Haemodynamic and/or tonometric monitoring in cardiac surgery.
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Biomedical subjects
Publications and source records attributed to R G Fiddian-Green.
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OBJECTIVE: To 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 SOURCES: Review and analysis of current medical literature on shock and organ failure, combined with the author's prior research and expertise in the areas of tissue oxygenation and tonometric monitoring in the critically ill. CONCLUSIONS: In 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.
OBJECTIVE: To 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 SOURCES: Review and analysis of current medical literature on shock and organ failure, combined with the author's prior research and expertise in the areas of tissue oxygenation and tonometric monitoring in the critically ill. CONCLUSIONS: The 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.
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OBJECTIVE: To examine the possibility that nosocomial pneumonias might be caused by the translocation of enteric bacteria and their toxins. DESIGN: Prospectively collected previous database was examined by logistic regression analysis. SETTING: University medical center. PATIENTS: Sixty-two ICU patients. MEASUREMENTS AND MAIN RESULTS: The best stand-alone predictors for nosocomial pneumonia were bleeding from stress ulceration (p less than .001), the severity of illness present (p less than .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. CONCLUSIONS: The 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.
Transient episodes of gut mucosal ischemia occur in many patients having cardiac surgery. Ischemic mucosal injury increases mucosal permeability and promotes the translocation of bacterial toxins and bacteria and, hence, the release of mediators. Collectively these substances are the putative cause of LOS, nosocomial infections, and MSOF. Circumstantial evidence suggests that the morbidity and mortality from cardiac surgery might be greatly reduced by preventing or limiting in duration the episodes of gut mucosal ischemia. This objective is unlikely to be reliably achieved in clinical practice without monitoring the adequacy of gut mucosal oxygenation. The adequacy of gut mucosal oxygenation can be conveniently monitored in the stomach with a Tonomitor incorporated into a nasogastric tube, because changes induced in this organ by disturbances in DO2 reflect changes occurring in other parts of the gut. Preventative measures currently possible in routine clinical practice include maintaining an intramucosal pH at normal levels by optimizing DO2, preventing the release of splanchnic vasoconstrictors and the formation of cellular aggregates by the use of pulsatile perfusion during bypass, and minimizing oxygen requirements with cooling and muscle relaxation. The translocation of bacterial toxins and bacteria across injured mucosa may be minimized by gut lavage before surgery. Therapeutic measures for gut mucosal ischemia currently possible in routine clinical practice include, in addition to the preventative measures outlined above, the prevention of free radical-induced mucosal injury during resuscitation, parenteral antibiotics, the treatment of sepsis, and the resection of infarcted gut.
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We tested the hypothesis that lipopolysaccharide (LPS) leads to an imbalance between mesenteric oxygen delivery (DO2) and gut metabolic demand for oxygen, even when cardiac index (CI) is within the normal range. Two groups of pentobarbital-anesthetized pigs (13 to 17 kg) were studied. The first group (LPS; n = 9) was infused over 20 min with Escherichia coli LPS (100 micrograms/kg) and resuscitated with normal saline (1.2 ml/kg.min). The second group (NS; n = 5) was not infused with LPS, but was resuscitated in the same way as the LPS group. Superior mesenteric arterial (SMA) blood flow and ileal intramucosal hydrogen ion concentration, [H+], were determined using a Doppler-shift probe and a tonometric catheter, respectively. Infusing LPS did not affect CI, although mean arterial pressure and systemic vascular resistance were significantly reduced. SMA flow and mesenteric DO2 decreased significantly in the LPS group. Although mesenteric oxygen utilization was well preserved in both groups, ileal intramucosal [H+] was significantly higher in endotoxic animals. These data support the idea that mesenteric oxygen consumption is flow-limited in this clinically relevant porcine model of septic shock.
Strictures of the Intrahepatic ducts, centrally located hepatic tumors, and intrahepatic stones present difficult management problems. The median hepatotomy can be easily and safely performed with the aid of an ultrasonic liver dissector and a knowledge of hepatic anatomy. The approach allows the confluence of the right and left hepatic ducts and primary and secondary bifurcations thereof to be exposed precisely without dissecting the porta or compromising the blood supply to the liver. We employed this technique without mortality and with minimal morbidity in eight patients, of whom two had Klatskin's tumors, one had an iatrogenic stricture of the right hepatic duct, one had sclerosing cholangitis, one had Intrahepatic gallstones, and three had centrally located tumors. The technique is recommended as an aid in the management of complex hepatobiliary problems.
The development of a safe and simple tonometric method of monitoring the adequacy of gastrointestinal mucosal perfusion has provided a new perspective of splanchnic ischaemia in the critically ill. It would appear that splanchnic hypoxia, identified by the presence of intramucosal acidosis in the gut, may be one of the most consistent and earliest indications of impaired tissue perfusion in the critically ill and be causally related to the development of sepsis and multiple organ failure.
We compared intramural pH (pHI) measured through a silicone balloon placed in the lumen of the sigmoid colon with risk factor analysis and inferior mesenteric artery (IMA) stump pressures as predictors of ischemic colitis in 34 patients undergoing elective or emergency operations on the abdominal aorta. All patients had preoperative and postoperative flexible sigmoidoscopy, IMA stump pressure measurements, and serial measurements of pHI. Logistic regression analysis showed that aortic aneurysm, age, and stenosis of the superior mesenteric artery were the only risk factors that bore a statistical relationship to ischemic colitis. Ligation of a patent IMA did not increase the likelihood of ischemic colitis. The IMA stump pressure criteria for predicting ischemic colitis were absent in nine of the ten patients in whom ischemic colitis developed and were present in five of the 24 in whom it did not develop. Intraoperative pHI dropped below 6.86 in all three patients in whom severe ischemic colitis developed. Mild colitis developed in seven patients whose minimum pH was 6.99 +/- 0.12 (mean +/- SD). No colitis developed in the remaining 24, whose minimum pH was 7.21 +/- 0.13. Thus, stump pressure is not a reliable means of predicting ischemic colitis. Aortic aneurysm, age, and superior mesenteric artery stenosis were significant risk factors. The average minimum intraoperative pHI and its duration were the best predictors for the development of ischemic colitis.
Endogenously synthesized prostaglandins are potential mediators of gastrointestinal mucosal protection. Some data suggest that gastric ulceration caused by stressful stimuli is due to diminished mucosal synthesis of prostaglandins. To examine this hypothesis, we determined the effect of hemorrhage, an ulcerogenic stimulus, on ex vivo production of immunoreactive prostaglandin E2 by gastric tissue in the rat. Macroscopic gastric ulcers were reproducibly observed in Sprague-Dawley rats subjected to hemorrhage (3 ml/100 g body weight). The number of ulcers was linearly related to the duration of shock. Prostaglandin E2 synthesis was significantly increased during in vitro incubation of oxyntic and nonoxyntic stomach tissue excised from rats subjected to hemorrhage for 30 minutes (p less than 0.05). These results indicate that damage to the gastric mucosa in rats subjected to hemorrhage occurs despite augmented endogenous secretion of prostaglandin E2. Mechanisms other than impaired prostaglandin biosynthesis were probably responsible for mucosal injury in this model.