- Ventilator-associated pneumonia
Ventilator-associated pneumonia (VAP) is a sub-type of
hospital-acquired pneumonia(HAP) which occurs in people who are on mechanical ventilationthrough an endotracheal or tracheostomytube for at least 48 hours. VAP is a medical condition that results from infectionwhich floods the small, air-filled sacs ( alveoli) in the lungresponsible for absorbing oxygenfrom the atmosphere. VAP is distinguished from other kinds of infectious pneumonia because of the different types of microorganismsresponsible, antibiotics used to treat, methods of diagnosis, ultimate prognosis, and effective preventive measures. In the community pneumonia is most often caused by "S. pneumoniae", "H. influenzae", or "S. aureus". However, in the hospital the organism associated with pneumonia is most often " Pseudomonas", regardless of whether or not the patient is ventilated. In order for a patient to have VAP they have to be on a ventilator; it’s not the organism that distinguishes VAP, it's the fact that the patient is on a ventilator.
Symptoms and Signs
People who are on mechanical ventilation are often sedated and are rarely able to communicate. As such, many of the typical symptoms of pneumonia will either be absent or unable to be obtained. The most important symptoms are
fever, low body temperature, new purulent sputum, and hypoxia (decreasing amounts of oxygen in the blood).
VAP should be suspected in any person with symptoms of VAP, increasing numbers of
white blood cells on blood testing, and new shadows (infiltrates) on a chest x-ray. Blood cultures may reveal the microorganism causing VAP.
Two strategies exist for diagnosing VAP. One strategy collects cultures from the trachea of people with symptoms of VAP plus a new or enlarging infiltrate on chest x-ray. The other is more invasive and advocates a
bronchoscopyplus bronchoalveolar lavage(BAL) for people with symptoms of VAP plus a new or enlarging infiltrate on chest x-ray. In both cases, VAP is not diagnosed when cultures are negative and another source of the symptoms is sought.
VAP primarily occurs because the endotracheal or tracheostomy tube allows 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, as of
2005, controversial. However, spread to the lungs from the blood streamor the gutis 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 exchangewith resulting symptoms.
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).
Pseudomonas aeruginosa" is the most common MDR Gram-negativebacterium 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 cephalosporinsand aztreonammay arise through induction of a plasmid-based extended spectrum beta-lactamase(ESBL) or plasmid-based ampC-type enzyme:*" Serratia marcescens" has an ampC genewhich 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 imipenemand 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 mecAgene.
Treatment of VAP should be matched to known causative bacteria. However, when VAP is first suspected, the bacteria causing infection is typically not known and broad-spectrum antibiotics are given (
empiric therapy) until the particular bacterium and its sensitivities are determined. Empiric antibiotics should take into account both the risk factors a particular individual has for resistant bacteria as well as the local prevalence of resistant microorganisms. If a person has previously had episodes of pneumonia, information may be available about prior causative bacteria. The choice of initial therapy is therefore entirely dependent on knowledge of local flora and will vary from hospital to hospital.
Risk factors for infection with an MDR strain include ventilation for more than five days, recent hospitalization (last 90 days), residence in a
nursing home, treatment in a hemodialysisclinic, and prior antibiotic use (last 90 days).
Possible empirical therapy combinations include (but are not limited to):
vancomycin/ linezolidand ciprofloxacin,
cefepimeand gentamicin/ amikacin/ tobramycin
vancomycin/ linezolidand ceftazidime
Ureidopenicillinplus β-lactamase inhibitor such as piperacillin/tazobactamor ticarcillin/clavulanate
* a carbapenem (e.g.,
Therapy is typically changed once the causative bacteria are known and continued until symptoms resolve (often 7 to 14 days).
People who do not have risk factors for MDR organisms may be treated differently depending on local knowledge of prevalent bacteria. Appropriate antibiotics may include
ceftriaxone, ciprofloxacin, levofloxacin, or ampicillin/sulbactam.
2005, there is ongoing research into inhaled antibiotics as an adjunct to conventional therapy. Tobramycinand polymyxin Bare commonly used in certain centres but there is no clinical evidence to support their use.
Prevention of VAP involves limiting exposure to resistant bacteria, discontinuing mechanical ventilation as soon as possible, and a variety of strategies to limit infection while intubated. Resistant bacteria are spread in much the same ways as any communicable disease. Proper
hand washing, sterile techniquefor invasive procedures, and isolation of individuals with known resistant organisms are all mandatory for effective infection control. A variety of aggressive weaning protocols to limit the amount of time a person spends intubation have been proposed. One important aspect is limiting the amount of sedation that a ventilated person receives.
Other recommendations for preventing VAP include raising the head of the bed to at least 45 degrees and placement of feedings tubes beyond the pylorus of the
stomach. Antiseptic mouth washes such as chlorhexidinemay also reduce the incidence of VAP. One recent study suggests that using heat and moisture exchangers instead of heated humidifiers, may increase the incidence of VAP. [cite journal | author=Lorente L, Lecuona M, Jimenez A, Mora ML, Sierra A. | title=Ventilator-associated pneumonia using a heated humidifier or a heat and moisture exchanger: a randomized controlled trial | journal=Crit Care | year=2006 | volume=10 | pages=4 ]
American and Canadian guidlines strongly recommend the use of supraglottic secretion drainage (SDD) Special tracheal tubes with an incorporated suction lumen as the EVAC tracheal tube form Covidien / Mallinckrodt can be used for that reason. New cuff technology based on polyurethane material in combination with subglottic drainage (SealGuard Evac tracheal tube from Covidien/Mallinckrodt)showed significant delay in early and late onset of VAP.cite journal |author=Lorente L, Lecuona M, Jiménez A, Mora ML, Sierra A |title=Influence of an endotracheal tube with polyurethane cuff and subglottic secretion drainage on pneumonia |journal=Am. J. Respir. Crit. Care Med. |volume=176 |issue=11 |pages=1079–83 |year=2007 |pmid=17872488 |doi=10.1164/rccm.200705-761OC]
A recent clinical trial indicates that the use of
silver-coated endotracheal tubes may also reduce the incidence of VAP.cite journal |author=Kollef MH, Afessa B, Anzueto A, "et al" |title=Silver-coated endotracheal tubes and incidence of ventilator-associated pneumonia: the NASCENT randomized trial |journal=JAMA |volume=300 |issue=7 |pages=805–13 |year=2008 |month=August |pmid=18714060 |doi=10.1001/jama.300.7.805 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18714060]
Epidemiology and prognosis
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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