Antacid, sucralfate, and prostaglandin E2 effects on the growth and potential for translocation of Pseudomonas aeruginosa, Escherichia coli, and Staphylococcus aureus in an in vitro gastric simulation.
Viable bacteria in the gut of thermally injured patients may be translocated through the gut mucosa, causing widespread infection. Increased flora from optimization of bacterial growth by pH elevation, coupled with the decreased intestinal motility common among patients whose mucosal integrity has been compromised, may increase the incidence of translocation. Gastric pH in these patients is monitored and maintained around pH 6 by various agents to reduce susceptibility to stress ulceration. Whole milk, given as a nutrient source, also raises pH. An in vitro trial simulating gastric fluid under conditions found in patients with burns was conducted to evaluate the growth of commonly ingested bacteria. Bicarbonate buffer containing pepsin and adjusted to pH 2, 4, or 7 with HCl was dosed with magnesium and aluminum hydroxide antacid (Maalox) (10 ml), sucralfate (Carafate) (0.4 gm), or prostaglandin E2 (PGE2) (10 ng) before inoculation with Escherichia coli (3 x 10(2) organisms), Pseudomonas aeruginosa (3 x 10(2) organisms), or Staphylococcus aureus (2 x 10(1) organisms). Bacterial growth and pH were determined periodically over the 24-hour trial. Milk was added at intervals in half the samples to simulate patient feeding. Maalox increased pH in all samples containing milk (initially pH 2, 4, or 7) to over 7.0 in 2 hours, and increased pH more slowly without milk. Carafate had a moderating effect, increasing pH 2 and pH 4 and decreasing pH 7, with a narrower pH range found in the milk groups. PGE2 treatments combined with milk also increased pH 2 and pH 4, but slightly elevated pH 7 within 24 hours. Without milk, PGE2 did not alter pH from initial values.(ABSTRACT TRUNCATED AT 250 WORDS)
Goeger
M P
MP
Shriners Burns Institute, Galveston, TX 77550.
Dupuis
G K
GK
Herndon
D N
DN
Robson
M C
MC
Heggers
J P
JP
D000818:Animals; D000863:Antacids / Q000494:pharmacology*; D002056:Burns / Q000382:microbiology* / Q000503:physiopathology; D015169:Colony Count, Microbial; D015232:Dinoprostone / Q000494:pharmacology*; D004926:Escherichia coli / Q000187:drug effects / Q000254:growth & development* / Q000502:physiology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D008892:Milk; D011550:Pseudomonas aeruginosa / Q000187:drug effects / Q000254:growth & development*; D013211:Staphylococcus aureus / Q000187:drug effects / Q000254:growth & development* / Q000502:physiology; D013270:Stomach / Q000382:microbiology* / Q000503:physiopathology; D013392:Sucralfate / Q000494:pharmacology*
D000863:Antacids; D013392:Sucralfate; D015232:Dinoprostone