equipment. This disease can be progressive and arouse ¬ abscesses and cavities. Complications such as empyema, bacteremia usually also in ¬ come across. Drugs chosen to address this infection is kanamycin mg/kgbb/12 7.5 hours for 10-12 days or gentamicin.
7. Pneumonia psendomonas aeroginosa
Bronchopneumonia is heavy, progressive accompanied by necrosis and usually cause death. Usually found as infections.

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Clinical Manifestations  pneumonia
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