Aspiration is defined as the inhalation of either oropharyngeal or gastric contents into the lower airways, that is, the act of taking foreign material into the lungs. This can cause a number of syndromes determined by the quantity and nature of the aspirated material, the frequency of aspiration, and the host factors that predispose the patient to aspiration and modify the response.
There are four types of aspiration syndromes. Aspiration of gastric acid causes a chemical pneumonitis which has also been called Mendelson syndrome. Aspiration of bacteria from oral and pharyngeal areas causes aspiration pneumonia. Aspiration of oil (eg, mineral oil or vegetable oil) causes exogenous lipoid pneumonia, an unusual form of pneumonia. Aspiration of a foreign body may cause an acute respiratory emergency and, in some cases, may predispose the patient to bacterial pneumonia. The pathophysiology, clinical presentation, treatment, and complications of each of these entities are different.
Aspiration pneumonia is an inflammation of the lungs and bronchial tubes. It results from inhaling vomit, food, or liquid. While this can happen to anyone, people with acid reflux are at a heightened risk for developing it. This is because reflux makes it possible for the stomach’s contents to make it up the esophagus, through the larynx, between the vocal cords, and into the lungs.
Aspiration pneumonia is actually a very common form of pneumonia, accounting for approximately 15 percent of all pneumonia cases. It’s more commonly found in men, young children, and the elderly, or those who are weakened by health issues.
A variety of symptoms are associated with aspiration pneumonia. The most common symptoms are
Bluish tint of the skin
Chest pain
Coughing
Fatigue
Fever
Gurgling
Shortness of breath
Wheezing
The micro-organisms that commonly cause these pneumonias, such as Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus, and gram-negative bacteria, are relatively virulent so that only a small inoculum is required to result in a pneumonia. The aspiration episode is often subtle. The inoculum in what was traditionally recognized as aspiration pneumonia was larger and typically apparent.
Patients who develop aspiration pneumonia have increased mor-bidity, mortality and costs of care. Surgical patients, especially those requiring general anesthesia, may be at particularly high risk. The prevalence of risk factors for and impact of aspiration pneumonia remains unclear.
Ventilator-associated pneumonia (VAP) is defined as pneumonia that occurs 48-72 hours or thereafter follow¬ing endotracheal intubation, characterized by the pre¬sence of a new or progressive infiltrate, signs of systemic infection (fever, altered white blood cell count), changes in sputum characteristics, and detection of a causative agent. VAP contributes to approximately half of all cases of hospital-acquired pneumonia.VAP is estimated to occur in 9-27 % of all mechanically ventilated patients, with the highest risk being early in the course of hospitalization. It is the second most common nosocomial infection in the intensive care unit (ICU) and the most common in mechanically ventilated patients. VAP rates range from 1.2 to 8.5 per 1,000 ventilator days and are reliant on the definition used for diagnosis. Risk for VAP is greatest during the first 5 days of mechanical ventilation (3 %) with the mean duration between intubation and development of VAP being 3.3 days. This risk declines to 2 %/day between days 5 to 10 of ventilation, and 1 %/day thereafter. Earlier studies placed the attributable mortality for VAP at between 33-50 %, but this rate is variable and relies heavily on the underlying medical illness. Over the years, the attributable risk of death has decreased and is more recently estimated at 9-13 %, largely because of implementation of preventive strategies. Approximately 50 % of all antibiotics adminis¬tered in ICUs are for treatment of VAP. Early onset VAP is defined as pneumonia that occurs within 4 days and this is usually attributed to antibiotic sensitive pathogens whereas late onset VAP is more likely caused by multidrug resistant (MDR) bacteria and emerges after 4 days of intubation. Thus, VAP poses grave implications in endotracheally intubated adult patients in ICUs worldwide and leads to increased adverse outcomes and healthcare costs. Independent risk factors for development of VAP are male sex, admission for trauma and intermediate underlying disease severity.
Pathogenesis
The complex interplay between the endotracheal tube, presence of risk factors, virulence of the invading bacteria and host immunity largely determine the development of VAP. The presence of an endotracheal tube is by far the most important risk factor, resulting in a violation of natural defense mechanisms (the cough reflex of glottis and larynx) against micro aspiration around the cuff of the tube. Infectious bacteria obtain direct access to the lower respiratory tract via: (1) micro aspiration, which can occur during intubation itself; (2) development of a biofilm laden with bacteria (typically Gram-negative bacteria and fungal species) within the endotracheal tube; (3) pooling and trickling of secretions around the cuff; and (4) impairment of mucociliary clearance of secretions with gravity dependence of mucus flow within the airways. Pathogenic material can also collect in surrounding anatomic structures, such as the stomach, sinuses, nasopharynx and oropharynx, with replacement of normal flora by more virulent strains. This bacterium-enriched material is also constantly thrust forward by the positive pressure exerted by the ventilator. Whereas reintubation following extubation increases VAP rates, the use of non-invasive positive pressure ventilation has been associated with significantly lower VAP rates. Host factors such as the severity of underlying disease, previous surgery and antibiotic exposure have all been implicated as risk factors for development of VAP.
In addition, it has recently been noted that critically ill patients may have impaired phagocytosis and behave as functionally immunosuppressed even prior to emergence of nosocomial infection. This effect is attributed to the detrimental actions of the anaphylatoxin, C5a, which impairs neutrophil phagocytic activity and impairs phagocytosis by neutrophils. More recently, a combined dysfunction of T-cells, monocytes, and neu¬trophils has been noted to predict acquisition of noso¬comial infection. For example, elevation of regula¬tory T-cells (Tregs), monocyte deactivation (measured by monocyte HLA-DR expression) and neutrophil dysfunc¬tion (measured by CD88 expression), have cumulatively shown promise in predicting infection in the critically ill population, as compared to healthy controls.
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