30-day adverse events,length of stay and re-admissions following surgical management of pelvic/acetabular fractures

IntroductionPelvic/acetabular fractures are associated with significant morbidity, mortality and cost to the society. We sought to utilize a national surgical database to assess the incidence and factors associated with prolonged length of stay (LOS), non-home discharge destination, 30-day adverse events and readmissions following surgical fixation of pelvic/acetabular fractures.Materials & methodsThe 2011–2016 ACS-NSQIP database files were queried using CPT codes (27215, 27217, 27218, 27226, 27227, 27228) for patients undergoing open reduction/internal fixation (ORIF) for pelvic/acetabular fractures. Patients undergoing additional procedures for associated fractures (vertebral fractures, distal radius/ulna fractures or femoral neck/hip fractures) were excluded from the analysis to ensure that a relevant population of patients with isolated pelvic/acetabular injuries were included in the analysis. A total of 572 patients were included in the final cohort. Severe adverse events (SAE) were defined as: death, ventilator use >48 h, unplanned intubation, stroke, deep venous thrombosis, pulmonary embolism, cardiac arrest, myocardial infarction, acute renal failure, sepsis, septic shock, re-operation, deep SSI and organ/space SSI. Minor adverse events (MAE) included – wound dehiscence, superficial SSI, urinary tract infection (UTI) and progressive renal insufficiency. An extended LOS was defined as >75th centile (>9days).ResultsFactors associated with AAE were partially dependent functional health status pre-operatively (p = 0.020), transfusion ≥1 unit of packed RBCs (p = 0.001), and ASA > II (p < 0.001). Experiencing a SAE was associated with congestive heart failure (CHF) pre-operatively [p = 0.005), total operative time >140 min (p = 0.034) and Hct <36 pre-operatively (p = 0.003). MAE was associated with transfusion≥1 unit of packed RBCs (p = 0.022) and ASA > II (p = 0.007). Patients with an ASA > II (p = 0.001), total operative time>140 min (p < 0.001) and Hct <36 (p = 0.006) were more likely to have a LOS >9 days. Male gender (p = 0.026), prior history of CHF (p = 0.024), LOS >9 days (p = 0.030) and >10% bodyweight loss in last 6 months before the procedure (p = 0.002) were predictors of 30-day mortality.ConclusionPatients with ASA grade > II, greater co-morbidity burden and prolonged operative times were likely to experience adverse events and have a longer length of stay. Surgeons can utilize this data to risk stratify patients so that appropriate pre-operative and post-operative medical optimization can take place.     

The rate of hepatic artery complications is higher in pediatric liver transplant recipients with metabolic liver diseases than with biliary atresia

Background

Liver transplantation (LT) is an excellent treatment option for patients with biliary atresia (BA) who fail portoenterostomy surgery. LT is also increasingly performed in patients with metabolic liver diseases. This study compared the outcomes in pediatric patients who underwent LT for metabolic liver diseases and BA.

Laparoscopic sleeve gastrectomy as a viable option for an ambulatory surgical procedure: our 52-month experience

Background

We present our experience with same-day discharge (without an overnight stay) after laparoscopic sleeve gastrectomy (SG) in 821 consecutive patients from 2011 to 2015. This is the largest series published to date of patients undergoing ambulatory surgery for such a procedure.

Outcomes of liver transplantation for Alagille syndrome after Kasai portoenterostomy: Alagille Syndrome with agenesis of extrahepatic bile ducts at porta hepatis

BackgroundAlagille syndrome (ALGS) is an autosomal dominant disorder, characterized by a paucity of intrahepatic bile ducts, resulting in significant cholestasis, and peculiar extrahepatic features. Some ALGS patients show a considerable overlap with biliary atresia (BA), and they can undergo Kasai procedure. The purpose of this study is to show the manifestations of BA overlapped ALGS cases in our institution, and to compare the outcomes of ALGS patients following liver transplantation (LT) between those who previously underwent Kasai surgery (ALGS-Kasai group) and those who did not (ALGS-non-Kasai group).MethodsMedical records of ALGS patients who underwent LT in Kyoto University Hospital, Japan from January 1992 to March 2018 were analyzed. ALGS diagnosis was determined according to physical, radiologic, and histopathological findings.ResultsThirty-one patients were ascertained (ALGS-Kasai: 4 males and 5 females vs. ALGS-non-Kasai: 14 males and 8 females, p = 0.43). Of 31 ALGS patients, 96.8% of children had pulmonary artery stenosis, 54.8% showed facial features, 29% revealed skeletal anomalies and 9.7% demonstrated ocular anomalies. The age at LT was significantly younger in ALGS-Kasai than ALGS-non-Kasai group (1.47 [interquartile range (IQR), 0.75–1.92] vs. 5.1 [IQR, 1.4–9.29] years; p = 0.038). Overall patient survival did not significantly differ between ALGS-Kasai (88.9%) and ALGS-non-Kasai patients (86.4%) (p = 0.84). Furthermore, the 1-year, 5-year, and 10-year patient survival rates for ALGS-Kasai group were 100%, 88.9%, and 88.9%, respectively, whereas those for ALGS-non-Kasai group were 90.9%, 90.9%, and 86.4%, respectively, with p-values of 0.36, 0.90, and 0.84, respectively.ConclusionsBA overlapped ALGS cases had neonatal progressive cholestasis which prompted Kasai procedure, and early liver dysfunction after Kasai led to performing LT. The ALGS-Kasai patients undergo LT at earlier ages than the ALGS-non-Kasai patients, however, overall patients' survival rates are similar between groups. Overall ALGS patients' survival rate after LT is considered high.Levels of EvidenceLevel III; Case–control study or Retrospective comparative study.     

Intraventricular ascorbic acid administration decreases hypoxic-ischemic brain injury in newborn rats

Neuronal cell damage following hypoxic-ischemic (HI) brain injury is partly caused by production of free radicals and reactive oxygen species (ROS). Ascorbic acid (AA) is a potent antioxidant, which scavenges various types of ROS. Some studies have shown that it is neuroprotective, however, the issue is still controversial. In this study, we examined the effect of intraventricular AA administration on immature HI brain using the Rice-Vannucci model. After unilateral carotid artery ligation under isoflurane anesthesia, 7-day-old rat pups received varying concentrations of AA (0.04, 0.2, 1 and 5 mg/kg) by intraventricular injection and were exposed to 8% oxygen for 90 min. Vehicle controls received an equal volume of phosphate saline buffer. We assessed the neuroprotective effect of AA at 7 days post-HI. The percent brain damage measured by comparing the wet weight of the ligated side of hemisphere with that of contralateral one was reduced in both 1 and 5 mg/kg groups but not in either 0.04 or 0.2 mg/kg groups compared to vehicle controls (5 mg/kg 16.0 +/- 4.3%, 1 mg/kg 10.9 +/- 5.0%, vs. controls 36.7 +/- 3.6%, P < 0.05). Macroscopic evaluation of brain injury revealed the neuroprotective effect of AA in both 1 and 5 mg/kg groups (5 mg/kg 1.1 +/- 0.4, 1 mg/kg 0.4 +/- 0.3, vs. controls 2.9 +/- 0.3, P < 0.05). Western blots of fodrin on the ligated side also showed that AA significantly suppressed 150/145-kDa bands of fodrin breakdown products, which suggested that AA suppressed activation of calpain. Neuropathological quantitative analysis of cell death revealed that 1 mg/kg of AA injection significantly reduced the number of necrotic cells in cortex, caudate putamen, thalamus and hippocampus CA1, whereas that of apoptotic cells was only reduced in cortex. These findings show that intraventricular AA injection is neuroprotective after HI in immature rats.     

Nocturnal hyperactivity, increased social novelty preference and delayed extinction of fear responses in post-weaning socially isolated mice

When rodents are reared in isolation from young age onwards, they manifest a number of behavioural alterations in adulthood. Since some of these alterations resemble symptoms of psychiatric disorders, the post-weaning social isolation (ISO) manipulation is often applied to create rodent models of these disorders. In rats, ISO effects have been thoroughly characterised, but in mice they are less well documented. Therefore, we further evaluated behaviour of adult ISO mice with a test battery that focussed on abnormalities relevant to schizophrenia. We found that ISO mice were hyperactive during the dark phase. Also, ISO mice showed alterations in magnitude, habituation and prepulse-inhibition of the acoustic startle reflex, increased anxiety, increased social preference and changes in extinction of fear responses. We did not observe increased sensitivity to locomotor-activating effects of amphetamine. It is concluded that ISO of mice might serve as a useful model to test further hypotheses regarding pathogenesis occurring at specific developmental timeframes.     

Adolescent development,hypothalamic-pituitary-adrenal function,and programming of adult learning and memory

Chronic exposure to stress is known to affect learning and memory in adults through the release of glucocorticoid hormones by the hypothalamic-pituitary-adrenal (HPA) axis. In adults, glucocorticoids alter synaptic structure and function in brain regions that express high levels of glucocorticoid receptors and that mediate goal-directed behaviour and learning and memory. In contrast to relatively transient effects of stress on cognitive function in adulthood, exposure to high levels of glucocorticoids in early life can produce enduring changes through substantial remodeling of the developing nervous system. Adolescence is another time of significant brain development and maturation of the HPA axis, thereby providing another opportunity for glucocorticoids to exert programming effects on neurocircuitry involved in learning and memory. These topics are reviewed, as is the emerging research evidence in rodent models highlighting that adolescence may be a period of increased vulnerability compared to adulthood in which exposure to high levels of glucocorticoids results in enduring changes in adult cognitive function.     

Differential regulation of HCN channel isoform expression in thalamic neurons of epileptic and non-epileptic rat strains

Hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels represent the molecular substrate of the hyperpolarization-activated inward current (I_h). Although these channels act as pacemakers for the generation of rhythmic activity in the thalamocortical network during sleep and epilepsy, their developmental profile in the thalamus is not yet fully understood. Here we combined electrophysiological, immunohistochemical, and mathematical modeling techniques to examine HCN gene expression and I_h properties in thalamocortical relay (TC) neurons of the dorsal part of the lateral geniculate nucleus (dLGN) in an epileptic (WAG/Rij) compared to a non-epileptic (ACI) rat strain. Recordings of TC neurons between postnatal day (P) 7 and P90 in both rat strains revealed that I_h was characterized by higher current density, more hyperpolarized voltage dependence, faster activation kinetics, and reduced cAMP-sensitivity in epileptic animals. All four HCN channel isoforms (HCN1-4) were detected in dLGN, and quantitative analyses revealed a developmental increase of protein expression of HCN1, HCN2, and HCN4 but a decrease of HCN3. HCN1 was expressed at higher levels in WAG/Rij rats, a finding that was correlated with increased expression of the interacting proteins filamin A (FilA) and tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b). Analysis of a simplified computer model of the thalamic network revealed that the alterations of I_h found in WAG/Rij rats compensate each other in a way that leaves I_h availability constant, an effect that ensures unaltered cellular burst activity and thalamic oscillations. These data indicate that during postnatal developmental the hyperpolarizing shift in voltage dependency (resulting in less current availability) is compensated by an increase in current density in WAG/Rij thereby possibly limiting the impact of I_h on epileptogenesis. Because HCN3 is expressed higher in young versus older animals, HCN3 likely does not contribute to alterations in I_h in older animals.     

Protective effect of N-acetylcysteine against BDE-209-induced neurotoxicity in primary cultured neonatal rat hippocampal neurons in vitro

Globally, brominated diphenyl ether-209 (BDE-209) is the most widely used polybrominated diphenyl ether (PBDEs). It has been reported that BDE-209 induces developmental neurotoxicity in vivo. The purpose of this study was to use an antioxidant, N-acetylcysteine (NAC), as an antidote for the neurotoxic effect of BDE-209. We used primary hippocampal neurons from rats for the in vitro cultures. BDE-209 was added to the cultures in increasing concentrations and co-cultured with NAC in order to assess the effect of NAC on BDE-209-induced neurotoxicity. We measured cell viability, apoptosis, expression of phosphorylated p38 mitogen-activated protein kinases (MAPK), intracellular calcium content, and intracellular reactive oxygen species (ROS) levels. The difference between the BDE-209 groups without NAC and the blank control groups was significant (P < 0.05). The difference between the NAC treatment groups and the BDE-209 groups without NAC was also significant (P < 0.05), showing that BDE-209 increased apoptosis, the expression of p38 MAPK, the calcium ion concentration, and the ROS level and decreased cell viability. In contrast, NAC reduced the degree of cellular cytotoxicity induced by BDE-209. The results suggested that NAC may be able to attenuate BDE-209-induced neurotoxicity.