A temporal study of TPN-induced changes in gut-associated lymphoid tissue and mucosal immunity

BACKGROUND: Total parenteral nutrition (TPN) is associated with decreases in small-intestinal gut-associated lymphoid tissue (GALT) T cells, B cells, and IgA levels and impairs IgA-mediated defenses in the respiratory tract. The impaired respiratory tract defenses are speculated to be due to reduced respiratory tract IgA levels. OBJECTIVES: To determine the time course of GALT cell reductions and document any changes in respiratory tract IgA levels in mice receiving TPN. DESIGN: Prospective randomized trial. SETTING: Animal research laboratory. MATERIALS: Thirty-five male ICR mice weighing 25 to 35 g. INTERVENTIONS: Mice underwent cannulation with intravenous catheters and received chow for 2 days followed by TPN for 0 (n=6), 1 (n=6), 2 (n=6), 3 (n=6), 4 (n=6), or 5 (n=5) days. Mice were killed after receiving TPN their respective number of days. The small intestine was harvested, and washings were obtained from the small intestine and the respiratory tract. Lymphocytes and IgA levels were analyzed by flow cytometry and enzyme-linked immunosorbent assay, respectively. MAIN OUTCOME MEASURES: Lymphocyte yields from Peyer patches, intraepithelial spaces, and the lamina propria; IgA levels from the small intestine and the respiratory tract. RESULTS: T- and B-cell yields in the Peyer patches and lamina propria were significantly reduced by day 2 (P<.05) and thereafter compared with day 0. The lamina propria CD4+/CD8+ ratio declined significantly by day 4 (P<.05) compared with day 0. Small-intestinal and respiratory tract IgA levels were significantly diminished by day 3 (P<.05) and thereafter compared with day 0. CONCLUSION: Total parenteral nutrition produces rapid changes in GALT cell profiles and reduces respiratory tract IgA levels consistent with the impairment of respiratory IgA-mediated defenses.     

Effect of lipid-free total parenteral nutrition on hepatic drug conjugation in rats

The effect of total parenteral nutrition (TPN) on drug conjugation in male Sprague-Dawley rats was examined using a nutrition solution composed of amino acids and glucose. The overall disposition of acetaminophen including the formation kinetics of the sulfate and glucuronide metabolites was used as an in vivo probe. Selected drug metabolizing enzyme activities also were examined in vitro. TPN, 200 kcal/kg/day, was administered by continuous i.v. infusion for 14 days and changes elicited were compared to control animals allowed free access to rat chow. TPN decreased the total clearance of acetaminophen by 34% and the formation clearance to acetaminophen sulfate by 47%. The formation clearance of acetaminophen to acetaminophen glucuronide was unaffected by TPN. Cytochrome P450 concentration and oxidative demethylase activity toward p-nitroanisole were decreased in parallel, 47 and 53%, respectively, and UDP-glucuronosyltransferase activity with p-nitrophenol and acetaminophen as the acceptor aglycones was decreased 44 and 25%, respectively in the animals receiving TPN. Sulfotransferase activity toward both p-nitrophenol and acetaminophen decreased 28% in animals receiving TPN vs. ad libitum rat chow. Administration of the parenteral nutrition solution as a continuous enteral infusion via a doudenal catheter slightly decreased p-nitroanisole demethylase activity (26%), but had no other significant effects on either cytochrome P450 concentration or on drug conjugating enzyme activities determined in vitro. These results show that parenteral nutrition administered i.v. depresses drug conjugation and suggest that alterations in both hepatic oxidative and conjugative biotransformation arising from total parenteral nutrition are largely attributable to bypassing the intestinal route for nutrient intake.     

Protracted diarrhea and malnutrition in infancy: Changes in intestinal morphology and disaccharidase activities during treatment with total intravenous nutrition or oral elemental diets

Two therapeutic regimens were compared in 16 infants with protracted diarrhea and malnutrition. Eight patients were treated with total parenteral nutrition given via a central vein (group A); the remaining eight patients received a combination of dilute parenteral nutrients given in a peripheral vein plus continuous enteral feedings of an elemental diet (group B). All patients recovered although two infants in group B were switched to TPN treatment after a poor response to the elemental diet. Intestinal biopsies were performed: (1) before treatment; (2) after 2 to 3 weeks of TPN or elemental diet; and (3) after 2 to 3 weeks of Nutramigen feedings. Before treatment, all patients had atrophic changes in the jejunal epithelium and deficient disaccharidase and trypsin activities. The second biopsy showed morphologic recovery in all patients, incomplete recovery of lactase and trypsin in both treatment groups, and complete recovery of sucrase and maltase activities only in group B patients. The third biopsy showed normal morphology and complete recovery of all enzymes measured. The mean number of hospital days was 46 +/- 4.8 for group A and 34 +/- 1.6 for group B (p less than 0.05) suggesting that patients given enteral feedings early tended to have a more rapid return of intestinal function and of some intestinal enzymes.     

Addition of glucagon to lipid-free total parenteral nutrition reduces production of prostaglandin E2 by stimulated splenic macrophages

Sepsis is a major complication of total parenteral nutrition (TPN). Impaired immunity has been suggested as being responsible for TPN-related sepsis, but it is unknown how the immune system is affected by TPN. We recently found that administration of lipid-free TPN resulted in an increase in prostaglandin E2 (PGE2) release by stimulated splenic macrophages. This observation suggested that TPN may impair immunity through the prominent immunosuppressive effects of PGE2. In the present study, we tested the hypothesis that addition of glucagon to TPN solution may protect against the immunosuppressive effect of TPN by modifying PGE2 secretion. Adult, male Sprague-Dawley rats (n = 18) underwent jugular vein cannulation: group 1 (n = 7) received intravenous saline and chow ad libitum; group 2 (n = 6) received TPN (80 mL/24 h); and group 3 (n = 5) received TPN (80 mL/24 h) plus glucagon (100 micrograms/24 h). After 10 days, spleens were removed and splenic macrophages were isolated and cultured for 24 h in plain M199 medium (nonstimulated) or in medium containing Escherichia coli lipopolysaccharide (5 micrograms/mL) (stimulated). PGE2 release was determined by enzyme-linked immunosorbent assay. There were no differences in PGE2 release between the groups of nonstimulated cells, but when stimulated with lipopolysaccharide, the macrophages from the TPN rats (group 2) released more PGE2 (81.68 +/- 25.99 ng/2.5 x 10(6) cells) than the control group (16.04 +/- 3.26 ng/2.5 x 10(6) cells). The release of PGE2 was normalized in the TPN animals treated with glucagon (15.71 +/- 3.33 ng/2.5 x 10(6) cells). This difference was significant, with p < .05 by Tukey's test after analysis of variance.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of minimum luminal nutrition on mucosal cellularity and immunity of the gut

Many catabolic patients can only consume small volumes of enteral nutrients. The aim of this study was to evaluate markers of cellularity and immunity in the small intestine of rats randomized to receive 6 days of parenteral nutrition, 25% enteral and 75% parenteral nutrition (i.e. minimum luminal nutrition) or enteral nutrition. The same glutamine-enriched solution was used for both parenteral and enteral nutrition. Enteral nutrition was associated with the least amount of jejunal atrophy (P<0.01), with the results from the minimum luminal nutrition group approximating those of the parenteral nutrition group. Parenteral nutrition was associated with the greatest number of CD2+ cells (P< 0.05) and the lowest CD4/CD8 cell ratio (P< 0.01) in the jejunal mucosa. In essence, we failed to demonstrate that there are any appreciable benefits associated with the enteral consumption of 25% of a nutrient load.     

Hepatobiliary dysfunction during total parenteral nutrition is caused by infusate, not the route of administration

Cholestatic jaundice is the major complication of total parenteral nutrition (TPN). Both the intravenous (IV) route of nutrition and the enteral fast have been implicated as causes of TPN-associated cholestasis (TPN-AC). The purpose of this study was to determine whether TPN-AC is caused by the TPN solution itself or the IV route of administration and enteral fast. Prepubescent rabbits (n = 24) were divided into four groups: CONTROL, fed standard lab chow; TPN, received a standard hyperalimentation solution of dextrose, Aminosyn, and lipids via the jugular vein; ENT, received the same hyperalimentation solution via a duodenostomy tube; and OSM, received a polymeric formula (Osmolite) via a duodenostomy tube. After 14 days on these diets, we measured bile flow, bile acid excretion, sulfobromophthalein (BSP) excretion, plasma amino acid profile, serum liver enzymes, and liver histology. Statistical analysis was by analysis of variance. Hyperalimentation solution significantly depressed hepatobiliary function, whether it was given IV or by gut. Bile flow in both the TPN (36.4 microL/kg/min) and ENT (46.2) groups was significantly less than CONTROL (84.5) or OSM (62.9). Hepatic secretory function, measured by excretion of the cholephilic dye BSP, was depressed in both TPN and ENT (57% and 55% of IV dose excreted in bile over 60 minutes, respectively) compared with CONTROL (84%) or OSM (71%). Serum liver enzymes were normal in all groups. Histological injury similar to TPN-AC in humans (portal inflammation and hepatocyte degeneration) was seen in both groups receiving the hyperalimentation solution.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum insulin-like growth factor I and physical performance in prepubertal Bolivian girls of a high and low socio-economic status

Leptin, a putative satiety hormone in rodents, is acutely regulated by fasting and refeeding. To determine the role of satiety hormones that are secreted by the gastrointestinal tract on leptin regulation, leptin mRNA and serum concentrations were measured after feeding rats similar calories with standard chow or infusion of total parenteral nutrition into the duodenum or intravenously. We have demonstrated that leptin gene expression and hormone secretion into the circulation are stimulated equally in the three experimental paradigms; it is unlikely that satiety factors secreted by the intestinal tract play a significant role in leptin regulation. Furthermore, intravenous infusion of individual components of TPN demonstrated that intravenous glucose infusion was mostly responsible for stimulation of the leptin gene and hormone secretion.     

Prostaglandin and tumor necrosis factor levels in early wound inflammatory fluid: effects of parenteral omega-3 and omega-6 fatty acid administration

Monokines are important mediators of wound healing. Specifically, the proportions of proinflammatory (tumor necrosis factor and PGE2) and antiinflammatory (PGF2 alpha) monokines may modulate its early phases. Using a polyvinyl alcohol sponge model of rat wounding, the authors determined the temporal changes in the levels of monokines in wound inflammatory fluid, and examined whether dietary manipulation for 6 days with the precursors (omega 6 fatty acids) and inhibitors (fish oil omega 3 fatty acids) of the prostaglandin-2 series influenced monokine composition of wound fluid. For 3 days before the wounding, adult rats received isocaloric, isovolemic, and isonitrogenous total parenteral nutrition (TPN), in which lipids supplied either 35% (Intralipid [IL] or fish oil emulsion [FO]) or 8% (minimal essential fatty acid; EFA) of the total calories. Control rats received isocaloric enteral chow. The controls were studied at 24, 48, 72, and 96 hours, and the experimentals at 72 hours after wounding. Cell counts were performed, and cell-free fluid was analyzed for PGE2, PGF2 alpha, and TNF. In control rats, the total WBC count was highest at 24 to 48 hours, and decreased significantly by 96 hours. The percentage of mononuclear cells progressively increased throughout the 96 hours, and the total mononuclear cell count peaked at 72 hours. The TNF and prostaglandin levels were highest at 24 hours; these decreased rapidly by 72 hours. At all time-points, the levels of PGE2 remained higher than those of PGF2 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)     

The intestine as an immunological organ]

The intestinal mucosa is in close contact with a large number of foreign antigens and mitogenic substances in the gut lumen. To protect the host against invasion of potential pathogens or an inappropriate immune response to the enormous number of antigens, a highly specialized immune system in the intestinal mucosa has developed, the so-called gut-associated lymphoid tissue (GALT). The passage of viable bacteria from the gastrointestinal tract through the epithelial mucosa is called bacterial translocation. Bacterial translocation in critically ill patients may lead to a significant incidence of systemic sepsis. This has attracted much clinical interest, as it has been shown that disturbances of the GALT and malnutrition itself, impair various aspects of barrier function. Enteral nutrition seems to be superior to parenteral nutrition in maintaining the functional barrier of the gut. Defined dietary variable (fibre, glutamine) influence bacterial translocation. Future therapeutic strategies should therefore concentrate on early enteral feeding in traumatised patients to reduce the incidence of bacterial translocation and septic complications.     

Regulation of albumin mRNA and its promoter-binding nuclear factors under different perioperative nutritional methods in hepatectomized rats

BACKGROUND: Regulation of perioperative albumin synthesis under parenteral (PN) and enteral (EN) nutrition was investigated. METHODS: Rats were divided into PN and EN groups. Both groups received the same regimen of artificial nutrition for 7 days and then underwent 70% hepatectomy. Serum albumin and mRNA levels of albumin and its promoter-binding nuclear factors (C/EBPalpha, beta, and DBP) were measured. RESULTS: Serum albumin and albumin mRNA in the PN group were significantly lower than those in the EN group at 72 hours after hepatectomy. Preoperative and postoperative DBP and C/EBPalpha mRNA levels in the EN group were significantly higher than those in the PN group. CONCLUSION: Serum albumin was well maintained by EN after hepatectomy owing to an early recovery of albumin mRNA level and its nuclear factor mRNA levels (C/EBPalpha and DBP). Compared with PN, EN is a more advantageous from of perioperative nutrition as pertains to albumin synthesis.     

Enteral or parenteral feeding after total gastrectomy: prospective randomised pilot study

OBJECTIVE: To compare the efficacy and cost of enteral and parenteral feeding after total gastrectomy. DESIGN: Prospective randomised open study. SETTING: University hospital, Finland. SUBJECTS: 29 patients undergoing curative total gastrectomy for gastric cancer. INTERVENTIONS: 13 patients were given early enteral feeding by nasojejunal tube and 16 patients parenteral nutrition by central venous catheter. MAIN OUTCOME MEASURES: Postoperative complications, duration of hospital stay, serum CRP and albumin concentrations, cost, and postoperative abdominal symptoms. RESULTS: One patient in the enteral feeding group discontinued the study on day 1. Oesophagojejunal leaks developed in one patient in each group. Infective complications occurred in 3 (23%) in the enteral group and 5 (31%) in the parenteral group. Serum CRP concentration on day six was lower in the enteral feeding group than in the parenteral feeding group (32 (16) g/L compared with 61 (41) g/L; p = 0.02). Enteral feeding was well tolerated. Diarrhoea developed earlier in the enteral than in the parenteral group (days 3-5 compared with 5-7, respectively) but there was a tendency to an increased risk of diarrhoea in the parenteral group. Parenteral feeding was more than four times as expensive as enteral feeding. CONCLUSION: Enteral nasojejunal feeding is safe and well tolerated after total gastrectomy. It is also cheaper than parenteral nutrition.     

Trimucytin: a collagen-like aggregating inducer isolated from Trimeresurus mucrosquamatus snake venom

OBJECTIVE: This study tested the hypothesis that gut stasis induced by parenteral morphine sulfate (MS) leads to enhanced bacterial translocation in rats on total parenteral nutrition (TPN). SUMMARY BACKGROUND DATA: TPN and MS are common adjuncts in the care of critically ill patients. TPN is known to provoke a variable degree of translocation. MS induces gut stasis with an accompanying bacterial overgrowth. The effect of these two treatments in combination on translocation is not known. METHODS: Rats were provided with central and subcutaneous lines for the continuous infusion of nutrients and drugs, respectively. Intestinal transit was assessed by the caudal movement of a fluorescent marker intubated into the proximal duodenum. Quantitative bacteriology was carried out from various segments of the gut and from ileocecal mesenteric lymph nodes (MLN), spleen, liver, and systemic blood obtained by cardia puncture on sacrifice at 96 hours. RESULTS: Transit was unchanged by TPN alone but prolonged when given in combination with MS. Bacterial overgrowth was also enhanced by MS and increased the bacterial translocation to MLN from 50% of animals with TPN, to 100% in those receiving both TPN and MS; the colony-forming units per MLN increased from 33 +/- 14 with TPN alone to 2079 +/- 811 (STD) with TPN plus MS. Furthermore, no bacteria were found at systemic sites with TPN alone, but in 93.3% of animals receiving TPN and MS. In a subgroup of rates provided with glutamine in TPN, the TPN plus MS effects on translocation were not reversed. CONCLUSIONS: These observations demonstrate the important role that morphine plays in promoting translocation, presumably by disrupting fasting motility and enhancing bacterial overgrowth.     

Carnitine supplementation accelerates normalization of food intake depressed during TPN

When total parenteral nutrition (TPN; containing glucose, fat, and amino acids; caloric ratio 50:30:20) providing 100% of the rat's daily caloric intake is given for 3-4 days, food intake rapidly decreases by approximately 85%. After stopping TPN, there is a lag period of 3-4 days before food intake returns to previous level, which appears to be related to fatty acid oxidation and fat deposition. Carnitine plays a key role in the oxidation of fatty acids, and was demonstrated to reduce fat deposition in rats receiving TPN, by increasing beta oxidation. We therefore investigated whether rats receiving TPN supplemented with carnitine may prevent either the decrease or speed up the resumption or normalization of food intake, after TPN is stopped. Fourteen adult Fischer-344 rats had a central venous catheter inserted. After 10 recovery days, controls (n = 7) were infused with TPN providing 100% of rat's daily caloric intake for 3 consecutive days, followed by 4 more days of normal saline. The carnitine group (n = 7) received the same solution, but which provided 100 mg/kg/day carnitine. Daily food intake was measured and data were analyzed using ANOVA and Student's t-test. Both parenteral solutions depressed food intake maximally by almost 90% by day 3. Carnitine accelerated the normalization of food intake by decreasing the lag period by 1 day. We conclude that the addition of carnitine enhanced the normalization of post-TPN food intake and argue that this may be on the basis of enhanced fatty acid oxidation, a substrate known to play a significant role in the anorexia induced by TPN.     

Absorption, tolerability, and effects on mitochondrial activity of oral coenzyme Q10 in parkinsonian patients

Venous thrombosis and bacterial infections are common complications of parenteral nutrition. To test the hypothesis that infection facilitates activation of coagulation during parenteral nutrition, healthy subjects were intravenously injected with endotoxin (2 ng/kg) after they had received either 1 week of standard parenteral nutrition (n = 7) or normal enteral feeding (n = 8). Compared with enteral feeding, parenteral nutrition was associated with a selectively enhanced activation of the coagulation system (plasma levels of thrombin-antithrombin III complexes) during endotoxemia. Activation of the fibrinolytic system (plasminogen activator activity, tissue-type plasminogen activator, plasminogen activator inhibitor type 1) proceeded similarly in both study groups. In patients receiving parenteral nutrition, one common complication (bacterial infection) may facilitate the occurrence of another common complication (venous thrombosis) by synergistic stimulation of the coagulation system.     

Intravenous ursodeoxycholic acid reduces cholestasis in parenterally fed newborn piglets

BACKGROUND & AIMS: Cholestasis complicates total parenteral nutrition (TPN) in preterm infants. Ursodeoxycholic acid (UDCA) is used for several cholestatic problems. The hypothesis of this study was that intravenous UDCA prevents TPN-induced cholestasis by (1) maintaining normal basal and stimulated bile flow, (2) altering bile composition, and (3) changing hepatocyte membrane composition and Na+,K(+)-adenosine triphosphatase (ATPase) activity. METHODS: Three groups of piglets were studied: group 1 received sow's milk, groups 2 and 3 received TPN, and group 3 also received 100 mumol.kg-1.day-1 UDCA intravenously. After 3 weeks, basal and stimulated bile flow were measured. Cholesterol, bile acids, phospholipids, and phospholipid fatty acids were analyzed in bile, and fluidity, phospholipid fatty acid composition, and Na+,K(+)-ATPase were analyzed in hepatocyte membranes. RESULTS: Bile acid secretion and basal and stimulated bile flow were similar in control and UDCA-treated animals but reduced to < 50% in the TPN group. Bile acid-dependent and -independent bile flow were lower in the TPN group. UDCA did not normalize abnormalities in TPN-induced bile composition. Sinusoidal but not canalicular membrane fluidity was different in TPN than in control and UDCA-treated animals. UDCA also increased Na+,K(+)-ATPase activity. Bile and membrane phospholipid fatty acids reflected dietary fatty acids. CONCLUSIONS: Intravenous UDCA improves bile flow and reduces bilirubin levels in the serum and liver in piglets with TPN-induced cholestasis.     

Parenteral versus enteral nutrition: morphological changes in human adult intestinal mucosa

In animal experiments total parenteral nutrition induces an atrophy of the small intestinal mucosa. In humans morphological data are few and controversial. Therefore, the aim of this study was to investigate the effect of parenteral nutrition on the intestinal mucosa of human adults. For this purpose samples of the proximal jejunum of a) patients with chronic pancreatitis receiving total parenteral nutrition as presurgical treatment, b) enterally nourished patients without (controls) and c) with chronic pancreatitis were compared using light and scanning electron microscopy. Statistical differences were assessed applying computer-assisted morphometry. The results demonstrated that the thickness of the jejunal mucosa decreased already in enterally nourished patients with chronic pancreatitis. However, after total parenteral nutrition the decrease (atrophy) was enhanced due to a strong reduction in villus height albeit the crypt length increased. In addition, scanning electron microscopy revealed distinctive changes in mucosal surface pattern, whereby finger-like villi were replaced by leaf-like villi and by long, winding bifurcating ridges. Cell shedding was absent. In conclusion, total parenteral nutrition in humans induces 1) an atrophy and 2) a remodelling of the intestinal mucosa (epithelium and lamina propria) with a decrease in the absorbing surface. These alterations involve both cell proliferation and cell shedding. The response of the mucosa to parenteral nutrition is immediate and the effect of the treatment in bringing about morphological alterations is more efficacious at the beginning than in the successive period. The basic disorder (chronic pancreatitis) of the patients nourished parenterally contributes to mucosal atrophy, but not to remodelling.     

Nutritional depletion in staged spinal reconstructive surgery. The effect of total parenteral nutrition

STUDY DESIGN: A prospective randomized study evaluating nutritional depletion in spine surgery patients. OBJECTIVE: To determine whether use of total parenteral nutrition (TPN) in patients undergoing staged spinal reconstructive procedures could affect their nutritional parameters or decrease their complication rates. SUMMARY OF BACKGROUND DATA: Several studies have shown that nutritional depletion occurs after major spinal surgery and that patients undergoing staged spinal surgery may be at particular risk of nutritional loss and its complications. METHODS: Forty adult patients undergoing staged spinal reconstructive surgery were randomized as to whether they received TPN postoperatively. Nutritional parameters, including skin fold measurement and albumin, pre-albumin, transferrin, and total lymphocyte counts, were obtained pre-operatively and at regular intervals. RESULTS: Five patients did not complete the study, leaving 35 patients for analysis. There was a significant decrease in incidence of albumin and pre-albumin depletion for the patients who did not receive TPN compared with those who did receive TPN (P < 0.025, P < 0.006, respectively). Patients with depleted albumin or pre-albumin counts were more likely to develop other postoperative infectious complications such as pneumonia or urinary tract infections (P < 0.035). There were no statistically significant differences in wound complications in this small patient study. There were no complications secondary to use of the TPN. CONCLUSIONS: For complex patients requiring staged anterior/posterior surgery, TPN appears to significantly lessen the decrease in nutritional parameters. Because depletion of nutritional parameters appears to correlate with an increased likelihood of perioperative infectious complications, use of TPN may result in a decrease of such complications in these patients.     

Enteral nutrition is superior to parenteral nutrition in severe acute pancreatitis: results of a randomized prospective trial

BACKGROUND: Parenteral nutrition is well established for providing nutritional support in acute pancreatitis while avoiding pancreatic stimulation. However, it is associated with complications and high cost. Benefits of enteral feeding in other disease states prompted a comparison of early enteral feeding with total parenteral nutrition in this clinical setting. METHODS: Thirty-eight patients with acute severe pancreatitis were randomized into two groups. The first (n = 18) received enteral nutrition through a nasoenteric tube with a semi-elemental diet, while the second group (n = 20) received parenteral nutrition through a central venous catheter. Safety was assessed by clinical course of disease, laboratory findings and incidence of complications. Efficacy was determined by nitrogen balance. The cost of nutritional support was calculated. RESULTS: Enteral feeding was well tolerated without adverse effects on the course of the disease. Patients who received enteral feeding experienced fewer total complications (P < 0.05) and were at lower risk of developing septic complications (P < 0.01) than those receiving parenteral nutrition. The cost of nutritional support was three times higher in patients who received parenteral nutrition. CONCLUSION: This study suggests that early enteral nutrition should be used preferentially in patients with severe acute pancreatitis.     

Delayed gastric emptying in a neonate, associated with a partial defect in the gastric smooth muscle

A girl born after 36 weeks' gestation had emesis 15 hours after birth. She required total parenteral nutrition (TPN) because of persistent gastric retention. When milk was given, the volume of gastric aspirate 3 hours after feeding often was greater than the volume given. Domperidon and erythromycin were ineffective. Upper gastrointestinal series showed slow gastric emptying but no abnormalities in the stomach. No stenosis or obstruction below pylorus was found. Endoscopy showed normal gastric mucosa. Manometry showed normal antroduodenal motility patterns. Transpyloric feeding, which started at age 73 days, was successful and enabled cessation of the TPN. Laparotomy at 119 days of age showed partial absence of the muscle and serosal layer in the anterior wall of the gastric body (1 x 4 cm). The mucosal layer was intact and partly adhered to the peritoneum and the left lobe of the liver. The defect was surgically corrected by plicating the place. The postoperative course was excellent, and oral feeding was fully established within 2 weeks. Although the cause of the partial muscle defect in the case is unclear, this case suggests that this rare condition can cause severe chronic gastric retention.