Influence of ERAS protocol on postoperative outcomes after elective colorectal resection surgery: A prospective cohort study- two years single center experience

Background ERAS (Enhanced Recovery After Surgery) protocol is a multimodal pathway of perioperative surgical care consisting of evidence-based procedures. ERAS protocol is hardly accepted by medical staff because it often opposes well established practice. Methods We analyzed length of hospital stay, postoperative complications, time until first stool passage and introduction of normal nutrition in patients undergoing elective colorectal resection surgery in University Hospital Center Split from October 2016. to October 2018. Patients were divided into 4 groups considering operation type (open/laparoscopic) and application of ERAS protocol (good/poor). Application of 60% or more ERAS steps was considered as well performed protocol. Results Groups Laparoscopy/ERAS and Open/ERAS had shorter postoperative hospital stay (Median, IQR; days) than groups Laparoscopy/non-ERAS and Open/non-ERAS (LE 5, 4-8 , OE 6, 5-9 vs LNE 7, 5-8,5 , ONE 7, 6-12). Similar difference was shown in times until first stool passage. Patients operated laparoscopically had shorter times until normal food tolerance (Median, IQR; days): LE 3, 2-3, LNE 3, 2-4 than patients who underwent open surgery (OE 3, 3-4, ONE 4, 3-5). In addition, laparoscopically operated patients had lower overall morbidity (P<0.001). Incidence of unplanned operations and hospital readmissions did not differ significantly among groups. Conclusions Well performed ERAS protocol can improve length of hospital stay and time until first stool passage in both open and laparoscopic types of operation. Optimal combination for colorectal resection is laparoscopic surgery with ERAS protocol. If open surgery is done, it should be preferably applied with ERAS protocol as well

Effect of remifentanil on rat long-term phrenic nerve facilitation in acute repeated hypoxia model

Cilj istraživanja bio je utvrditi hoće li intravenska infuzija agonista μ-opioidnih receptora remifentanila spriječiti pojavu dugoročne facilitacije freničkoga živca (pLTF) u modelu ponavljanih hipoksija u odraslih mužjaka štakora vrste Sprague-Dawley, koji su obostrano vagotomizirani, paralizirani i mehanički ventilirani te anestezirani uretanom. Remifentanilska (n=12) i naloksonska skupina životinja (n=4) primale su trajnu infuziju remifentanila u dozi 0,5 μg/kg/min, dok je kontrolna skupina životinja (n=6) primala infuziju 0,9% NaCl. Sve životinje bile su podvrgnute protokolu akutne ponavljane hipoksije (AIH protokol). Vršna aktivnost freničkog živca (pPNA), frekvencija disanja (f), trajanje inspirija (Ti), ekspirija (Te) te ukupno trajanje respiracijskog ciklusa (Ttot) mjereni su tijekom svih pet hipoksijskih epizoda, te 15, 30 i 60 minuta nakon poslijednje hipoksije. Dobivene vrijednosti uspoređivane su s početnim vrijednostima prije izlaganja životinja protokolu akutne ponavljane hipoksije. U remifentanilskoj skupini određena još jedna točka mjerenja u kojoj se nakon zaustavljanja infuzije remifentanila, nakon 15 minuta mjerila vršna aktivnost freničkoga živca kao i trajanje pojedinih faza u ciklusu disanja koje su uspoređene s aktivnošću freničkoga živca prije početka primjene infuzije remifentanila. U naloksonskoj skupini primjenjena je jednokratna doza anatagonista μ-opioidnih receptora naloksona u dozi 0,1 mg/kg. U kontrolnoj skupini životinja, vršna aktivnost freničkog živca (pPNA) bila je statistički značajno veća 60 minuta nakon poslijednje hipoksije (T60, povećanje od 138,8±28,3 %, p=0,006) u odnosu na početne vrijednosti, tj. primjećena je pojava pLTF-a. U remifentanilskoj skupini životinja, nije primjećena statistički značajna razlika vrijednostima pPNA u vremenskoj točki T60 u usporedbi s početnim vrijednostima (smanjenje od 5,3±16,5%, p>0,05), tj. nije došlo do nastanka pLTF-a. Vršna aktivnost freničkog živca petnaest minuta nakon zaustavljanja infuzije remifentanila povećala se u odnosu na početne vrijednosti za 93,2±40,2% (p<0,05), te je ostala povećana tijekom slijedećih 30 minuta. To je značilo da nakon prestanka infuzije remifentanila a nakon izlaganja životinja AIH protokolu dolazi do nastanka pLTF-a. Primjena antagonista μ-opioidnih receptora naloksona 60 minuta nakon posljednje hipoksije dovela je do statistički značajnog povećanja vrijednosti pPNA (povećanje od 309±21,3%, p<0,05), odnosno došlo je do nastanka pLTF-a- Možemo zaključiti kako je primjena remifentanila, kratkodjelujućeg agonista μ-opioidnih receptora, reverzibilno spriječila pojavu freničkog LTF-a.The aim was to investigate whether intravenous infusion of remifentanil would depress phrenic long term facilitation (pLTF) evoked by acute intermittent hypoxia (AIH) in adult, male, urethane anaesthetized Sprague-Dawley rats, bilaterally vagotomized, paralyzed and mechanically ventilated. The remifentanil (n=12) and naloxone group (n=4) received a remifentanil infusion (0,5 μg/kg/min i.v., n=12), whereas the control group (n=6) received saline. Rats were exposed to AIH protocol. Phrenic nerve amplitude (PNA), burst frequency (f) and breathing rhythm parameters (Ti, Te, Ttot) were analyzed during 5 hypoxias and at 15, 30, and 60 minutes after the final hypoxia, and compared to baseline values. At the end of the experiment, the infusion of remifentanil was stopped and phrenic nerve activity was compared to baseline values prior to remifentanil infusion, whereas in the naloxone group opioid antagonist naloxone was applied (0,1 mg/kg). In the control group, peak phrenic nerve activity (pPNA) significantly increased at 60 min (T60, increase by 138,8±28,3%, p=0,006) after the last hypoxic episode compared to baseline values, i.e. pLTF was induced. In remifentanil treated rats, there were no significant changes in peak phrenic nerve activity at T60 compared to baseline values (decrease by 5,3±16,5%, p>0.05), i.e.pLTF was abolished. Fifteen minutes following cessation of remifentanil infusion, pPNA increased by 93,2±40,2% (p<0,05) and remained increased compared to pre-remifentanil-infusion values for more than 30 minutes, i.e. pLTF could be observed after cessation of the remifentanil infusion. Naloxone reversed remifentanil action, and few minutes after iv. injection, i.e. pPNA increased by 309±21,3% (p<0,05) and pLTF was observed. In conclusion, the short acting μ-opioid receptor agonist, remifentanil, reversibly abolished phrenic long term facilitation in urethane anesthetized rats

Effect of remifentanil on rat long-term phrenic nerve facilitation in acute repeated hypoxia model

Cilj istraživanja bio je utvrditi hoće li intravenska infuzija agonista μ-opioidnih receptora remifentanila spriječiti pojavu dugoročne facilitacije freničkoga živca (pLTF) u modelu ponavljanih hipoksija u odraslih mužjaka štakora vrste Sprague-Dawley, koji su obostrano vagotomizirani, paralizirani i mehanički ventilirani te anestezirani uretanom. Remifentanilska (n=12) i naloksonska skupina životinja (n=4) primale su trajnu infuziju remifentanila u dozi 0,5 μg/kg/min, dok je kontrolna skupina životinja (n=6) primala infuziju 0,9% NaCl. Sve životinje bile su podvrgnute protokolu akutne ponavljane hipoksije (AIH protokol). Vršna aktivnost freničkog živca (pPNA), frekvencija disanja (f), trajanje inspirija (Ti), ekspirija (Te) te ukupno trajanje respiracijskog ciklusa (Ttot) mjereni su tijekom svih pet hipoksijskih epizoda, te 15, 30 i 60 minuta nakon poslijednje hipoksije. Dobivene vrijednosti uspoređivane su s početnim vrijednostima prije izlaganja životinja protokolu akutne ponavljane hipoksije. U remifentanilskoj skupini određena još jedna točka mjerenja u kojoj se nakon zaustavljanja infuzije remifentanila, nakon 15 minuta mjerila vršna aktivnost freničkoga živca kao i trajanje pojedinih faza u ciklusu disanja koje su uspoređene s aktivnošću freničkoga živca prije početka primjene infuzije remifentanila. U naloksonskoj skupini primjenjena je jednokratna doza anatagonista μ-opioidnih receptora naloksona u dozi 0,1 mg/kg. U kontrolnoj skupini životinja, vršna aktivnost freničkog živca (pPNA) bila je statistički značajno veća 60 minuta nakon poslijednje hipoksije (T60, povećanje od 138,8±28,3 %, p=0,006) u odnosu na početne vrijednosti, tj. primjećena je pojava pLTF-a. U remifentanilskoj skupini životinja, nije primjećena statistički značajna razlika vrijednostima pPNA u vremenskoj točki T60 u usporedbi s početnim vrijednostima (smanjenje od 5,3±16,5%, p>0,05), tj. nije došlo do nastanka pLTF-a. Vršna aktivnost freničkog živca petnaest minuta nakon zaustavljanja infuzije remifentanila povećala se u odnosu na početne vrijednosti za 93,2±40,2% (p<0,05), te je ostala povećana tijekom slijedećih 30 minuta. To je značilo da nakon prestanka infuzije remifentanila a nakon izlaganja životinja AIH protokolu dolazi do nastanka pLTF-a. Primjena antagonista μ-opioidnih receptora naloksona 60 minuta nakon posljednje hipoksije dovela je do statistički značajnog povećanja vrijednosti pPNA (povećanje od 309±21,3%, p<0,05), odnosno došlo je do nastanka pLTF-a- Možemo zaključiti kako je primjena remifentanila, kratkodjelujućeg agonista μ-opioidnih receptora, reverzibilno spriječila pojavu freničkog LTF-a.The aim was to investigate whether intravenous infusion of remifentanil would depress phrenic long term facilitation (pLTF) evoked by acute intermittent hypoxia (AIH) in adult, male, urethane anaesthetized Sprague-Dawley rats, bilaterally vagotomized, paralyzed and mechanically ventilated. The remifentanil (n=12) and naloxone group (n=4) received a remifentanil infusion (0,5 μg/kg/min i.v., n=12), whereas the control group (n=6) received saline. Rats were exposed to AIH protocol. Phrenic nerve amplitude (PNA), burst frequency (f) and breathing rhythm parameters (Ti, Te, Ttot) were analyzed during 5 hypoxias and at 15, 30, and 60 minutes after the final hypoxia, and compared to baseline values. At the end of the experiment, the infusion of remifentanil was stopped and phrenic nerve activity was compared to baseline values prior to remifentanil infusion, whereas in the naloxone group opioid antagonist naloxone was applied (0,1 mg/kg). In the control group, peak phrenic nerve activity (pPNA) significantly increased at 60 min (T60, increase by 138,8±28,3%, p=0,006) after the last hypoxic episode compared to baseline values, i.e. pLTF was induced. In remifentanil treated rats, there were no significant changes in peak phrenic nerve activity at T60 compared to baseline values (decrease by 5,3±16,5%, p>0.05), i.e.pLTF was abolished. Fifteen minutes following cessation of remifentanil infusion, pPNA increased by 93,2±40,2% (p<0,05) and remained increased compared to pre-remifentanil-infusion values for more than 30 minutes, i.e. pLTF could be observed after cessation of the remifentanil infusion. Naloxone reversed remifentanil action, and few minutes after iv. injection, i.e. pPNA increased by 309±21,3% (p<0,05) and pLTF was observed. In conclusion, the short acting μ-opioid receptor agonist, remifentanil, reversibly abolished phrenic long term facilitation in urethane anesthetized rats

Effect of remifentanil on rat long-term phrenic nerve facilitation in acute repeated hypoxia model

Cilj istraživanja bio je utvrditi hoće li intravenska infuzija agonista μ-opioidnih receptora remifentanila spriječiti pojavu dugoročne facilitacije freničkoga živca (pLTF) u modelu ponavljanih hipoksija u odraslih mužjaka štakora vrste Sprague-Dawley, koji su obostrano vagotomizirani, paralizirani i mehanički ventilirani te anestezirani uretanom. Remifentanilska (n=12) i naloksonska skupina životinja (n=4) primale su trajnu infuziju remifentanila u dozi 0,5 μg/kg/min, dok je kontrolna skupina životinja (n=6) primala infuziju 0,9% NaCl. Sve životinje bile su podvrgnute protokolu akutne ponavljane hipoksije (AIH protokol). Vršna aktivnost freničkog živca (pPNA), frekvencija disanja (f), trajanje inspirija (Ti), ekspirija (Te) te ukupno trajanje respiracijskog ciklusa (Ttot) mjereni su tijekom svih pet hipoksijskih epizoda, te 15, 30 i 60 minuta nakon poslijednje hipoksije. Dobivene vrijednosti uspoređivane su s početnim vrijednostima prije izlaganja životinja protokolu akutne ponavljane hipoksije. U remifentanilskoj skupini određena još jedna točka mjerenja u kojoj se nakon zaustavljanja infuzije remifentanila, nakon 15 minuta mjerila vršna aktivnost freničkoga živca kao i trajanje pojedinih faza u ciklusu disanja koje su uspoređene s aktivnošću freničkoga živca prije početka primjene infuzije remifentanila. U naloksonskoj skupini primjenjena je jednokratna doza anatagonista μ-opioidnih receptora naloksona u dozi 0,1 mg/kg. U kontrolnoj skupini životinja, vršna aktivnost freničkog živca (pPNA) bila je statistički značajno veća 60 minuta nakon poslijednje hipoksije (T60, povećanje od 138,8±28,3 %, p=0,006) u odnosu na početne vrijednosti, tj. primjećena je pojava pLTF-a. U remifentanilskoj skupini životinja, nije primjećena statistički značajna razlika vrijednostima pPNA u vremenskoj točki T60 u usporedbi s početnim vrijednostima (smanjenje od 5,3±16,5%, p>0,05), tj. nije došlo do nastanka pLTF-a. Vršna aktivnost freničkog živca petnaest minuta nakon zaustavljanja infuzije remifentanila povećala se u odnosu na početne vrijednosti za 93,2±40,2% (p<0,05), te je ostala povećana tijekom slijedećih 30 minuta. To je značilo da nakon prestanka infuzije remifentanila a nakon izlaganja životinja AIH protokolu dolazi do nastanka pLTF-a. Primjena antagonista μ-opioidnih receptora naloksona 60 minuta nakon posljednje hipoksije dovela je do statistički značajnog povećanja vrijednosti pPNA (povećanje od 309±21,3%, p<0,05), odnosno došlo je do nastanka pLTF-a- Možemo zaključiti kako je primjena remifentanila, kratkodjelujućeg agonista μ-opioidnih receptora, reverzibilno spriječila pojavu freničkog LTF-a.The aim was to investigate whether intravenous infusion of remifentanil would depress phrenic long term facilitation (pLTF) evoked by acute intermittent hypoxia (AIH) in adult, male, urethane anaesthetized Sprague-Dawley rats, bilaterally vagotomized, paralyzed and mechanically ventilated. The remifentanil (n=12) and naloxone group (n=4) received a remifentanil infusion (0,5 μg/kg/min i.v., n=12), whereas the control group (n=6) received saline. Rats were exposed to AIH protocol. Phrenic nerve amplitude (PNA), burst frequency (f) and breathing rhythm parameters (Ti, Te, Ttot) were analyzed during 5 hypoxias and at 15, 30, and 60 minutes after the final hypoxia, and compared to baseline values. At the end of the experiment, the infusion of remifentanil was stopped and phrenic nerve activity was compared to baseline values prior to remifentanil infusion, whereas in the naloxone group opioid antagonist naloxone was applied (0,1 mg/kg). In the control group, peak phrenic nerve activity (pPNA) significantly increased at 60 min (T60, increase by 138,8±28,3%, p=0,006) after the last hypoxic episode compared to baseline values, i.e. pLTF was induced. In remifentanil treated rats, there were no significant changes in peak phrenic nerve activity at T60 compared to baseline values (decrease by 5,3±16,5%, p>0.05), i.e.pLTF was abolished. Fifteen minutes following cessation of remifentanil infusion, pPNA increased by 93,2±40,2% (p<0,05) and remained increased compared to pre-remifentanil-infusion values for more than 30 minutes, i.e. pLTF could be observed after cessation of the remifentanil infusion. Naloxone reversed remifentanil action, and few minutes after iv. injection, i.e. pPNA increased by 309±21,3% (p<0,05) and pLTF was observed. In conclusion, the short acting μ-opioid receptor agonist, remifentanil, reversibly abolished phrenic long term facilitation in urethane anesthetized rats

Effects on Recovery of Pediatric Patients Undergoing Total Intravenous Anesthesia with Propofol versus Ketofol for Short—Lasting Laparoscopic Procedures

Background: Combining ketamine and propofol (ketofol) was suggested as a new concept for sedation and general anesthesia in pediatric populations for various conditions. The aim of the present study was to determine the effect of total intravenous anesthesia (TIVA) with propofol and ketofol on recovery after laparoscopic surgery in pediatric patients. Methods: Two hundred children with median age of 5 years who underwent laparoscopic surgery were randomized into two groups. Propofol 1% was used for induction and maintenance of anesthesia in group I, while ketamine-propofol combination (ketofol) was used in group II. Ketamine-propofol combination (ketofol) was prepared in the same applicator for group II. Ketofol ratios of 1:4 and 1:7 were used for induction and maintenance of anesthesia, respectively. A reduced McFarlan infusion dose was used in group I (1.2, 1.0, and 0.8 mL/kg/h for 15, 15, and 30 min, respectively), while a McFarlan infusion dose was used in group II (1.5, 1.3, and 1.1 mL/kg/h for 15, 15, and 30 min, respectively). Extubating time, duration of anesthesia, and length of stay in post-anesthesia care unit (PACU) were recorded. Results: Extubating time was significantly lower in the ketofol group than in the propofol group (240 s vs. 530 s; p &lt; 0.00001). Significantly shorter duration of anesthesia (47 min vs. 60 min; p &lt; 0.00001) as well as length of stay in the PACU (35 min vs. 100 min; p &lt; 0.00001) were recorded in ketofol compared to the propofol group. Total fentanyl (100 µg (interquartile range, IQR 80, 125) vs. 50 µg (IQR 40, 60); p &lt; 0.00001) and propofol (260 mg (IQR 200, 350) vs. 160 mg (IQR 120, 210); p &lt; 0.00001) consumption per body weight were significantly lower in the ketofol group. Conclusions: TIVA with ketamine-propofol combination (ketofol) using a reduced McFarlan dose regimen shortened extubating time, duration of anesthesia, as well as length of stay in the PACU in pediatric anesthesia after laparoscopic surgery

Nonelective surgery at night and in-hospital mortality - Prospective observational data from the European Surgical Outcomes Study

BACKGROUND Evidence suggests that sleep deprivation associated with night-time working may adversely affect performance resulting in a reduction in the safety of surgery and anaesthesia. OBJECTIVE Our primary objective was to evaluate an association between nonelective night-time surgery and in-hospital mortality. We hypothesised that urgent surgery performed during the night was associated with higher in-hospital mortality and also an increase in the duration of hospital stay and the number of admissions to critical care. DESIGN A prospective cohort study. This is a secondary analysis of a large database related to perioperative care and outcome (European Surgical Outcome Study). SETTING Four hundred and ninety-eight hospitals in 28 European countries. PATIENTS Men and women older than 16 years who underwent nonelective, noncardiac surgery were included according to time of the procedure. INTERVENTION None. MAIN OUTCOME MEASURES Primary outcome was in-hospital mortality; the secondary outcome was the duration of hospital stay and critical care admission. RESULTS Eleven thousand two hundred and ninety patients undergoing urgent surgery were included in the analysis with 636 in-hospital deaths (5.6%). Crude mortality odds ratios (ORs) increased sequentially from daytime [426 deaths (5.3%)] to evening [150 deaths (6.0%), OR 1.14; 95% confidence interval 0.94 to 1.38] to night-time [60 deaths (8.3%), OR 1.62; 95% confidence interval 1.22 to 2.14]. Following adjustment for confounding factors, surgery during the evening (OR 1.09; 95% confidence interval 0.91 to 1.31) and night (OR 1.20; 95% confidence interval 0.9 to 1.6) was not associated with an increased risk of postoperative death. Admittance rate to an ICU increased sequentially from daytime [891 (11.1%)], to evening [347 (13.8%)] to night time [149 (20.6%)]. CONCLUSION In patients undergoing nonelective urgent noncardiac surgery, in-hospital mortality was associated with well known risk factors related to patients and surgery, but we did not identify any relationship with the time of day at which the procedure was performed