Ventilator-associated PNEUMONIA

Vol. 10 •Issue 4 • Page 49
Ventilator-associated PNEUMONIA

Targeting a Dreaded Invader

By Francie Scott

A respiratory therapist making rounds notes the ventilator patient in the neuro ICU has a high fever and purulent secretions. These symptoms could point to ventilator-associated pneumonia, a dangerous infection that plagues intubated patients. This is where the controversy begins. What should the care team do next to keep the patient alive?

According to one school of thought, a course of antibiotics should be initiated if patients present with two or more clinical symptoms of ventilator-associated pneumonia (VAP). These include temperatures greater than 38 degrees Celsius or lower than 36 degrees Celsius, leukopenia, leukocytosis, purulent tracheal secretions and decreased PaO2. Many clinicians also culture endotracheal tube aspirates.

Another clinical strategy, one advocated particularly by European physicians, contends the presence of bacteria should be confirmed by an invasive test such as bronchoscopy or protected specimen brush sampling before antibiotics are administered. That way, clinicians can target the actual pathogens attacking the patient rather than trying to hit it with a broad spectrum antimicrobial. If they skip the invasive testing, clinicians may be contributing to antibiotic resistance and missing other clinical problems.

The American College of Chest Physicians hoped to put the controversy to rest by appointing a panel of doctors to examine the current literature and prepare guidelines for the diagnosis and management of VAP. Members of the panel conscientiously examined 155 references but found no conclusive answer to their question.

“We couldn’t determine which approach is best, based on our understanding of the literature,” says panel chair Ronald F. Grossman, MD, professor of medicine at the University of Toronto and a pulmonologist at Toronto’s Mt. Sinai Hospital. Panel findings are published in a supplement included with the April 2000 edition of Chest.1 Although Dr. Grossman said some people would be disappointed with the results, panel members suggested hospitals continue their current practice until more randomized controlled trials are conducted to clarify the issue.


While the debate continues, RTs at the bedside should look for early warning signs of VAP and maintain stringent universal precautions to keep mortality and morbidity from VAP at a minimum. Dr. Grossman recommends keeping ventilator patients in a semi-upright position and carefully washing hands before approaching patients as “the two most effective ways” of preventing VAP.

Richard G. Wunderink, MD, director of the research department at Methodist Healthcare in Memphis, Tenn., offers similar advice. He urged RTs to look for increased secretions and high-minute ventilation in patients with healthy lungs.

Therapists also must pay scrupulous attention to cleaning respiratory equipment. Invasive medical devices are considered important contributors to the pathogenesis and development of VAP. These culprits include nasogastric tubes that predispose patients to gastric reflux and aspiration, endotracheal tubes that fall prey to bacterial colonization, and pools of contaminated secretions generated by a mucosal above the endotracheal tube-cuff and ventilator circuits.

However, both doctors said tubing and circuits should be changed as infrequently as possible because studies show that frequent changes increase the risk of VAP. “It makes good sense when you think about it in terms of handling the airway,” Dr. Wunderink says.

Writing in Chest,2 Dr. Wunderink suggested continuous aspiration of subglottic secretions can reduce the incidence of VAP, especially in surgical patients. In the same edition of Chest,3 Marin Kollef, MD, of Barnes-Jewish Hospital in St. Louis, described how clinicians employed that method to “significantly” delay the occurrence of VAP in patients undergoing cardiac surgery.

The study involved 343 patients who required mechanical ventilation. Of that group, 160 patients received continuous aspiration and 183 received routine post-operative care. Clinicians identified VAP in eight patients in the study group and 15 in the control group.

“A lot of people have this false impression that a cuffed tube prevents aspiration,” Dr. Wunderink says, but the cuffed tube prevents only “macro aspiration,” not small leaks every time patients turn their heads. “Millions of bugs just got down to the lower respiratory tract,” when that happened, he describes. He recommends placing patients in a semi-upright position to reduce the risk of such leaks.

Dr. Kollef discussed prevention of VAP in detail in the New England Journal of Medicine4 including a description of the pathogenesis plus pharmacologic and non-pharmacologic strategies. He included continuous subglottic suctioning, humidification with heat and moisture exchangers to minimize condensate within ventilator circuits and postural changes among the non-pharmacologic strategies. On the pharmacologic side, Dr. Kollef noted stress ulcer prophylaxis could be administered because ventilator patients are at risk for gastrointestinal bleeding from stress ulcers. He also suggested the role of gastric pH in the pathogenesis of VAP is controversial.

On the cutting edge, Dr. Kollef reports some clinicians have tried immunoglobulin, which reduced the overall incidence of VAP but proved expensive and fraught with side effects. Others have tried vaccines against specific pathogens such as Haemophilus influenzae and Streptococcus pneumoniae. Prophylactic treatment of neutropenia has also been tried because the presence of the condition has been linked to increased risk for community-acquired and nosocomial infections.


VAP appears to follow two paths: First is early onset VAP, which occurs within two to four days of intubation and is often due to antibiotic-sensitive bacteria such as Staphylococcus aureus, according to Dr. Kollef’s NEJM article. Second is late-onset VAP, which may be linked to antibiotic-resistant pathogens such as Pseudomonas aeruginosa, Acinetobactor species and Enterobacter species.

Dr. Wunderink favors two high doses of one antibiotic to treat early onset VAP because it’s usually associated with bacteria from aspirating gastric contents or leaking from secretions above the cuff. At this early stage, the pathogens are sensitive to antibiotics and the patient recovers from the pneumonia.

“Frankly, early onset pneumonia doesn’t often kill patients,” he said.

When late onset VAP invades the body, clinicians must consider several sites of infection, including sites of indwelling catheters and central lines, and the sinuses. Late onset VAP often involves drug-resistant pathogens, so heavy-hitting and expensive antibiotics may be necessary to reverse the disease process.

Clinicians have no successful strategies for preventing late onset VAP, except, as Dr. Wunderink wrote, “an accurate diagnosis of early onset VAP and avoidance of antibiotics as much as possible.”

Dr. Grossman says some clinicians have tried rotating beds, but he considers this “a very expensive option.”

Ideally, rapid extubation is the goal for all ventilator patients. The longer the tube is in place, the more vulnerable patients are to VAP and other complications.


In the big picture, nosocomial pneumonia is a killer at large in the nation’s hospitals, accounting for approximately 30 percent of deaths from hospital-acquired infections. Much of the pneumonia occurs in the ICU, and critical care clinicians view it as a particularly nasty enemy they find difficult to tame.

“Dreaded,” is the adjective Dr. Kollef chooses.

Depending on the population studied, the prevalence of VAP may range from as low as six patients per 100 to as high as 52 patients per 100, according to Dr. Grossman and his team. They noted the crude rate of VAP increases from 1 percent to 3 percent for every day a patient receives mechanical ventilation; the death rate increases from twofold to tenfold during the same time period.

These statistics paint a sobering picture for ICU clinicians as they strive to reduce the incidence of VAP infection.


1. Grossman RF, et al. Evidence-based assessment of diagnostic tests for ventilator-associated pneumonia. Chest. 2000 Apr;117(4 Suppl 2): 117S-81S.

2. Wunderink RG. Prevention of ventilator-associated pneumonia: does one size fit all? Chest. 1999 Nov;116:1155-6.

3. Kollef MH, et al. A randomized clinical trial of continous aspiration of subglottic secretions in cardiac surgery patients. Chest. 1999 Nov;116:1339-46.

4. Kollef MH. The prevention of ventilator-associated pneumonia. N Engl J Med. 1999 Feb. 25;8(340) 627-34.

Francie Scott is senior editor of ADVANCE.