Hospital-acquired pneumonia is also known as nosocomial pneumonia and it is a type of pneumonia that is acquired during or after hospitalization for treatment of another illness or procedure. The causes, microbiology, treatment and prognosis differ from those of community-acquired pneumonia. It is studied that up to 5% of patients who are admitted in a hospital for other causes, gradually develop pneumonia. Hospitalized patients are at higher risk for pneumonia, including mechanical ventilation, malnutrition for a prolonged time, underlying heart and lung diseases, fewer amounts of stomach acid, and immune system disturbances. In addition, a person is exposed to different types of microorganisms than those at home. Resistant bacteria such as MRSA, Pseudomonas, Enterobacter, and Serratia are some of the hospital-acquired microorganisms. Hospitalized patients are being treated for underlying illnesses and the exposure to the dangerous bacteria in the hospitals, tends to be more fatal than community-acquired pneumonia. Ventilator-associated pneumonia (VAP) is a subset of hospital-acquired pneumonia, which occurs after at least 48 hours of mechanical ventilation and intubation.
Hospital-acquired infections include clinically evident infections that do not originate from patient’s original admitting diagnosis. After admission in the hospital, a patient’s flora begins to acquire characteristics of the surrounding bacterial pool and this happens within hours. Infections that are clinically evident, after 48 hours of hospitalization are considered hospital-acquired. Patients being infected after the discharge from the hospital are considered to have infection of nosocomial origin, if the organisms were acquired during the hospital stay.
Hospital acquired pneumonia mostly develops in patients who are severely debilitated or who have low immunity.
Given below are the different organisms that are responsible for causing hospital acquired pneumonia:
The organism may be antibiotic-resistant; an intravenous, broad spectrum agent such as cefotaxmime or ceftazidine is indicated. In addition to the antibiotic, Metronidazole should be used to cover anaerobic infection, if any.
Hospital-acquired pneumonia (HAP) is linked to high morbidity and mortality rate. Early, appropriate, and adequate empiric therapy can ensure and increase the chances of survival. In 1995, the American Thoracic Society provided guidelines to the physicians in the management of HAP. However, these guidelines have certain drawbacks such as lack of recommendations for duration of therapy and no recognition of newer drugs such as cefepime, trovafloxacin, and meropenem. Furthermore, they are not able to distinguish similar compounds (ie, ß-lactam/ß-lactamase inhibitor combinations) or they fail to recommend specific antibiotics. The clinician following these guidelines needs to tackle local patterns of antimicrobial resistance, especially in ICUs. Efficient computerized antibiotic management programs that include information on local patterns of antimicrobial resistance can be of help for physicians in empiric therapy decision making, to improve patient quality of care, and to reduce the medical costs.
Pneumonia that is contracted in the hospital or any other type of institution is more severe than pneumonia acquired in the community. The organisms in the hospitals are more aggressive in nature and therefore are harder to treat. Generally, people in hospitals and nursing homes have low immunity and they tend to be sick even without pneumonia. Therefore, they are not able to fight the infection.
Staphylococcal Pneumonia: Staphylococcus aureus is known to cause only 2% of community-acquired pneumonias and about 10 to 15% of hospital-acquired pneumonia. This type of pneumonia usually occurs in people who are hospitalized for another disorder. This pneumonia usually affects the very young, the very old, and people who are already debilitated by other illnesses. It also tends to develop in alcoholics. Although uncommon, it can be serious; the death rate is about 15 to 40%. The patients who develop staphylococcal pneumonia are usually already seriously ill.
Staphylococcus pneumonia symptoms are typical. It has been noticed that the chills and fever are more persistent in staphylococcal pneumonia than in pneumococcal pneumonia. Sometimes, the symptoms may worsen quickly accompanied with severe and potentially fatal deterioration in lung function. Staphylococcus may sometimes cause collections of pus (abscesses) in the lungs and, in children; it may produce lung cysts that contain air (pneumatoceles). The bloodstream may carry the bacteria from the lung to produce pus elsewhere. In the pleural space, there are collections of pus and this is called as empyema, and is relatively common. These collections can be drained using a needle or a chest tube.
Antibiotics that fight against Staphylococcus are usually a type of penicillin known as oxacillin or its equivalent. However, there are an increased number of strains of staphylococcus becoming resistant to these penicillins and hence use of other antibiotics, such as vancomycin is recommended.
Bacterial Pneumonia is caused by Gram-negative bacteria, such as Klebsiella (Friedländer’s pneumonia), Pseudomonas, Enterobacter, Proteus, Serratia, and Acinetobacter. This type of pneumonia tends to be serious.
Gram-negative Bacterial Pneumonia Gram-negative bacterial pneumonia usually occurs in hospitalized patients and patients who live in nursing homes. Fortunately, they rarely infect the lungs of healthy adults. People who are on breathing machines like ventilators that are used in intensive care units are usually susceptible to Gram-negative bacterial pneumonia. Other people who are at high risk of contracting this disease are infants, older people, alcoholics, and people with chronic diseases, especially immune system disorders.
The symptoms of gram-negative bacterial pneumonia, though similar to gram-positive pneumonia, the people tend to be sicker and worsen quickly. Gram-negative bacteria quickly destroy the lung tissue, so gram-negative pneumonia tends to become serious quickly. Fever, coughing, and shortness of breath are common. The sputum that is coughed up may appear thick and red, the color and consistency similar to that of currant jelly.
Since the infection is serious in nature, the person is treated intensively in the hospital with antibiotics, supplemental oxygen, and intravenous fluids. Sometimes, the patient may be put on a ventilator. Unfortunately, despite receiving excellent treatment, people dying of gram-negative pneumonia account to about 25 to 50%, which is relatively high.
Nosocomial pneumonia symptoms are as follows:
In diagnosing hospital acquired pneumonia, the physicians may face difficulty because there is no reliable method to diagnose all cases. Initially, the diagnosis is based on clinical grounds that are evident by the finding of a new infiltrate on chest radiograph, fever, purulent sputum, or other signs of clinical deterioration. However, in a series reported by Fagon et al, this clinical method was found to be specific for hospital acquired pneumonia in only 27 of 84 patients. That may be because many other conditions such as congestive heart failure, pulmonary embolism, atelectasis, ARDS, pulmonary hemorrhage, or drug reactions may mimic pneumonia, particularly in critically ill patients. Since, specificity is lacking, it may give rise to the need to have more reliable diagnostic tools so that incidences of the use of antibiotics for noninfectious diseases can be lowered. While there are many different testing modalities that can be used in the diagnosis, there are their own limitations and none of the method is good enough and sufficiently sensitive and specific to be considered as a “gold standard” test.
Blood cultures are known to have diagnostic and prognostic value; however, their sensitivity is reported to be only 8% to 20%. Therefore, their role is limited. Similarly, examination of expectorated sputum is neither specific nor sensitive. Therefore, this test should not be routinely used. In such scenarios, the most useful noninvasive test is the examination of tracheobronchial aspirates (TBA). This method is highly sensitivity, and it has been demonstrated in a recent study, where the organism causing infection was recovered from tracheal secretions in 29 of 31 patients. Unfortunately, this test also has its drawback. The inability of this test to differentiate between the organism responsible for causing the pneumonia and harmless colonizers, has put the use of TBA in its negative predictive value, its ability to exclude the presence of resistant organisms, and thus to narrow antibiotic coverage.
In invasive bronchoscopic techniques, samples are taken directly from the lower respiratory tract without the contamination from upper airway or oral secretions. This test would seem like an advanced technique in identifying the responsible pathogen. When bronchoscopic methods like the bronchoalveolar lavage (BAL) or the use of protected specimen brushes (PSB) were compared to less invasive methods, surprisingly, they did not appear to differ much in terms of sensitivity, specificity or, more importantly, patient morbidity and mortality. The current lack of consensus on the role of invasive diagnostic testing for hospital acquired pneumonia is the subject of ongoing debate.
One study compared the results of bronchoscopically obtained PSB with those of TBA in 76 mechanically ventilated patients, which were already put on empiric antibiotic therapy. It was found that more patients who received bronchoscopy with PSB changed their antibiotic regimen, but there were no significant change in length of stay, mortality between the two groups or the days requiring mechanical ventilation. This study concluded that the outcome is not influenced by techniques used for microbial investigation.
Another study showed a comparison between the use of invasive testing, such as PSB and BAL, with the use of noninvasive TBA in 413 patients. There was an initial decrease in antibiotic use, mortality, and organ dysfunction at 14 days among patients using invasive techniques. But, at 28-days, analysis of the difference in mortality could not be similarly demonstrated. This study along with other studies has concluded that noninvasive and invasive tools achieve similar diagnostic performance. Therefore, using invasive techniques cannot be justified in every patient with hospital acquired pneumonia. There are many who disagree and suggests that if invasive testing is done within the first 12 hours after diagnosis and before antibiotics are administered, the improvement in diagnostic yield may be sufficient to merit its use.
In a recent review by Ewig and Torres, he stated that invasive and noninvasive techniques do not differ significantly. Both of them are less sensitive than specific. He also states that the false-negative rate for these tests ranges from 30% to 40% and the false-positive rate from 20% to 30%. The review suggested that invasive diagnostic testing should not be performed early in the course of hospital acquired pneumonia and the best way to make adjustments to the empiric antibiotic regimen is by TBA rather than invasive techniques. Further, they stated that due to low degree of sensitivity linked with invasive methods, empiric therapy should not be stopped on the basis of negative diagnostic testing alone. The potential role for invasive diagnostic evaluation, it says, lies in cases of non response to initial treatment.
After hospital acquired pneumonia is diagnosed, it is absolutely essential that microbial therapy is begun promptly since delays in commencing antibiotics end up with worse results. One study in support of this observation confirmed a mortality rate of 30% in patients who received prompt, appropriate treatment as against 91% among patients who did not. The initial selection of an antimicrobial agent is mostly always made on an empiric basis and is determined by factors such as severity of infection, patient-specific risk factors, and the duration of stay in hospital before onset of infection.
All empiric treatment regimens must provide coverage against a group of core organism that includes gram negative bacilli (Escherichia coli, Enterobacter spp, Klebsiella spp, Serratia marcescens, Proteus spp, and Hemophilius influenzae) and gram-positive organisms such as streptococcus pneumonia and Staphylococcus aureus.
In patients with relatively mild and moderate infections and no particular risk factors for resistant or unusual pathogens, a nonpseudomonal third-generation cephalosporin such as ceftriaxone; monotherapy with a second-generation cephalosporin such as cefuroxime; or piperacillin/tazobactam; or a beta-lactam/beta-lactamase inhibitor such as ampicillin/sulbactam, ticarcillin/clavulanate may be appropriate. For patients in low risk category like this who are allergic to penicillin, it is recommended to start treatment with clindamycin or fluoroquinolone and aztreonam. While the use of flouroquinolone in the empiric regimen of patients with penicillin allergies is considered acceptable, a recent report studied the use of penicillin skin testing in such patients and concluded that most patients with a history of penicillin allergy could be safely treated with penicillin antibiotics. Therefore penicillin skin testing may be a method by which the administration of fluoroquinolones could be decreased.
Patients with mild or moderate infections having specific risk factors should have a wider empiric coverage. For patients with witnessed aspiration or in those having undergone recent thoracoabdominal surgery, adding clindamycin to cover anaerobes may be recommended, although even the use of a beta-lactam may be sufficient. For patients with head trauma, coma, recent influenza virus infections, chronic renal failure or diabetes, or those who are users of injection drugs, are vulnerable to infection by Staphylococcus aureus the addition of vancomycin to cover methicillin-resistant strains until sensitivities are known may be advised. Patients who have been on a prolonged course of steroids should include a macrolide as part of their initial therapy due to their heightened susceptibility to Legionella spp.
The severity of the infection notwithstanding, patients who have been on antibiotic medication prior to developing pneumonia, patients suffering from structural lung disease, those on steroids and those with a prolonged ICU course (more than 5 days) should be administered a combination of antibiotics to cover core pathogens along with infection from Pseudomonas aeruginosa or Acinetobacter spp. The high rate of acquired resistance among these organisms is the major reason why combination therapy is advised. For this category of patients, appropriate combinations include, ciprofloxacin, aminoglycoside in addition to a beta-lactam with antipseudomonal coverage. In case the patient shows risk factors that indicate that methicillin-resistant Staphylococcus aureus could be a likelypathogen, vancomycin could also be considered.
The criteria for pneumonia to be diagnosed as severe are if the patient needs to be shifted into the ICU, there is radiographic evidence of rapid progression, if mechanical ventilation or high level of inspired oxygen is required or if there is any evidence of sepsis. Patients suffering from severe pneumonias who have been hospitalized for less than 5 days, should be treated for empiric coverage to target the core group of organisms only; although monotherapy would in most cases not suffice for these patients and hence a combination therapy would be advised. Any patient diagnosed with severe pneumonia and having any one risk factor including a hospitalization of more than 5 days, should be re-administered with a combination of antibiotics that cover infections by P aeruginosa and Acinetobacter spp.
There happens to be no consensus about the duration of antibiotic therapy for patients suffering from hospital acquired pneumonia, but if the initial clinical suspicion was low, and if the clinical symptoms have not deviated drastically, antibiotics may be safely discontinued after 72 hrs. The Recommendations of the American Thoracic Society indicate that the duration of treatment should be determined by severity, the pathogenic organism and the time taken for clinical response. However a panel of experts differs with this view and states that the main factor determining the duration of therapy should be the time taken for clinical response and not the pathogen involved. They further state that patients be treated for a minimum of 72 hours after a clinical response is achieved.
Clinical response to antimicrobial therapy is not very likely to be achieved in the initial 48 to 72 hours, so the empiric antibiotic treatment should not be altered at this time unless prompted by results of microbiologic investigation. For patients failing to respond after the initial period, a broader antibiotic coverage may be recommended, invasive diagnostic testing may be performed and non infectious causes considered. Appropriate diagnostic testing may include radiographic tests to assess the possibility of pleural effusions or abscesses that hamper response, bronchoscopy with PSB and BAL, CTs of the sinuses to evaluate for sinusitis, as this may be a cause of recurring, persistent symptoms. After eliminating all other etiologies in the non responsive patient, an open lung biopsy for diagnostic purposes may be recommended although this method has not shown any marked improvement in the outcomes.