Hospital-acquired pneumonia

Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. ; Philip Marcus, M.D., M.P.H.

Hospital-acquired pneumonia (HAP) or nosocomial pneumonia refers to any pneumonia contracted by a patient in a hospital at least 48–72 hours after being admitted. It is thus distinguished from community-acquired pneumonia. It is usually caused by a bacterial infection, rather than a virus.^[1][2] HAP is the second most common nosocomial infection (after urinary tract infections ) and accounts for 15–20% of the total.^[1][2][3] It is the most common cause of death among nosocomial infections and is the primary cause of death in intensive care units.^[1][3] HAP typically lengthens a hospital stay by 1–2 weeks.^[1][3]

Most nosocomial respiratory infections are caused by so-called skorvatch microaspiration of upper airway secretions, through inapparent aspiration, into the lower respiratory tract. Also, “macroaspirations” of esophageal or gastric material is known to result in HAP. Since it results from aspiration either type is called aspiration pneumonia. Although gram-negative bacilli are a common cause they are rarely found in the respiratory tract of people without pneumonia, which has led to speculation of the mouth and throat as origin of the infection.

The majority of cases related to various gram-negative bacilli (52%) and S. aureus (19%). Others are Haemophilusspp. (5%). In the ICU results were S. aureus(17.4%), P. aeruginosa (17.4%), Klebsiella pneumoniae andEnterobacter spp. (18.1%), and Haemophilus influenzae (4.9%). Viruses –influenza and respiratory syncytial virus and, in the immunocompromised host, cytomegalovirus– cause 10-20% of infections.

Hospital-acquired pneumonia must be differentiated from other conditions that cause fever, cough, chest pain, tachycardia, and leukocytosis in hospitalized patients, such as atelectasis, congestive heart failure, pulmonary embolism, aspiration pneumonitis, among others. ^[4][5]

The epidemiology of health-care-associated pneumonia varies considerably according to the type of health-care setting. Nosocomial pneumonia has been the second most common hospital-associated infection after that of the urinary tract. The primary risk factor for the development of hospital-associated bacterial pneumonia is mechanical ventilation. In long-term care facilities such as nursing homes, pneumonia is the first or second most common infection (after those of the urinary tract) acquired by patients, and accounts for 13-48% of all nursing home-associated infections. ^[6]

Among the factors contributing to contracting HAP are mechanical ventilation (ventilator-associated pneumonia), old age, decreased filtration of inspired air, intrinsic respiratory, neurologic, or other disease states that result in respiratory tract obstruction, trauma, (abdominal) surgery, medications, diminished lung volumes, or decreased clearance of secretions may diminish the defenses of the lung. Also poor hand-washing and inadequate disinfection of respiratory devicescauses cross-infection and is an important factor.

The natural history of HAP depends on many factors and occurs 48 hours or more after hospitalization. Complications include sepsis, respiratory failure, pleural effusion, empyema, and lung abscess. Healthcare-associated pneumonia seems to have fatality rates similar to hospital-acquired pneumonia, worse than community-acquired pneumonia but less severe than pneumonia in ventilated patients. Besides clinical markers like tachypnea (fast breathing) or a high white cell count (leukocytosis), the prognosis seems to be influenced by the underlying associated diseases (comorbidities) and functional capacities.^[7][8][9] Many patients have a decreased health condition after the episode.^[10]

In hospitalised patient who develop respiratory symptoms and fever one should consider the diagnosis. The likelyhood increases when upon investigation symptoms are found of respiratory insufficiency, purulent secretions, newly developed infiltrate on the chest X-Ray, and increasing leucocyte count. If pneumonia is suspected material from sputum or tracheal aspirates are sent to the microbiology department for cultures. In case ofpleural effusion thoracentesis is performed for examination of pleural fluid. In suspected ventilator-associated pneumonia it has been suggested that bronchoscopy(BAL) is necessary because of the known risks surrounding clinical diagnoses.

People with pneumonia often have a productive cough, fevershaking chills, shortness of breath, pleuritic chest pain, hemoptysis, headaches, sweaty, and clammy skin. Other possible symptoms are loss of appetite, fatigue, cyanosis, nausea, vomiting, mood swings, and joint pains or muscle aches. In elderly people manifestations of pneumonia may not be typical. They may develop a new or worsening confusion or may experience unsteadiness, leading to falls. Infants with pneumonia may have many of the symptoms above, but in many cases they are simply sleepy or have a decreased appetite. In VAP, often no history is available in patients with ventilator-associated pneumonia as they are often sedated and are rarely able to communicate.

Physical examination is important in diagnosing hospital-acquired pneumonia, finding include fever, tachypnea, rhonchi, crackles and wheezes. For ventilator-associated pneumonia, a deterioration in ventilator parameters such as, tachypnea, decreased tidal volume, increased minute ventilation, or decreased oxygen saturation could be the first indicators of a new onset ventilator-associated pneumonia.^[11]

Current guidelines recommend a combination of chest X-ray, laboratory data as well as clinical judgment in diagnosis and management of community acquired pneumonia. Laboratory tests include CBC, metabolic panel, sputum gram-stain and culture, serology for mycoplasma, chlamydia, and legionella. Additional test include bronchial samples and HIV testing for special conditions.

An important test for making a diagnosis of pneumonia is a chest x-ray. Chest x-rays can reveal areas of opacity (seen as white) which represent consolidation, pleural effusion, air bronchogram and/or cavitations. Pneumonia is not always seen on x-rays, either because the disease is only in its initial stages, or because it involves a part of the lung not easily seen by x-ray.

The medical regimen in patients with hospital-acquired pneumonia will depend on the risk factors and the likelihood of drug resistance pathogens. For patients with no risk factors for MDR pathogens, the regimen consists of one antibiotic medication, usually ceftriaxone or a fluoroquinolone. For patients with risk of MDR pathogens, a three drug combination regimen is preferred; which includes an antipseudomonal cephalosporin or carbapenem plus a fluoroquinolone plus linezolid or vancomycin (for MRSA coverage).

The prevention for HAP includes education of health-care workers about the epidemiology and infection-control procedures, and involve the workers in the implementation of interventions to prevent HAP by using performance-improvement tools and technique. Disinfection and maintenance of equipment and devices, as well as preventive measures of person to person transmission, are part of the preventive recommendations given by the CDC for HAP.

Linezolid was compared to vancomycin for the treatment of VAP, and showed cost-effectiveness as an alternative to vancomycin treatment as it had a higher cure rate and prices per treatment were similar.^[12][13] One study reported that oropharingeal decontamination decreased the incidence of ventilator-associated pneumonia from 4% to less than 1% in the studied population. The cost of the intervention was less than $2500. ^[14]

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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. ; Philip Marcus, M.D., M.P.H.; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [1]

Most nosocomial respiratory infections are caused by so-called skorvatch microaspiration of upper airway secretions, through inapparent aspiration, into the lower respiratory tract. Also, “macroaspirations” of esophageal or gastric material is known to result in HAP. Since it results from aspiration either type is called aspiration pneumonia. Although gram-negative bacilli are a common cause they are rarely found in the respiratory tract of people without pneumonia, which has led to speculation of the mouth and throat as origin of the infection.

Adapted from CDC^[1]

• Bacteria may invade the lower respiratory tract by micro- or bolus-aspiration of oropharyngeal organisms, inhalation of aerosols containing bacteria, or, less frequently, by hematogenous spread from a distant body site.
• Bacterial translocation from the gastrointestinal tract had been hypothesized as a mechanism for infection; however, its occurrence in patients with health-care-associated pneumonia has not been shown.
• Of the plausible routes, micro-aspiration is believed to be the most important for both health-care-associated and community-acquired pneumonia.
• In studies using radioisotope tracers, 45% of healthy adults were found to aspirate during sleep^[2].
• Persons with abnormal swallowing, such as those who have depressed consciousness, respiratory tract instrumentation and/or mechanically assisted ventilation, gastrointestinal tract instrumentation or diseases, or who have just undergone surgery, especially thoracic and/or abdominal surgery, are particularly likely to aspirate.
• The high incidence of Gram-negative bacillary pneumonia in hospitalized patients appears to be the result of factors that promote colonization of the pharynx by Gram-negative bacilli and the subsequent entry of these microorganisms into the lower respiratory tract.
• Although aerobic Gram-negative bacilli are recovered infrequently or are found in small numbers in pharyngeal cultures of healthy persons, colonization dramatically increases in patients with acidosis, alcoholism, azotemia, coma, diabetes mellitus, hypotension, leukocytosis, leukopenia, pulmonary disease, or endotracheal or nasogastric tubes in place, and in patients given antimicrobial agents.
• Oropharyngeal or tracheobronchial colonization by Gram-negative bacilli begins with the adherence of the microorganisms to the host’s epithelial cells.
• Adherence may be affected by multiple factors related to the bacteria (e.g., presence of pili, cilia, or capsule, or production of elastase or mucinase), host cell (e.g., surface proteins and polysaccharides), and environment (e.g., pH and presence of mucin in respiratory secretions).
• Studies indicate that certain substances (e.g., fibronectin) can inhibit the adherence of Gram-negative bacilli to host cells.
• Conversely, certain conditions (e.g., malnutrition, severe illness, or post-operative state) can increase adherence of gram-negative bacteria.
• In addition to the oropharynx, the stomach has been postulated to be an important reservoir of organisms that cause health-care-associated pneumonia, although the exact role of the stomach in the causation of health-care-associated pneumonia, specifically VAP, has been critically investigated and debated.
• The stomach’s role may vary depending on the patient’s underlying condition(s) and on the prophylactic or therapeutic interventions that the patient receives.
• In healthy persons, few bacteria entering the stomach survive in the presence of hydrochloric acid at pH<2.
• However, whe gastric pH increases from the normal levels to >4, microorganisms are able to multiply to high concentrations in the stomach.
• This can occur in patients with advanced age, achlorhydria, ileus, or upper gastrointestinal disease, and in patients receiving enteral feeding, antacids, or histamine-2 (H-2) antagonists.
• The contribution of other factors, such as duodeno-gastric reflux and the presence of bile, to gastric colonization in patients with impaired intestinal motility also has been suggested.

• Ventilator-associated pneumonia is primarily caused by the endotracheal or tracheostomy tube allowing free passage of bacteria into the lower segments of the lung in a person who often has underlying lung or immune problems.
• Bacteria travel in small droplets both through the endotracheal tube and around the cuff.
• Often, bacteria colonize the endotracheal or tracheostomy tube and are embolized into the lungs with each breath.
• Bacteria may also be brought down into the lungs with procedures such as deep suctioning or bronchoscopy.
• Whether bacteria also travel from the sinuses or the stomach into the lungs is, controversial.
• However, spread to the lungs from the blood stream or the gut is uncommon.
• Once inside the lungs, bacteria then take advantage of any deficiencies in the immune system (such as due to malnutrition or chemotherapy) and multiply.
• A combination of bacterial damage and consequences of the immune response lead to disruption of gas exchange with resulting symptoms.

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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. ; Philip Marcus, M.D., M.P.H.

The majority of cases related to various gram-negative bacilli (52%) and S. aureus (19%). Others are Haemophilus spp. (5%). In the ICU results were S. aureus(17.4%), P. aeruginosa (17.4%), Klebsiella pneumoniae and Enterobacter spp. (18.1%), and Haemophilus influenzae (4.9%). Viruses –influenza and respiratory syncytial virus and, in the immunocompromised host, cytomegalovirus– cause 10-20% of infections.

• Commonly polymicrobial
• Common microbial agents include:
  • Pseudomonas aeruginosa
  • Escherichia coli
  • Klebsiella pneumoniae
  • Acinetobacter

• Staphylococcus aureus
• Methicillin resistant staphylococcus aureus (common in patients with diabetes mellitus, head trauma, and in ICU)

• S. aureus
• Enteric gram-negative rods
• Streptococcus pneumoniae
• Pseudomonas

• The microbiologic flora responsible for VAP is different from that of the more common community-acquired pneumonia (CAP). In particular, viruses and fungi are uncommon causes in people who do not have underlying immune deficiencies.
• Though any microorganism that causes CAP can cause VAP, there are several bacteria which are particularly important causes of VAP because of their resistance to commonly used antibiotics. These bacteria are referred to as multidrug resistant (MDR).
• VAP has been classified into either early-onset pneumonia (EOP), if pneumonia develops within 96 hours of the patient’s admission to an ICU or intubation for mechanical ventilation, and late-onset pneumonia (LOP), if pneumonia develops after 96 hours of the patient’s admission to an ICU or intubation for mechanical ventilation. ^[2]
• This categorization can be helpful to clinicians in initiating empiric antimicrobial therapy for cases of pneumonia, when the results of microbiologic diagnostic testing are not yet available.
• EOP has been associated usually with non-multi-antimicrobial-resistant microorganisms such as Escherichia coli, Klebsiella spp., Proteus spp., S. pneumoniae, H. influenzae, and oxacillin-sensitive S. aureus.
• On the other hand, LOP has been associated with Pseudomonas aeruginosa, oxacillin-resistant S. aureus, and Acinetobacter spp (strains that are usually multi-antibiotic-resistant).

The following is a list of the most MDR common pathogens associated with ventilator-associated pneumonia:

• Pseudomonas aeruginosa is the most common MDR gram-negative bacterium causing VAP. Pseudomonas has natural resistance to many antibiotics and has been known to acquire resistance to every antibiotic except for polymixin B. Resistance is typically acquired through upregulation or mutation of a variety of efflux pumps which pump antbiotics out of the cell. Resistance may also occur through loss of an outer membrane porin channel (OprD)
• Klebsiella pneumoniae has natural resistance to some beta-lactam antibiotics such as ampicillin. Resistance to cephalosporins and aztreonam may arise through induction of a plasmid-based extended spectrum beta-lactamase (ESBL) or plasmid-based ampC-type enzyme.
• Serratia marcescens has an ampC gene which can be induced by exposure to antibiotics such as cephalosporins. Thus, culture sensitivities may initially indicate appropriate treatment which fails due to bacterial response.
• Enterobacter as a group also have an inducible ampC gene. Enterobacter may also develop resistance by acquiring plasmids.
• Citrobacter also has an inducible ampC gene.
• Stenotrophomonas maltophilia often colonizes people who have endotracheal tubes or tracheostomies but can also cause pneumonia. It is often resistant to a wide array of antibiotics but is usually sensitive to co-trimoxazole.
• Acinetobacter are becoming more common and may be resistant to carbapenems such as imipenem and meropenem.
• Burkholderia cepacia is an important organism in people with cystic fibrosis and is often resistant to multiple antibiotics.
• Methicillin-resistant Staphylococcus aureus is an increasing cause of VAP. As many as fifty percent of Staphylococcus aureus isolates in the intensive care setting are resistant to methicillin. Resistance is conferred by the mecA gene.

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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. ; Philip Marcus, M.D., M.P.H.; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [1]

Hospital-acquired pneumonia must be differentiated from other conditions that cause fever, cough, chest pain, tachycardia, and leukocytosis in hospitalized patients, such as atelectasis, congestive heart failure, pulmonary embolism, aspiration pneumonitis, among others. ^[1][2]

• Atelectasis
• Congestive heart failure
• Pulmonary embolism
• Acute respiratory distress syndrome
• Aspiration pneumonitis
• Cryptogenic organizing pneumonia
• Drug reaction
• Infiltrative tumor
• Lung contusion
• Pulmonary embolism
• Pulmonary hemorrhage
• Radiation pneumonitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]

The epidemiology of health-care-associated pneumonia varies considerably according to the type of health-care setting. Nosocomial pneumonia has been the second most common hospital-associated infection after that of the urinary tract. The primary risk factor for the development of hospital-associated bacterial pneumonia is mechanical ventilation. In long-term care facilities such as nursing homes, pneumonia is the first or second most common infection (after those of the urinary tract) acquired by patients, and accounts for 13-48% of all nursing home-associated infections. ^[1]

• Pneumonia has accounted for approximately 20% of all hospital-associated infections and 27% and 24% of all infections acquired in the medical intensive-care unit (ICU) and coronary care unit, respectively. ^[2]

• The incidence of HAP is 5-15 cases per 1 000 hospital admissions. ^[3]
• The incidence of VAP is 6 to 20 times more than in patients without mechanical support.

• HAP and VAP are nosocomial infections with a high mortality in contrast with other nosocomial infections.
• This higher mortality rate is associated with MDR pathogens.

• HAP is more commonly reported in patients > 65 years, probably due to the fact that this age population is more commonly hospitalized.

• There is no predominance in gender, although some data reports a higher incidence among females.

• VAP occurs in up to 25% of all people who require mechanical ventilation.
• VAP can develop at any time during ventilation, but occurs more often in the first few days after intubation.
• This is because the intubation process itself contributes to the development of VAP.
• VAP occurring early after intubation typically involves fewer resistant organisms and is thus associated with a more favorable outcome.
• Because respiratory failure requiring mechanical ventilation is itself associated with a high mortality, determination of the exact contribution of VAP to mortality has been difficult.
• As of 2006, estimates range from 33% to 50% death in patients who develop VAP.
• Mortality is more likely when VAP is associated with certain microorganisms (Pseudomonas, Acinetobacter), blood stream infections, and ineffective initial antibiotics.
• VAP is especially common in people who have acute respiratory distress syndrome (ARDS).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]

Among the factors contributing to contracting HAP are mechanical ventilation (ventilator-associated pneumonia), old age, decreased filtration of inspired air, intrinsic respiratory, neurologic, or other disease states that result in respiratory tract obstruction, trauma, (abdominal) surgery, medications, diminished lung volumes, or decreased clearance of secretions may diminish the defenses of the lung. Also poor hand-washing and inadequate disinfection of respiratory devicescauses cross-infection and is an important factor.

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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. ; Philip Marcus, M.D., M.P.H.

The natural history of HAP depends on many factors and occurs 48 hours or more after hospitalization. Complications include sepsis, respiratory failure, pleural effusion, empyema, and lung abscess. Healthcare-associated pneumonia seems to have fatality rates similar to hospital-acquired pneumonia, worse than community-acquired pneumonia but less severe than pneumonia in ventilated patients. Besides clinical markers like tachypnea (fast breathing) or a high white cell count (leukocytosis), the prognosis seems to be influenced by the underlying associated diseases (comorbidities) and functional capacities.^[1][2][3] Many patients have a decreased health condition after the episode.^[4]

• The natural course of hospital-acquired pneumonia will depend on several factors, such as the causative pathogen, the host immune status and the choice of antibiotic therapy.
• By definition, hospital-acquired pneumonia occurs 48 hours or more since hospital admission; and ventilator-associated pneumonia occurs 48 to 72 hours after the patient was intubated. ^[5]
• Physicians should suspect of hospital-acquired pneumonia in hospitalized patients that develop fever (> 38° C), productive cough and/or leukocytosis associated with a new chest X-ray infiltration.
• Empirical antibiotic therapy should be started in case of high suspicion, as it has shown improvement of patient survival.

Despite appropriate antibiotic therapy, severe complications can result from HAP, including:

• Sepsis can occur when microorganisms enter the blood stream and the immune system responds.
• Sepsis most often occurs with bacterial pneumonia
• Streptococcus pneumoniae is the most common cause.
• Individuals with sepsis require hospitalization in an intensive care unit. They often require medications and intravenous fluids to keep their blood pressure from going too low. Sepsis can cause liver, kidney, and heart damage among other things.

• If enough of the lung is involved, it may not be possible for a person to breathe enough to live without support.
• Non-invasive machines such as a bilevel positive airway pressure machine may be used.
• Otherwise, placement of a breathing tube into the mouth may be necessary and a ventilator may be used to help the person breathe.

• Occasionally, microorganisms from the lung will cause fluid to form in the space surrounding the lung, called the pleural cavity.
• If the microorganisms themselves are present, the fluid collection is often called an empyema.
• If pleural fluid is present in a person with CAP, the fluid should be collected with a needle (thoracentesis) and examined.
• Depending on the result of the examination, complete drainage of the fluid may be necessary, often with a chest tube. If the fluid is not drained, bacteria can continue to cause illness because antibiotics do not penetrate well into the pleural cavity.

• Rarely, microorganisms in the lung will form a pocket of fluid and bacteria called an abscess.
• Abscesses can be seen on an x-ray as a cavity within the lung. Abscesses typically occur in aspiration pneumonia and most often contain a mixture of anaerobic bacteria.
• Usually antibiotics are able to fully treat abscesses, but sometimes they must be drained by a surgeon or radiologist.

With treatment, most types of bacterial pneumonia can be cured within one to two weeks. Viral pneumonia may last longer, and mycoplasmal pneumonia may take four to six weeks to resolve completely. The eventual outcome of an episode of pneumonia depends on how ill the person is when he or she is first diagnosed.

In the United States, about one of every twenty people with pneumococcal pneumonia will die.^[6] In cases where the pneumonia progresses to blood poisoning (bacteremia), one of every five will die. The death rate (or mortality) also depends on the underlying cause of the pneumonia. Pneumonia caused by Mycoplasma, for instance, is associated with little mortality. However, about half of the people who develop methicillin-resistantStaphylococcus aureus (MRSA) pneumonia while on a ventilator will die.^[7] In regions of the world without advanced health care systems, pneumonia is even deadlier.

• Fever typically responds in the first two days of therapy and other symptoms resolve in the first week.
• The x-ray, however, may remain abnormal for at least a month, even when HAP has been successfully treated.
• When HAP does not respond as expected, there are several possible causes.
  • A complication of HAP may have occurred or a previously unknown health problem may be playing a role.
  • Additional causes include inappropriate antibiotics for the causative organism (ie DRSP), a previously unsuspected microorganism (such as tuberculosis), or a condition which mimics HAP (such as Wegener’s granulomatosis).
  • Additional testing may be performed and may include additional radiologic imaging (such as a computed tomography scan) or a procedure such as a bronchoscopy or lung biopsy.

Clinical prediction rules have been developed to more objectively prognosticate outcomes in Hospital-acquired pneumonia. Pneumonia severity index^[8] –online calculator

• CURB-65 score, which takes into account the severity of symptoms, any underlying diseases, and age^[9] –online calculator

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