ABC of colorectal diseases. Intestinal stomas.
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Biomedical subjects
Publications and source records attributed to M H Irving.
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We have studied gut hormone profiles in a small number of patients on treatment with home parenteral nutrition following near-total enterectomy who had no evidence of inflammatory bowel disease and who were otherwise healthy. These and age- and sex-matched controls had gut hormone profiles measured after an overnight fast and a standard test meal. Circulating pancreatic glucagon concentrations and profiles were the same in both groups as were the neurotensin and VIP. Peptide YY (PYY) concentrations and profiles were markedly raised in the short bowel group. It is suggested that the normal glucagon responses reflect the integrity of the remaining duodenum and pancreas. Circulating neurotensin and VIP originate largely from outside the bowel and so the removal of the gut source does not significantly affect their profiles. Enteroglucagon and PYY are secreted from terminal ileum and colon in response to unabsorbed food residues. The elevated circulating levels and profiles are consistent with those observed by others in patients with jejunoileal bypass or major resections in whom unabsorbed nutrients reach the colon.
Metabolic effects of a commercially available amino acid infusate were investigated in five preoperative patients with abdominal sepsis and five healthy subjects. Oxygen consumption (VO2) was measured continuously during the 3-h study, and blood samples were taken regularly for hormone and metabolite analyses. During 1 h of preinfusion measurements, VO2 was 15% higher (P less than 0.05) in the septic patients. Preinfusion plasma cortisol, glucagon, and catecholamines were also significantly elevated in the septic group. The amino acid solution (9 g nitrogen; 950 kJ; 227 kcal) was infused into each subject through their central venous catheter during the 2nd and 3rd h of the study. VO2 increased similarly in both groups by approximately 21% during the infusion (P less than 0.05), whereas respiratory quotient increased significantly in only the controls (P less than 0.05). Plasma insulin and glucagon concentrations rose significantly in both groups during the infusion, despite little change in glucose levels. Plasma norepinephrine increased in both groups, although the response was significant in only the control subjects. In summary, the amino acid infusate stimulated metabolic rate similarly in the septic and nonseptic subjects.
Intestinal failure can be the end result of a wide variety of disease processes that impair the ability of the gut to adequately digest and absorb food. Patients with established intestinal failure may require parenteral nutrition support and/or abdominal surgery to reverse the disease process involved. Selected patients with irreversible intestinal failure can be managed in experienced units by home parenteral nutrition.
300 consecutive admissions over 7 years to a purpose-built intestinal failure unit are reviewed. The commonest underlying condition was Crohn's disease (42%), and the commonest complication precipitating admission was intestinal fistula (42%). Total parenteral nutrition was used in 85% and surgery in 50%. A multidisciplinary approach to management gave a high success rate--90% of patients were discharged from hospital, although nearly 25% needed home parental nutrition. These results suggest that chronic intestinal failure should be managed in specialised units in the same manner as other types of organ failure.
Cyclic neutropenia, a rare blood disorder, may be complicated by spontaneous necrosis of the cecum and ascending colon. We describe one such case, where a staged surgical approach achieved a successful outcome. The importance of recognition of this disorder is stressed, since this allows both performance of appropriate surgery and consultation with hematologic colleagues.
This investigation compared the metabolic effects of lipid infusion in five septic and five nonseptic patients. Oxygen consumption was determined by indirect calorimetry over 1 h of rest and during 2 h when Intralipid (20%) was infused [166 mL/h; 23 kJ/min (5.5 kcal/min)]. Septic patients had a resting metabolic rate 17% higher than that of their nonseptic control subjects and a significant (P less than 0.05) rise (13%) in oxygen uptake was measured in both groups of subjects during the 2-h infusion of lipid. Preinfusion respiratory quotient (RQ) was 7% higher in the septic patients (P less than 0.05), and during the infusion period RQ decreased similarly (approximately 6%; P less than 0.05) in both groups. Plasma catecholamines were elevated in the septic patients preinfusion and the concentrations remained unaltered during the infusion. Norepinephrine rose significantly in the nonseptic group with the lipid infusion. The results show that sepsis has little or no influence on the characteristic rise in metabolic rate that occurs with intravenous lipid.
During treatment of the injured patient it is assumed that the cardiovascular responses follow recognized physiological principles. Studies in humans have shown that injury causes a profound suppression of arterial baroreflex function which alters the normal relationship between heart rate and blood pressure and casts doubt on this assumption. To investigate the mechanism of baroreflex suppression, we have studied the effects of the two major components of injury, blood loss and tissue damage, on baroreflex function in healthy volunteers. Baroreflex function was assessed using suction stimulation of the carotid sinus. The loss of 500 ml blood had no effect on baroreflex sensitivity. A human laboratory model of tissue injury reduced the ability of the baroreflex to compensate for a rise in blood pressure (P less than 0.05, Wilcoxon signed rank test). We conclude that tissue damage, rather than hypovolaemia, appears to mediate the effect of injury on baroreflex function in the injured. Blockade of neural signals from damaged tissue may have a role in the treatment of injury.
The collagen content of resected strictured intestine, with and without fistulas, from patients with Crohn's disease has been compared with that in macroscopically normal intestine removed from the same patients and from others without inflammatory bowel disease. Collagen content per unit wet or dry weight of tissue was significantly increased in all grossly diseased tissue whether fistulated or not. Although there was a significant increase in collagen types I, III, and V in diseased tissue, the relative proportions of major collagen types extracted by limited pepsin digestion were similar for both Crohn's and non-Crohn's intestine (type I, 65 to 70 percent; type III, 25 to 30 percent; type IV, 2 to 3 percent; and type V, 2.5 to 3 percent). CNBr digestion of pepsin insoluble material showed a similar relative abundance of types I and III, indicating no major change in collagen type distribution between older (insoluble) and more newly synthesized collagen. There was no evidence of the presence of type I trimer collagen. Type VI collagen, although not quantitated, was observed in 70 percent of intestinal specimens. The proportion of total collagen solubilized by pepsin treatment was significantly greater in both grossly diseased and macroscopically normal Crohn's bowel compared with non-inflammatory bowel disease bowel. These findings suggest that there are disturbances of collagen metabolism in Crohn's intestine, which account for the stricturing process and which may predate gross pathologic changes.
Survival from injury depends on the interaction between the patient's own homeostatic responses and treatment given. The function of the principal homeostatic reflex of the cardiovascular system, the arterial baroreflex, was studied in 22 healthy controls and in 21 moderately injured patients (ISS range, 9 to 17; median, 9) using suction stimulation of the carotid sinus baroreceptors. When compared to controls, marked baroreflex suppression was evident 3 hours after injury (p less than 0.05), at 3 days after injury (p less than 0.001), and even 15 days after injury (p less than 0.05, all Wilcoxon rank sum test). Partial recovery of baroreflex function occurred between 3 and 15 days after injury (p less than 0.005, all Wilcoxon signed rank test) and was complete by 5 months after injury. The suppression of baroreflex activity was accompanied by a "fixed" rise in heart rate and a rise in systolic blood pressure. This study has shown that moderate injury results in a profound and prolonged suppression of baroreflex function. Further advances in the resuscitation and critical care of the injured may need to take account of such derangements of cardiovascular physiology.
The place of somatostatin and its analogues in the management of gastrointestinal fistulae is reviewed, drawing attention to the difficulty of assessing treatments that influence spontaneous closure. Sixteen patients with gastric, small bowel, and pancreatic fistulae were randomized to receive octreotide injections (100 micrograms t.i.d.) or placebo for 12 days. Spontaneous fistula closure occurred in 7 at a mean of 37 days after entering the trial. A second study is underway with greater patient numbers recruited from peripheral hospitals and with an increased period of octreotide medication (21 days).
Total body pool and intestinal absorption of ascorbic acid were studied in 12 patients undergoing operation for Crohn's disease (six with fistulae and six without) and in six control patients undergoing operation for reasons other than Crohn's disease. L-[carboxyl-14C]Ascorbic acid, 0.19-0.40 megabecquerels (MBq), was given orally. After a period of equilibration, the labeled ascorbic acid was flushed out of the patient's body tissues using large doses of unlabeled ascorbic acid. Intestinal absorption of ascorbic acid, assessed from the total cumulative urinary 14C recovery, was found to be similar in patients with fistulizing Crohn's disease (73.9 +/- 8.45%), those without fistulas (72.8 +/- 11.53%), and in controls (80.3 +/- 8.11%). Total body pools of ascorbic acid, calculated using the plasma 14C decay curves, were similar in patients with Crohn's disease with fistulas (17.1 +/- 5.91 mg/kg), patients without fistulas (9.6 +/- 3.58 mg/kg), and in controls (13.3 +/- 4.28 mg/kg). The results indicate that ascorbic acid absorption is normal in patients with both fistulizing and nonfistulizing Crohn's disease. The results suggest that routine supplements of vitamin C are not necessary unless oral ascorbic acid intake is low.
A total of 1000 deaths from injury in England and Wales have been reviewed to establish the incidence and pattern of penetrating injury and the adequacy of its management. Of the 1000 deaths, 71 (7.1 per cent) were due to penetrating injury. There were 32 knife wounds and 30 firearm injuries. Most of the latter were suicides. Only 17 patients (24 per cent) reached hospital alive. Of these cases, 10 had extracranial injury and all 10 deaths were considered to have been potentially preventable when reviewed by four external assessors. One of seven patients with cranial injury was considered to have been a potentially preventable death. The median age of the 11 cases of potentially preventable death was 37 years (range: 7-61 years). Of these, three did not have any surgery for surgically treatable injuries. Seven patients underwent operation and difficulty was encountered in six of these. It appears from our figures that whilst penetrating injury is an uncommon cause of death, it is poorly managed. The implications of this finding for systems of injury care in the United Kingdom are discussed.
This study compared the metabolic responses to parenteral nutrition in five septic and six nonseptic individuals. Oxygen uptake (VO2) was measured for 1 h preinfusion and during the first 2 h of parenteral nutrition infusion. While baseline VO2 was 19% higher in the septic compared with nonseptic patients (p less than 0.01), both groups responded similarly to nutrition: VO2 increased 25% and 27% above baseline in the nonseptic and septic groups, respectively (NS between groups). Respiratory quotient increased 9% in the nonseptic (p less than 0.01) and 5% in the septic (p less than 0.05) patients during infusion. Plasma glucose and insulin increased identically in both groups. Cortisol was consistently higher in the septic patients whereas glucagon decreased similarly in both groups with feeding. Norepinephrine increased 25% in response to the nutrition and remained elevated in the nonseptic group. The results illustrate the effect nutrient-induced thermogenesis may have in the energy balance of parenterally fed patients.