STRESS ULCER PROPHYLAXIS AS A RISK FACTOR FOR TRACHEAL COLONIZATION AND HOSPITAL-ACQUIRED PNEUMONIA IN INTENSIVE CARE PATIENTS: IMPACT ON LATENCY TIME FOR PNEUMONIA.

Abstract

SUMMARYStress ulcer prophylaxis is associated with bacterial colonization of respiratory tract. The aims of our study were to determine risk factors for trachea colonization (TC), colonization of pharynx (CP) or stomach (CD) and hospital-acquired pneumonia (HAP), and divide the factors into those with high risk and low risk. The study population (ventilated intensive care unit (ICU) patients eligible to receive stress ulcer prophylaxis) was randomized to receive one of three different treatment protocols: ranitidine, sucralfate, and no stress ulcer prophylaxis (control group). Clinical data relative to pre-specified risk factors for TC or HAP were recorded, as follows: APACHE II score (second risk factor), duration of intubation or tracheotomy (third risk factor), duration of mechanical ventilation (fourth risk factor) and duration of hospitalization in the ICU (fifth risk factor). Gastric pH was recorded and microbiological data regarding stomach, pharynx and trachea were collected on the 1st, 2nd, 3rd and 5th day. Fifty-eight out of 81 patients developed HAP (including ventilator-associated pneumonia), which occurred later in patients with gastric content pH <4 or those that were tracheotomized. Stress ulcer prophylaxis was not associated with HAP; however, it was proved as a risk factor for TC. TC was detected in tracheotomized patients and was caused by gram-negative pathogens. CP was associated with TC, since the majority of patients had CP before TC. A combination of risk factors (APACHE II >18, age >65, mechanical ventilation and sedation) caused a higher incidence of HAP and lower incidence of TC. HAP was more frequent in patients staying in the ICU for >10 days and those with cardiovascular disease as the underlying disorder. Sedation and previous antibiotic therapy correlated with longer latent period (LAT), while higher values of gastric content pH were related to shorter LAT. The longest LAT was found in patients colonized with Acinetobacter spp. Risk factors that accelerated the occurrence of HAP were found to have caused previous colonization. A combination of risk factors increased the likelihood of TC and HAP, and shortened LAT between TC and HAP.