title: Gastric alkalinization after major trauma.
abstract: BACKGROUND
  Gastric function in trauma patients is poorly understood. In animals, shock causes gastric luminal alkalinization and bile reflux. In trauma patients, studies of stress gastritis prophylaxis demonstrated with continuous gastric pH monitoring that the stomach became alkaline even without antisecretory therapy. Therefore, we hypothesized that trauma patients have an alkaline gastric environment that may be because of bile reflux.
  
  
  METHODS
  A prospective observational study at an urban Level I trauma center was performed. All major torso trauma patients (severe head injuries excluded) who met the criteria for standardized shock resuscitation were eligible for inclusion. A 12.5 Fr silastic pH probe (Sandhill Scientific) was placed in the stomach and the gastric pH continuously monitored for 7 days. Patients received no stress gastritis prophylaxis. Gastric samples were obtained each day and assayed for total bile acids and pH.
  
  
  RESULTS
  Twelve patients were entered into the study. Mean age was 31 years +/- 4 years, 67% men, 75% blunt mechanism of injury, and mean Injury Severity Score 28 +/- 3. Three patients (25%) developed multiple organ failure and four acquired ventilator-associated pneumonia. During the first day of continuous pH monitoring, 9 of 12 patients had a gastric pH >4 for the majority of the day with 7 patients having essentially no acid production. During subsequent days, gastric pH began to drop and by the 4th day the majority of each day was spent at a pH <4. Additionally, gastric pH of patients with ventilator-associated pneumonia or multiple organ failure tended to be more alkaline. Bile acid was present in the gastric fluid of all patients in varying amounts. However, there was no significant correlation between gastric pH and bile acid concentration.
  
  
  CONCLUSIONS
  Traumatic injury causes gastric luminal alkalinization that may be related, only in part, to bile acid reflux. Other alkalinizing factors remain to be elucidated.
authors.affiliation: Department of Surgery, UC Davis Medical Center, Sacramento, California, USA. christine.cocanour@ucdmc.ucdavis.edu
authors.forename: Christine S
authors.initials: CS
authors.lastname: Cocanour
authors.forename: Elizabeth D
authors.initials: ED
authors.lastname: Dial
authors.forename: Lenard M
authors.initials: LM
authors.lastname: Lichtenberger
authors.forename: Ernest A
authors.initials: EA
authors.lastname: Gonzalez
authors.forename: Rosemary A
authors.initials: RA
authors.lastname: Kozar
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Moore
authors.forename: David W
authors.initials: DW
authors.lastname: Mercer
mesh_terms: D000136:Acid-Base Equilibrium; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005745:Gastric Acidity Determination; D005764:Gastroesophageal Reflux / Q000209:etiology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D015601:Injury Severity Score; D016018:Least-Squares Analysis; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D011446:Prospective Studies; D012042:Registries; D012151:Resuscitation / Q000379:methods*; D012307:Risk Factors; D013898:Thoracic Injuries / Q000150:complications*