Muzlovič Igor, Štubljar David
1Department of Infectious Diseases, University Medical Centre, Ljubljana, Slovenia; 2Department of Research and Development, In-Medico, Metlika, Slovenia.
Acta Clin Croat. 2019 Mar;58(1):72-86. doi: 10.20471/acc.2019.58.01.10.
Stress 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 1, 2, 3 and 5 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 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.
应激性溃疡预防与呼吸道细菌定植有关。我们研究的目的是确定气管定植（TC）、咽部定植（CP）或胃部定植（CD）以及医院获得性肺炎（HAP）的危险因素，并将这些因素分为高风险和低风险因素。研究人群（符合接受应激性溃疡预防条件的机械通气重症监护病房（ICU）患者）被随机分为接受三种不同治疗方案之一：雷尼替丁、硫糖铝和不进行应激性溃疡预防（对照组）。记录与预先指定的TC或HAP风险因素相关的临床数据，如下：急性生理与慢性健康状况评分系统（APACHE）II评分（第二个风险因素）、插管或气管切开持续时间（第三个风险因素）、机械通气持续时间（第四个风险因素）以及在ICU住院时间（第五个风险因素）。记录胃内pH值，并在第1、2、3和5天收集有关胃、咽部和气管的微生物学数据。81名患者中有58例发生HAP（包括呼吸机相关性肺炎），在胃内容物pH<4的患者或接受气管切开术的患者中发生时间较晚。应激性溃疡预防与HAP无关；然而，它被证明是TC的一个危险因素。在接受气管切开术的患者中检测到TC，且由革兰氏阴性病原体引起。CP与TC相关，因为大多数患者在发生TC之前就有CP。多种风险因素（APACHE II>18、年龄>65岁、机械通气和镇静）导致HAP发生率较高而TC发生率较低。在ICU住院>10天的患者以及以心血管疾病为基础疾病的患者中HAP更为常见。镇静和先前的抗生素治疗与较长的潜伏期（LAT）相关，而较高的胃内容物pH值与较短的LAT相关。在感染 spp.的患者中发现最长的LAT。发现加速HAP发生的风险因素曾导致先前的定植。多种风险因素的组合增加了TC和HAP的可能性，并缩短了TC和HAP之间的LAT。
