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PubMed1995

Minimally invasive surgery for gastroesophageal reflux disease.

BACKGROUND: The goal of this study was to determine if the outcome of antireflux surgery can be improved by: (1) conducting a careful preoperative workup to characterize gastroesophageal reflux disease (GERD) in the individual patient; and (2) tailoring the operation to the results of the preoperative function tests. PATIENTS AND METHODS: Sixty-eight patients had operations for GERD by minimally invasive techniques. RESULTS: A Rossetti fundoplication was performed in 22 patients. Sixty-eight percent became asymptomatic. Twenty-seven percent developed dysphagia or gas bloat. Thirty-five patients had a Nissen fundoplication. Ninety-one percent are asymptomatic. Eleven patients with severe abnormalities of esophageal peristalsis underwent a Guarner fundoplication with relief of symptoms in 82% of patients. No patients in the Nissen or Guarner group developed postoperative persistent dysphagia or gas bloat. A pyloromyotomy was performed in 3 patients because of severe delayed gastric emptying. CONCLUSIONS: Minimally invasive surgery for GERD gives good-to-excellent results even in patients with abnormal esophageal body function, provided that the operation is tailored to the individual patient based on the results of the preoperative function tests.

Adult↗

PubMed2001

Intragastric pH in critically ill neonatal foals and the effect of ranitidine.

OBJECTIVE: To characterize intragastric pH profiles in critically ill foals and determine whether administration of ranitidine altered pH profiles. DESIGN: Prospective observational study. ANIMALS: 23 hospitalized neonatal foals < or = 4 days of age. PROCEDURE: Intragastric pH was measured continuously for up to 24 hours by use of an indwelling electrode and continuous data recording system. In 21 foals, ranitidine was administered IV. RESULTS: 10 foals had predominantly or exclusively alkaline profiles, 10 had profiles typical of those reported for healthy foals, with periods of acidity (hourly mean pH < 5.0 at least once), and 3 had atypical profiles with periods of acidity. All 10 foals that had intragastric pH profiles typical of healthy foals survived, whereas only 2 foals with alkaline profiles survived, and none of the foals with atypical profiles survived. The effects of ranitidine administration could not be assessed in 13 foals because of a high baseline intragastric pH. In 7 of the remaining 9, ranitidine administration resulted in an alkalinizing response, but this response was often of blunted duration. Ranitidine administration did not appear to alter the intragastric pH profile in the remaining 2 foals. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that hospitalized critically ill foals often have intragastric pH profiles different from those reported for healthy foals and may respond differently to ranitidine administration than do healthy foals. Many critically ill foals have continuously alkaline intragastric pH profiles, questioning the need for prophylactic administration of ranitidine in all critically ill foals.

Animals↗

PubMed1997

Type of solution and PCO2 measurement errors during tonometry.

OBJECTIVE: The choice of solution for gastrointestinal tonometry influences the PCO2 measurement bias, precision and the time required for equilibration. We compared saline with buffered solutions during in vitro tonometry, with respect to systematic and accidental measurement errors and equilibration time. DESIGN: A prospective laboratory study. MEASUREMENTS: Saline, phosphate, phosphate bicarbonate and succinylated gelatin solutions were equilibrated in a specialized blood gas tonometer at PCO2s of 2.7, 3.6, 4.5, 6.2 and 9.0 kPa, using calibration gases. Accidental errors were determined: the within-syringe decline of PCO2 and the effects of handling errors (five up and down movements of the plunger). The PCO2 build up in gastrointestinal tonometers was determined in 5000 ml saline baths with fixed PCO2 levels of 2.7 and 9.0 kPa. RESULTS: The build up of PCO2 in phosphate bicarbonate and gelatin was about 4 and 2 times slower than in saline and phosphate, respectively, both for gas and gastrointestinal tonometers. The bias of the measured PCO2 at equilibrium was -15% for saline, and between -1 and 3% for phosphate, phosphate bicarbonate and gelatin. The precision was comparable among the solutions: 2 +/- 1% for saline, 2 +/- 1% for phosphate, 1 +/- 0% for phosphate bicarbonate and 1 +/- 1% for gelatin. The accidental errors were virtually absent with phosphate bicarbonate, intermediate with gelatin and largest with saline and phosphate. CONCLUSION: Phosphate bicarbonate buffer and succinylated gelatin allow accurate PCO2 measurements, but their equilibration is too slow for clinical application. The advantage of phosphate over saline solution is a smaller bias only. Thus, both saline and phosphate are currently the tonometer solutions of choice, provided that strictly anaerobic conditions are applied and the bias by the blood gas analyzer is known.

Analysis of Variance↗

PubMed1983

False-positive serum gastrin elevation during secretin stimulation due to Boots secretin.

Five patients with hypochlorhydria, chronic gastritis, and high serum gastrin levels and four control subjects underwent secretin stimulation testing. Gastrin determinations were made by a commercially available radioimmunoassay kit. Intravenous Boots secretin gave positive stimulation tests in all patients and controls. Positive Boots secretin stimulation tests in two of the control subjects were confirmed by a different gastrin assay kit. Synthetic secretin stimulation in two of the patients and the four control subjects showed no rise in postsecretin gastrin. Gastrin assay of pure Boots secretin from three different lots gave values ranging from 170,000 to 1,620,000 pg/ml. Gastrin assay of synthetic CCK 8 gave values of 718,600 and 1,300,000 pg/ml. Gastrin-like activity was undetectable in synthetic and GIH secretin and the normal saline used as a diluent. We conclude: 1) Boots secretin contains a contaminating substance or substances exhibiting immunoreactivity with commercially available gastrin assay kits, 2) cholecystokinin or cholecystokinin-like peptides are the leading candidates for contaminating substances in some assays, and 3) Boots secretin can cause false-positive secretin stimulation tests and should not be used in the secretin stimulation test for hypergastrinemia. We have switched exclusively to Kabi (GIH) secretin.

False Positive Reactions↗

PubMed1995

Do isolated gastric mucosal surface cells from rabbits secrete HCO3-?

Only indirect observations suggest that gastric surface cells secrete HCOH3-, which, if the case, should result in an alteration of intracellular pH. This study attempts to determine if HCO3- transport is notable in intracellular pH regulation by isolated surface cells. Maintenance of cellular pH during perfusion with HCO3(-)-free Ringer's solution is unaffected by either the absence of Cl- or the presence of an inhibitor of HCO3- transport, 4,4'-diisothiocyanostilbene-2-2'-disulfonate (DIDS). This implies the absence of Cl-/HCO3- exchange and HCO3- transport related to Na+. Addition of HCO3-/CO2 to the perfusate results in acidification due to CO2. The pH then drifts upward, which is prevented by amiloride, an inhibitor of Na+/H+ exchange. Calculated H+ efflux is not significantly affected by HCO3-/CO2. Removal of HCO3-/CO2 results in alkalinization, which is unaffected by the absence of Cl-. Alkalinization following HCO3-/CO2 removal is significantly impaired by acetazolamide. Once alkalinization occurs, the pH declines slowly and is unaffected by a Cl(-)-free perfusate or amiloride or conductance but is markedly accelerated by a Na(+)-free perfusate. The latter is prevented by amiloride but not by DIDS. Thus, under isolated conditions, gastric mucosal surface cells do not appear to be a major source of HCO3- secretion. Alkalinization of the cells can occur as a result of carbonic anhydrase activity, but the alkalinization is maintained by an extracellular Na+ gradient that prevents exchange of intracellular Na+ with extracellular H+.

Amiloride↗

PubMed2004

Cyclooxygenase 1 is required for pH control at the mouse gastric surface.

BACKGROUND: Endogenous cyclooxygenase (COX) activity is required to maintain a relatively alkaline surface pH at the gastric luminal surface. AIMS: The purpose of this study was to determine which COX isoform, COX-1 or COX-2, is responsible for regulating the protective surface pH gradient and to test if COX inhibitors also had non-COX mediated effects in vivo. METHODS: Immunofluorescence and western blot analysis showed constitutive expression of both COX isoforms in the normal mouse stomach. We used in vivo confocal microscopy to measure pH near the mucosal surface of anaesthetised COX-1 (-/-), COX-2 (-/-), or wild-type mice of the same genetic background. RESULTS: When the gastric mucosal surface was exposed and superfused (0.2 ml/min) with a weakly buffered saline solution (pH 3) containing the pH indicator Cl-NERF, the pH directly at the gastric surface and thickness of the pH gradient were similar in wild-type and COX-2 (-/-) mice, but COX-1 (-/-) mice had a significantly thinner pH gradient. Addition of indomethacin had minimal effects on the residual surface pH gradient in COX-1 (-/-) mice, suggesting no role for COX-2 in surface pH regulation. Whole stomach perfusion studies demonstrated diminished net alkali secretion in COX-1 (-/-) mice, and application of SC-560 or rofecoxib to wild-type mice and mutant mice confirmed that only COX-1 inhibition reduced alkali secretion. CONCLUSION: COX-1 is the dominant isoform regulating the normal thickness of the protective surface pH gradient in mouse stomach.

Animals↗

PubMed1993

Gastric intramural pH as a predictor of success or failure in weaning patients from mechanical ventilation.

OBJECTIVE: To determine whether gastric intramural pH (pHi), an indirect measure of gastric mucosal ischemia, can be used to predict the success of weaning from mechanical ventilation. Gastric mucosal ischemia (and, therefore, acidosis) may develop in patients during unsuccessful attempts to wean them from mechanical ventilation because blood flow from nonvital areas (for example, splanchnic bed) is diverted to meet the increased demands of respiratory muscles. DESIGN: Cohort study. SETTING: Intensive care unit. PATIENTS: Twenty-nine patients receiving assisted mechanical ventilation for respiratory failure who were thought by their physicians to be weanable from mechanical ventilation. MEASUREMENTS: Simultaneous samples of arterial blood and gastric juice were obtained from patients during assisted mechanical ventilation, as well as during weaning trials. The predictor variable, pHi, was calculated using the following equation: 6.1 + log HCO3/(gastric PCO2 x 0.0307). The outcome was success or failure of weaning, decided by physicians blinded to the study. RESULTS: Patients who could not be weaned from mechanical ventilation had a substantially reduced gastric pHi (7.36 during mechanical ventilation compared with 7.09 during weaning [difference, 0.27; 95% Cl, 0.12 to 0.42; P < 0.01]). Patients who were successfully weaned from mechanical ventilation showed no change in pHi (7.45 during mechanical ventilation compared with 7.46 during weaning [difference, 0.01; Cl, -0.01 to 0.03; P = 0.29]). The sensitivity and specificity of pHi in predicting weaning success or failure were both 100% (Cl, 81 to 100 and 72 to 100, respectively). CONCLUSION: Gastrointestinal acidosis may be an early sign of weaning failure. Measurement of pHi, which is simple and rapid, may be of practical value in predicting the likelihood of weaning success or failure during weaning trials.

Acidosis↗

PubMed1992

Indomethacin accelerates clearance of labeled cells and increases DNA synthesis in gastrointestinal mucosa of the rat.

Sprague-Dawley rats treated with placebo, parenteral indomethacin, or oral prostaglandin E2 for six days were given an intraperitoneal injection of [3H] methyl-thymidine and killed at 45 min and 96 hr after labeling. Treatments were continued until death. The dpm/DNA index was determined in mucosal scrapings of the stomach, duodenum, and jejunum and used to estimate DNA synthesis (45 min) and the clearance of labeled cells (96 hr). Indomethacin increased the DNA synthesis in both the duodenal and jejunal mucosa (P less than 0.05). In comparison to the controls, the clearance of labeled cells from the antral, duodenal, and jejunal mucosa was accelerated by indomethacin treatment, whereas the elimination of labeled cells from the antral and jejunal mucosa was slowed by PGE2 treatment (P less than 0.05). DNA synthesis of the antral mucosa was significantly reduced by PGE2 (P less than 0.05). The cyclooxygenase blocker did not affect the cell kinetic parameters of the oxyntic mucosa. The plasma levels of somatostatin were significantly higher both in PGE2- and indomethacin-treated rats than in controls (P less than 0.05). It is concluded that indomethacin treatment increases the cell losses from the epithelial surface, which in turn trigger a compensatory trophic reaction. It is suggested that an important physiological action of endogenous prostaglandins is to regulate the outflow of cells from the superficial zones of the epithelium. Finally, this study disclosed the presence of hitherto unknown regulatory mechanisms that promote cell proliferation in the gastrointestinal mucosa despite inhibition of the synthesis of endogenous prostaglandins.

Animals↗

PubMed1994

Intra-operative gut mucosal hypoperfusion is associated with increased post-operative complications and cost.

OBJECTIVES: To determine CO and gastric mucosal perfusion in patients during elective major surgery; to seek a relationship with subsequent outcome. DESIGN: Prospective descriptive study. SETTING: University hospital. PATIENTS: 51 patients undergoing elective major surgery of an anticipated duration of greater than 2 h who were at risk of developing gut mucosal hypoperfusion and postoperative organ failure. MEASUREMENTS AND RESULTS: CO was determined by oesophageal Doppler measurement of aortic blood flow. Gastric mucosal perfusion was determined by tonometric assessment of gastric mucosal pH (pHi). Blood pressure and urine flow were measured. At the end of surgery no patients were oliguric or hypotensive. Post-operatively morbidity, mortality, duration and cost of stay in the ITU and hospital were assessed. There were 32 patients with evidence of gastric mucosal ischaemia at the end of surgery (pHi < 7.32) despite maintenance of CO. This group of patients spent a mean of 4.7 (range 0-33) days in the ITU, 14 developed major complications (7 with multiple organ failure [MOF] and 6 died. In 19 patients gut mucosal perfusion was maintained during surgery (pHi > or = 7.32); these patients demonstrated an increase in CO of 48.4% (95% confidence interval 21.3 -75.6) and spent a mean of 1.0 (range 0-4) days in the ITU. Only one developed a major complication and none died. The total cost of post-operative care for the 51 patients was estimated at pounds 356650. Mean cost per patient in the low pHi group was significantly greater at pounds 8845 (range pounds 600--pounds 42,700) compared to pounds 3874 (range pounds 2,600--pounds 9,600) in the normal pHi group. The total.cost of post-operative care for the 7 patients who developed MOF was pounds 171,450 i.e. 48% of the total cost. CONCLUSION: A low gastric pHi measured during the intraoperative period in a group of patients undergoing major (mainly cardiovascular) surgery is associated with increased post-operative complications and cost.

Adult↗

PubMed1983

Role of luminal alkalinization in repair process of ethanol-induced mucosal damage in rat stomach.

Changes in transmucosal potential difference (PD) and luminal pH after intragastric application of ethanol were simultaneously determined in stomachs of anesthetized rats. When the stomachs were exposed to 5-50% ethanol for 10 min, the PD was abruptly reduced and gradually returned to the basal levels, while the luminal pH gradually increased; these responses were concentration-dependent. The reduction of PD with 10% ethanol rapidly returned to the basal level without any changes in luminal pH. The PD after 50% ethanol gradually returned to the basal level in 3 hr, during which time luminal pH was kept at around 6. In cimetidine plus atropine-treated rats, considerably greater amounts of HCO3- were evident in the perfusate. The surface mucosal cells damaged by 50% ethanol recovered in parallel with the recovery of PD. When the stomach pH was maintained at a low level by an intravenous infusion of histamine or intragastric perfusion of 0.01 N HCl, the PD remained at a reduced level and the mucosal damage was aggravated. The perfusion of 0.01 N NaHCO3 kept the luminal pH at around 8-9, but it did not affect the recovery process of PD after 50% ethanol. These results suggest that application of ethanol induces luminal alkalinization, probably by HCO3- diffusion through the broken barrier, which in turn plays a role in the recovery from damage.

Acid-Base Equilibrium↗

PubMed1994

[Gastric pH changes during and after extracorporeal circulation. What is its clinical meaning?].

OBJECTIVE: To determine the relationship between gastric pH (pHm) and several other indices of blood perfusion in patients undergoing cardiopulmonary bypass (CPB). To evaluate the importance of pHm as a prognostic index for elective cardiac surgery. DESIGN: Prospectives study. SETTING: Cardiac surgery ICU of a Regional Hospital in Italy. PATIENTS: Nineteen patients were sequentially studies in a 4-month period. METHOD: Before anesthetic induction, a pH probe incorporated in the tip of a nasogastric tube (GrapHprobe SH, GrapHometer, Zinetics Medical, USA) was inserted in the stomach. Results, collected during the CPB and in the postoperative period until 1 hour after extubation, were compared to the peripheral tissue perfusion and oxygenation data (transcutaneous: PtcO2), hemodynamic variations (Swan-Ganz catheter), pharyngeal temperature, and blood gases. RESULTS: No significant variations of pHm were reported during the study. Significant relations were found only after surgery between pHm and PaO2 (p < 0.001), hemoglobin (p < 0.001), and blood pH (p < 0.05). No statistical correlations were reported between pHm and hemodynamic variations. CONCLUSIONS: Although a significant variation of peripheral and pulmonary vascular resistance and transcutaneous oxygenation was reported throughout the study, no correlations were found to pHm. At present it is not possible to confirm the importance of pHm as a prognostic index for elective cardiac patients, even though it is necessary to examine whether the additional data of pHm variation could be considered a true marker of visceral perfusion.

Aged↗

PubMed1985

Prostaglandin protection of the gastric mucosa against alcohol injury--a dynamic time-related process. Role of the mucosal proliferative zone.

The aim of the present study was first to resolve controversies regarding the extent of prostaglandin protection ("cytoprotection") of the gastric mucosa against injury produced by 100% ethanol and second to determine time sequence and histologic, ultrastructural, and functional features of this protection. Fasted rats received intragastrically (A) 0.9% NaCl alone as a control, (B) 5 micrograms/kg of 16,16-dimethyl prostaglandin E2 dissolved in 0.9% NaCl, and (C) 100 micrograms/kg of 16,16-dimethyl prostaglandin E2 dissolved in 0.9% NaCl. Thirty minutes later, 2 ml of 100% ethanol was instilled. The gastric mucosa was assessed macroscopically, by quantitative histology, and by scanning and transmission electron microscopy for [3H]thymidine uptake, mitotic activity, ion fluxes, and gastric potential difference determined at several time intervals (between 10 min and 16 h) after ethanol administration. Between 10 min and 16 h after ethanol administration macroscopic necrosis involved 27% +/- 3% to 41% +/- 4% of the mucosal area in controls (group A), but necrosis was prevented in groups receiving 16,16-dimethyl prostaglandin E2 (groups B and C). In the control group, histology and electron microscopy showed extensive disruption of the surface epithelium and deep necrosis (greater than 0.2 mm) involving greater than 46% +/- 4% of the mucosa between 15 min and 16 h after ethanol administration. Deep necrotic lesions were completely prevented by either dose of 16,16-dimethyl prostaglandin E2 (groups B and C). The mucosal proliferative zone was severely damaged in controls (68% +/- 5%) within the first hour after ethanol administration, whereas 16,16-dimethyl prostaglandin E2 protected the zone from damage (less than 5% +/- 1%). Neither dose of 16,16-dimethyl prostaglandin E2 prevented the occurrence of initial (at 15-30 min) morphologic and functional disruption of the surface epithelium after ethanol administration. However, initial disruption of the surface epithelium by 16,16-dimethyl prostaglandin E2 (groups B and C) was followed by migration of cells from the mucosal proliferative zone; the result was prompt restoration of the surface epithelium and resumption of its barrier and transport functions.

16,16-Dimethylprostaglandin E2↗

PubMedDate not supplied

What is known about methods of correctly placing gastric tubes in adults and children.

An abdominal radiograph is considered the "gold standard" for determining the position of flexible small-bore nasogastric/orogastric tubes. However, placement must be checked frequently while a tube is in place, and the summative radiation risk of multiple radiographs, as well as their expense, make the development of adequate bedside placement-locating methods imperative. Several methods of detecting tube placement have been investigated in adults, including: aspirating gastric contents and measuring the pH, bilirubin, pepsin, and trypsin levels; examining the visual characteristics of aspirate; placing the proximal end of the tube under water and observing for bubbles in synchrony with expirations; measuring the carbon dioxide level at the proximal end of the nasogastric/orogastric tube; auscultation for a gurgling sound over the epigastrium or left upper quadrant of the abdomen; and measuring the length from the nose/mouth to the proximal end of the tube. Many researchers have already concluded simple auscultation is not a reliable method to assess tube position because injection of air into the tracheobronchial tree or into the pleural space can produce a sound indistinguishable from that produced by injecting air into the gastrointestinal tract. In adults, only pH and bilirubin of aspirate have been shown both to reliably predict tube position and to have inexpensive simple bedside tests. In children, only pH of aspirate has been shown to be reliable. Research on gastric tube placement in children is relatively new because children are challenging to study in that they are considered a vulnerable population. This review of the literature includes results of both adult and pediatric studies. Tube placement error rates varied from 1.9% to 89.5% in adults and between 20.9% and 43.5% in children.

Adult↗

PubMed1996

Role of adenosine and nitric oxide in the hyperemic response to superficial and deep gastric mucosal injury and H+ back-diffusion in cats.

BACKGROUND: This study was undertaken to examine the role of adenosine and nitric oxide (NO) in the hyperemic response to H+ back-diffusion into superficially or deeply injured gastric mucosa, and the role of adenosine in mucosa when blood flow was reduced with indomethacin. METHODS: Cat stomachs were exposed to 2 M NaCl for 10 min followed by luminal perfusion at pH 1. Gastric mucosal blood flow was determined by radioactive microspheres, portal vein blood flow by transit-time flowmetry, and H+ back-diffusion/secretion by pH-stat titration, and concentrations of histamine in aortic and portal vein blood were measured. RESULTS: In the antrum pretreatment with the adenosine blocker 8-phenyltheophylline (8-PT) or with NG-methyl-L-arginine (L-NMMA), a specific inhibitor of NO formation, had no effect on the hyperemic response or mucosal injury. However, pretreatment with 8-PT in addition to indomethacin produced extensive deep lesions in the antrum. In the corpus/fundus 8-PT had no effect on the hyperemic response and did not increase indomethacin-induced lesions. L-NMMA significantly reduced the hyperemic response in corpus/fundus. In areas with deep lesions very high blood flow was observed in the vital part of the mucosa below the necrotic tissue. This hyperemia was reduced by L-NMMA but not by 8-PT. Indomethacin increased the release of histamine during base-line conditions, whereas 8-PT reduced histamine release after damage. CONCLUSIONS: This study indicates that usually adenosine is not involved in the hyperemic response to mucosal damage, but it appears to have important protective functions in the antral mucosa under marginal circulatory conditions. NO is one of the mediators of the hyperemic response to mucosal injury in the corpus/fundus.

Adenosine↗

PubMed2000

Changes in gastric intramucosal pH and circulating blood volume following coronary artery bypass grafting.

PURPOSE: To determine the changes in gastric intramucosal pH (pHi) following coronary artery bypass grafting (CABG) in comparison with systemic hemodynamic variables and circulating blood volume (BVc). METHODS: Twenty patients who underwent CABG under mild hypothermic cardiopulmonary bypass (CPB) were included. Hemodynamic variables and the values of pHi were obtained at 3,6, 12 and 24 hr after admission to the intensive care unit (ICU). The pHi was measured by gastric tonometric catheter. The BVc was measured by carbon monoxide (CO)-labeled hemoglobin (CO-Hb) dilution method (CO method) at 6 and 24 hr after ICU admission. RESULTS: Systemic vascular resistance index (SVRI) and pulmonary vascular resistance index (PVRI) decreased with time. Systemic oxygen delivery index (DO2I) and systemic oxygen consumption index (VO2I) showed a gradual increase during the study period. By contrast, pHi decreased to the lowest value (7.26+/-0.05) at six hours and returned to normal levels (7.34+/-0.04) at 24 hr after ICU admission. Changes in BVc between six and 24 hr ranged from -242 ml to 978 ml (mean, 334+/-338 ml). The pHi increased in patients whose BVc increased by > 300 ml. Mean fluid balance was negative in this period (-386+/-667 ml; range, -1786 - + 423 ml). CONCLUSION: The pHi showed the lowest value at six hours and returned to normal at 24 hr after ICU admission. The pHi increased with the decrease in vascular resistance and with the increases in BVc in this period. The improvement of pHi, an indicator of splanchnic perfusion, appears to be related to systemic vasodilatation and an increase in BVc.

Aged↗

PubMed1996

[Measurement of gastric mucosal pH by tonometry in major abdominal surgery].

OBJECTIVE: To investigate whether changes in gastric intramucosal pH (pHim) occur during major abdominal surgery, and if so, to determine the relationship between classic global indices of tissue perfusion such as mean arterial blood pressure (MAP), heart rate (HR), central venous pressure (CVP), urine flow (UF) and arterial pH (pHa). STUDY DESIGN: Prospective descriptive study. PATIENTS: Seven ASA2 patients undergoing major abdominal surgery. METHODS: After induction of anaesthesia and endotracheal intubation, a tonometer nasogastric tube was positioned in the stomach. Measurements of tonometric PCO2 (PCO2ss), end-tidal PCO2 (PETCO2), PaCO2, bicarbonates [bicarb], pHa, MAP, HR, CVP and UF were collected at baseline (HO), and one, two, three, and 24 hours (H1, H2, H3, and H24) after the beginning of surgery. RESULTS: Haemodynamics did not significantly change during anaesthesia. During recovery HR increased and CVP decreased significantly. The pHim decreased significantly from 7.42 +/- 0.03 at H0 to 7.30 +/- 0.02 at H3. This was associated with a significant decrease in pHa (from 7.43 +/- 0.02 at H0 to 7.33 +/- 0.02 at H3) and in [bicarbo] from 22 +/- 1 mmol at H0 to 20 +/- 1 mmol at H3). The PaCO2 increased significantly from 33.5 +/- 1.5 mmHg at H0 to 39.5 +/- 2.8 at H3. On the other hand, pHimcorr (7.40- (pHa-pHim) and delta CO2 (PCO2ss-PETCO2) did not vary during anaesthesia. Postoperative organ failure did not occur in these patients. CONCLUSIONS: The pHim may decrease during anaesthesia without evidence of abnormal tissue perfusion. In order to avoid.

Abdomen↗

PubMed2005

Sensitive pepsin immunoassay for detection of laryngopharyngeal reflux.

OBJECTIVES/HYPOTHESIS: To determine whether measurement of pepsin in throat sputum by immunoassay could be used as a sensitive and reliable method for detecting laryngopharyngeal reflux (LPR) compared with 24-hour double-probe (esophageal and pharyngeal) pH monitoring. STUDY DESIGN: Patients with clinical LPR undergoing pH monitoring provided throat sputum samples during the reflux-testing period for pepsin measurement using enzyme-linked immunoadsorbent assay. RESULTS: Pepsin assay results from 63 throat sputum samples obtained from 23 study subjects were compared with their pH monitoring data. Twenty-two percent (14/63) of the sputum samples correlated the presence of pepsin with LPR (pH < or = 4 at the pharyngeal probe), of which the median concentration of pepsin was 0.18 microg/mL (range 0.003-22 microg/mL). Seventy-eight percent (49/63) of the samples unassociated with (pharyngeal) reflux contained no detectible pepsin. Mean pH values for pepsin-positive samples were significantly lower than negative samples at both esophageal probe (pH 2.2 vs. pH 5.0) (P < .01) and the pharyngeal probe (pH 4.4 vs. pH 5.8) (P < .01). When the pepsin assay results were compared with the pharyngeal pH data for detecting reflux (events pH < or = 4), the pepsin immunoassay was 100% sensitive and 89% specific for LPR. CONCLUSIONS: Detection of pepsin in throat sputum by immunoassay appears to provide a sensitive, noninvasive method to detect LPR.

Acid-Base Equilibrium↗

PubMed1996

Effect of tube feedings on the measurement of gastric intramucosal pH.

OBJECTIVE: To determine the effect of enteral tube feedings on the measurement of gastric intramucosal pH. DESIGN: Interventional study. SETTING: Two intensive care units of a university-affiliated teaching hospital. PATIENTS: Twenty hemodynamically stable patients undergoing mechanical ventilation, with a nasogastric tonometer in situ, in whom enteral feeding was initiated. INTERVENTIONS: The baseline fasting gastric intramucosal pH and gastric fluid pH were determined in the study population. The patients then received enteral feedings for 2 hrs, after which the gastric intramucosal pH and gastric fluid pH measurements were repeated. The tube feedings were then withheld for 2 hrs. The data set was repeated 1 and 2 hrs after the feedings had been stopped. Finally, tube feedings were retarded and the data set was repeated after 4 hrs. All patients received a histamine-2 (H2)-receptor antagonist-blocking agent during the study. To investigate the possibility that a direct reaction between gastric fluid and enteral feedings may generate CO2, 30-mL aliquots of gastric fluid from an independent sample of 14 patients (seven receiving cimetidine) were mixed with 60 mL of enteral feeding in an airtight container; the PCO2 of the gastric fluid before and after adding enteral feeding was measured tonometrically. MEASUREMENTS AND MAIN RESULTS: The mean +/- SD gastric intramucosal pH decreased from 7.40 +/- 0.08 to 7.33 +/- 0.12 (p < .005), and from 7.38 +/- 0.07 to 7.31 +/- 0.1 (p < .005) after the first and second feeding challenges, respectively. The gastric intramucosal pH returned to the baseline value after 1 hr of fasting. The mean in vitro PCO2 of the gastric fluid increased from 11.9 +/- 3.0 to 16.2 +/- 2.0 torr (1.6 +/- 0.4 to 2.1 +/- 0.27 kPa) (p = .003) after the addition of tube feedings in the samples from those patients who were not receiving H2 receptor antagonists, but did not change significantly in those samples from the patients who were receiving H2 receptor antagonists. CONCLUSIONS: Enteral feeding stimulates the secretion of hydrogen ions, which are then buffered by ionized bicarbonate secreted by the nonparietal gastric cells generating CO2. In addition, the enzymatic digestion of nutrients in the stomach may also generate CO2. The increased intraluminal CO2 following enteral feeding results in a spuriously low gastric intramucosal pH reading. Our data suggest that tube feedings should be temporarily discontinued for at least 1 hr when measuring the gastric intramucosal pH. These data should, however, be used with caution when extrapolating to hemodynamically unstable patients. Furthermore, the consequences of frequent interruptions of enteral feeding need to be weighed against the possible benefits derived from the use of this monitoring tool.

APACHE↗