A literature review of recent advances in enteral feeding and the increased understanding of the gut A. Howood
literature review focuses on recent advances in enteral feeding and increased understanding of the role of the gut. The gut is beginning to be seen as a reservoir for bacteria and a source which contributes to multi-organ failure (MOF) due to translocation of bacteria, in addition to its usual functions. Enteral feeding as discussed in this article is a method of feeding which frequently involves nurses at the bedside, yet so many seem unfamiliar with recent research on the topic. A simple change to intermittent enteral feeding could be more beneficial for patients than continuous feeding. Indeed, continuous feeding may even be harmful, and as Florence Nightingale stated in her book Notes on Ho$ituls in 1858, hospitals should do no harm to patients. This
INTRODUCTION
CASE STUDIES
The aim of this literature review is to look at current research into enteral feeding and gut stability. A vast amount of research has been undertaken in this area over the last few years, but many practitioners seem unaware of the findings that have repeatedly been shown. The gut is now thought to play a major role in the progression of patients into MOF or sepsis due to translocation of bacteria and the chain reaction this can result in. It is not intended in this paper to discuss the release of endotoxins and chemical mediators.
Jacobs et al (1990) completed a study of 24 patients who were all continuously enterally fed, specifically looking at the effect of their gastric pH on determining bacterial colonisation. He noted that the cause of pneumonia in patients in intensive therapy units (ITUs) can be hand contamination through bad practice or adhesion of bacteria to an endotracheal tube (ET) which is dislodged during suction. Colonisation of bacteria could also be due to the use of antacids as they decrease the acidity of the stomach and allow the overgrowth of bacteria. In this study no antacids were given to the 24 patients. The study was small but significant in its findings that the patients were divided into two groups depending on gastric pH. Group A had intermittent pH > 3.5 and group B had intermittent pH < 3.5. All but one patient in group A (12
A. Horwood Staff Nurse ITU, St Hsliars Hospital, Wryth Lane, Carshelton, Surrey (Requests for offprints to AH) Manuscript
accepted 7 May 1992
186
INTENSlVEANDCRITICALCARENURSlNG
patients) developed pneumonia, while in group B (12 patients) only one patient developed though there was no statistical pneumonia, difference between the mortality in group A and group B patients. It was hypothesised that the drop in pH experienced by the patients in group B killed bacteria which had been allowed to grow during the previous hours. Others have identifed that the ‘translocation of bacteria from the lumen of the stomach to the trachea via the oropharynx is a major cause of pneumonia among ventilated ITU patients’ (Lee et al, 1990). The study by Lee et al (1990) of 50 patients also showed a dramatic reduction in the incidence of pneumonia with intermittent feeding which results in a drop of pH when feeding stops, This took the hypothesis one step further as the drop in pH seemed to be what killed the bacteria and prevented the development of In the continuously fed group pneumonia. 13124 patients developed pneumonia whilst only 3/26 of those fed intermittently developed pneumonia. There was no significant difference between the Apache II scores (Knaus et al, 1985) and associated risk of death of the two groups, but the mortality of the intermittently fed group was less. The time they spent in the ITU was also less, due to the lack of complications such as pneumonia: ‘The reduction of gastric acidity by antacids and H receptor antagonists as prophylaxis against stress ulceration has been shown to promote pneumonia among ventilated ITU patients so none was given in this study’ (Lee et al, 1990). There were no instances of bleeding or ulceration in these patients. Nobody is totally sure of the mechanism by which enteral feeding prevents stress ulceration, but it certainly appears to work effectively. It has been suggested that ‘receptors in the antrum and/or duodenum may be stimulated by the enteral nutrients and directly initiate neural reflexes protective to the gastric muscosa (Ephgrave, 1990). Ephgrave’s (1990) study on rats noted that antacids and H receptor antagonists which became popular due to their effect in reducing the incidence of bleeding from stress
ulceration also reduced gastric acidity. In so doing they contribute to the incidence of nosocomial pneumonia by allowing overgrowth of gram negative organisms. Perhaps the cause of stress ulceration was never due entirely to gastric pH and with other advances in intensive care many of the precipitating factors have been resolved without recognition of this. A study by Harvey et al (1989) was small containing only 25 patients but there was a strong correlation between the occurrence of organisms in the stomach and their incidence in other sites. The patients were fed 2-hourly enterally so not gaining the possible benefits of intermittent feeding as it was neither well-spaced intermittent nor continuous feeding - which must be a design weakness in the study. Nevertheless a staggering number and amount of organisms were isolated in these 25 patients in which ‘the first positive bacterial culture occurred in all patients within the first 4 days of 1TU admission’ (Garvey et al, 1989). A correlation was found to exist between the occurrence of organisms in the stomach and occurrence elsewhere in the body, particularly the lower respiratory tract. The same type of organisms as those found in the stomach in these 25 patients could be cultured in 44 other different places, and this was not affected by systemic antibiotic therapy that the patients were receiving. It was found that gastric contents of critically ill patients receiving antacid therapy were uniformly colonised with bacteria or fungi with the potential to colonise other sites. These findings suggest that if prophylactic antacids are confined to high risk patients only, this may reduce the infective complications of the majority of patients and therefore improve outcome. The gut is ‘essential as a barrier to enteric flora and prevention of host invasion by microorganisms or soilage by their toxins’ (Wilmore, 1988). It has been suggested that as the enteric flora is destroyed so the gut becomes a source of unlimited bacteria and toxins. ‘Bacterial translocation from the gut is a process whereby indigenous intestinal microflora relocate extralumenally when the gut is not active or well perfused’ (Wilmore, 1988). This has impli-
INTENSlVEANDCRITlCALCARENURSlNG
cations for the long-term use of parenteral nutrition alone, as this method of feeding would encourage bacterial relocation, perhaps even contributing further to MOF in the patients concerned. In critically ill, stressed patients the intestinal barrier may be less than perfect and in those who are not enterally fed to help maintain the normal flora they ‘may continually contaminate themselves by way of a leaky or permeable gastrontestinal tract’ (Wilmore, 1988). It has been suggested that bowel rest produces changes in host resistance to injury unrelated to those associated with malnutrition, which calls into question the rationale for the method of feeding chosen (Fong, 1989). Perhaps it is unwise to induce bowel rest in patients, as occurs when parenteral nutrition is used alone. As enteral feeding maintains the intestinal mucosa and so supports the gut barrier, this could suggest the idea of minimal enteral/jejostomy feeding taking place when possible as well as parenteral nutrition to try and maintain the intestinal mucosa while feeding the patient parenterally. However as yet this area needs more research, as it is unclear if there are any real benefits for patients who are fed this way. The gut is now beginning to be seen as a portal of entry for bacteria possibly causing bacteraemia unless the normal state of gut mucosa can be maintained. In a small study of 20 patients enteral feeding was found to give adequate protection against the stress ulceration syndrome without using antacids (Valentine, 1986). Understanding of the relevance of gastric pH to the prevention of stress ulcers has come a long way in recent years, but the pathogenesis of stress ulceration is multifactorial. There are many factors which work together to cause ulceration such as ‘decreased gastric blood flow, impaired gastroduodenal defence mechanism against acidity and increased luminal acid concentration’ (Rigaud, 1986). Rigaud (1986) investigated 12 patients in ITU respiratory failure, giving half ranitidine whilst the other half were fed enterally and given as placebo. The study is extremely small so it is unwise to draw any firm conclusion from the fact that no conclusive benefit for the giving of
187
ranitidine was demonstrated; but the profile of intragastric pH in patients given ranitidine was very little modified as compared with patients who were just enterally fed (Rigaud, 1986). The study needs to be repeated using a larger number of patients before the use of ranitidine for selected high risk patients is stopped. However, it has been reported elsewhere that the ‘treatment of seriously ill patients with antacids or cimetidine may encourage airway colonisation and predispose the patient to pneumonia’ caused by gram negative bacilli (Moulin et al 1982). Moulin et al (1982) studied 60 ITU patients of whom 48 received standard antacids, 3 received cimetidine while 9 received both: ‘In 8 patients there was no evidence that any organism was present in both stomach and upper airway during any 24h period, but in the other 52 patients at least one organism was cultured simultaneously form both tracheal and gastric aspirate’ (Moulin, 1982). It was shown in the Moulin et al 1982 study that the maintenance of a high ‘gastric pH appeared to lead to increasing populations of gram negative bacilli’. Pneumonia developed in over half of the 60 patients, due to bacteria that had previously been isolated. The incidence of pneumonia within 31 patients meant these patients stayed in the unit for longer. Prophylactic use of antacids and H receptor antagonists may no longer be justified routinely for every patient who comes into an ITU as according to the papers cited here, they raise the pH of the stomach and allow bacteria to colonise the gut.
DISCUSSION Feeding the patient enterally for 16 h and resting for 8 h seems to be the best policy. The gastric pH would have time to drop below 3.5 during the rest period and this would allow the gastricjuices to kill any bacteria in the stomach. It is also a good idea to return any gastric aspirate when giving enteral feeding, up to 500m1, and reduce the feed down to 30ml an hour preferably when there is much gastric aspirate. This would give
188
INTENSIVE AND CRITICAL CARE NURSING
patients the benefit of retaining ted food, allowing them more Switching the feed off totally mean that the patient would not of either effective continuous feeding.
partially digestime to digest it. would probably gain the benefits or intermittent
CONCLUSION More research is needed into the role of gastrointestinal hormones and the natural protection thev, seem to aive the eastrointenstinal tract when stimulated during enteral feeding, as this seems to be the way forward in the prevention and treatment of stress ulcers. More research is needed to investigate the more recently identified role the gut may be seen to have in allowing translocation of bacteria to occur, as this is poorly understood, and may provide the answer to many questions. ”
References Alverdy J et al 1988 Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 104: 185-190 Ephg% K S et al 1990 Enteral nutrients prevent stress ulceration and increase intragastric volume. Critical Care Medicine 1990 18 (6): 621-624 Fong Y et al 1989 TPN and bowel rest modify the metabolic response to endotoxin in humans. Annals of Surgery 1989 210 (4): 449-457 Garvev B M et al 1989 Effects of gastric alkalization on bacierial colonization in criticali; ill patients. Critical Care Medicine 17 (3): 21 I-216 Jacobs S, Rene W, Chang S, Lee B, Bartlett F W 1990 Continuous enteral feeding : a major cause of
pneumonia among ventilated intensive care unit patients. Journal of Parenteral and Enteral Nutrition. 14 (4): 353-356 Knaus W A, Draper E A, Wagner D P, Zimmerman J E 1985 APACHE II: a severity of disease classification system. Critical Care Medicine 13 (10): 818-827 Lee B, Chang R W S, Jacobs S 1990 Intermittent nasogastric feeding: a simple and effective method to reduce pneumonia among ventilated ICU patients. Clinical Intensive Care: 100-102 Moulin G et al 1982 Aspiration of gastric bacteria in antacid - treated patients: a frequent cause of postoperative colonisation of the airway. The Lancet (Jan): 242-245 Nightingale F 1859 Notes on hospitals. Parker and Son In Woodham-Smith C 1950 Florence Nightingale. Constable, London p 333 Rigaud D et al 1986 Intragastric pH profile during acute respiratory failure in patients with chronic obstructive pulmonary disease. Chest 90: 58-63 Valentine J et-al 1986 Dbes nasoenteral feeding afford adequate gastroduodenal stress prophylaxis?Critical Care Medicine 14 (7): 599-601 Wilmore D et al 1988 The gut: a central organ after surgical stress. Surgery 154: 917-923 -
Further reading Bower R et al 1986 Postoperative enteral ves parenteral nutrition. Archives of Surgery 121 (Sept): 1040-1045 Brinson R, Pitts M 1989 Enteral nutrition in the critically ill patients: role of hypalbuminemia. Critical Care Medicine 17 (4): 367-370 Creagh T 1988 Nasogastric warnings. Nursing Times 84 (7): 46-47 Deitch E 1988 Hemorrhagic shock - induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation. Surgery 104 (2): 191-198 Deitch E et al 1987 Endotoxin oromotes the translocation of bacteria from the gut. Archives Surgery 122: 185-l 90 Deitch E et al 1987 The gut as a portal of entry for bacteremia. Annals Surgery 205: 68 l-69 I Gaffany I 1988 Knotted tubes. Nursing Times 84 (7): 48
literature review focuses on recent advances in enteral feeding and increased understanding of the role of the gut. The gut is beginning to be seen as a reservoir for bacteria and a source which contributes to multi-organ failure (MOF) due to translocation of bacteria, in addition to its usual functions. Enteral feeding as discussed in this article is a method of feeding which frequently involves nurses at the bedside, yet so many seem unfamiliar with recent research on the topic. A simple change to intermittent enteral feeding could be more beneficial for patients than continuous feeding. Indeed, continuous feeding may even be harmful, and as Florence Nightingale stated in her book Notes on Ho$ituls in 1858, hospitals should do no harm to patients. This
INTRODUCTION
CASE STUDIES
The aim of this literature review is to look at current research into enteral feeding and gut stability. A vast amount of research has been undertaken in this area over the last few years, but many practitioners seem unaware of the findings that have repeatedly been shown. The gut is now thought to play a major role in the progression of patients into MOF or sepsis due to translocation of bacteria and the chain reaction this can result in. It is not intended in this paper to discuss the release of endotoxins and chemical mediators.
Jacobs et al (1990) completed a study of 24 patients who were all continuously enterally fed, specifically looking at the effect of their gastric pH on determining bacterial colonisation. He noted that the cause of pneumonia in patients in intensive therapy units (ITUs) can be hand contamination through bad practice or adhesion of bacteria to an endotracheal tube (ET) which is dislodged during suction. Colonisation of bacteria could also be due to the use of antacids as they decrease the acidity of the stomach and allow the overgrowth of bacteria. In this study no antacids were given to the 24 patients. The study was small but significant in its findings that the patients were divided into two groups depending on gastric pH. Group A had intermittent pH > 3.5 and group B had intermittent pH < 3.5. All but one patient in group A (12
A. Horwood Staff Nurse ITU, St Hsliars Hospital, Wryth Lane, Carshelton, Surrey (Requests for offprints to AH) Manuscript
accepted 7 May 1992
186
INTENSlVEANDCRITICALCARENURSlNG
patients) developed pneumonia, while in group B (12 patients) only one patient developed though there was no statistical pneumonia, difference between the mortality in group A and group B patients. It was hypothesised that the drop in pH experienced by the patients in group B killed bacteria which had been allowed to grow during the previous hours. Others have identifed that the ‘translocation of bacteria from the lumen of the stomach to the trachea via the oropharynx is a major cause of pneumonia among ventilated ITU patients’ (Lee et al, 1990). The study by Lee et al (1990) of 50 patients also showed a dramatic reduction in the incidence of pneumonia with intermittent feeding which results in a drop of pH when feeding stops, This took the hypothesis one step further as the drop in pH seemed to be what killed the bacteria and prevented the development of In the continuously fed group pneumonia. 13124 patients developed pneumonia whilst only 3/26 of those fed intermittently developed pneumonia. There was no significant difference between the Apache II scores (Knaus et al, 1985) and associated risk of death of the two groups, but the mortality of the intermittently fed group was less. The time they spent in the ITU was also less, due to the lack of complications such as pneumonia: ‘The reduction of gastric acidity by antacids and H receptor antagonists as prophylaxis against stress ulceration has been shown to promote pneumonia among ventilated ITU patients so none was given in this study’ (Lee et al, 1990). There were no instances of bleeding or ulceration in these patients. Nobody is totally sure of the mechanism by which enteral feeding prevents stress ulceration, but it certainly appears to work effectively. It has been suggested that ‘receptors in the antrum and/or duodenum may be stimulated by the enteral nutrients and directly initiate neural reflexes protective to the gastric muscosa (Ephgrave, 1990). Ephgrave’s (1990) study on rats noted that antacids and H receptor antagonists which became popular due to their effect in reducing the incidence of bleeding from stress
ulceration also reduced gastric acidity. In so doing they contribute to the incidence of nosocomial pneumonia by allowing overgrowth of gram negative organisms. Perhaps the cause of stress ulceration was never due entirely to gastric pH and with other advances in intensive care many of the precipitating factors have been resolved without recognition of this. A study by Harvey et al (1989) was small containing only 25 patients but there was a strong correlation between the occurrence of organisms in the stomach and their incidence in other sites. The patients were fed 2-hourly enterally so not gaining the possible benefits of intermittent feeding as it was neither well-spaced intermittent nor continuous feeding - which must be a design weakness in the study. Nevertheless a staggering number and amount of organisms were isolated in these 25 patients in which ‘the first positive bacterial culture occurred in all patients within the first 4 days of 1TU admission’ (Garvey et al, 1989). A correlation was found to exist between the occurrence of organisms in the stomach and occurrence elsewhere in the body, particularly the lower respiratory tract. The same type of organisms as those found in the stomach in these 25 patients could be cultured in 44 other different places, and this was not affected by systemic antibiotic therapy that the patients were receiving. It was found that gastric contents of critically ill patients receiving antacid therapy were uniformly colonised with bacteria or fungi with the potential to colonise other sites. These findings suggest that if prophylactic antacids are confined to high risk patients only, this may reduce the infective complications of the majority of patients and therefore improve outcome. The gut is ‘essential as a barrier to enteric flora and prevention of host invasion by microorganisms or soilage by their toxins’ (Wilmore, 1988). It has been suggested that as the enteric flora is destroyed so the gut becomes a source of unlimited bacteria and toxins. ‘Bacterial translocation from the gut is a process whereby indigenous intestinal microflora relocate extralumenally when the gut is not active or well perfused’ (Wilmore, 1988). This has impli-
INTENSlVEANDCRITlCALCARENURSlNG
cations for the long-term use of parenteral nutrition alone, as this method of feeding would encourage bacterial relocation, perhaps even contributing further to MOF in the patients concerned. In critically ill, stressed patients the intestinal barrier may be less than perfect and in those who are not enterally fed to help maintain the normal flora they ‘may continually contaminate themselves by way of a leaky or permeable gastrontestinal tract’ (Wilmore, 1988). It has been suggested that bowel rest produces changes in host resistance to injury unrelated to those associated with malnutrition, which calls into question the rationale for the method of feeding chosen (Fong, 1989). Perhaps it is unwise to induce bowel rest in patients, as occurs when parenteral nutrition is used alone. As enteral feeding maintains the intestinal mucosa and so supports the gut barrier, this could suggest the idea of minimal enteral/jejostomy feeding taking place when possible as well as parenteral nutrition to try and maintain the intestinal mucosa while feeding the patient parenterally. However as yet this area needs more research, as it is unclear if there are any real benefits for patients who are fed this way. The gut is now beginning to be seen as a portal of entry for bacteria possibly causing bacteraemia unless the normal state of gut mucosa can be maintained. In a small study of 20 patients enteral feeding was found to give adequate protection against the stress ulceration syndrome without using antacids (Valentine, 1986). Understanding of the relevance of gastric pH to the prevention of stress ulcers has come a long way in recent years, but the pathogenesis of stress ulceration is multifactorial. There are many factors which work together to cause ulceration such as ‘decreased gastric blood flow, impaired gastroduodenal defence mechanism against acidity and increased luminal acid concentration’ (Rigaud, 1986). Rigaud (1986) investigated 12 patients in ITU respiratory failure, giving half ranitidine whilst the other half were fed enterally and given as placebo. The study is extremely small so it is unwise to draw any firm conclusion from the fact that no conclusive benefit for the giving of
187
ranitidine was demonstrated; but the profile of intragastric pH in patients given ranitidine was very little modified as compared with patients who were just enterally fed (Rigaud, 1986). The study needs to be repeated using a larger number of patients before the use of ranitidine for selected high risk patients is stopped. However, it has been reported elsewhere that the ‘treatment of seriously ill patients with antacids or cimetidine may encourage airway colonisation and predispose the patient to pneumonia’ caused by gram negative bacilli (Moulin et al 1982). Moulin et al (1982) studied 60 ITU patients of whom 48 received standard antacids, 3 received cimetidine while 9 received both: ‘In 8 patients there was no evidence that any organism was present in both stomach and upper airway during any 24h period, but in the other 52 patients at least one organism was cultured simultaneously form both tracheal and gastric aspirate’ (Moulin, 1982). It was shown in the Moulin et al 1982 study that the maintenance of a high ‘gastric pH appeared to lead to increasing populations of gram negative bacilli’. Pneumonia developed in over half of the 60 patients, due to bacteria that had previously been isolated. The incidence of pneumonia within 31 patients meant these patients stayed in the unit for longer. Prophylactic use of antacids and H receptor antagonists may no longer be justified routinely for every patient who comes into an ITU as according to the papers cited here, they raise the pH of the stomach and allow bacteria to colonise the gut.
DISCUSSION Feeding the patient enterally for 16 h and resting for 8 h seems to be the best policy. The gastric pH would have time to drop below 3.5 during the rest period and this would allow the gastricjuices to kill any bacteria in the stomach. It is also a good idea to return any gastric aspirate when giving enteral feeding, up to 500m1, and reduce the feed down to 30ml an hour preferably when there is much gastric aspirate. This would give
188
INTENSIVE AND CRITICAL CARE NURSING
patients the benefit of retaining ted food, allowing them more Switching the feed off totally mean that the patient would not of either effective continuous feeding.
partially digestime to digest it. would probably gain the benefits or intermittent
CONCLUSION More research is needed into the role of gastrointestinal hormones and the natural protection thev, seem to aive the eastrointenstinal tract when stimulated during enteral feeding, as this seems to be the way forward in the prevention and treatment of stress ulcers. More research is needed to investigate the more recently identified role the gut may be seen to have in allowing translocation of bacteria to occur, as this is poorly understood, and may provide the answer to many questions. ”
References Alverdy J et al 1988 Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 104: 185-190 Ephg% K S et al 1990 Enteral nutrients prevent stress ulceration and increase intragastric volume. Critical Care Medicine 1990 18 (6): 621-624 Fong Y et al 1989 TPN and bowel rest modify the metabolic response to endotoxin in humans. Annals of Surgery 1989 210 (4): 449-457 Garvev B M et al 1989 Effects of gastric alkalization on bacierial colonization in criticali; ill patients. Critical Care Medicine 17 (3): 21 I-216 Jacobs S, Rene W, Chang S, Lee B, Bartlett F W 1990 Continuous enteral feeding : a major cause of
pneumonia among ventilated intensive care unit patients. Journal of Parenteral and Enteral Nutrition. 14 (4): 353-356 Knaus W A, Draper E A, Wagner D P, Zimmerman J E 1985 APACHE II: a severity of disease classification system. Critical Care Medicine 13 (10): 818-827 Lee B, Chang R W S, Jacobs S 1990 Intermittent nasogastric feeding: a simple and effective method to reduce pneumonia among ventilated ICU patients. Clinical Intensive Care: 100-102 Moulin G et al 1982 Aspiration of gastric bacteria in antacid - treated patients: a frequent cause of postoperative colonisation of the airway. The Lancet (Jan): 242-245 Nightingale F 1859 Notes on hospitals. Parker and Son In Woodham-Smith C 1950 Florence Nightingale. Constable, London p 333 Rigaud D et al 1986 Intragastric pH profile during acute respiratory failure in patients with chronic obstructive pulmonary disease. Chest 90: 58-63 Valentine J et-al 1986 Dbes nasoenteral feeding afford adequate gastroduodenal stress prophylaxis?Critical Care Medicine 14 (7): 599-601 Wilmore D et al 1988 The gut: a central organ after surgical stress. Surgery 154: 917-923 -
Further reading Bower R et al 1986 Postoperative enteral ves parenteral nutrition. Archives of Surgery 121 (Sept): 1040-1045 Brinson R, Pitts M 1989 Enteral nutrition in the critically ill patients: role of hypalbuminemia. Critical Care Medicine 17 (4): 367-370 Creagh T 1988 Nasogastric warnings. Nursing Times 84 (7): 46-47 Deitch E 1988 Hemorrhagic shock - induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation. Surgery 104 (2): 191-198 Deitch E et al 1987 Endotoxin oromotes the translocation of bacteria from the gut. Archives Surgery 122: 185-l 90 Deitch E et al 1987 The gut as a portal of entry for bacteremia. Annals Surgery 205: 68 l-69 I Gaffany I 1988 Knotted tubes. Nursing Times 84 (7): 48
