In addition, a quantitative approach to assessing the culture (performing a bacterial count of the pathogen that is causing the pneumonia) does not appear to be superior to a qualitative approach (determining the presence of the pathogen). In recent years there has been a focus on rapid diagnostics, allowing for detection of significant levels of pathogens before this becomes apparent on microbial cultures. Several approaches have been used, including using host biomarkers such as IL-1β and IL-8. Alternatively, molecular detection of bacteria has been undertaken, with reports that amplifying the pan-bacterial 16S gene can provide a measure of bacterial load. A trial of biomarker-based exclusion of VAP (VAP-RAPID2) has recently finished recruitment, and results are awaited (https://clinicaltrials.gov/ct2/show/NCT01972425). Blood cultures may reveal the microorganisms causing VAP, but are often not helpful as they are positive in only 25% of clinical VAP cases. Even in cases with positive blood cultures, the bacteremia may be from a source other than the lung infection. Prevention
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 technique for 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 intubated have been proposed. One important aspect is limiting the amount of sedation that a ventilated person receives.
Habit-induced individuals generally have a history of bulimia nervosa or of intentional regurgitation (magicians and professional regurgitators, for example), which though initially self-induced, forms a subconscious habit that can continue to manifest itself outside the control of the affected individual. Trauma-induced individuals describe an emotional or physical injury (such as recent surgery, psychological distress, concussions, deaths in the family, etc. ), which preceded the onset of rumination, often by several months. Pathophysiology
Rumination syndrome is a poorly understood disorder, and a number of theories have speculated the mechanisms that cause the regurgitation, which is a unique symptom to this disorder. While no theory has gained a consensus, some are more notable and widely published than others.The most widely documented mechanism is that the ingestion of food causes gastric distention, which is followed by abdominal compression and the simultaneous relaxation of the lower esophageal sphincter (LES). This creates a common cavity between the stomach and the oropharynx that allows the partially digested material to return to the mouth. There are several offered explanations for the sudden relaxation of the LES. Among these explanations is that it is a learned voluntary relaxation, which is common in those with or having had bulimia. While this relaxation may be voluntary, the overall process of rumination is still generally involuntary. Relaxation due to intra-abdominal pressure is another proposed explanation, which would make abdominal compression the primary mechanism. The third is an adaptation of the belch reflex, which is the most commonly described mechanism.