Effect of enteral feeding on hepatic steatosis induced by total parenteral nutrition.

This study was designed to test the hypothesis that deprivation of enteral feeding contributes to the development of total parenteral nutrition (TPN)-induced hepatic dysfunction and that alterations of gut hormones are involved in its pathogenesis. Twenty-one adult Sprague-Dawley rats were randomized into three groups: group 1 received chow feeding ad libitum (288 kcal/kg per day); group 2 received dextrose-based TPN (320 +/- 5 kcal/kg per day); and group 3 received TPN (315 +/- 15 kcal/kg per day) plus chow feeding ad libitum (74 +/- 1 kcal/kg per day). After 7 days, portal blood was assayed for insulin, glucagon, gastrin, peptide YY, secretin, and vasoactive intestinal polypeptide; systemic blood for determination of liver function tests and serum lipid analysis. Liver biopsies were taken for histology and staining for fat, and the remainder of the livers were removed for tissue lipid analysis. TPN induced striking hepatic steatosis with prominent histologic changes and accumulation of lipids, mainly triglycerides and cholesterol ester, in the liver. Addition of enteral feeding to TPN-treated animals significantly reduced the histologic changes as well as lipid accumulation in the liver. Portal plasma levels of gastrin and peptide YY were reduced in animals maintained on TPN alone, with no change in secretin or vasoactive intestinal polypeptide levels. Enteral supplementation increased peptide YY levels in group 3, but not to normal, while gastrin secretion remained decreased. The serum triglyceride levels were decreased in both TPN groups; no differences were detected in the serum cholesterol levels or liver function tests.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

Myocardial calcification: a predictor of poor outcome for myocarditis treated with extracorporeal life support.

Myocarditis is an inflammatory disease of the myocardium with a variety of causes. It is potentially reversible, and has been treated successfully with extracorporeal life support (ECLS). With increasing severity, myocarditis results in significant damage to myocardial cells. Dystrophic calcification of the myocardium may occur, serving as a marker of severe damage. At the authors' institution, from July 1990 to January 1992, five patients (four neonates, one 5 year old) with severe myocarditis refractory to medical management were treated with venoarterial ECLS. Three survived (60%) and two died. All patients were female, and their age range was 2 weeks to 5 years. Nonsurvivors had significant myocardial calcification, which was detected by a chest roentgenogram as well as a two-dimensional echocardiogram; the three survivors had no evidence of calcification. The nonsurvivors had minimal recovery of myocardial function and subsequently had their ECLS discontinued at 83 and 169 hours, respectively. The authors conclude that the development of progressive myocardial calcification in conjunction with a lack of recovery of cardiac function is a sign of severe myocardial damage and poor prognosis. Continuation of ECLS in this setting may not be warranted.

Helium-oxygen and conventional mechanical ventilation in the treatment of large airway obstruction and respiratory failure in an infant.

The application of 70% helium-30% oxygen mixtures by tight-fitting face mask in the emergency management of large airway obstruction is well known. We present the case of an infant with severe large airway obstruction and respiratory failure that was unresponsive to the more traditional approaches of airway management, including the delivery of He-O2 by face mask, endotracheal intubation, and conventional mechanical ventilation with oxygen alone. This case was successfully managed with He-O2, when concentrations of O2 were lower than those previously reported in association with conventional mechanical ventilation, until the obstruction could be surgically corrected. We suggest using a new combination of the low-density helium-oxygen gas mixtures and conventional mechanical ventilation, both of which are readily available in most intensive care units.

Sepsis in rats stimulates cellular proliferation in the mucosa of the small intestine.

BACKGROUND/AIMS: Increased protein synthesis in intestinal mucosa during sepsis may reflect increased cell turnover. The influence of sepsis and endotoxemia on cellular proliferation in the mucosa of the small intestine was studied. METHODS: Sepsis was induced in rats by cecal ligation and puncture. Control rats were sham-operated. Other rats were treated with endotoxin (total dose, 2 mg/kg), human recombinant tumor necrosis factor alpha, or human recombinant interleukin 1 alpha at a dose of 100 micrograms/kg each. Villus height and crypt depth in the jejunum were measured as the number of cells along the side of the villus and crypt, respectively. Cellular proliferation was assessed by measuring the rate of [3H]thymidine incorporation into DNA of the jejunal mucosa and performing autoradiographic studies after intravenous administration of [3H]thymidine. RESULTS: Sepsis resulted in reduced villus height, increased crypt depth, and increased incorporation of [3H]thymidine into DNA in the jejunal mucosa. Autoradiography after administration of [3H]thymidine showed labeled cells almost exclusively in the crypts; the number of labeled cells per crpt was higher in septic than in control rats. Administration of endotoxin or recombinant interleukin 1 alpha, but not recombinant tumor necrosis factor alpha, stimulated the incorporation of [3H]-thymidine into DNA in the jejunal mucosa. CONCLUSION: Sepsis and endotoxemia stimulate cellular proliferation in the mucosa of the small intestine. This response to sepsis and endotoxemia may be partly mediated by interleukin 1.

Inspiratory work and response times of a modified pediatric volume ventilator during synchronized intermittent mandatory ventilation and pressure support ventilation.

Volume ventilation by demand flow ventilators significantly increases work of breathing during inspiration. Although various ventilator modifications and different modes of ventilation have been developed, there have been few studies regarding imposed work of breathing in infants and children. This study was designed to evaluate several modifications of a commercially available demand flow ventilator designed to shorten response time (tr) and decrease the imposed work (Wi) involved in opening the demand valve. Minimum withdrawal volume (Vmin), maximum negative pressure (P mneg), and tr were measured. Wi was defined as the product of Vmin and P mneg. Seven Siemens Servo 900C ventilators were tested under 16 different trial conditions with four variables: 1) mode of ventilation (synchronized intermittent mandatory ventilation [SIMV] vs. pressure support ventilation [PSV]); 2) caliber of circuit tubing (adult vs. pediatric); 3) location of airway pressure monitor (distal vs. proximal); and 4) ventilator trigger sensitivity (0 cm H2O--high vs. -2 cm H2O--low). Vmin, Pmneg, and Wi were all decreased (P less than .05) while tr was unaffected by changing ventilator trigger sensitivity from low to high. Wi was decreased by pediatric tubing and proximal airway pressure monitoring only when low trigger sensitivity was used. PSV and proximal airway monitoring shortened tr. The authors conclude that the use of pediatric circuit tubing and proximal airway pressure monitoring with a Siemens Servo 900C ventilator significantly improved ventilator performance.

Pudendal nerve terminal motor latency influences surgical outcome in treatment of rectal prolapse.

PURPOSE: This study was undertaken to document the effect of pudendal nerve function on anal incontinence after repair of rectal prolapse. METHODS: Patients with full rectal prolapse (n = 24) were prospectively evaluated by anal manometry and pudendal nerve terminal motor latency (PNTML) before and after surgical correction of rectal prolapse (low anterior resection (LAR; n = 13) and retrorectal sacral fixation (RSF; n = 11)). RESULTS: Prolapse was corrected in all patients; there were no recurrences during a mean 25-month follow-up. Postoperative PNTML was prolonged bilaterally (> 2.2 ms) in six patients (3 LAR; 3 RSF); five patients were incontinent (83 percent). PNTML was prolonged unilaterally in eight patients (4 LAR; 4 RSF); three patients were incontinent (38 percent). PNTML was normal in five patients (3 LAR; 2 RSF); one was incontinent (20 percent). Postoperative squeeze pressures were significantly higher for patients with normal PNTML than for those with bilateral abnormal PNTML (145 vs. 66.5 mmHg; P = 0.0151). Patients with unilateral abnormal PNTML had higher postoperative squeeze pressures than those with bilateral abnormal PNTML, but the difference was not significant (94.8 vs. 66.5 mmHg; P = 0.3182). The surgical procedure did not affect postoperative sphincter function or PNTML. CONCLUSION: Injury to the pudendal nerve contributes to postoperative incontinence after repair of rectal prolapse. Status of anal continence after surgical correction of rectal prolapse can be predicted by postoperative measurement of PNTML.