Nosocomial Pneumonia in Intubated Patients Given Sucralfate as Compared with Antacids or Histamine Type 2 Blockers

Abstract

Gram-negative nosocomial pneumonia may result from retrograde colonization of the pharynx from the stomach, and this may be more likely when the gastric pH is relatively high. We studied the rate of nosocomial pneumonia among 130 patients given mechanical ventilation in an intensive care unit who were receiving as prophylaxis for stress ulcer either sucralfate (n = 61), which does not raise gastric pH, or conventional treatment with antacids, histamine type 2 (H2) blockers, or both (n = 69). At the time of randomization to treatment, the two groups were similar in age, underlying diseases, and severity of acute illness. Patients in the sucralfate group had a higher proportion of gastric aspirates with a pH less than or equal to 4 (P less than 0.001) and significantly lower concentrations of gram-negative bacilli (P less than 0.05) in gastric aspirates, pharyngeal swabs, and tracheal aspirates than did patients in the antacid-H2-blocker group. The rate of pneumonia was twice as high in the antacid-H2 group as in the sucralfate group (95 percent confidence interval, 0.89 to 4.58; P = 0.11). Gram-negative bacilli were isolated more frequently from the tracheal aspirates of patients with pneumonia who were receiving antacids or H2 blockers. Mortality rates were 1.6 times higher in the antacid-H2 group than in the sucralfate group (95 percent confidence interval, 0.99 to 2.50; P = 0.07). Although our results fell just short of statistical significance when they were analyzed according to intention to treat, they suggest that agents that elevate gastric pH increase the risk of nosocomial pneumonia in patients receiving ventilation by favoring gastric colonization with gram-negative bacilli. We conclude that in patients receiving mechanical ventilation, the use of a prophylactic agent against stress-ulcer bleeding that preserves the natural gastric acid barrier against bacterial overgrowth may be preferable to antacids and H2 blockers.

Role of Gastric Colonization in Nosocomial Infections and Endotoxemia: A Prospective Study in Neurosurgical Patients on Mechanical Ventilation

“…The results of this study confirm that intragastric microbial growth is pH-dependent [18][19][20] and promoted by treatment with Hs-receptor blockers or antacids [3][4][5][6][7][8]. However, our data do not support results from previous studies on intubated ICU patients, which suggested that gastric colonization was a significant risk factor for subsequent tracheal colonization or pneumonia [5,[8][9][10].…”

“…However, none of the three reports mentioned oropharyngeal culturing, so the oropharynx as an important source of pathogens [21][22][23] may have contributed to gastric and tracheal colonization in all three studies. Treatment with H zreceptor blockers or antacids may predispose to pneumonia in intubated patients [7,11,12), but the * DIC score as defined [16], ranging from 0 to 13; 13 = most severe DIe.…”

“…The rise of gastric pH induced by such treatment promotes microbial colonization of the stomach [3][4][5][6][7][8]. Gastric microbial growth may predispose to tracheal colonization in intubated patients [5,[8][9][10], and possibly increase the risk for nosocomial pneumonia.…”

“…HI-receptor blockers or antacids, but whether the stomach was a source of the pathogens causing pneumonia was not evaluated [7,11,12).…”

Early gastrostomy reduces the rate of ventilator-associated pneumonia in stroke or head injury patients

“…These mechanisms include: 1) disturbance of the physiological pharyngoglottal reflexes that prevent aspiration [22]; 2) dysfunction of the upper and lower oesophageal sphincters and associated gastro-oesophageal reflux secondary to the presence of the tube [9]; and 3) colonisation of the stomach by bacteria that may subsequently migrate to the oropharynx and into the lower respiratory tract (gastropulmonary hypothesis) [23,24].…”