Richard G. Fiddian-Green

Predictive value of the stomach wall pH for complications after cardiac operations: comparison with other monitoring

The ability to predict impending complications after elective cardiac operations from measurements of BP, cardiac index, arterial pH, and urine output on the day of operation was compared with that of indirect measurement of stomach wall pH in 85 patients. We found that acidosis in the stomach wall was the most sensitive predictor for complications. The specificity of this predictive test increased exponentially as the duration and degree of intramural acidosis increased. Hypotension, acidosis, and oliguria, but not cardiac index, also predicted postsurgical problems. Stepwise logistic regression analysis of the data that showed postoperative complications were best predicted by the duration of hypotension, and the predictive ability was significantly improved when the duration of intramural acidosis was included.

Back-diffusion of CO2 and its influence on the intramural pH in gastric mucosa

We have examined the back-diffusion of CO2 generated by buffering HCI with NaHCO, in the stomach, observed its influence on the pH in the wall of the gastric mucosa, and compared its effects with those of HCl. Isolated stomachs of 17 anesthetized dogs were exposed to either ( I ) 250 ml NaCl at pH 7, or (2) 125 ml HCl (12.5 meq) + 125 ml NaHCO, (12.5 meq) to generate 12.5 meq CO2 in the stomach, or (3) 250 ml HCI alone to give either 12.5 or 35 meq HCl in the stomach. Samples of gastric fluid and arterial blood were collected every 20 min for 6 hr and analyzed for pH and pC02. The intramural pH of the gastric wall was measured by hollow viscus tonometry. The pC02 in gastric juice rose to 1184 + 139 mm Hg upon the generation of CO2 in the stomach. The till of the CO2 generated by the buffering of acid was 32 + 4 min and of the pC02 was 18.7 f 0.7 min. The till of an equimolar amount of HCI was 2 hr 42 min f 40 min. The disappearance of the CO, was accompanied by a rise in intragastric pH from 6.0 f 0.01 to 6.8 + 0.09 (P < 0.05). and by a fall in intramural pH in the gastric wall from control values of 7.31 + 0.05 to 6.3 f 0.8 (P .Z 0.001). In contrast the pH in gastric fluid did not change and the pH in the intramural fluid did not fall below control values following the administration of 12.5 or 35 meq HCI alone.

Goals for the resuscitation of shock.

ObjectiveTo remind practitioners of the conventional goals of resuscitation of overt hypotensive or uncompensated shock (“ABC,” for airway, breathing, and circulation) and to introduce additional goals, represented by successive letters of the alphabet, to aid clinicians in recognizing the persistence of compensated shock in the splanchnic organs and in achieving more complete resuscitation by eliminating inadequate tissue perfusion in these organs. Data SourcesReview and analysis of current medical literature on shock and organ failure, combined with the authors prior research and expertise in the areas of tissue oxygenation and tonometric monitoring in the critically ill. ConclusionsIn traumatic and septic shock, multiple system organ failure is associated with a persistent state of compensated shock in which hypotension and oliguria are corrected, but in which inadequate perfusion persists in the splanchnic organs and especially in the mucosal lining of the gut. The additional goals recommended include “D” for increasing the delivery of oxygen to levels that meet the metabolic demand by all tissues in the body, especially those tissues within the splanchnic circulation, and “E” for ensuring extraction and utilization of oxygen by the tissues. Future needs for goals that address reperfusion injury, translocation of bacterial toxins, and the release of toxic mediators are also considered. (Crit Care Med 1993; 21:S25-S31)

Associations between intramucosal acidosis in the gut and organ failure

ObjectiveTo alert health professionals to the need for early detection and prevention of shock in critically ill patients. By describing the associations between intramucosal acidosis in the gut and multiple system organ failure, the author demonstrates how noninvasive measurement of gut intramucosal pH can be used to monitor the adequacy of tissue oxygenation in the splanchnic organs and predict splanchnic ischemia within minutes of its onset. Data SourcesReview and analysis of current medical literature on shock and organ failure, combined with the authors prior research and expertise in the areas of tissue oxygenation and tonometric monitoring in the critically ill. ConclusionsThe presence of defective tissue oxygenation in splanchnic organs and in gut ischemia may be detected within minutes of its occurrence via measurements of intramucosal pH in the gut. Measurement of intramucosal pH, obtained noninvasively with an intraluminally located gastrointestinal tonometer, provides an absolute metabolic measure of the adequacy of mucosal oxygenation. The putative consequences of intramucosal acidosis and associated mucosal injury include nosocomial pneumonia, myocardial depression, sepsis from enteric organisms, multiple system organ failure, and death. Through the use of routine monitoring of the adequacy of gut mucosal oxygenation, ischemic mucosal injury and its putative consequences can be prevented, resulting in reduced frequency of multiple organ failure and improved outcome. (Crit Care Med 1993; 21:S103-S107)

Transient episodes of sigmoid ischemia and their relation to infection from intestinal organisms after abdominal aortic operations

We examined the possibility that disruption of the mucosal barrier confining bacteria to the lumen of the colon, which occurs during the transient episodes of sigmoid ischemia after abdominal aortic operations, might be causally related to the appearance of infections from intestinal organisms. Six (18%) of 33 patients after elective operations developed transient sigmoid ischemia identified by the development of acidosis in the sigmoid colon wall on the day of operation and the appearance of guaiac-positive liquid stool a few days after the surgery. Three patients developed infections from intestinal organisms, all of whom had an antecedent episode of sigmoid ischemia (p < .004, Fishers exact test). The degree of acidosis in the wall of the sigmoid colon on the day of surgery was greater (p < .004) and the duration longer (p < .004) in these patients than in the others. The duration of sigmoid ischemia was the best predictor of infection (p < .0001). These data are consistent with the hypothesis in question.

Nosocomial pneumonia in the critically ill: product of aspiration or translocation?

ObjectiveTo examine the possibility that nosocomial pneumonias might be caused by the translocation of enteric bacteria and their toxins. DesignProspectively collected previous database was examined by logistic regression analysis. SettingUniversity medical center. PatientsSixty-two ICU patients. Measurements and Main ResultsThe best stand-alone predictors for nosocomial pneumonia were bleeding from stress ulceration (p < .001), the severity of illness present (p < .001), and intramucosal acidosis in the stomach (p = .023), a metabolic indication of mucosal ischemia. Mechanical ventilation (p = .038) and the administration of antacids/cimetidine (p = .054) were also of stand-alone predictive value, but did not significantly improve the best predictive model for nosocomial pneumonia derived from the severity of illness present and the intramucosal pH in the stomach. ConclusionsThe findings are consistent with the hypothesis that ischemic mucosal injury and its associated translocation of enteric bacteria and toxins might be more important in the pathogenesis of nosocomial pneumonia in the critically ill than the aspiration of contaminated nasopharyngeal secretions. (Crit Care Med 1991; 19:763)

Cystic neuroendocrine neoplasms of the pancreas and liver.

Four cases involving cystic endocrine neoplasms of the pancreas and liver are reported. Because of their rich collateral blood supply, islet cell tumors of the pancreas, even if large in size, rarely undergo central or cystic degeneration. However, failure to appreciate that a small percentage of these neoplasms may mimic benign pancreatic pseudocysts by their clinical and radiological appearance can lead to inappropriate surgical therapy. Ultrasound, computerized tomography, and/or angiography are rarely helpful in distinguishing between benign and neoplastic cysts. The definitive diagnosis can be made with assurance only by obtaining a generous biopsy of the cyst wall or any intracystic excrescences for histologic examination. Functional cystic tumors of the pancreas or liver should be excised totally whenever possible, and efforts should be made to remove as much of the tumor mass as possible even when a curative resection cannot be accomplished. Internal drainage may be acceptable as palliation for large, unresectable tumors.

Effect of Luminal Somatostatin on Acid Secretion and Gastrin Release

The mechanisms by which somatostatin inhibits acid secretion when infused into the lumen of the stomach have been examined in 20 healthy subjects. The acid secretory response to distension with 500 ml of neutral water was examined in nine successive 10-min test periods in each subject. Samples of serum and boiled neutral gastric juice were collected and frozen for later immunoassay for gastrin. Somatostatin was added to the distending fluid in a concentration of 600 pg/ml in the middle 3 test periods in 10 test subjects, and placebo added in the same 3 test periods in 10 control subjects. The addition of somatostatin inhibited the rate of acid secretion as compared with placebo alone in the control subjects (p < 0.025) without altering the concentration of immunoreactive gastrin in the serum but reducing the concentration of immunoreactive gastrin in gastric juice (p < 0.02). The data are consistent with the suggestions that the intraluminal administration of somatostatin inhibits antral gastrin release in a paracrinic manner and inhibits acid secretion indirectly by inhibiting lumina gastrin-mediated acid secretory activity.

Release of Human Pancreatic Polypeptide and Gastrin in Response to Intraduodenal Stimuli: A Case Report

A recent clinical case afforded an opportunity to study the effects of duodenal stimulation on plasma human pancreatic polypeptide and gastrin concentrations, independent of gastric stimulation. A distension stimulus was provided by rapid injection of 100 ml of water and saline via a T-tube into an isolated duodenal afferent limb. In a third experiment, the saline contained 200 pg/ml of heptadecapeptide human gastrin. Within 2 min after each injection, a rapid rise in circulating human pancreatic polypeptide levels appeared that fell promptly towards basal thereafter. Injections of 100 ml of Flexical, a supplemental tube feeding, resulted in a biphasic human pancreatic polypeptide response, the initial peak comparable to that seen following distension with water, saline, or saline containing gastrin, and a second peak of much greater magnitude and duration followed the initial peak. Plasma gastrin concentrations were not influenced following any of the stimuli. Duodenal distension alone may induce an early transient increase in plasma human pancreatic polypeptide concentrations, while intraduodenal nutrients per se may induce a later increment of greater magnitude and duration.

The effect of pyloromyotomy on serum and luminal gastrin in infants with hypertrophic pyloric stenosis

Previous studies of the pathogenesis of congenital hypertrophic pyloric stenosis (CHPS) have implicated immunoreactive gastrin, although no consistent relationship has been demonstrated. In this study we have examined the effect which pyloromyotomy has on serum and luminal gastrin concentration after a mechanical and protein stimulus. Seventeen infants were examined preoperatively, and 1 week after pyloromyotomy. On each occasion, samples of serum and gastric contents were collected from fasting infants. Sixty cubic centimeters of water was placed into the stomach and further samples collected 20 min later. The water was then aspirated and replaced by 60 cc of 10% peptone broth and a third set of samples collected after 20 min. All samples from each patient were analyzed for immunoreactive gastrin in the same assay. Pyloromyotomy did not alter fasting serum gastrin (119.3 pg 2 11.9 preop vs 164.7 f 29.9 postop) nor did it alter the gastrin response to water. Pyloromyotomy decreased the incremental serum gastrin response to peptone broth (66.6 + 16.9 preop vs 18.9 + 11.7 postop). Luminal gastrin concentration was not significantly affected by pyloromyotomy. When the pre- and postoperative serum gastrin increments for water and peptone were plotted against the fasting gastrin levels, an inverse relationship was apparent which was statistically significant by regression analysis. Seen in this way, intragastric water and peptone have a dual effect on serum gastrin; a rise if the fasting serum gastrin concentration is low; a fall or lesser rise if the fasting serum gastrin concentration is high. The data suggest that the direction and magnitude of serum gastrin response to intragastric water or peptone is set by the fasting level, and is independent of pyloromyotomy.