Thursday, October 21, 2010

Extensive and detailed clinical highlights on Pneumonia

Pneumonia is usually triggered when a patient's defense system is weakened, most often by a simple viral upper respiratory tract infection or a case of influenza. Such infections or other triggers do not cause pneumonia directly but they alter the mucous blanket, thus encouraging bacterial growth. Other factors can also make specific people susceptible to bacterial growth and pneumonia.
Aetiology
· Viral (most common)
· Bacterial
· Pneumococcus
· Haemophilus influenzae (untypable or type b)
· Staphylococcus aureus
· Group A streptococcus
· Atypical
· Mycoplasma pneumoniae
· Chlamydia pneumoniae
· Chlamydia trachomatis
Classification of pneumonia:
community-acquired pneumonias;
Pneumonia in immunocompromised host
Nosocomial pneumonia
Pneumonia due to aspiration
Community-acquired pneumonia has become a major health problem throughout the world. Each year in the United States, an estimated 4 million cases occur. About 20% of these cases require hospitalization, the condition resulting in more than 65 million days of restricted activity overall. Mortality rates range from 1% to 5% in outpatients and from 15% to 30% in inpatients, making it the sixth leading cause of death. Many experts divide therapy for community-acquired pneumonia into two categories: inpatient and outpatient.

Problems in establishing a cause The etiology of community-acquired pneumonia is a long- and often-debated topic. Some researchers imply that outpatients contract different causative agents than do inpatients, while other investigators do not make major distinctions between the two categories. Other experts have attempted to elucidate the causes according to patient age. Even after examination of virtually every study completed on community-acquired pneumonia, it is extremely difficult to posit any useful probability of cause on the basis of age or outpatient versus inpatient setting.

The difficulty arises from a simple fact: in most patients with community-acquired pneumonia (about 98% of those treated as outpatients and 50% to 60% of those treated as inpatients), the causative organism is not known. Even in studies at academic centers where every effort is made to culture samples from all conceivable sites, the success rate in determining a cause is only about 50%. In most cases with an "established" cause, testing has been done on expectorated sputum, and this source of sample material always has the potential of contamination with upper-airway organisms. Correlation is not high between findings in expectorated sputum and findings in specimens from lower in the respiratory tract, obtained by bronchoscopy with a protected brush or by fine-needle or transtracheal aspiration.

A variety of organisms can cause community-acquired pneumonia. A review of studies during the past 20 years that included more than 100 subjects (total, >4,900 patients) reveals that the following are the most common pathogens(1): Streptococcus pneumoniae (9% to 75%; mean, 33%), Haemophilus influenzae (0 to 50%; mean, 10%), Legionella species (0 to 50%; mean, 7%), and Chlamydia pneumoniae (0 to 20%; mean, 5%) (1,3,5,8). Other organisms reported, in no particular order, wereMycoplasma pneumoniae, other gram-positive organisms, gram-negative organisms, anaerobes, mycobacteria, fungi, and viruses. The incidence of so-called "atypical" (legionellal, chlamydial, and mycoplasmal) pneumonias is particularly difficult to ascertain, because diagnosis of these infections is usually made by serologic testing. This method indicates only whether there has been exposure to these organisms and an immunologic response; it does not necessarily establish that they are causative agents of the pneumonia under scrutiny.
Despite all the contradictory statistics on etiology, most investigators agree that S pneumoniaeis the leading cause of community-acquired pneumonia in both inpatients and outpatients.

Considerations in choosing outpatient therapy

Perhaps the greatest debate concerning community-acquired pneumonia has been over therapeutic options. Because outpatient therapy must be chiefly empirical, antibiotics should be chosen that provide adequate coverage against the putative treatable organisms known to cause community-acquired pneumonia. The Infectious Diseases Society of America recommends selecting from among the macrolides erythromycin, clarithromycin (Biaxin), and azithromycin (Zithromax); the fluoroquinolones levofloxacin (Levaquin), trovafloxacin mesylate (Trovan), grepafloxacin (Raxar), sparfloxacin (Zagam), and any other fluoroquinolone with enhanced activity against S pneumoniae;and (in patients between the ages of 17 and 40) doxycycline.
Duration of therapy
The preferred duration of therapy for community-acquired pneumonia is an unresolved issue, and surprisingly, applicable prospective studies are not available. The Infectious Diseases Society of America recommends 7 to 10 days. However, one study found that clinical outcomes were as good with a 3- to 5-day course of azithromycin as with the usual 7- to 10-day course of comparable antibiotics. Outcome research is urgently needed, because both cost and resistance could be minimized by using shorter courses of antibiotic therapy.

Antibiotic resistance

Development of bacterial resistance has been a significant problem related to antibiotic use. The frequency of resistance among community-acquired pathogens is increasing and has been linked to inappropriate use of antibiotics, such as the following:

To treat viral infections

To treat resistant organisms
For longer periods than necessary
To treat a particular organism with a much-wider-spectrum agent than needed
Unnecessary use of antibiotics for viral illnesses is common and has led to increasing rates of antibiotic resistance among S pneumoniae and other community-acquired pathogens. In addition, boundaries between community and hospital environments are blurring, with potential negative consequences regarding resistance. Resistance genes occur in both pathogenic and commensal organisms to which people are exposed continually through food, the environment, and animals. The multitude of genetic mechanisms available for evolution and reassortment of antibiotic resistance genes virtually ensures that genes useful to survival of bacteria are rapidly disseminated.
On the bright side, resistance to newer fluoroquinolones (eg, trovafloxacin) may be slow to develop because bacteria might be required to mutate more than once to achieve a significant level of resistance. Encouragingly, one recent multicenter study found (theoretical considerations notwithstanding) that resistance to antibiotics did not parallel antibiotic use.
antibiotic regimens for community-acquired pneumonia
Erythromycin: 500 mg q6h
Clarithromycin (Biaxin): 500 mg q12h
Azithromycin (Zithromax): Day 1, 500 mg; then 250 mg qd
Levofloxacin (Levaquin): 500 mg qd
Sparfloxacin (Zagam): Day 1, 400 mg; then 200 mg qd
Trovafloxacin mesylate (Trovan): 200 mg qd
Grepafloxacin (Raxar): 600 mg qd
Doxycycline: 100 mg bid
Many experts believe that empirical outpatient treatment of community-acquired pneumonia must include coverage for the common causative organisms, which include such gram-positive bacteria as S pneumoniae and such atypical organisms as Legionella, Mycoplasma, and Chlamydia. Since S pneumoniae is conceded to be the most common causative agent in community-acquired pneumonia, the organism deserves particular attention in therapeutic considerations.
In general, choosing antibiotics to which organisms are highly resistant should be avoided. However, there is little clinical evidence demonstrating that using antibiotics to which recovered organisms have high or intermediate resistance results in more treatment failures than using antibiotics to which the organisms are sensitive. In one recent study, a few clinical failures occurred among patients who had highly penicillin-resistant S pneumoniae infection. It seems intuitively obvious that treating infections with antibiotics to which organisms are highly resistant will eventually result in significant numbers of treatment failures.
Differences by location
Resistance to different antibiotics may vary by hospital and by locale, so the pattern of resistance in a geographic area of practice must be known to make a rational selection among antibiotics. Information on resistance patterns can be obtained from each hospital's microbiology department and each state's board of health.
Surveillance studies show almost exponential increases in penicillin-resistant S pneumoniaeover the past 3 years in the United States. This trend is also true worldwide. If a location has considerable (eg, more than 5% to 10%) resistance to S pneumoniae, use of another antibiotic should be considered. High-level resistance to penicillin is associated with high-level resistance to macrolides, cephalosporins, and doxycycline as well. In contrast, to date, high-level resistance to the newer fluoroquinolones is less than 1%, and cross-resistance between these agents and penicillin has not, as yet, been recognized.
Minimizing resistance
Theoretically, choosing doses of antibiotics on the basis of pharmacodynamics should increase eradication of bacteria and thus minimize development of resistance. Preventing antibiotic resistance through rapid DNA-based testing is an emerging and potentially promising biotechnologic tool. Additional new techniques under way to combat resistance include development of products that block bacterial adherence to tissues, design of drugs to fit model chemicals into the crystal structures of the catalytic sites of key enzymes from bacteria, and use of other highly sophisticated molecular biology tools.
More general solutions to the problem of increasing antibiotic resistance include intensive education of healthcare providers, enhanced education of patients, institution of mandatory surveillance programs, and funding of appropriate research.

Preventive measures

Virtually all experts on community-acquired pneumonia recommend use of polyvalent pneumococcal vaccine (Pneumovax 23, Pnu-Imune 23) in patients considered at increased risk. Some authors question the usefulness of pneumococcal vaccine, particularly in the elderly, but case-control and cohort studies have documented its efficacy. Prospective studies evaluating the impact of immunization on disease incidence, antibiotic resistance, and overall treatment cost are under way.

Summary

Most patients with community-acquired pneumonia are treated as outpatients, and choice of therapy is usually empirical because the etiologic agent is unknown. Therapy should include coverage for both typical and atypical organisms. In geographic areas with highly resistant S pneumoniae, one of the newer fluoroquinolones should be considered, since resistance to penicillin is associated with cross-resistance to macrolides and tetracyclines. Once-daily dosing should be given strong preference because more-frequent dosing results in poor compliance, which may lead to inadequate therapy and increased resistance. At present, the duration of therapy should probably be no less than 7 days.
Patients should be categorized for mortality risk with objective scoring methods, and the need for hospitalization should be decided accordingly. Greater use of observational and intermediate-care beds is encouraged, as is improved utilization of pneumococcal vaccine. The main types of pneumonia are presented.
PNEUMOCOCCAL PNEUMONIA
Essentials of Diagnosis
• Sudden onset of shaking chills, fever, chest pain, and cough with rust-colored sputum.
• X-rays show infiltration, often lobar in distribu- tion, but sometimes patchy.
• Pneumococci are present in the sputum and often in the blood.
• Leukocytosis.
General Considerations
Pneumonia is an inflammatory process in lung parenchyma most commonly caused by infection. The consolidation of pneumonia must be differentiated from pulmonary infarction, atelectasis with bronchial obstruction, and congestive heart failure, but it may coexist with any of these conditions. The pneumococcus accounts for 50-80% of community-acquired bacterial pneumonias; types 1-9 and 12are most commonly found in adults, whereas types 6, 14, 19, and 23 are most common in children. These bacteria frequently are in the normal flora of the respiratory tract. The development of pneumonia must therefore usually be attributed to an impairment of natural resis- tance. Conditions leading to aspiration of secretions include suppression of the cough or epiglottic reflex, impairment of upward migration of mucous sheets (propelled by cilia), and impairment of alveolar phagocyte function. Among conditions that predis- pose to pneumonia are viral respiratory diseases, mal- nutrition, exposure to cold, noxious gases, alcohol intoxication, depression of cerebral functions by drugs, and cardiac failure. Pulmonary consolidation may be in one or more lobes or may be patchy in distribution.
Clinical Findings
A. Symptoms and Signs: The onset is usually sudden, with shaking chills, "stabbing" chest pain (exaggerated by respiration but sometimes referred to the shoulder, abdomen, or flank), high fever, cough and "rusty" sputum, and occasionally vomiting. A history of recent upper respiratory illness can often be elicited.
The patient appears severely ill, with marked tachypnea (30-40/min) but no orthopnea. Respi- rations are grunting, nares flaring, and the patient often lies on the affected side in an attempt to splint the chest. Herpes simplex facial lesions are often present.
Initially, chest excursion is diminished on the involved side, breath sounds are suppressed, and fine inspiratory rales are heard. Later, the classic signs (absent breath sounds, dullness, etc) of consolidation appear. A pleural friction rub or abdominal distention may be present. During resolution of the pneumonia, the signs of consolidation are replaced by rales. Physical findings are often inconclusive, and repeated x-ray examination is helpful.
B. Laboratory Findings: Blood cultures are positive for pneumococci in 15-25% of cases early in the disease. In peripheral blood, leukocytosis (20-35 thousand/^L) is the rule, and a low white blood cell count carries a poorer prognosis.
Sputum must be examined by Gram's stain and by culture. In the smears, the presence of many squamous epithelial cells suggests heavy contamination with saliva, and such specimens are of no value. Typical sputum from pneumococcal pneumonia contains many red and white cells (PMNs) and many pneumococci. If good sputum specimens are not obtainable, a trans- tracheal aspirate may reveal the causative agent, but this procedure is not without risk. A microscopic "quellung" reaction with pooled antiserum rapidly identifies pneumococci in fresh sputum.
C. X-Ray Findings (picture 1): Initially, there may be only a vague haziness across the involved part of the lung field. Later typical consolidation is well defined either in lobar or in patchy distribution. Fluid shadows in the costophrenic angles may appear before pleural exudate can be detected by physical examination. During reso lution of the consolidation, which may require 8-10 weeks, areas of radiolucency may appear, suggesting ' 'pseudocavitation.''
Treatment
A blood culture and a good sputum specimen for smear and culture should always be obtained before treatment is started. The dosage and route of administration of antimicrobial drugs are influenced to some extent by the clinical severity of the disease, the pres- ence of unfavorable prognostic signs (see below), and the presence of complications.

Drug Category: Antibiotics

The initial antibiotic to treat low-risk patients is a macrolide. Macrolides are effective against most likely organisms in community-acquired bacterial pneumonia. Macrolides are used for gram-positive organisms, Legionella, and Mycoplasma. Azithromycin administered IV has the advantage of once-daily dosing over IV erythromycin.
normal chest x-ray (lateral view)

normal chest x-ray (antero-posterior view)
Macrolides, as a class, have the potential to cause adverse GI effects. Newer agents are expensive, have fewer adverse GI effects, and fewer drug interactions compared to erythromycin. Macrolides are used for community-acquired pneumonia in patients younger than 60 years who are nonsmokers and have no comorbidity. Newer macrolides offer better compliance through reduced dosing frequency and improved activity against H influenzae andMycoplasma.
Patients with community-acquired pneumonia who are older than 60 years or have comorbidity still are susceptible to S pneumoniae, but broader coverage is required to includeHaemophilus, Moraxella,and other gram-negative organisms. Therefore, empiric therapy would include one of the macrolide agents outlined above plus one of the second-generation or third-generation cephalosporins, amoxicillin-clavulanate, or respiratory fluoroquinolone.
The choice of antimicrobial agent is based on the severity of patient illness, host factors (eg, comorbidity, age), and presumed causative agent (see Tables 1-3 in Medical Care). Outpatients are prescribed oral agents, and parenteral antibiotics are prescribed to patients admitted to the hospital.
Second-generation cephalosporins have added activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis in addition to the gram-positive activity of first-generation cephalosporins.
Third-generation cephalosporins have wider activity against most gram-negative bacteria, such asEnterobacter, Citrobacter, Serratia, Neisseria, Providencia, and Haemophilus species, including beta-lactamase–producing strains.
Second-generation cephalosporins are not effective against Legionella or Mycoplasma. Generally, they are well tolerated but expensive. Oral second-generation and third-generation cephalosporins offer increased activity against gram-negative agents and may be effective against ampicillin-resistant S pneumoniae.
IV cephalosporins may be combined with a macrolide agent in patients with community-acquired pneumonia who are admitted to the hospital. They broaden the gram-negative coverage and, in the case of third-generation agents, may be effective against resistant S pneumoniae. Also, ceftazidime, a third-generation agent, is effective against Pseudomonas.
When a severely ill patient has features of sepsis, respiratory failure, or neutropenia, treatment with an IV macrolide is combined with an IV third-generation cephalosporin. An alternative regimen may include imipenem, meropenem, or piperacillin/tazobactam plus a macrolide plus vancomycin. A fulminant course should lead to consideration of Legionella, Mycoplasma, psittacosis, and Q fever as the cause of bacterial pneumonia.
Pediatric respiratory system

Respiratory system

B. General Supportive Treatment:
1. Ventilation and oxygenation-An adequate airway must be maintained—if necessary, by tracheal suction, endotracheal tube, or tracheostomy. Oxygen must be supplied to any patient with severe pneumonia, cyanosis with Pao2 below 60, or marked dyspnea;
this will also help to prevent pulmonary edema. Oxygen may be supplied by nasal catheter, soft rubber mask, or oxygen tent. With masks, a 95% oxygen concentration can be maintained, whereas with nasal tubes or tents the concentration will reach only 40- 50%. However, masks are difficult to tolerate because of cough and expectoration. Oxygen must be humidified to prevent drying of secretions.
2. Management of shock and pulmonary edema-These are the most frequent causes of death in pneumonia. Oxygen administration tends to prevent pulmonary edema; impending right heart failure must be managed, and digitalization is urgent.
3. Management of toxic delirium-Toxic delirium occurs in any severe pneumonia and may be particularly difficult to manage in alcoholics. Delirium, anxiety, and restlessness during waking hours may be treated with diazepam, 5 mg, or chlordiazepoxide, 10 mg, or phenobarbital, 15-30 mg orally 4-6 times daily. Pentobarbital, 0.1 g, or flurazepam (Dalmane), 30 mg, at bedtime helps to ensure adequate rest. If sedatives or tranquilizers are given, it is helpful to check the patient's sensorium frequently for any change suggestive of meningitis, which-requires a diagnostic lumbar puncture.
4. Fluids-Patients with pneumococcal pneumonia may perspire profusely and lose much fluid and salt. Sufficient fluid must be given to maintain a daily urinary output of at least 1500 mL. Electrolytes must be kept in balance.
5. Diet-Initially, the dyspneic patient is anorectic, and a liquid diet is preferred. With improvement, a normal diet will be tolerated. If complications suggest a long illness, a high-protein, high-calorie diet with vitamin supplementation is indicated.
6. Cough-If cough interferes with sleep and rest, it may be suppressed with codeine phosphate, 15-30mg every 3-4 hours subcutaneously or orally;
or by elixir of terpin hydrate with codeine, 4 mL every 3—4 hours as necessary.
7. Pleuritic pain-For mild pain, spray ethyl chloride over the area of greatest pain for about 1 minute or inject a local anesthetic to anesthetize the involved dermatomes to provide temporary relief. Codeine phosphate, 15-30 mg, may be given as necessary for pain. For very severe pain, use meperidine, 50-100 mg subcutaneously, or morphine sulfate, 10-15 mg subcutaneously.
8. Abdominal distention-Abdominal disten- tion is usually due to air swallowing in severe dyspnea and is a frequent problem in patients with pneumonia. Neostigmine methylsulfate, 1:2000, 1 mL subcutane- ously, and insertion of a rectal tube will usually pro- duce rapid initial decompression. Gastric dilatation can be relieved by suction through a nasal tube passed into the stomach.
9. Congestive failure- (Distinguish from shock and pulmonary edema.) In elderly patients or patients with preexisting heart disease, congestive failure may be precipitated by pneumonia. Rapid digitalization is indicated.
10.Cardiac arrhythmias-Extrasy stoles usually require no treatment. If atrial fibrillation or flutter develops, rapid failure may be precipitated. Rapid digitalization is usually indicated in these cases.

Further Inpatient Care

  • Hospitalization versus ambulatory care
·
  • The decision to hospitalize patients with community-acquired pneumonia is dictated by a series of well-recognized risk factors that increase either the risk of death or the risk of a complicated course for a patient with community-acquired pneumonia. Specific risk factors for mortality or a complicated course of pneumonia include the following:
o
  • Advanced age (>65 y)
  • Comorbid illness or other findings - (1) COPD, including chronic suppurative diseases of the lung (eg, bronchiectasis, cystic fibrosis); (2) diabetes mellitus; (3) chronic renal failure; (4) congestive heart failure; (5) chronic liver disease of any etiology; (6) suspicion of aspiration; (7) postsplenectomy state; and (8) chronic alcohol abuse or malnutrition
Certain physical findings may predict a poor outcome from community-acquired bacterial pneumonia. These physical findings include the following:
o
  • Respiratory rate in excess of 30 breaths per minute
  • Diastolic blood pressure less than 60 mm Hg or systolic blood pressure less than 90 mm Hg
  • Temperature higher than 38.3°C (101°F)
  • Evidence of extrapulmonary sites of disease (eg, septic arthritis, meningitis)
  • Confusion, decreased level of consciousness, or both
The following series of laboratory findings predicts severe disease and, possibly, a complicated course of illness:
o
  • WBC count of fewer than 4000/μL or more than 30,000/μL, absolute neutrophil count of fewer than 1000/μL
  • ABG determinations showing a PaO2 of less than 60 mm Hg or PaCO2 of greater than 50 mm Hg on room air
  • Respiratory failure requiring mechanical ventilation
  • Abnormal renal function as indicated by serum creatinine of greater than 1.2 mg/dL or blood nitrogen of greater than 20 mg/dL (>7 mmol/L)
  • Chest radiographic findings for multilobar involvement, the presence of a cavity, rapid radiographic progression, and the presence of a pleural effusion
  • Evidence of sepsis or organ dysfunction as manifested by a metabolic acidosis, an increased prothrombin time, increased partial thromboplastin time, or decreased platelets (a picture of disseminated intravascular coagulation).
viral pneumonia

Pneumonia I


Chicken Pox-Acute Pneumonia

Lobar Pneumonia

X-ray showing Pneumonia 



The decision to hospitalize also should take in to account social considerations, which include the absence of a responsible caregiver and or an unstable home situation. The Pneumonia Severity of Illness Scoring System (PSISS) was developed by Fine et al (Fine, 1997). This scoring system evaluates 20 different clinical and laboratory indices that are readily available. The PSISS is used to assist in deciding whether patients can be safely treated in an outpatient setting. Demographic factors Age Men: Age in years Woman: Age in years minus 10 Nursing home resident: 10 Coexisting Illnesses (definitions listed below) Neoplastic disease: 30 Liver disease: 20 Congestive heart failure: 10 Cerebrovascular disease: 10 Renal disease: 10 Physical Examination Findings Altered mental status: 20 Respiratory rate >30 breaths per min: 20 Systolic blood pressure <90 mm Hg: 20 Temperature <35°C (95°F) or >40°C (104°F): 15 Pulse rate >125 breaths per min: 10 Laboratory and Roentgenographic Findings Arterial pH <7.35: 30 Blood urea nitrogen >30 mg/dL (11 mmol/L): 20 Sodium <130 mmol/L: 20 Glucose >250 mg/dL (14 mmol/L): 10 Hematocrit <30%: 10 PaO2 <60 mm Hg: 10 Pleural effusion: 10 Coexisting illnesses: The diagnosis of congestive heart failure is documented by history or by findings on physical examination, chest radiograph, echocardiogram, multiple-gated acquisition scan, or left ventriculogram. The clinical diagnosis of stroke or transient ischemic attack is documented by magnetic resonance imaging or CT scan findings. A history of chronic renal disease or abnormal blood urea nitrogen and creatinine concentrations should be documented in the medical record. Altered mental status is defined as disorientation to person, place, or time that is not known to be chronic or as stupor or coma. Hospitalization versus ambulatory care is determined by the total points calculated from the PSISS. Patients are categorized in to 5 risk classes, as follows: o Risk class I - Older than 50 years, no preexisting illness or vital sign abnormality Risk class II - Fewer than 70 points Risk class III - 71-90 points Risk class IV - 91-130 points Risk class V - More than 131 points Although further epidemiologic studies are required to make definite recommendations for hospital versus home care for patients with community-acquired pneumonia, preliminary data (Fine, 1997) indicate that patients in risk classes I and II can be treated at home with planned outpatient follow-up evaluations. Patients in risk class III should be observed in the emergency department before their disposition is decided. Patients in risk classes IV and V are ill and usually require admission to the hospital. Response to therapy
·
  • Having initiated a course of therapy based on empiric guidelines, carefully evaluating the patient's response to therapy is essential. With appropriate antibiotic therapy, improvement in the clinical manifestations of pneumonia should be observed in 48-72 hours. Because of the time required for antibiotics to act, antibiotics should not be changed within the first 72 hours unless marked clinical deterioration occurs.
  • With pneumococcal pneumonia, the cough usually resolves within 8 days and crackles heard on auscultation clear within 3 weeks. The timing of radiologic resolution of the pneumonia varies with patient age and the presence or absence of an underlying lung disease. The chest radiograph usually clears within 4 weeks in patients younger than 50 years without underlying pulmonary disease. In contrast, resolution may be delayed for 12 weeks or longer in older individuals and those with underlying lung disease.
Patients who do not respond to treatment
·
  • A common concern is patients who do not improve despite antibiotic treatment. If patients do not improve within 72 hours, consider an organism that is not covered by the initial empiric antibiotic regimen. Lack of response also could be secondary to drug resistance, nonbacterial infection, unusual pathogens (eg, P carinii, M tuberculosis), drug fever, or a complication such as empyema or abscess formation. One must broaden the differential diagnosis to include noninfectious etiologies such as malignancies, inflammatory conditions, or congestive heart failure.
  • When reevaluating a patient who is not responding, a careful history of travel and animal exposure should be obtained to rule out unusual pathogens. If this is unrevealing, then further diagnostic procedures may be required. Bronchoscopy helps evaluate the airway for obstruction due to a foreign body or malignancy. Infection with previously unsuspected pathogens such as P carinii or M tuberculosis often is diagnosed using bronchoscopy. During bronchoscopy, protected brushing and bronchioalveolar lavage specimens may be obtained for microbiologic examination and quantitative cultures. Transbronchial biopsy also may be helpful in some cases. Routine bacterial cultures have limited utility when obtained from bronchoscopy after antibiotics have already been administered.
  • A retrospective study evaluated the use of fiberoptic bronchoscopy in nonresolving pneumonia. A specific diagnosis that could account for the prolonged course was found in 12 of 14 patients. The etiologies included Pneumocystis, mycobacteria, cytomegalovirus, and actinomycosis and noninfectious entities such as bronchioalveolar carcinoma, adenocarcinoma, and eosinophilic pneumonia. A second prospective study found the diagnostic sensitivity of video bronchoscopy after the initiation of antibiotics to be 41%.
  • In addition to bronchoscopy, further imaging studies, such as CT scan of the thorax, may be helpful. Finally, open or thoracoscopic lung biopsy may need to be performed if all other procedures do not aid in diagnosis and the patient continues to be ill. Thoracoscopic lung biopsy is associated with less morbidity compared to the open lung biopsy.
Other inpatient care
·
  • Antibiotic therapy should be reevaluated based on laboratory data and clinical response.
  • Adequate respiratory support (eg, low-flow oxygen, assisted ventilation) is provided as dictated by the patient's clinical situation.
  • Bronchial hygiene includes suctioning of secretions, chest physiotherapy, and positioning to encourage dependent drainage. These are used to optimize the elimination of purulent sputum and to avoid atelectasis.
  • General supportive measures include proper hydration, nutrition, and patient ambulation.

Further Outpatient Care

  • When treated in an outpatient setting, arranging adequate follow-up evaluations for the patient is mandatory. Patients also should be instructed to return if their condition deteriorates.
  • Patients should have a follow-up chest radiograph in approximately 6 weeks to ensure resolution of consolidation.
  • Chest radiograph findings indicating nonresolution of symptoms should raise the consideration of an endobronchial obstruction as a cause of postobstructive pneumonia. A CT scan may be of benefit in these cases.

Deterrence/Prevention

  • Prevention of community-acquired pneumonia·
  • Influenza vaccination for elderly individuals results in a reduction of the rate of hospitalization for pneumonia and influenza by 48-57%.
  • S pneumoniae is the most common cause of pneumonia overall and fatal pneumonia. The incidence of pneumococcal disease is the highest in children younger than 2 years and in adults older than 65 years. Other important risk factors are chronic heart disease, chronic lung disease, cigarette smoking, and asplenia. A 23-valent capsular polysaccharide vaccine and a heptavalent protein-polysaccharide conjugate vaccine are currently available. Both vaccines are efficacious in prevention of invasive pneumococcal disease. The role of the pneumococcal vaccine has not been defined as clearly as that of the influenza vaccine in adults. However, the advisory committee on immunization practice recommends pneumococcal vaccination for persons older than 65 years and for younger patients with chronic illnesses.
Prevention of nosocomial pneumonia·
  • A number of preventative strategies have been applied. Some of these probably are effective or promising, and some are currently being evaluated.
  • The efficacious regimens are hand washing and isolation of patients with multiple resistant respiratory tract pathogens. Hand washing between patient contacts is a basic and often neglected behavior by medical personnel.
  • Interventions that should be considered or undertaken include nutritional support, attention to the size and nature of the GI reservoir of microorganisms, careful handling of ventilator tubing and associated equipment, subglottic secretion drainage, and lateral-rotation bed therapy.
  • The regimens of unproven value in preventing nosocomial pneumonia, although used on limited investigational bases, are selective digestive decontamination with a regimen of topical and systemic antibiotic prophylaxis. Selective digestive contamination has been studied for many years with a goal of eliminating all potential pathogens from the GI tract. Incidence of nosocomial pneumonia is not always reduced; therefore, efficacy of these regimens has been questioned. Also, mortality reduction often is not observed.
  • Some experimental regimens are undergoing clinical evaluation. These are monoclonal antibodies to specific bacterial antigens and reduction of endogenous sources of bacterial infection by mechanical means. The development of new biomaterials for endotracheal tubes is one such therapy, leading to the eradication of a reservoir of a large number of bacteria in the airway.
Smoking cessation

Complications

  • Destruction of lung tissue from infection (leading to bronchiectasis)
  • Necrotizing pneumonia
  • Empyema
  • Pulmonary abscess
  • Respiratory failure
  • Acute respiratory distress syndrome
  • Ventilator dependence
  • Superinfection with gram-negative organisms
  • Death

Prognosis

  • Generally, prognosis is good in otherwise healthy patients with uncomplicated pneumonia.
  • Advanced age, aggressive organisms (eg, Klebsiella, Legionella, resistant S pneumoniae), comorbidity, respiratory failure, neutropenia, and features of sepsis, alone or in combination, increase morbidity and mortality.

Patient Education

  • For excellent patient education resources, visit eMedicine's Pneumonia Center and Procedures Center. Also, see eMedicine's patient education articles Bacterial Pneumonia and Bronchoscopy.

Medical/Legal Pitfalls

  • The guidelines for empiric management of community-acquired bacterial pneumonia are formed with the intent of following evidence-based recommendations, but the recommendations of these guidelines are not based on a firm scientific foundation. Future studies should focus on the following issues:·
  • Duration of therapy
  • Duration of therapy related to severity of initial illness
  • Appropriate time to switch hospitalized patients from parenteral therapy to oral therapy
  • Pathogens responsible for pneumonia when no organism is identified with extensive diagnostic testing
In the future, a number of unresolved questions about nosocomial pneumonia need to be examined. These should focus on the diagnosis of nosocomial pneumonia, determinants of specific pathogens, duration of therapy, and timing of switch to oral therapy. Ultimately, prevention of nosocomial pneumonia is the most effective way to avoid disease associated with mortality. In patients who are elderly or debilitated, if bacteremia is present with pneumococcus, the mortality rate remains approximately 40% even if treated. Empiric therapy for hospitalized patients initially should be broad and cover the likely causative organisms. Always consider the possibility of Legionella when evaluating community-acquired pneumonia because delayed treatment increases mortality significantly. Remember that the most prevalent causative organism is pneumococcus, regardless of the host; empiric therapy must be selected with this consideration in mind.

Special Concerns

  • Relative adrenal insufficiency occurs in a high proportion of patients with severe CAP. Median cortisol levels were 15.5 mcg/dL; 65% met the criteria for adrenal insufficiency, 75% had cortisol levels below 25 mcg/dL and 47.5% had cortisol levels below 15 mcg/dL. These finding highlight the importance of measuring cortisol levels and may help explain the potential benefits of hydrocortisone infusion in these patients.
OTHER BACTERIAL PNEUMONIAS
Primary bacterial pneumonias caused by single bacterial species other than the pneumococcus may account for up to 25% of community-acquired and 80% of hospital-acquired pneumonias. All of these pneumonias may have somewhat similar physical find- ings and x-ray evidence of pulmonary infiltration or •consolidation. For proper treatment, it is crucial to identify the causative agent by blood culture and by sputum examination with stained smear and culture. Transtracheal aspiration, fiberoptic bronchoscopy, or even lung biopsy may be needed for specific diagnosis and treatment.
Streptococcal Pneumonia
Pneumonia due to hemolytic streptococci occurs usually as a sequela to viral infection of the respiratory tract, especially influenza or measles, or in persons with underlying pulmonary disease. The patients are usually in a severely toxic condition and cyanotic. Pleural effusion develops frequently and early and progresses to empyema in one-third of untreated pa- tients. The diagnosis rests on finding large numbers of streptococci in smears of sputum and culturing hemolytic streptococci from blood and sputum.
The treatment of choice is with penicillin G in a dosage similar to that for pneumococcal pneumonia. If treatment is started early, the prognosis is good.
Staphylococcal Pneumonia
Pneumonia caused by Staphylococcus aureus occurs as a sequela to viral infections of the respiratory tract (eg, influenza) and in debilitated (eg, postsurgical) patients or hospitalized infants, especially after antimicrobial drug administration. There is often a history of a mild illness with headache, cough, and generalized aches that abruptly changes to a very se- vere illness with high fever, chills, and exaggerated cough with purulent or blood-streaked sputum and deep cyanosis. There may be early signs of pleural effusion, empyema, or tension pneumothorax. X-ray examination reveals lung consolidation, pneumatoceles, abscesses, empyema, and pneumothorax. The demonstration of pyopneumothorax and of cavities with air-fluid levels by x-ray is highly suggestive of Staphylococcal pneumonia. The diagnosis must be confirmed by stained smear of sputum (masses of white cells and gram-positive cocci, many intra- cellular) and culture (predominantly S aureus), and
also by means of cultures of pleural fluid and blood. The white count is usually more than 20,000//zL.
Initial therapy (based on sputum smear) consists of nafcillin, 6-12 g/d, or vancomycin, 2 g/d, given intravenously in divided doses as a bolus. If the staphylococcus proves to be penicillin-sensitive by laboratory test, penicillin G, 20-60 million units/d intravenously, is the antibiotic of choice. Drugs should be continued for several weeks. If empyema develops, drainage must be established. The prognosis varies with the underlying condition of the patient and the drug susceptibility of the organism.
Legionella Pneumonia
The eponym legionnaires' disease has been given to a serious pneumonia that afflicted people attending the American Legion Convention in Philadelphia in 1976. Other outbreaks have been diagnosed ret- rospectively at least since 1965, and sporadic infec- tions have occurred at least since 1947 in many places.
Legionella pneumophila is a poorly staining gram-negative bacterium that grows slowly on special media (eg, charcoal-yeast extract) at 35 °C. There are at least 8 species of Legionella, some with multiple serotypes. These organisms can be recovered in human disease from sputum, bronchial washings, pleural fluid, lung biopsies, or blood. Legionella species occur in the environment and are acquired by humans from aerosols, dust from air-conditioning systems, water, or soil. The infection is not usually communi- cable from patient to contacts. Asymptomatic infec- tion is common at all ages, whereas symptomatic infection is most often an opportunistic pneumonia in immunocompromised individuals.
Asymptomatic infection is evident only by a rise in specific antibodies. Symptomatic infection is ob- served mainly in elderly persons, smokers, and pa- tients undergoing hemodialysis or renal transplant.
The incubation period is estimated to be 2-10 days. Initial symptoms are malaise, diffuse myalgias, and headache, followed in 12-48 hours by high, non- remittent fever and chills. Nausea, vomiting, and diarrhea are frequent early in the illness. On the third day a dry cough begins that is nonproductive or produces scanty mucoid, sometimes blood-streaked sputum. Dyspnea and hypoxia become marked as signs of consolidation develop. Pleuritic chest pain occurs in one-third of patients. Severe confusion or delirium may occur.
There is leukocytosis with a shift to the left, hyponatremia, abnormal liver function tests, and, occasionally, microscopic hematuria. Chest x-rays reveal patchy, often multilobar pulmonary con- solidation, and, occasionally, small pleural effusions. The illness usually worsens for 4-7 days before im- provement begins in those who recover. During severe outbreaks, the mortality rate has been 10%in those with manifest disease. Death is attributed to respi- ratory or renal failure or shock, with disseminated intravascular coagulation.
The diagnosis is based on a clinical picture com- patible with the specific features of the disease and on negative results of bacteriologic laboratory tests for other pneumonias. The organism can be identified by immunofluorescence in cultures, lung biopsy, and, rarely, sputum specimens. A retrospective diagnosis is based on a significant rise in specific serum antibodies detected by immunofluorescence.
The treatment of choice is erythromycin, 0.5-1 g every 6 hours intravenously or orally for 2-3 weeks. This usually results in improvement in 2-3 days. Rifampin, 10-20 mg/kg/d, has been suggested for patients who fail to respond to erythromycin. Assisted ventilation and management of shock are essential. fulminant course should lead to consideration ofLegionella, Mycoplasma, psittacosis, and Q fever as the cause of bacterial pneumonia.
Pneumocystis carinii Pneumonia
This parasitic infection occurs in debilitated children or immunodeficient adults. It has been a prominent opportunistic infection in AIDS patients. The diagnosis is made by lung biopsy and the demonstration of typical cysts of P carinii in impression smears of lung tissue stained with methena- mine-silver. Early treatment with sulfamethoxazole- trimethoprim can cure the pneumonia. The same drug has been effective in prophylaxis during immunosuppression. An alternative, more toxic drug is pentamidine isethionate (available through the Centers for Disease Control, Atlanta, GA 30333).
"MIXED" BACTERIAL PNEUMONIAS (Hypostatic Pneumonia, "Terminal" Pneumonia, Bronchopneumonia)
Essentials of Diagnosis
• Variable onset of fever, cough, dyspnea, expectoration.
• Symptoms and signs often masked by primary (debilitating) disease.
• Greenish-yellow sputum (purulent) with mixed flora.
• Leukocytosis (often absent in aged and debilitated patients).
• Patchy infiltration on chest x-ray.
General Considerations
Mixed bacterial pneumonias include those in which culture and smear reveal several organisms, not one of which can clearly be identified as the causative agent. These pneumonias usually appear as complica- tions of anesthesia, surgery, aspiration, trauma, or various chronic illnesses (cardiac failure, advanced carcinoma, uremia). They are common complications of chronic pulmonary diseases such as bronchiectasis and emphysema. Old people are most commonly affected ("terminal" pneumonia). Patients treated with intermittent positive pressure breathing apparatus or immunosuppressive drugs may develop pneumonia caused by gram-negative rods.
The following findings in a debilitated, chroni- cally ill, or aged person suggest a complicating pneumonia: (1) worsening of cough, dyspnea, cyanosis; (2) low-grade, irregular fever; (3) purulent sputum; and (4) patchy basal densities on a chest film (in addition to previously noted densities caused by a primary underlying disease, if any), sometimes with local necrosis and cavitation.
Clinical Findings
A. Symptoms and Signs: The onset is usually insidious, with low-grade fever, cough, expectoration, and dyspnea that may become marked and lead to cyanosis. Physical findings are extremely variable and may not be impressive against a background of cardiac or pulmonary disease. The signs listed under Other Bacterial Pneumonias may also be present.
B. Laboratory Findings: The appearance of a greenish or yellowish (purulent) sputum should suggest a complicating pneumonia. Smears and cul- tures reveal a mixed flora, often including anaerobes. Predominant types should be noted. Leukocytosis is often absent in the aged and debilitated patient present- ing with a mixed infection.
C. X-Ray Findings: X-ray (Picture 3) shows patchy, irregular infiltrations, most commonly posterior and basal (in bedridden patients). Abscess formation may be observed. Careful interpretation will avoid confusion with shadows due to preexisting heart or lung disease.
Differential Diagnosis
Mixed bacterial pneumonias must be differ- entiated from tuberculosis, carcinoma, and other spe- cific mycotic, bacterial, and viral pulmonary infec- tions (to which they may be secondary).
Treatment
Clear the airway and correct hypoxia. Unless a probably significant etiologic agent can be identified, give one of the new cephalosporins (eg, cefotaxime, 12 g/d intravenously) as initial therapy. This will be modified according to clinical and laboratory results.
Prognosis
The prognosis depends upon the nature and sever- ity of the underlying pulmonary disease and varies with the predominating organism.
ASPIRATION PNEUMONIA
Aspiration pneumonia is an especially severe type of pneumonia, often with a high mortality rate. It results from the aspiration of gastric contents in addition to aspiration of upper respiratory flora in secretions. Important predisposing factors include impairment of the swallowing mechanism (eg,esopha- geal disease), inadequate cough reflex (eg, anesthesia, postoperative state, central nervous system disease, drug abuse), and impaired gastric emptying (eg, pyloric obstruction). Pulmonary injury is due in large part to the low pH (< 2.5) of gastric secretions.
Scattered areas of pulmonary edema and bron- chospasm occur, and the x-ray appearance (pictures 4-5) may be confused with that of pulmonary emboli, atelectasis, bronchopneumonia, and congestive heart failure.
Removal of aspirated material by catheter suction or bronchoscopy may be attempted, but this usually fails to remove all aspirate completely. Corticosteroids (eg, prednisone, 100 mg orally on the first or second day) may reduce the intensity of the inflammatory reaction to acidic gastric secretion, but the value of corticosteroids in the treatment of aspiration pneumo- nia is not proved, and they increase the risk of superinfection. Some aspiration pneumonias have no bacterial component, but in many others a mixed bacterial flora is involved. Antimicrobial drugs directed against the latter (eg, penicillin G plus an aminoglycoside or the best available cephalosporin) are sometimes adminis- tered without waiting for evidence of progressive pul- monary infection. In doing so, however, there is a risk of favoring the development of resistant mi- croorganisms. Therefore, administration of antimi- crobials should not continue without laboratory and clinical evidence of microbial infection. Assisted ventilation and supplementary oxygen are beneficial.

Infection in the immunocompromised host

Viral Pneumonias
Viruses are a common cause of serious infections of the lower respiratory tract among immunocompromised patients. Pathogens most commonly implicated are the herpesviruses--herpes simplex, varicella-zoster, and cytomegalovirus. These viruses belong to the familyHerpesviridae,which consists of large, enveloped, double-stranded DNA viruses.
Herpesviruses vary widely in their ability to infect different types of cells. Further, they share the common ability to establish lifelong latent infection. This latter aspect is of particular concern for seropositive immunosuppressed persons, whose immune systems may be unable to contain the virus in its latent form.
Other viruses that cause significant lower respiratory tract disease in immunocompromised patients include adenoviruses and measles virus.
Epidemiologic, etiologic, and clinical characteristics
Immunocompromised patients are at particular risk for virus pneumonia. These include patients who are receiving cancer chemotherapy, those who are neutropenic, those infected with HIV, burn victims, those with congenital cell-mediated immunodeficiency, and those who are severely debilitated or malnourished as a result of prolonged hospitalization. Although the lung is often involved in disseminated HSV infection, disseminated disease seldom occurs among those with mucocutaneous HSV infections. Visceral dissemination develops in fewer than 10% of virus -seropositive transplant recipients with infection.
HSV pneumonia develops by two principal mechanisms. First, the presence of focal or multifocal infiltrates correlates with antecedent upper airway infection with virus. This pattern is most likely due to direct extension of viral infection from the upper to the lower respiratory tract, aspiration of infectious secretions, or reactivation of dormant HSV in vagal ganglia. Tracheitis or esophagitis and oral mucocutaneous lesions often precede development of pulmonary disease. Second, diffuse interstitial infiltrates may develop following viremia secondary to dissemination of HSV from genital or oral lesions or transfusion of HSV-infected blood. Early dissemination also may be reflected by other organ dysfunction, such as elevated liver enzyme levels.
The spectrum of respiratory diseases due to HSV infection ranges from oropharyngitis to membranous tracheobronchitis and diffuse or localized pneumonia. Usually the trachea and large bronchi are involved in creating a thick inflammatory membrane that can ultimately cause significant resistance to ventilation. Community-acquired pneumonia caused by HSV is uncommon, occurring usually only after a prolonged and complicated hospital stay.
Dyspnea and cough are the most common symptoms of HSV pneumonia. Fever, tachypnea, intractable wheezing, chest pain, and hemoptysis also occur. Cutaneous, genital, or oral lesions may herald pulmonary or disseminated disease.
Focal lesions on chest film begin as small nodules that are best seen in the periphery, away from normal vascular markings. As the disease progresses, the nodules may coalesce to form extensive infiltrates. HSV pneumonia may initially present as a focal or segmental pneumonia that has spread from upper airway lesions. However, it can ultimately extend to other areas of the lung, producing diffuse infiltrates similar to the pattern seen with viremic HSV infection.
Diagnosis
The diagnosis of virus pneumonia should be based on clinical suspicion, radiographic findings (picture 6), isolation of HSV from the lungs, and histologic findings of a necrotizing or hemorrhagic pneumonia. Since virus can be isolated from oropharyngeal secretions in 2% to 25% of normal hosts, positive sputum cultures are often difficult to interpret. The use of tracheal aspirates to bypass the upper respiratory tract can yield samples with significantly improved specificity. Bronchoscopy is especially useful for direct sampling of bronchial mucosal lesions and for obtaining bronchial brushings, washings, and biopsy specimens for histologic and cytologic examination. Scrapings from the base of ulcerated lesions can be examined with Wright or Giemsa stain for multinucleated giant cells and intranuclear inclusions. Specimens also can be examined by immunofluorescent staining with polyclonal- or monoclonal-specific antibodies or by electron microscopy. Appropriate viral cultures of mucosal lesions, blood, and respiratory secretions should always be obtained in cases of suspected herpetic pneumonia. Serologic assays are of little diagnostic use.
Treatment
Acyclovir (Zovirax), after it is metabolized to acyclovir triphosphate, inhibits viral DNA synthesis by competitively binding to viral DNA polymerase. Since oral acyclovir is poorly absorbed, intravenous acyclovir at a dosage of 250 mg/m2 every 8 hours is currently the treatment of choice for HSV pneumonia (table 2). Adverse reactions are infrequent, but patients should be well hydrated to prevent renal impairment secondary to precipitation of acyclovir in the tubules, which occurs in 5% to 10% of patients. The dosage of acyclovir must be decreased in patients with underlying renal insufficiency.
Treatment of severe viral infections of the lower respiratory tract
Herpes simplex: Acyclovir (Zovirax)
Varicella-zoster: Acyclovir, VZIG
Cytomegalovirus: Ganciclovir (Cytovene), IVIG, foscarnet sodium (Foscavir)
Adenovirus: Supportive care, ribavirin (Virazole)*
Measles: Supportive care, IVIG, ribavirin
IVIG, intravenous immunoglobulin: VZIG, varicella-zoster immune globulin.
*Currently not considered standard care or still under investigation.
More than half of all cases of viral pneumonia are complicated by other infections. Empirical broad-spectrum antibiotic therapy that includes an antistaphylococcal drug should be instituted in patients with progressive virus pneumonia that does not respond to antiviral therapy. If deterioration continues despite the addition of antibiotics, a definitive diagnostic procedure such as bronchoscopy or open lung biopsy should be pursued to search for other opportunistic organisms, such as Aspergillus, Candida, and Pneumocystis carinii.
The role of adjunctive corticosteroids is still controversial. These agents should not be considered as standard care, especially in an already immunocompromised host. Ventilatory support is often required for severe hypoxemia. Fluid management is of special concern because fulminant pneumonia is often associated with pulmonary edema and alveolar hemorrhage.
Preventive efforts should be directed toward chemoprophylaxis of high-risk seropositive patients during induction of immunosuppression for transplantation. Passive or active immunization has not been proved to be helpful.

Summary

Three herpesviruses (herpes simplex, varicella-zoster, and cytomegalovirus) commonly cause respiratory tract infections in immunocompromised patients. Adenoviruses and measles virus are also significant causes of respiratory disease in this population.
Diagnosis of herpesvirus infections is difficult because these viruses can establish latency and are often shed intermittently in the absence of invasive disease. A positive respiratory tract culture of herpesviruses alone is not diagnostic of active invasive disease. Preventive measures should focus on limiting the patient's exposure to active infection, broad use of available vaccines in children and susceptible adults, and use of hyperimmune globulin and chemoprophylaxis in high-risk patients.
Adenovirus pneumonia is diagnosed by viral culture and rapid antigen detection assays, whereas measles pneumonia is often identifiable by the characteristic rash. Treatment of either adenovirus or measles pneumonia is primarily supportive.
THE GENERAL GUIDELINES FOR TREATING PNEUMONIA
Studies are indicating that many patients are hospitalized unnecessarily for pneumonia and those that are could be released sooner. One study, for example, estimated that one-third of patients who are now routinely hospitalized for pneumonia could be treated safely at home, and another 20% could be released from the hospital with only a short period of observation. A number of strategies are being devised to determine when and which patients can be safely discharged.
Categorizing Severity
Ruling out the Least Severe Cases. The procedure for deciding on hospitalization or not starts by ruling out patients in the lowest risk groups (class 1 and 2), who can be discharged with outpatient care only. This can often be done with a simple physical examination, which can often rule out a severe condition. Patients in low-risk categories have the following characteristics:
· No other major illnesses are present.
· No serious symptoms are present (eg, altered mental state, rapid pulse or breathing rate, very low blood pressure, very high fever).
As examples, the following chioldren with signs of pneumonia should be hospitalized, class 1 categories:
· Any infant under a month.
· Child with severe psychiatric conditions.
· children with abnormal heart rhythms.
· children who are vomiting heavily.
· Children who are dehydrated.
Determining The Next Levels of Severity. If a patient cannot be categorized in class I, the next step is to determine which of the other four higher classes the patient fits. This step involves assigning points to other findings, including the following:
· Laboratory test results.
· X-ray findings.
· Demographics (ie, boy or girl, nursing home patient).
The essential form of treatment is the use of effective antibiotics. Unfortunately, many hospital germs are resistant to many of the commonly used antibiotics. In such cases the mortality rate may be as high as 40 per cent.
As well as intensive antibiotic treatment, good nursing, inhaled oxygen to raise oxygen blood levels and fluids by transfusion, other supportive measures may be essential. Patients who recover from lobar pneumonia often do so suddenly.
· Supportive:
· oxygen to maintain SaO2 95%
· IV fluids if necessary
· clinical and radiological monitoring.
· Antibiotics:
· should be used if bacterial infection suspected or child unwell
· young children — ampicillin ± flucloxacillin (Staph suspected)
· older children — penicillin or ampicillin
· cefotaxime should be reserved for children who are severely ill, responding poorly or at risk.
· Complications:
· Pleural effusion
· Early diagnostic and therapeutic aspiration (ideally under ultrasound control)
· Large bore intercostal catheter for large effusions or if fluid "thick"
· Surgical decortication is rarely necessary if early drainage and appropriate antibiotic therapy is used.
· Pneumatoceles
· Generally conservative
· Drainage for pneumothorax or decompression occasionally needed.
The treatments include:
o Give an antibiotic.
o Advise the mother to give homecare.
o Treatfever.
o Treatwheezing.
Refer to the fold-out chart and find the heading, ``Treatmentinstructions''. Then look at the boxes underneath this heading,and find the box that matches each of the four treatments listedabove. Use these boxes when treating a child with a respiratoryinfection.
Give an antibiotic
WHO recommends treating pneumonia by giving one of the following antibiotics for 5 days:
- co-trimoxazole
- amoxycillin,(in tablet or syrup form)
- ampicillin, or
- procainepenicillin (by daily intramuscular injection).
You need to learn how to give only the antibiotic(s) used in your health centre. The instructions presented here are for giving anoral antibiotic.
If the child cannot take an oral antibiotic (e.g. if the child is unable to drink or will not wake up), however, you will need to give a parenteral antibiotic, such as procaine penicillin. If you are unable to give parenteral antibiotics, refer the child as quickly as possible without giving the first dose.
Cautions about giving an antibiotic:
o Do not give co-trimoxazole to a baby with jaundice, or to a premature baby less than one month old.
o Do not give amoxycillin, ampicillin, procaine penicillin, benzathinepenicillin or phenoxymethylpenicillin if the child has a history of breathing problems or anaphylaxis (allergic reaction) afte rtreatment with penicillin.
Treat fever
Fever is common in acute respiratory infections. The method of treating fever in a child aged 2 months up to 5 years will depend on whether the fever is high or low If the fever is high(39"C or more):
o The child will feel better and eat better if the fever is lowered with paracetamol.It is harder for a child with pneumonia to breathe when he or she has a high fever.
Tell the mother to give the child paracetamol every 6 hours in the appropriate dosage until the child's temperature drops below39". Give the mother enough paracetamol for 2 days.
If the fever is low(38 39"C):
o Advise the mother to give the child more fluids than usual. Paracetamol is not needed.
Tell the mother to keep the child with any fever(38"C or more) lightly clothed. She should notoverwrap or overdress the child, since this will make him or her uncomfortable and may make the fever worse.
Children aged 2 months up to 5 years should not be given antibiotics if they have fever alone. However, fever is a danger sign in young infants, so young infants with fever should be given a first dose of antibiotic and referred to a hospital. They should not be given paracetamol for fever.
Treat wheezing
Children with a first episode of wheezing
Use a bronchodilator to treat children with a first episode of wheezing. A bronchodilator is a drug that helps children with wheezing to breathe more easily by opening the air passages of their lungs and relaxing the bronchospasm.
Before giving the bronchodilator, look to see if the child is in respiratory distress. Signs of respiratory distress are:
- the child is uncomfortable,
- the child is obviously not getting enough air into the lungs,
- the child may have difficulty feeding or talking.
This condition can usually be recognized by simple observation.However, most children who wheeze are not in respiratory distress. They are alert and are getting enough air into their lungs.
If the child is in respiratory distress, give a rapid-acting bronchodilator and refer the child immediately to a hospital. The bronchodilator should be given in rapid-acting form so that the child begins to breathe more easily before he or she is referred. If you are unable to administer a rapid-acting bronchodilator,give the first dose of an oral bronchodilator (see below), and refer the child immediately to a hospital.
If the child is not in respiratory distress, give an oral bronchodilator (preferably salbutamol) in the appropriate and show the mother how to give it.
If the child will be referred for other reasons (e.g. danger signs or chest indrawing), give a single dose of oral salbutamol.If there is no other reason for referral, treat the child based on other signs you see (e.g. fast breathing or fever) and givethe mother enough salbutamol for 5 days of treatment. Tell her to give it three times daily.
If a child with recurrent wheezing also has adanger sign, you should remember that this child needs urgent referral to a hospital.Since the assessment process for recurrent wheezing requiresadditional time, it may cause an unacceptable delay in referral.You will learn with clinical experience which children with recurrent wheezing and a danger sign should be further assessed with a rapid-acting bronchodilator, and which should be referred without any further assessment.
However, most children with recurrent wheezing have asthma. They may come often to the health centre with wheezing. You will cometo recognize these children and treat them promptly with abronchodilator.

1 comment:

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