Pneumonia Sumber

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Pneumonia

PATHOGENESIS.

The lower respiratory tract is normally kept sterile by physiologic defense mechanisms,including the mucocil iary clearance, the properties of normal secretions such as secretory

immunoglobulin A (IgA), and clearing of the airway by coughing. Immunologic defensemechanisms of the lung that limit invasion by pathogenic organisms include macrophages

that are present in alveoli and bronchioles, secretory IgA, and other immunoglobulins.

Viral pneumonia usually results from spread of infection along the airways, accompanied by

direct injury of the respiratory epithelium, resulting in airway obstruction from swelling,

abnormal secretions, and cellular debris. The small caliber of airways in young infants makes

them particularly susceptible to severe infection. Atelectasis, interstitial edema, and

ventilation-perfusion mismatch causing significant hypoxemia often accompany airway

obstruction. Viral infection of the respiratory tract can also predispose to secondary bacterial

infection by disturbing normal host defense mechanisms, altering secretions, and modifying

the bacterial flora.

When bacterial infection is established in the lung parenchyma, the pathologic process varies

according to the invading organism. M. pneumoniae attaches to the respiratory epithelium,

inhibits ciliary action, and leads to cellular destruction and an inflammatory response in the

submucosa. As the infection progresses, sloughed cellular debris, inflammatory cells, and

mucus cause airway obstruction, with spread of infection occurring along the bronchial tree,

as it does in viral pneumonia.

S. pneumoniae produces local edema that aids in the proliferation of organisms and their

spread into adjacent portions of lung, often resulting in the characteristic focal lobar

involvement.

Group A streptococcus infection of the lower respiratory tract results in more diffuse

infection with interstitial pneumonia. The pathology includes necrosis of tracheobronchial

mucosa; formation of large amounts of exudate, edema, and local hemorrhage, with extension

into the interalveolar septa; and involvement of lymphatic vessels and the increased

likelihood of pleural involvement.

S. aureuspneumonia manifests in confluent bronchopneumonia, which is often unilateral and

characterized by the presence of extensive areas of hemorrhagic necrosis and irregular areas

of cavitation of the lung parenchyma, resulting in pneumatoceles, empyema, or, at times,

bronchopulmonary fistulas.

Recurrent pneumoniais defined as 2 or moreepisodes in a single yr or 3 or moreepisodes

ever, with radiographic clearing between occurrences.

CLINICAL MANIFESTATIONS.

Viral and bacterial pneumonias are often preceded by several days of symptoms of an upper

respiratory tract infection, typically rhinitis and cough. In viral pneu monia, fever is usually

present; temperatures are generally lower than in bacterial pneumonia. Tachypnea is the most

consistent clinical manifestation of pneumonia. Increased work of breathing accompanied by

intercostal, subcostal, and suprasternal retractions, nasal flaring, and use of accessory muscles


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is common. Severe infection may be accompanied by cyanosis and respiratory fatigue,

especially in infants. Auscultation of the chest may reveal crackles and wheezing, but it is

often difficult to localize the source of these adventitious sounds in very young children with

hyperresonant chests. It is often not possible to distinguish viral pneumonia clinically from

disease caused byMycoplasmaand other bacterial pathogens.

Bacterial pneumonia in adults and older children typically begins suddenly with a shaking

chill followed by a high fever, cough, and chest pain. In older children and adolescents, a

brief upper respiratory tract illness is followed by the abrupt onset of shaking chills and high

fever accompanied by drowsiness with intermittent periods of restlessness; rapid respirations;

a dry, hacking, unproductive cough; anxiety; and, occasionally, delirium. Circumoral

cyanosis may be observed. Many children are noted to be splinting on the affected side to

minimize pleuritic pain and improve ventilation; they may lie on their side with their knees

drawn up to their chest.

Physical findings depend on the stage of pneumonia. Early in the course of illness,

diminished breath sounds, scattered crackles, and rhonchi are commonly heard over theaffected lung field. With the development of increasing consolidation or complications of

pneumonia such as effusion, empyema, or pyopneumothorax, dullness on percussion is noted

and breath sounds may be diminished. A lag in respiratory excursion often occurs on the

affected side. Abdominal distention may be prominent because of gastric dilation from

swallowed air or ileus. Abdominal pain is common in lower lobe pneumonia. The liver may

seem enlarged because of downward displacement of the diaphragm secondary to

hyperinflation of the lungs or superimposed congestive heart failure. Nuchal rigidity, in the

absence of meningitis, may also be prominent, especially with involvement of the right upper

lobe.

Symptoms described in adults with pneumococcal pneumonia may be noted in older children

but are rarely observed in infants and young children, in whom the clinical pattern is

considerably more variable. In infants, there may be a prodrome of upper respiratory tract

infection and diminished appetite, leading to the abrupt onset of fever, restlessness,

apprehension, and respiratory distress. These infants appear ill with respiratory distress

manifested by grunting; nasal flaring; retractions of the supraclavicular, intercostal, and

subcostal areas; tachypnea; tachycardia; air hunger; and often cyanosis. Results of physical

examination may be misleading, particularly in young infants, with meager findings

disproportionate to the degree of tachypnea. Some infants with bacterial pneumonia may

have associated gastrointestinal disturbances characterized by vomiting, anorexia, diarrhea,

and abdominal distention secondary to a paralytic ileus. Rapid progression of symptoms ischaracteristic in the most severe cases of bacterial pneumonia

DIAGNOSIS.

The chest radiograph confirms the diagnosis of pneumonia and may indicate a complication

such as a pleural effusion or empyema. Viral pneumonia is usually characterized by

hyperinflation with bilateral interstitial infiltrates and peribronchial cuffing ( Fig. 397-1 ).

Confluent lobar consolidation is typically seen with pneumococcal pneumonia ( Fig. 397-2 ).

The radiographic appearance alone is not diagnostic and other clinical features must be

considered. Repeat chest x-rays are not required for proof of cure for patients with

uncomplicated pneumonia.


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The peripheral white blood cell (WBC) count can be useful in differentiating viral from

bacterial pneumonia. In viral pneumonia, the WBC count can be normal or elevated but is

usually not higher than 20,000/mm3, with a lymphocyte predominance. Bacterial pneumonia

(occasionally, adenovirus pneumonia) is often associated with an elevated WBC count in the

range of 15,000-40,000/mm3and a predominance of granulocytes. A large pleural effusion,

lobar consolidation, and a high fever at the onset of the illness are also suggestive of abacterial etiology. Atypical pneumoniadue to C. pneumoniaeorM. pneumoniaeis difficult

to distinguish from pneumococcal pneumonia by x-ray and other labs, and although

pneumococcal pneumonia is associated with a higher WBC count, erythrocyte sedimentation

rate (ESR), and Creactive protein (CRP), there is considerable overlap.

The definitive diagnosis of a viral infection rests on the isolation of a virus or detection of the

viral genome or antigen in respiratory tract secretions. Growth of respiratory viruses in tissue

culture usually requires 510 days. Reliable DNA or RNA tests for the rapid detection of

RSV, parainfluenza, influenza, and adenoviruses are available and accurate. Serologic

techniques can also be used to diagnose a recent respiratory viral infection but generally

require testing of acute and convalescent serum samples for a rise in antibodies to a specificviral agent. This diagnostic technique is laborious, slow, and not generally clinically useful

because the infection usually resolves by the time it is confirmed serologically. Serologictesting may be valuable as an epidemiologic tool to define the incidence and prevalence of

the various respiratory viral pathogens.

The definitive diagnosis of a bacterial infection requires isolation of an organism from the

blood, pleural fluid, or lung. Culture of sputum is of little value in the diagnosis of

pneumonia in young children. Blood cultures are positive in only 10% of children with

pneumococcal pneumonia. InM. pneumoniaeinfections, cold agglutinins at titers >1 : 64 are

found in the blood in 50% of patients. Cold agglutinins are nonspecific, however, because

other pathogens such as influenza viruses may also cause increases. Acute infection caused

byM. pneumoniaecan be diagnosed on the basis of a positive PCR test or seroconversion in

an IgG assay. Serologic evidence such as the anti-streptolysin O (ASO) titer may be useful in

the diagnosis of group A streptococcal pneumonia

Atelektasis

Definition

Atelectasis is a collapse in part of the lungs. Normally, air passes through the airways into small sacs

of the lungs. Oxygen from the air passes through these sacs into the blood. Carbon dioxide alsopasses from the blood to the sacs to leave the body. With atelectasis, these sacs are collapsed.

Oxygen and carbon dioxide cannot pass through the collapsed sacs.

A collapse over large areas of the lungs can lead to serious problems. In infants, atelectasis may be:

Congenitalpresent at birth

Acquiredcaused by an acquired condition

Causes

Atelectasis is not a disease. It is the result of a disease or abnormality in the body. It can be causedby:


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Blockage in airwaysas a result of an inhaled stool during birth, inhaled object, or a mucus plug

that keeps air from moving into sacs

Lung infectionsmay cause fluid build-up that blocks air to lung sacs

Lack of surfactant (common in premature infants)surfactant is a fluid that lines the inside of the

lungs and helps them function properly

Impaired breathingair is not pulled deep enough into the lungs to open all sacs

Damage to nerve and muscles that control breathingmay prevent coughing, deep breathing, or

yawning

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Risk Factors

Factors that increase the chance of congenital atelectasis include:

Inhaled meconium or amniotic fluid

Prolonged or difficult labor

Birth injury to central nervous system

Children under 3 years old are more likely to develop atelectasis than older children or adults. Factors

that may increase your babys chance of atelectasis include:

Premature birth

Lung condition or infectionparticularly if coughing is impaired

Injury to chest wall

Having anesthesia

Inhaling a foreign object, such as a peanut or marble

Respiratory distress syndrome Being on ventilatorair does not move into lungs in a normal pattern

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Symptoms

Atelectasis may not have obvious symptoms.

Larger areas of atelectasis may lead to:

Rapid breathing

Taking shallow breaths

Agitation

Coughing

Decreased chest movement during breathing

Wheezing

Fever

Blueness of the skin

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PATHOPHYSIOLOGY

In order to understand the pathophysiology of atelectasis, a review of the normal mechanisms thatprevent lung collapse is required. Elastin fibers within alveolar walls result in a tendency for the alveoli
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to recoil inwards. This is balanced by the outward recoil of the chest wall and the interaction between

the parietal and visceral pleura. In addition, the primary mechanism that keeps the lung from

collapsing at low volumes is surfactant.

Surfactant is a complex phospholipid and protein mixture produced by type II alveolar epithelial cells.

It functions to lower surface tension, which is defined by the law of Laplace:

Pressure = 2 x (surface tension) / radius

As alveolar volume decreases with expiration, surface tension increases to the degree that, without

surfactant, the alveolus would collapse completely. This adhesive atelectasis becomes clinically

relevant in diseases that result in absent or deficient surfactant production and homeostasis, including

neonatal respiratory distress syndrome, congenital surfactant protein B deficiency, and pulmonary

alveolar proteinosis.

Obstructive atelectasis

Following obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli,leading to retraction of the lung and an airless state within a few hours. In the early stages, blood

perfuses the airless lung; this results in ventilation-perfusion mismatch and arterial hypoxemia. Afilling of the alveolar spaces with secretions and cells may occur, thereby preventing completecollapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing thesurrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm iselevated, and the chest wall flattens.

If the obstruction is removed, any complicating postobstructive infection subsides and the lung returnsto its normal state. If the obstruction is persistent and infection continues to be present, fibrosisdevelops and the lung becomes bronchiectatic.

Nonobstructive atelectasis

The loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructive

atelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleuraleffusions affect the lower lobes more commonly than pneumothorax, which affects the upper lobes. Alarge pleural-based lung mass may cause compression atelectasis by decreasing lung volumes.

Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoylphosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lackof production or inactivation of surfactant, which may occur in ARDS, radiation pneumonitis, and blunttrauma to the lung, cause alveolar instability and collapse.

Middle lobe syndrome (recurrent atelectasis and/or bronchiectasis involving the right middle lobeand/or lingula) has recently been reported as the pulmonary manifestation of primary Sjgrensyndrome.

Scarring of the lung parenchyma leads to cicatrization atelectasis.

Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolarcarcinoma.

Platelike atelectasis

Also called discoid or subsegmental atelectasis, this type is seen most commonly on chestradiographs. Platelike atelectasis probably occurs because of obstruction of a small bronchus and isobserved in states of hypoventilation, pulmonary embolism, or lower respiratory tract infection. Smallareas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactantformation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. A mild-to-severe gasexchange abnormality may occur because of ventilation-perfusion mismatch and intrapulmonaryshunt.


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Postoperative atelectasis

Atelectasis is a common pulmonary complication in patients following thoracic and upper abdominalprocedures.General anesthesiaand surgical manipulation lead to atelectasis by causingdiaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar andsegmental in distribution. After induction of anesthesia, atelectasis increases from 1 to 11% of total

lung volume. End-expiratory lung volume is also found to be decreased.

In 2009 study, a recruitment maneuver plus positive end-expiratory pressure (PEEP) reducedatelectasis to 3 4%, increased end-expiratory lung volume, and increased the PaO 2/FiO2ratio from266 70 mm Hg to 412 99 mm Hg. It was found that the PEEP alone did not reduce the amount ofatelectasis or improve oxygenation, but a recruitment maneuver followed by PEEP reducedatelectasis and improved oxygenation.[4]

Medical

Lobar atelectasis is a common problem caused by a variety of mechanisms including resorptionatelectasis due to airway obstruction, passive atelectasis from hypoventilation, compressiveatelectasis from abdominal distension, and adhesive atelectasis due to increased surface tension.

Evidence-based studies on the management of lobar atelectasis are lacking. Assessment of airbronchograms on a chest radiograph may be helpful to determine whether the airway obstruction isproximal or distal. Chest physiotherapy, nebulized dornase alfa (DNase), and, possibly, fiberopticbronchoscopy might be helpful in patients with mucous plugging of the airways. In passive andadhesive atelectasis, positive end-expiratory pressure might be a useful adjunct to treatment.

Nonpharmacologic therapies for improving cough and clearance of secretions from the airwaysinclude chest physiotherapy, including postural drainage, chest wall percussion and vibration, and aforced expiration technique (called huffing). Increased airway clearance as assessed by sputumcharacteristics (ie, volume, weight, viscosity) and clearance of the radioaerosol from the lung showthat the long-term efficacy of these techniques compared with unassisted cough alone is unknown.[9]

The treatment of atelectasis depends on the underlying etiology. Treatment of acute atelectasis,

including postoperative lung collapse, requires removal of the underlying cause.

For postoperative atelectasis, prevention is the best approach. Anesthetic agents associated withpostanesthesia narcosis should be avoided; narcotics should be used sparingly because they depressthe cough reflex. Early ambulation and use of incentive spirometry are important. Encourage thepatient to cough and to breathe deeply. Nebulized bronchodilators and humidity may help liquefysecretions and promote their easy removal. In the case of lobar atelectasis, vigorous chestphysiotherapy frequently helps reexpand the collapsed lung. When these efforts are not successfulwithin 24 hours, flexible fiberoptic bronchoscopy should be performed.

When a mechanically obstructed bronchus is suggested but coughing or suctioning is not successful,bronchoscopy should be performed. If bronchoscopy is successful, any underlying infection, ifpresent, is treated.

Prevention of further atelectasis involves (1) placing the patient in such a position that the uninvolvedside is dependent to promote increased drainage of the affected area, (2) giving vigorous chestphysiotherapy, and (3) encouraging the patient to cough and to breathe deeply.

Patients may require repeat bronchoscopy if atelectasis recurs. This is particularly true in patients withneuromuscular disease and poor cough.

Therapy with a broad-spectrum antibiotic is started and modified appropriately if a specific pathogenis isolated from sputum samples or bronchial secretions.

Postoperative atelectasis is treated with adequate oxygenation and reexpansion of the lungsegments. Supplemental oxygen should be titrated to achieve an arterial oxygen saturation of greaterthan 90%.

Severe hypoxemia associated with severe respiratory distress or hypoxemia should lead to intubationand mechanical support. Intubation not only provides oxygenation and ventilatory support, but also
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provides access for suctioning of the airways and facilitates performing bronchoscopy, if needed. Thepositive pressure and larger tidal volumes often help to reexpand collapsed lung segments.

Continuous positive airway pressure delivered via a nasal cannula or facemask may also be effectivein improving oxygenation and reexpanding the collapsed lung.

Broad-spectrum antibiotics should be prescribed if evidence of infection is present, such as fever,night sweats, or leukocytosis, because secondary atelectasis usually becomes infected regardless ofthe cause of obstruction. Obstruction of a major bronchus may cause severe hacking or coughing.

Antitussive therapy reduces the cough reflex and may produce further obstruction; thus, it should beavoided.

Fiberoptic bronchoscopy is commonly required for diagnosis, particularly if an endobronchial lesion issuggested. This procedure has a limited role in the management of postoperative atelectasis.Fiberoptic bronchoscopy is not more effective than standard chest physiotherapy, deep breathing,coughing, and suctioning of patients who are intubated. Therefore, simple and standard respiratorytherapy techniques should be administered to patients who spontaneously ventilate or patients onmechanical ventilation. Fiberoptic bronchoscopy should be reserved for those situations in whichchest physiotherapy is contraindicated (eg, chest trauma, immobilized patient), poorly tolerated, orunsuccessful.

Judicious use of perioperative analgesia is an essential adjunct, permitting patients to breathe deeply,cough forcefully, and participate in chest physiotherapy maneuvers. In patients with underlyingpulmonary disease, use of epidural analgesia has been shown to be a very effective pain controlmeasure, thereby aiding aggressive chest physiotherapy.

N-acetylcysteine aerosols commonly are administered in an effort to promote clearance of tenacioussecretions; however, their efficacy has not been documented. In addition, N-acetylcysteine maycause acute bronchoconstriction. Its use should be limited to direct instillation at the time of fiberopticbronchoscopy.

In a study of noncystic fibrosis in children who had atelectasis of infectious origin, treatment withDNase led to rapid clinical improvement observed within 2 hours and radiologic improvement

documented within 24 hours. DNase may be an effective treatment for infectious atelectasis inpediatric patients with noncystic fibrosis. Such data does not exist for adult patients, but DNase couldbe used as a trial of therapy in adults as well.[10]

Prophylactic maneuvers for reducing the incidence and magnitude of postoperative atelectasis inhigh-risk patients should be encouraged. These techniques are deep-breathing exercises, coughingexercises, and incentive spirometry.

For maximal benefit, prophylactic measures should be taught and instituted before surgery and usedregularly, on an hourly basis, after surgery.

Early ambulation of patients after surgery has also been found to be as effective as physical therapy.

Kato et al reported on the use of the RTX respirator for extensive atelectasis in elderly patients.

Patients were placed in the lateral decubitus position, and the RTX respirator was reported to be auseful tool to clear retained sputum in elderly patients

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