30-Day Outcomes of Revisional Bariatric Stapling Procedures: First Report Based on MBSAQIP Data Registry

Introduction

The number of bariatric revisional cases has nearly doubled since 2011, and now comprises 13.6% of the total number of cases. The objective of this study is to evaluate the outcomes and safety of the two most common stapling revisional procedures, namely, sleeve and gastric bypass in comparison to primary stapling procedures using the MBSAQIP data registry.

Methods

We reviewed all the sleeve and gastric bypass cases entered between January 1, 2015, and December 31, 2015, in the MBSAQIP data registry. We, then, identified sleeve and bypass patients who have had a previous bariatric procedure. Demographics and 30 day outcomes of all sleeve and gastric bypass patients were analyzed. We conducted within group comparisons comparing primary sleeve gastrectomy (PS) and primary gastric bypass (PB) patients to revisional sleeve (RS) and revisional gastric bypass (RB) patients, respectively. We, then, conducted group comparisons comparing RS to RB patients.

Results

The total number of patients analyzed was 141,577 (98,292 or 69% sleeve patients and 43,285 or 31% gastric bypass patients). Among the sleeve patients, 92,666 (94%) had a PS and 5626 (6%) had RS. Among the bypass patients, 39,567 (91%) had a PB and 3718 patients (9%) had RB. 30-day readmission rate of RS was significantly higher as compared to PS (4.1 vs 0.4%, p?<?0.05). The incidence of at least one complication requiring reoperation or reintervention within 30 days following RS was twice as high as compared to PS (1.9 and 2% for RS vs 0.9 and 1.1% for PS respectively, p?<?0.05). Length of stay and 30 day mortality rates for PS and RS were the same. 30-day readmission rate of RB as compared to PB was 8.3 vs 6.3% (p?<?0.05). Also, the incidence of at least one complication requiring reoperation or reintervention following RB was 3.9 and 4%, respectively vs 2.4 and 2.7% for PB (p?<?0.05). In addition, readmission rates and unplanned admission rates to the ICU were significantly higher for RB compared to RS (8.3 and 2% for RB vs 4.1 and 0.9% for RS respectively, p?<?0.05). The incidence of at least one reoperation or one intervention following RB were also significantly higher compared to RS (3.9 vs 1.9% and 4 vs 2% respectively, p?<?0.05).

Conclusion

Revisional stapling procedures are safe but the rates of complications following RS and RB are twice as high compared to PS and PB. Also, RB are more likely to develop complications compared to RS.

     

Delayed-type Necrosis after Soft-tissue Augmentation with Hyaluronic Acid

The growing use of dermal fillers, specifically the use of hyaluronic acid, can be explained by their effectiveness and versatility as well as their favorable safety profiles. Nevertheless, early and late complications with varying levels of severity may occur. The incidence of complications is low and the majority of adverse events are mild (edema, erythema, and local ecchymosis) and of limited duration. However, more severe events, such as ischemia and necrosis, may occur. The symptoms of ischemia can occur immediately after the injection or several hours after the procedure. Here, the authors report three cases of necrosis after hyaluronic acid injection with the first symptoms presenting only several hours after the procedure. The patients were treated immediately after the diagnosis. The aim of this review is to communicate the possibility of the delayed-type presentation of necrosis, present the signs and symptoms that lead to early diagnosis, and review the treatment possibilities of this severe complication.Dermal fillers have been injected with increasing frequency over the past three decades for soft-tissue augmentation by volume expansion in the management of the aging face. In 2012, there were about two million procedures using dermal fillers, according to the American Society of Plastic Surgeons, five percent more than in 2011 and 205 percent more than in 2000, second only to botulinum toxin type A. These minimally invasive and nonsurgical cosmetic procedures were the two most commonly performed in this range of time studied.1,2The growing use of dermal fillers, specifically the use of hyaluronic acid (HA), can be explained by their effectiveness and versatility as well as their favorable safety profiles. Nevertheless, early and late complications with varying levels of severity may occur. The incidence of complications is low and the majority of adverse events are mild (edema, erythema, and local ecchymosis) and of limited duration. However, more severe events, such as ischemia and necrosis, may occur.Injection necrosis is a rare, but important, complication associated with dermal fillers. Necrosis can be attributed to one of two factors—an interruption of vascular supply due to compression or frank obstruction of vessels by direct injection of the material into a vessel itself. The glabella is the injection site commonly believed to be at greater risk for necrosis, but it can also occur at the nasolabial fold.3 Risk factors for intravascular injection include site of application (deep injection of filler products at or near the site of named vessels), volume applied (larger amounts of product can cause a proportionally greater degree of arterial obstruction), and previous scarring (deep tissue scars may stabilize and fix arteries in place, making them easier to penetrate with small sharp needles).4The initial presentation of vascular events may include pain and discomfort disproportionate to what is typically experienced following filler treatments and clinical findings, including blanching, livedo pattern, or violaceous discoloration.4 Although many cases report this immediate post-injection presentation as the typical background seen in a necrosis event, there are few reports with the first symptom presenting only hours after augmentation. See Figures 1 through ​through3,3, where the authors present three cases of vascular compromise after soft-tissue augmentation with delayed-type presentation. Open in a separate windowOpen in a separate windowFigures 2Aand 2B.Case 2: Necrosis and secondary infection 48 hours after the HA injection (a). Discrete scars in the affected area after treatment (b). Open in a separate windowOpen in a separate windowFigures 1Aand 1B.Case 1: Edema, erythema, and progressive violaceous reticulated patch, livedoid area were observed on the left cheek 36 hours after the injection (a). Complete healing five days after hyaluronidase application and nine days after the HA injection (b). Open in a separate windowOpen in a separate windowFigures 3Aand 3B.Case 3: Necrosis and secondary infection 48 hours after the HA injection (a). Erythema, hipercromia, and discreet scars in the affected area after treatment (b).     

Temporal dissociation of salience and prediction error responses to appetitive and aversive taste

The feedback‐related negativity (FRN), a frontocentral ERP occurring 200–350 ms after emotionally valued outcomes, has been posited as the neural correlate of reward prediction error, a key component of associative learning. Recent evidence challenged this interpretation and has led to the suggestion that this ERP expresses salience instead. Here, we distinguish between utility prediction error and salience by delivering or withholding hedonistically matched appetitive and aversive tastes, and measure ERPs to cues signaling each taste. We observed a typical FRN (computed as the loss‐minus‐gain difference wave) to appetitive taste, but a reverse FRN to aversive taste. When tested axiomatically, frontocentral ERPs showed a salience response across tastes, with a particularly early response to outcome delivery, supporting recent propositions of a fast, unsigned, and unspecific response to salient stimuli. ERPs also expressed aversive prediction error peaking at 285 ms, which conformed to the logic of an axiomatic model of prediction error. With stimuli that most resemble those used in animal models, we did not detect any frontocentral ERP signal for utility prediction error, in contrast with dominant views of the functional role of the FRN ERP. We link the animal and human literature and present a challenge for current perspectives on associative learning research using ERPs.     

Variants in CIB2 cause DFNB48 and not USH1J

The genetic, mutational and phenotypic spectrum of deafness‐causing genes shows great diversity and pleiotropy. The best examples are the group of genes, which when mutated can either cause non‐syndromic hearing loss (NSHL) or the most common dual sensory impairment, Usher syndrome (USH). Variants in the CIB2 gene have been previously reported to cause hearing loss at the DFNB48 locus and deaf‐blindness at the USH1J locus. In this study, we characterize the phenotypic spectrum in a multiethnic cohort with autosomal recessive non‐syndromic hearing loss (ARNSHL) due to variants in the CIB2 gene. Of the 6 families we ascertained, 3 segregated novel loss‐of‐function (LOF) variants, 2 families segregated missense variants (1 novel) and 1 family segregated a previously reported pathogenic variant in trans with a frameshift variant. This report is the first to show that biallelic LOF variants in CIB2 cause ARNSHL and not USH. In the era of precision medicine, providing the correct diagnosis (NSHL vs USH) is essential for patient care as it impacts potential intervention and prevention options for patients. Here, we provide evidence disqualifying CIB2 as an USH‐causing gene.     

Fibroblast growth factor 2 decreases bleomycin‐induced pulmonary fibrosis and inhibits fibroblast collagen production and myofibroblast differentiation

Fibroblast growth factor (FGF) signaling has been implicated in the pathogenesis of pulmonary fibrosis. Mice lacking FGF2 have increased mortality and impaired epithelial recovery after bleomycin exposure, supporting a protective or reparative function following lung injury. To determine whether FGF2 overexpression reduces bleomycin‐induced injury, we developed an inducible genetic system to express FGF2 in type II pneumocytes. Double‐transgenic (DTG) mice with doxycycline‐inducible overexpression of human FGF2 (SPC‐rtTA;TRE‐hFGF2) or single‐transgenic controls were administered intratracheal bleomycin and fed doxycycline chow, starting at either day 0 or day 7. In addition, wild‐type mice received intratracheal or intravenous recombinant FGF2, starting at the time of bleomycin treatment. Compared to controls, doxycycline‐induced DTG mice had decreased pulmonary fibrosis 21 days after bleomycin, as assessed by gene expression and histology. This beneficial effect was seen when FGF2 overexpression was induced at day 0 or day 7 after bleomycin. FGF2 overexpression did not alter epithelial gene expression, bronchoalveolar lavage cellularity or total protein. In vitro studies using primary mouse and human lung fibroblasts showed that FGF2 strongly inhibited baseline and TGFβ1‐induced expression of alpha smooth muscle actin (αSMA), collagen, and connective tissue growth factor. While FGF2 did not suppress phosphorylation of Smad2 or Smad‐dependent gene expression, FGF2 inhibited TGFβ1‐induced stress fiber formation and serum response factor‐dependent gene expression. FGF2 inhibition of stress fiber formation and αSMA requires FGF receptor 1 (FGFR1) and downstream MEK/ERK, but not AKT signaling. In summary, overexpression of FGF2 protects against bleomycin‐induced pulmonary fibrosis in vivo and reverses TGFβ1‐induced collagen and αSMA expression and stress fiber formation in lung fibroblasts in vitro, without affecting either inflammation or epithelial gene expression. Our results suggest that in the lung, FGF2 is antifibrotic in part through decreased collagen expression and fibroblast to myofibroblast differentiation. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

MERTK mutation update in inherited retinal diseases

MER tyrosine kinase (MERTK) encodes a surface receptor localized at the apical membrane of the retinal pigment epithelium. It plays a critical role in photoreceptor outer segment internalization prior to phagocytosis. Mutations in MERTK have been associated with severe autosomal recessive retinal dystrophies in the RCS rat and in humans. We present here a comprehensive review of all reported MERTK disease causing variants with the associated phenotype. In addition, we provide further data and insights of a large cohort of 1,195 inherited retinal dystrophies (IRD) index cases applying state‐of‐the‐art genotyping techniques and summarize current knowledge. A total of 79 variants have now been identified underlying rod‐cone dystrophy and cone‐rod dystrophy including 11 novel variants reported here. The mutation spectrum in MERTK includes 33 missense, 12 nonsense, 12 splice defects, 12 small deletions, 2 small insertion–deletions, 3 small duplications, and 2 exonic and 3 gross deletions. Altogether, mutations in MERTK account for ～2% of IRD cases with a severe retinal phenotype. These data are important for current and future therapeutic trials including gene replacement therapy or cell‐based therapy.