Compliance with enhanced recovery after surgery criteria and preoperative and postoperative counselling reduces length of hospital stay in colorectal surgery: results of a randomized controlled trial.

AIM: The aim of this randomized clinical trial was to compare patients treated using a multimodal approach [enhanced recovery after surgery (ERAS)], with a special focus on counselling, to patients treated in a standard conventional care pathway, who underwent elective colorectal resection. METHOD: In a single-centre trial, adult patients eligible for open or laparoscopic colorectal resection were randomized to an ERAS programme or standard care. The primary end-point was postoperative total hospital stay. Identical discharge criteria were defined for both treatment groups. Secondary end-points included postoperative complications, postoperative C-reactive protein levels, postoperative hospital stay, readmission rate and mortality. All parameters were recorded before operation, on the day of surgery and daily thereafter until discharge. RESULTS: Total hospital stay was significantly shorter among patients randomized to ERAS than among the standard group [median 5 days (range 2-50 days) vs median 8 days (range 2-48 days); P = 0.001]. The two treatment groups exhibited similar outcomes regarding overall major and minor morbidity, reoperation rate, readmission rate and 30-day mortality. There were also no differences in tolerance of enteral nutrition or in the inflammatory response, as reflected by postoperative C-reactive protein levels. CONCLUSION: ERAS care was associated with a significantly shorter length of hospital stay. Without any difference in surgical or general complications, tolerance of enteral nutrition or postoperative C-reactive protein levels, peri-operative information and guidance for ensuring that patients comply with the ERAS approach appear to be important factors to reduce the length of hospital stay.

Identification of thoracic intervertebral spaces by means of surface anatomy: a magnetic resonance imaging study.

BACKGROUND: Successful thoracic epidural analgesia depends on the sensory blockage of specific dermatomes following appropriate placement of the epidural catheter. This study aimed to ascertain how accurately anaesthesiologists identify thoracic intervertebral spaces, and whether counting from the prominent vertebra is easier than using the iliac crest as an anatomical landmark. METHODS: Five anaesthesiologists attempted to locate one out of five consecutive intervertebral spaces (Th7-Th8 to Th11-Th12) on patients referred for magnetic resonance imaging of the vertebral column. The intended thoracic interspace and the counting reference point (C7-Th1 or L3-L4) were marked with oil capsules. The body mass index, gender and position of the patient were recorded. The exact capsule positions were determined by a radiologist after the study. RESULTS: In 92 patients, 26.7% of the thoracic interspaces were correctly identified. The counting reference point was the only variable studied with a significant influence on error. The accuracy increased when the iliac crest was used as an anatomical landmark rather than the prominent vertebra (odds ratio, 0.29). The majority (76.4%) of all the incorrectly placed capsules were found cephalad to the intended level. CONCLUSION: We recommend that the caudal of two to three possible interspaces should be used when placing an epidural catheter in the thoracic spine. Because of the inaccurate localization of the thoracic intervertebral spaces, documentation should state the site of puncture as being in the upper or lower thoracic spine instead of claiming to be in an exact interspace.

A randomised study of lidocaine and prilocaine for spinal anaesthesia.

BACKGROUND: Transient neurologic symptoms (TNS) are common after lidocaine-induced spinal anaesthesia (SA). Recent data indicate that TNS may be less frequent after prilocaine-induced spinal anaesthesia, for which reason the isobaric solution was compared with lidocaine. METHODS: One hundred patients scheduled for short urologic procedures under spinal anaesthesia were randomised to receive 80 mg prilocaine or lidocaine, both 20 mg/ml. The clinical course and the duration of anaesthesia were monitored. The following day an anaesthesiologist unaware of the randomisation interviewed the patients using a structured questionnaire. RESULTS: Following prilocaine spinal anaesthesia the mean time until 2-segment regression was 123(SD 42) min and total sensory block lasted 221(49) min, compared to 106(26) and 181(48) min following lidocaine. TNS occurred in 7/49 patients in the lidocaine group and in 2/50 in the prilocaine group (ns). CONCLUSION: TNS occurred also after isobaric prilocaine SA. The frequency was not significantly different from that following lidocaine SA but larger studies are needed to establish the relative risk of TNS following SA induced by the two local anaesthetics. Isobaric prilocaine has a longer duration of action than an equal dose of lidocaine and may be an alternative drug for spinal anaesthesia of intermediate or short duration.

Release of endothelin-1 in strangulation obstruction of the small bowel in pigs.

Evidence has been provided that increased portal vein pressure results in increased release of endothelin-1 (ET-1). Strangulation obstruction is associated with increased venous pressure, and we wanted to determine if it is associated with increased local release of ET-1 and elevated concentration of ET-1 in systemic blood. Strangulation obstruction was induced by elevating pressure in a gasket placed around a loop of ileum until venous pressure reached 50 mm Hg. Ischemia in a bowel loop was induced by arterial clamping, reducing blood flow by 70%. Blood samples were collected before and after 30, 90, and 180 min of strangulation or ischemia. ET-1 was determined by radioimmunoassay following acidification and extraction on C18 columns. In strangulated loop the blood flow decreased by 70%. ET-1 concentration remained around 5 pg/ml in arterial blood, increased fourfold in strangulated venous blood, and remained unchanged in venous blood from control bowel. The release of ET-1 from the strangulated loop to blood increased twofold. Ischemia resulted in reduced release of ET-1. It is concluded that strangulation obstruction causes increased release of ET-1 to venous blood in the strangulated loop, but not increased ET-1 concentration in systemic blood. The increased ET-1 release was probably due to increased venous pressure, not to low blood flow.

[Perioperative and postoperative normovolemic anemia. Physiological compensation, monitoring and risk evaluation]. / Per- og postoperativ normovolemisk anemi. Fysiologisk tilpasning, monitorering og risikovurdering.

We accept increasingly lower haemoglobin concentrations in order to avoid erythrocyte transfusions in surgical patients. Knowledge about the physiological adaptation to anaemia, and how this is affected by disease and anaesthesia, are necessary in order to foresee when compensation may be inadequate. Only a few methods are available at present for monitoring tissue oxygenation i.e. mixed venous oxygen saturation, systemic lactacidosis and ECG. In acute haemodilution, cardiac output increases by about 30%, mainly because of a drop in peripheral resistance. Increased contractility and heart rate may contribute to the hyperdynamic circulation and elevate myocardial oxygen demand. In acute anaemia the maximal oxygen extraction ratio in humans is approximately 0.5. Erythrocyte transfusion carries a small, but not negligible risk of infectious disease transmission and immunological incompatibility. Whether allogen transfusions increase the rate of postoperative infections and recurrence of cancer is still a debated issue. The low rate of complications associated with erythrocyte transfusions indicates that the margins of safety should not be too narrow, and that the transfusion trigger should be individualized between 5 and 10 g/100 ml.

Retention and distribution of polygeline (Haemaccel) in the rat.

The plasma substitute polygeline (Haemaccel registered) contains a large fraction of molecules sufficiently small to cross the capillary and glomerular membranes. Plasma volume expansion, tissue extravasation and renal elimination of this artificial colloid were quantified using 125I-labelled polygeline molecules. In pentobarbital anaesthetized rats, either 10 ml 3.5% polygeline (n = 8) or 10 ml 0.9% saline (n = 8) was infused intravenously over 60 min. The plasma volume was assessed by the 3 min distribution volume for I-albumin and the plasma volume changes over time were calculated from erythrocyte volume fractions. The plasma volume increased by 4.6 (2.0) ml (mean (SD)) at the end of the Haemaccel infusion compared with 2.1 (1.8) ml after the saline infusion (P = 0.02). One hour later the increase was 2.4 (1.5) and 1.6 (1.0) ml respectively, not significantly different (P = 0.20). Extravasation of labelled polygeline was greatest in the kidney, possibly due to cellular uptake. Skin and skeletal muscle contained 4-5 times more polygeline than could be attributed to intravascular radioactivity, but still uptake in these tissues did not reach one percent of the amount injected. Following a 60 min infusion and a 60 min interval, 23 (4)% of the polygeline was recovered intravascularly, 43 (9)% had been excreted in urine, leaving 33% to other compartments. Thus, more polygeline was distributed to the interstitium than remained in the circulation. This calls for further investigations into the handling and effect of polygeline in this extravascular compartment.

Interstitial fluid accumulation does not influence oxygen uptake in the rabbit small intestine.

Crystalloid resuscitation increases interstitial fluid volume. Intestinal ischemia and impaired barrier function may contribute to the precipitation of multiple organ failure. Accordingly, the intestine was chosen as target organ to test whether interstitial oedema impairs oxygen extraction by the tissue. The portal vein in anaesthetized rabbits was partially obstructed for 30 min along with an intravenous infusion of 0.9% saline 60-90 ml kg-1 (oedema group, n = 7). Total water content of the small intestine increased from 3.4 ml g-1 dry weight in control (n = 8) to 3.9 ml g-1 in the oedema group (P = 0.049). Small intestinal O2 uptake was calculated from the arteriovenous O2 content and electromagnetic flow measurements in the superior mesenteric artery. Mesenteric flow was reduced stepwise by a snare occluder around the artery. Intestinal oxygenation was monitored indirectly as well, by means of mesenteric venous lactate, arterial base excess and by mucosal pH (pHi) assessed tonometrically. The oxygen extraction ratios were similar in the oedema and control group at similar oxygen supplies. After a 45 min flow reduction to 15% of baseline mesenteric venous lactate and pHi did not differ between the groups. pHi averaged 7.31 and fell to 6.74. Below an intestinal O2 uptake of 2.5 ml min-1, pHi correlated somewhat better with O2 uptake (r = 0.66) than did arterial base excess (r = 0.50). The results indicate that acute elevation of extracellular volume to the extent in the present study, does not impede oxygen uptake in the gut.

Lymphatic transport and organ uptake of gelatin and hyaluronan injected into the rat mesentery.

The metabolic pathways of denatured collagen (gelatin) and hyaluronan were studied by injecting labelled macromolecules into the mesentery of rats. The label, [125]tyramine-cellobiose is trapped intracellularly after endocytosis, allowing localization of the site of uptake. Mesenteric and thoracic lymph was sampled for 6 h in anaesthetized rats. Separate rats were investigated after an awake period of 6 or 24 h. About 30% of the gelatin remained at the site of injection and of the remaining activity 1.7% was recovered in lymph, 11% in the liver and 15% in the kidneys, whereas 3 h after an intravenous injection of gelatin > 70% was recovered in the liver. The change in preferable site of uptake from the liver to the kidney was attributed to local degradation in the mesentery as confirmed by chromatography of tissue extracts and lymph. Following hyaluronan injection and 6 h lymph sampling approximately 30% was left at the site of injection and of the remaining activity 5.7% was recovered in lymph. After an awake period of 6 or 24 h, 30% was regained in the liver. The recoveries in other organs were negligible and mesenteric lymph nodes seem quantitatively unimportant in the uptake of hyaluronan or gelatin from lymph or blood. The liver has a central role in intestinal hyaluronan metabolism, while denatured collagen is more prone to local degradation with remote uptake shared between the liver and the kidney.

Increased lymphatic hyaluronan output and preserved hyaluronan content of the rat small intestine in prolonged hypoproteinaemia.

Nephrotic syndrome was induced in seven rats by daily aminonucleoside injections. Experiments were performed in anaesthesia 6 or 7 d later when protein loss in urine had reduced serum colloid osmotic pressure (COP) to 8.2 +/- 0.9 (SD) mmHg compared with 20.2 +/- 2.2 mmHg in controls (P < 0.01). Due to the decreased COP in the nephrotic rats, lymph flow in the main mesenteric lymphatic was 29.5 +/- 11.5 microliters min-1 compared with 4.2 +/- 2.2 microliters min-1 in the control rats (P < 0.01). The corresponding hyaluronan concentrations were 3.4 +/- 0.9 micrograms ml-1 and 12.0 +/- 3.5 micrograms ml-1, respectively (P < 0.01). Nevertheless lymphatic hyaluronan output was doubled in the nephrotic rats, but this did not affect the hyaluronan content of the small intestine of 192 +/- 58 micrograms g-1 dry wt compared with 215 +/- 69 micrograms g-1 in controls (P > 0.05). During a 20 min intravenous 0.9% saline infusion of 4 ml 100 g-1 rat, the hyaluronan concentration increased to 18.3 (6.0) micrograms ml-1 in mesenteric lymph in controls, whereas the concentration in lymph from the nephrotic rats remained unchanged. Lymphatic output increased, however, in this group as well due to the elevated flow. The amount of hyaluronan cleared daily by the main mesenteric lymphatic in awake rats corresponds to about half the tissue hyaluronan content in the drained area (østgaard & Reed 1993 b).(ABSTRACT TRUNCATED AT 250 WORDS)

Increased negatively of interstitial fluid pressure in rat skin contributes to the edema formation induced by Zymosan.

Increased negatively of interstitial fluid pressure (Pif) contributes to rapid edema formation in several acute inflammatory reactions attesting to an "active" role for the loose connective tissues in the transcapillary fluid exchange and edema formation under these circumstances. The present study reports the effect of the complement activator Zymosan on Pif, transcapillary fluid, and albumin flux. Micropipettes (tip diameter 5 to 7 microns) connected to a servo-controlled counterpressure system were used to measure Pif in rat dermis. When compared to saline injection, subdermal injection of 1 mg Zymosan in 10 microliters 0.15 M NaCl increased total tissue water by 1.6 ml/g dry weight in 5 min, corresponding to about 150% increase in interstitial fluid volume. Pif increased from +0.4 to +3.7 mm Hg. Increased negativity of Pif can be masked by the edema formation which will increase Pif. Measurements were therefore also performed after circulatory arrest, when transcapillary fluid flux and edema formation are abolished. Using this experimental protocol Pif fell from +0.3 mm Hg to -2.5 mm Hg 5 min after subdermal injection of Zymosan and remained at this level throughout the observation period of 90 min. Injection of saline alone after circulatory arrest increased Pif transiently by about 1 mm Hg. Thus, subdermal injection of Zymosan causes increased negativity of Pif by about 4 mm Hg. Although the lowering of Pif itself will explain a minor part of the increased fluid filtration, the results attest to the role of loose connective tissues being active in the edema-generating process also in the inflammatory reaction induced by Zymosan.

Hyaluronan turnover in the rat small intestine.

The main metabolic pathway for the interstitial matrix component hyaluronan seems to be via lymph. Present estimates of turnover of intestinal hyaluronan are based on isolated organs and/or experiments in anaesthesia over a few hours. In this study lymph was sampled from the main mesenteric lymphatic for 24 h in awake, restrained rats. The tissue content of hyaluronan averaged 28 micrograms g-1 in the duodenum/jejunum and 124 micrograms g-1 in the colon. Based on tissue content and lymphatic output, the turnover rate of hyaluronan in the small intestine was estimated at approximately 50%. In another experimental group anaesthetized rats were fed either phosphate buffer or triolein in buffer via a gastric tube. Lymph flow increased with fluid absorption from the gut and hyaluronan output in lymph was elevated correspondingly. However, no effect of acute fat administration on hyaluronan concentration or lymph flow could be demonstrated.

Intravenous saline infusion in rat increases hyaluronan efflux in intestinal lymph by increasing lymph flow.

The output of hyaluronan in mesenteric lymph was studied in anaesthetized rats to allow estimation of the turnover rate. The duodenum/jejunum contained 45 micrograms of this glycosaminoglycan per g wet tissue weight. In fasted rats the concentration of hyaluronan in postnodal lymph averaged 15 micrograms ml-1 and the mean efflux was 2.1 micrograms h-1, corresponding to a daily removal of 10% of the intestinal hyaluronan content. An intravenously injected bolus of 0.9% saline 4 ml 100 g-1 followed by an infusion of the same amount per hour increased the hyaluronan concentration in lymph transiently to 22 micrograms ml-1. During the 8-h i.v. infusion the hyaluronan output remained five times above control due to the high lymph flow. Water and hyaluronan content of the small intestine remained unaltered despite the saline load, the maintained tissue level of hyaluronan suggests an increased rate of synthesis.