Thirty-day readmissions following parathyroidectomy: Evidence from the National Readmissions Database, 2013-2014.

PURPOSE: Parathyroidectomy is one of the most common procedures performed in the United States, and are increasingly being performed safely in the outpatient setting. However, complications from surgery can be life-threatening, and thus an understanding of who may be at risk is essential. We analyzed and compared the risk factors for patients readmitted within 30 days following inpatient parathyroidectomy for primary or secondary hyperparathyroidism. MATERIALS AND METHODS: We reviewed the National Readmissions Database from 2013 to 2014 for patients who received inpatient parathyroidectomy for primary or secondary hyperparathyroidism. The primary outcome was non-elective readmission within 30 days. Multivariate logistic regression was used to analyze risk factor odds ratios for readmission. RESULTS: 7171 patients underwent inpatient parathyroidectomies in 2013 and 2014. 59.89% of parathyroidectomies were performed for primary hyperparathyroidism, with a 5.6% readmission rate. Most common causes of readmission were septicemia (13.69%), hypocalcemia (12.86%), heart failure (10.79%) and renal failure (9.54%). Having Medicare (OR: 1.71, CI:1.14-2.59, p = .01), Medicaid (OR: 3.24, CI: 2.03-5.17, p < .001), and self-paying (OR: 2.43, CI: 1.11-5.32, p = .02), were associated with increased odds of readmission for those with primary hyperparathyroidism. 21.99% of parathyroidectomies were performed for secondary hyperparathyroidism, with a 19.4% readmission rate. Most common causes of readmission were hypocalcemia (22.88%), hungry bone syndrome (14.38%), electrolyte disorders (13.73%), and renal failure (11.11%). CONCLUSION: Patients with secondary hyperparathyroidism are older, poorer and have more comorbidities than patients with primary hyperparathyroidism, and are more likely to be readmitted within 30 days of parathyroidectomy.

Two knockdown models of the autism genes SYNGAP1 and SHANK3 in zebrafish produce similar behavioral phenotypes associated with embryonic disruptions of brain morphogenesis.

Despite significant progress in the genetics of autism spectrum disorder (ASD), how genetic mutations translate to the behavioral changes characteristic of ASD remains largely unknown. ASD affects 1-2% of children and adults, and is characterized by deficits in verbal and non-verbal communication, and social interactions, as well as the presence of repetitive behaviors and/or stereotyped interests. ASD is clinically and etiologically heterogeneous, with a strong genetic component. Here, we present functional data from syngap1 and shank3 zebrafish loss-of-function models of ASD. SYNGAP1, a synaptic Ras GTPase activating protein, and SHANK3, a synaptic scaffolding protein, were chosen because of mounting evidence that haploinsufficiency in these genes is highly penetrant for ASD and intellectual disability (ID). Orthologs of both SYNGAP1 and SHANK3 are duplicated in the zebrafish genome and we find that all four transcripts (syngap1a, syngap1b, shank3a and shank3b) are expressed at the earliest stages of nervous system development with pronounced expression in the larval brain. Consistent with early expression of these genes, knockdown of syngap1b or shank3a cause common embryonic phenotypes including delayed mid- and hindbrain development, disruptions in motor behaviors that manifest as unproductive swim attempts, and spontaneous, seizure-like behaviors. Our findings indicate that both syngap1b and shank3a play novel roles in morphogenesis resulting in common brain and behavioral phenotypes.

Context-dependent hyperactivity in syngap1a and syngap1b zebrafish models of SYNGAP1-related disorder.

Background and aims: SYNGAP1-related disorder (SYNGAP1-RD) is a prevalent genetic form of Autism Spectrum Disorder and Intellectual Disability (ASD/ID) and is caused by de novo or inherited mutations in one copy of the SYNGAP1 gene. In addition to ASD/ID, SYNGAP1 disorder is associated with comorbid symptoms including treatment-resistant-epilepsy, sleep disturbances, and gastrointestinal distress. Mechanistic links between these diverse symptoms and SYNGAP1 variants remain obscure, therefore, our goal was to generate a zebrafish model in which this range of symptoms can be studied. Methods: We used CRISPR/Cas9 to introduce frameshift mutations in the syngap1a and syngap1b zebrafish duplicates (syngap1ab) and validated these stable models for Syngap1 loss-of-function. Because SYNGAP1 is extensively spliced, we mapped splice variants to the two zebrafish syngap1a and b genes and identified mammalian-like isoforms. We then quantified locomotory behaviors in zebrafish syngap1ab larvae under three conditions that normally evoke different arousal states in wild-type larvae: aversive, high-arousal acoustic, medium-arousal dark, and low-arousal light stimuli. Results: We show that CRISPR/Cas9 indels in zebrafish syngap1a and syngap1b produced loss-of-function alleles at RNA and protein levels. Our analyses of zebrafish Syngap1 isoforms showed that, as in mammals, zebrafish Syngap1 N- and C-termini are extensively spliced. We identified a zebrafish syngap1 α1-like variant that maps exclusively to the syngap1b gene. Quantifying locomotor behaviors showed that syngap1ab mutant larvae are hyperactive compared to wild-type but to differing degrees depending on the stimulus. Hyperactivity was most pronounced in low arousal settings, and hyperactivity was proportional to the number of mutant syngap1 alleles. Limitations: Syngap1 loss-of-function mutations produce relatively subtle phenotypes in zebrafish compared to mammals. For example, while mouse Syngap1 homozygotes die at birth, zebrafish syngap1ab-/- survive to adulthood and are fertile, thus some aspects of symptoms in people with SYNGAP1-Related Disorder are not likely to be reflected in zebrafish. Conclusion: Our data support mutations in zebrafish syngap1ab as causal for hyperactivity associated with elevated arousal that is especially pronounced in low-arousal environments.

Drugs prescribed for Phelan-McDermid syndrome differentially impact sensory behaviors in shank3 zebrafish models.

Background: Altered sensory processing is a pervasive symptom in individuals with Autism Spectrum Disorders (ASD); people with Phelan McDermid syndrome (PMS), in particular, show reduced responses to sensory stimuli. PMS is caused by deletions of the terminal end of chromosome 22 or point mutations in Shank3. People with PMS can present with an array of symptoms including ASD, epilepsy, gastrointestinal distress, and reduced responses to sensory stimuli. People with PMS are often medicated to manage behaviors like aggression and/or self-harm and/or epilepsy, and it remains unclear how these medications might impact perception/sensory processing. Here we test this using zebrafish mutant shank3ab PMS models that likewise show reduced sensory responses in a visual motor response (VMR) assay, in which increased locomotion is triggered by light to dark transitions. Methods: We screened three medications, risperidone, lithium chloride (LiCl), and carbamazepine (CBZ), prescribed to people with PMS and one drug, 2-methyl-6-(phenylethynyl) pyridine (MPEP) tested in rodent models of PMS, for their effects on a sensory-induced behavior in two zebrafish PMS models with frameshift mutations in either the N- or C- termini. To test how pharmacological treatments affect the VMR, we exposed larvae to selected drugs for 24 hours and then quantified their locomotion during four ten-minute cycles of lights on-to-off stimuli. Results: We found that risperidone normalized the VMR in shank3 models. LiCl and CBZ had no effect on the VMR in any of the three genotypes. MPEP reduced the VMR in wildtype (WT) to levels seen in shank3 models but caused no changes in either shank3 model. Finally, shank3 mutants showed resistance to the seizure-inducing drug pentylenetetrazol (PTZ), at a dosage that results in hyperactive swimming in WT zebrafish. Conclusions: Our work shows that the effects of drugs on sensory processing are varied in ways that can be highly genotype- and drug-dependent.

Context-dependent hyperactivity in syngap1a and syngap1b zebrafish autism models.

Background and Aims: SYNGAP1 disorder is a prevalent genetic form of Autism Spectrum Disorder and Intellectual Disability (ASD/ID) and is caused by de novo or inherited mutations in one copy of the SYNGAP1 gene. In addition to ASD/ID, SYNGAP1 disorder is associated with comorbid symptoms including treatment-resistant-epilepsy, sleep disturbances, and gastrointestinal distress. Mechanistic links between these diverse symptoms and SYNGAP1 variants remain obscure, therefore, our goal was to generate a zebrafish model in which this range of symptoms can be studied. Methods: We used CRISPR/Cas9 to introduce frameshift mutations in the syngap1a and syngap1b zebrafish duplicates (syngap1ab) and validated these stable models for Syngap1 loss-of-function. Because SYNGAP1 is extensively spliced, we mapped splice variants to the two zebrafish syngap1a and b genes and identified mammalian-like isoforms. We then quantified locomotory behaviors in zebrafish syngap1ab larvae under three conditions that normally evoke different arousal states in wild type larvae: aversive, high-arousal acoustic, medium-arousal dark, and low-arousal light stimuli. Results: We show that CRISPR/Cas9 indels in zebrafish syngap1a and syngap1b produced loss-of-function alleles at RNA and protein levels. Our analyses of zebrafish Syngap1 isoforms showed that, as in mammals, zebrafish Syngap1 N- and C-termini are extensively spliced. We identified a zebrafish syngap1 α1-like variant that maps exclusively to the syngap1b gene. Quantifying locomotor behaviors showed that syngap1ab larvae are hyperactive compared to wild type but to differing degrees depending on the stimulus. Hyperactivity was most pronounced in low arousal settings, with overall movement increasing with the number of mutant syngap1 alleles. Conclusions: Our data support mutations in zebrafish syngap1ab as causal for hyperactivity associated with elevated arousal that is especially pronounced in low-arousal environments.

A brain-wide analysis maps structural evolution to distinct anatomical module.

The vertebrate brain is highly conserved topologically, but less is known about neuroanatomical variation between individual brain regions. Neuroanatomical variation at the regional level is hypothesized to provide functional expansion, building upon ancestral anatomy needed for basic functions. Classically, animal models used to study evolution have lacked tools for detailed anatomical analysis that are widely used in zebrafish and mice, presenting a barrier to studying brain evolution at fine scales. In this study, we sought to investigate the evolution of brain anatomy using a single species of fish consisting of divergent surface and cave morphs, that permits functional genetic testing of regional volume and shape across the entire brain. We generated a high-resolution brain atlas for the blind Mexican cavefish Astyanax mexicanus and coupled the atlas with automated computational tools to directly assess variability in brain region shape and volume across all populations. We measured the volume and shape of every grossly defined neuroanatomical region of the brain and assessed correlations between anatomical regions in surface fish, cavefish, and surface × cave F2 hybrids, whose phenotypes span the range of surface to cave. We find that dorsal regions of the brain are contracted, while ventral regions have expanded, with F2 hybrid data providing support for developmental constraint along the dorsal-ventral axis. Furthermore, these dorsal-ventral relationships in anatomical variation show similar patterns for both volume and shape, suggesting that the anatomical evolution captured by these two parameters could be driven by similar developmental mechanisms. Together, these data demonstrate that A. mexicanus is a powerful system for functionally determining basic principles of brain evolution and will permit testing how genes influence early patterning events to drive brain-wide anatomical evolution.

Novel Husbandry Practices Result in Rapid Rates of Growth and Sexual Maturation Without Impacting Adult Behavior in the Blind Mexican Cavefish.

Animal model systems are dependent on the standardization of husbandry protocols that maximize growth and reduce generation time. The Mexican tetra, Astyanax mexicanus, exists as eyed surface and blind cave dwelling populations. The opportunity for comparative approaches between independently evolved populations has led to the rapid growth of A. mexicanus as a model for evolution and biomedical research. However, a slow and inconsistent growth rate remains a major limitation to the expanded application of A. mexicanus. Fortunately, this temporal limitation can be addressed through husbandry changes that accelerate growth rates while maintaining optimal health outcomes. Here, we describe a husbandry protocol that produces rapid growth rates through changes in diet, feeding frequency, growth sorting and progressive changes in tank size. This protocol produced robust growth rates and decreased the age of sexual maturity in comparison to our previous protocol. To determine whether changes in feeding impacted behavior, we tested fish in exploration and schooling assays. We found no difference in behavior between the two groups, suggesting that increased feeding and rapid growth will not impact the natural variation in behavioral traits. Taken together, this standardized husbandry protocol will accelerate the development of A. mexicanus as a genetic model.

Restoring Shank3 in the rostral brainstem of shank3ab-/- zebrafish autism models rescues sensory deficits.

People with Phelan-McDermid Syndrome, caused by mutations in the SHANK3 gene, commonly exhibit reduced responses to sensory stimuli; yet the changes in brain-wide activity that link these symptoms to mutations in the shank3 gene remain unknown. Here we quantify movement in response to sudden darkness in larvae of two shank3 zebrafish mutant models and show that both models exhibit dampened responses to this stimulus. Using brain-wide activity mapping, we find that shank3-/- light-sensing brain regions show normal levels of activity while sensorimotor integration and motor regions are less active. Specifically restoring Shank3 function in a sensorimotor nucleus of the rostral brainstem enables the shank3-/- model to respond like wild-type. In sum, we find that reduced sensory responsiveness in shank3-/- models is associated with reduced activity in sensory processing brain regions and can be rescued by restoring Shank3 function in the rostral brainstem. These studies highlight the importance of Shank3 function in the rostral brainstem for integrating sensory inputs to generate behavioral adaptations to changing sensory stimuli.

Intestinal dysmotility in a zebrafish (Danio rerio) shank3a;shank3b mutant model of autism.

Background and aims: Autism spectrum disorder (ASD) is currently estimated to affect more than 1% of the world population. For people with ASD, gastrointestinal (GI) distress is a commonly reported but a poorly understood co-occurring symptom. Here, we investigate the physiological basis for GI distress in ASD by studying gut function in a zebrafish model of Phelan-McDermid syndrome (PMS), a condition caused by mutations in the SHANK3 gene. Methods: To generate a zebrafish model of PMS, we used CRISPR/Cas9 to introduce clinically related C-terminal frameshift mutations in shank3a and shank3b zebrafish paralogues (shank3abΔC). Because PMS is caused by SHANK3 haploinsufficiency, we assessed the digestive tract (DT) structure and function in zebrafish shank3abΔC+/- heterozygotes. Human SHANK3 mRNA was then used to rescue DT phenotypes in larval zebrafish. Results: Significantly slower rates of DT peristaltic contractions (p < 0.001) with correspondingly prolonged passage time (p < 0.004) occurred in shank3abΔC+/- mutants. Rescue injections of mRNA encoding the longest human SHANK3 isoform into shank3abΔC+/- mutants produced larvae with intestinal bulb emptying similar to wild type (WT), but still deficits in posterior intestinal motility. Serotonin-positive enteroendocrine cells (EECs) were significantly reduced in both shank3abΔC+/- and shank3abΔC-/- mutants (p < 0.05) while enteric neuron counts and overall structure of the DT epithelium, including goblet cell number, were unaffected in shank3abΔC+/- larvae. Conclusions: Our data and rescue experiments support mutations in SHANK3 as causal for GI transit and motility abnormalities. Reductions in serotonin-positive EECs and serotonin-filled ENS boutons suggest an endocrine/neural component to this dysmotility. This is the first study to date demonstrating DT dysmotility in a zebrafish single gene mutant model of ASD.

Prenatal Neuropathologies in Autism Spectrum Disorder and Intellectual Disability: The Gestation of a Comprehensive Zebrafish Model.

Autism spectrum disorder (ASD) and intellectual disability (ID) are neurodevelopmental disorders with overlapping diagnostic behaviors and risk factors. These include embryonic exposure to teratogens and mutations in genes that have important functions prenatally. Animal models, including rodents and zebrafish, have been essential in delineating mechanisms of neuropathology and identifying developmental critical periods, when those mechanisms are most sensitive to disruption. This review focuses on how the developmentally accessible zebrafish is contributing to our understanding of prenatal pathologies that set the stage for later ASD-ID behavioral deficits. We discuss the known factors that contribute prenatally to ASD-ID and the recent use of zebrafish to model deficits in brain morphogenesis and circuit development. We conclude by suggesting that a future challenge in zebrafish ASD-ID modeling will be to bridge prenatal anatomical and physiological pathologies to behavioral deficits later in life.

Cost-aware care: critical core competency.

HYPOTHESIS: Resident core competence can be improved by learning to accurately estimate the costs of postoperative complications. DESIGN: Prospective, institutional review board-approved study. In step 1, residents were provided 3 clinical vignettes detailing specific treatment measures for postsurgical complications and asked to assign total cost estimates for the treatment for each vignette; in step 2 they were given a pocket-sized cost card listing hospital costs, and in step 3, after 2 weeks, they were retested using the same clinical vignettes as in step 1. SETTING: University of Connecticut, Farmington, and the Yale University School of Medicine, New Haven. PARTICIPANTS: Fifty-three general surgery residents. MAIN OUTCOME MEASURES: Cost estimates for steps 1 and 3 were compared using the paired t test and analysis of variance to examine whether there is a difference between the baseline cost estimates and the actual cost; whether introduction of the cost card improves performance; and whether responses correlate to postgraduate year level or to the clinical vignette. RESULTS: There was a statistically significant difference between the baseline cost estimates (before introduction of the cost card) and the actual cost of the treatment (P = .03). Introduction of the cost card resulted in a statistically significant improvement between the cost estimates before and after the intervention (P = .002), with a drop in average percentage error by 35% (range, 32%-38%). Level of postgraduate training or type of test vignette (at analysis of variance) did not seem to be a significant factor. CONCLUSIONS: There is a lack of awareness among surgical residents of the cost of treatment of postoperative complications. Introduction of a simple educational tool such as a cost card measurably improves their overall understanding of the cost of care and can be easily incorporated into the residency curriculum.

Small-bowel tumors: epidemiologic and clinical characteristics of 1260 cases from the connecticut tumor registry.

OBJECTIVE: To examine the epidemiology and clinical characteristics of small-bowel cancer. DESIGN: Patients with small-bowel tumors reported between 1980 and 2000, studied retrospectively. SETTING: Data from the Connecticut Tumor Registry. PATIENTS: One thousand sixty small-bowel cancer cases: 628 men (49.84%) and 632 women (50.16%). Mean age at presentation was 65.2 years. RESULTS: The most common location of small-bowel tumors was the ileum (374 cases; 29.7%), followed by the duodenum (320 cases; 25.4%) and the jejunum (193 cases; 15.3%). In 367 patient cases (29.1%: 192 men [30.6%] and 175 women [27.7%]), a prior or subsequent tumor of the gastrointestinal tract was reported. The most prevalent histologic type was carcinoid (417 cases; 33%), followed by adenocarcinoma (341 cases; 27%) and lymphoma (205 cases; 16.3%). The patient population was predominantly white (1159 patients; 92%), followed by African American patients (91 patients; 7.2%). Stratification by consecutive 7-year intervals showed the following: from 1980 to 1986, there were 10.5 cases per 100 000 individuals; from 1987 to 1993, there were 13.05 cases per 100 000 individuals; and from 1994 to 2000, there were 14.86 cases per 100 000 individuals. Men comprised 44.8% of cases from 1980 to 1986, 50.2% of cases from 1987 to 1993, and 53.3% of cases from 1994 to 2000. African American patients accounted for 7.5% of all cases from 1980 to 1986, 5.8% from 1986 to 1993, and 8.2% of cases from 1994 to 2000. In 1106 patients (87.7%), the primary therapy was surgical, including intestinal bypass, radical excision, excisional biopsy, and subtotal or total excision. CONCLUSIONS: The incidence of small-bowel tumors in Connecticut has increased during the past 2 decades, with the highest rate of increase in men. Carcinoid tumors are the most common small intestinal cancers identified histologically, followed by adenocarcinomas. The former seems to be more frequently seen in the ileum, the latter in the duodenum. Surgery is the treatment of choice for the cure or palliation of small-bowel cancers.

The efficacy of intraoperative methylene blue enemas to assess the integrity of a colonic anastomosis.

BACKGROUND: Intraoperative testing of colonic anastomoses is routine in assuring anastamotic integrity. We sought to determine the efficacy of the methylene blue enema (MBE) as an intraoperative test for anastomotic leaks. METHODS: This study is a retrospective review of consecutive colonic operations performed from January 2001 to December 2004 in a community hospital setting by a general surgical group that uses the MBE exclusively. All operations featuring a colonic anastomosis and an intraoperative MBE were studied (n = 229). Intraoperative MBE via a rectal tube was used as the diagnostic test. Intraoperative leak (IOL) rate and clinically significant postoperative leak (POL) rate were the outcome measures. RESULTS: The IOL rate was 4.5% for proximal anastomoses, 8% for distal anastomoses, and 7% of total anastomoses. The POL rate was 3% of anastomosis. There were no other testing methods employed. There were no POLs in cases where an IOL led to concomitant intraoperative repair. POL rate for proximal anastomosis was 0.8% and for distal 3%, for stapled 1% and hand sewn 5%. CONCLUSION: MBE IOL rate is comparable to published IOL rates for other methods of intraoperative testing. The MBE can be applied to proximal and distal anastomosis. Patients who were found to have an IOL, and underwent immediate repair, did not develop a clinical POL.

The Sestamibi Paradox: Improving Intraoperative Localization of Parathyroid Adenomas.

Accurate localization of parathyroid adenomas allows for minimally invasive parathyroidectomy. This results in a shorter length of stay and increased patient satisfaction. Preoperative Technetium (99mTc) sestamibi scans accurately localize parathyroid adenomas in 70 to 85 per cent of cases. If a patient has a negative scan, it is logical to believe that with a preoperative sestamibi injection, the gamma probe may fail to help find an adenoma. We hypothesized that the gamma probe would not be useful intraoperatively for patients with primary hyperparathyroidism (PHPTH) and a negative sestamibi scan. We retrospectively reviewed the cases of parathyroidectomy at our institution from 2010 to 2016. We selected patients with PHPTH and negative sestamibi scan. In all cases, an attempt was made to find adenomas intraoperatively with the gamma probe. A frozen section was obtained as well as intraoperative parathyroid hormone levels to confirm removal of hyperfunctioning parathyroid tissue. There were 132 parathyroidectomies of which 22 had PHPTH and a negative sestamibi scan. One case was excluded because of insufficient documentation of the intraoperative use of the gamma probe. In 19 of the 21 patients analyzed, the gamma probe successfully identified the adenoma in the operating room (sensitivity, 90.5%). In two patients, the gamma probe did not aid in localization. There were no false positives. In all cases, the parathyroid resected was confirmed by frozen section. The intraoperative parathyroid hormone levels dropped >50 per cent in all but three cases, two of which corresponded to those cases where the gamma probe did not help. Even in patients with negative sestamibi scans, intraoperative use of the gamma probe after preoperative sestamibi injection is effective in localizing parathyroid adenomas.

Surgical perspectives in peptic ulcer disease and gastritis.

For much of the twentieth century, surgery was frequently the solution for peptic ulcer disease. Our understanding of the pathophysiology of ulcers paralleled the development of potent pharmaceutical therapy. As the surgical world developed parietal cell vagotomy which would minimize the complications of surgery, patients failing medical therapy became rare. Emergent surgery for complicated peptic ulcers has not declined however. The development of proton pump inhibitors and the full understanding of the impact of H pylori has led to a trend towards minimalism in surgical therapy for complicated peptic ulcer disease. In addition to the changes in patient care, these developments have had an impact on the training of surgeons. This article outlines these trends and developments.

Function Over Form: Modeling Groups of Inherited Neurological Conditions in Zebrafish.

Zebrafish are a unique cell to behavior model for studying the basic biology of human inherited neurological conditions. Conserved vertebrate genetics and optical transparency provide in vivo access to the developing nervous system as well as high-throughput approaches for drug screens. Here we review zebrafish modeling for two broad groups of inherited conditions that each share genetic and molecular pathways and overlap phenotypically: neurodevelopmental disorders such as Autism Spectrum Disorders (ASD), Intellectual Disability (ID) and Schizophrenia (SCZ), and neurodegenerative diseases, such as Cerebellar Ataxia (CATX), Hereditary Spastic Paraplegia (HSP) and Charcot-Marie Tooth Disease (CMT). We also conduct a small meta-analysis of zebrafish orthologs of high confidence neurodevelopmental disorder and neurodegenerative disease genes by looking at duplication rates and relative protein sizes. In the past zebrafish genetic models of these neurodevelopmental disorders and neurodegenerative diseases have provided insight into cellular, circuit and behavioral level mechanisms contributing to these conditions. Moving forward, advances in genetic manipulation, live imaging of neuronal activity and automated high-throughput molecular screening promise to help delineate the mechanistic relationships between different types of neurological conditions and accelerate discovery of therapeutic strategies.

Postoperative day one: a high risk period for respiratory events.

BACKGROUND: In 2001, the Joint Commission on Accreditation of Healthcare Organizations released Pain Management Standards that has led to an increased focus on pain control. Since then the Institute for Safe Medication Practices has noted that overaggressive pain management has led to increases in oversedation and fatal respiratory depression. One of our previous studies found that postoperative patients may be reaching dangerously high levels of sedation as a result of pain management. Our hypothesis is that postoperative patients who have a respiratory event caused by analgesic use are more likely to have that event in the first postoperative day. METHODS: We performed a retrospective case-control analysis identifying 62 postoperative patients who had a respiratory event. A respiratory event was defined as respiratory depression caused by narcotic use in the postoperative period that was reversed by naloxone. Sixty-two postoperative patients with no such event were chosen randomly and frequency matched based on surgical procedure and diagnosis-related group. Risk factors for an event were identified. RESULTS: Of the cases, 77.4% had a respiratory event in the first 24 hours postoperatively. Significant risk factors for an event were as follows: 65 years of age or older, having chronic obstructive pulmonary disease, having 1 or more comorbidities, and being placed on hydromorphone. CONCLUSIONS: The first 24 hours after surgery represents a high-risk period for a respiratory event as a result of narcotic use. The realization of this risk can lead to the implementation of standards to increase patient safety in the first postoperative day.

Hyperparathyroidism but a negative sestamibi scan: a clinical dilemma.

BACKGROUND: The outcomes of patients with biochemically confirmed hyperparathyroidism but a negative Tc-99 Sestamibi scan are unclear. We examined the outcomes and quality of life of patients having surgery and those who had medical therapy. METHODS: Patients having a diagnosis of hyperparathyroidism with confirmed elevated calcium and parathormone levels, yet negative sestamibi scans were identified. The RAND SF-36 Health Survey was administered via mail to these patients. The patient's charts were then reviewed to verify treatments and to determine outcomes. RESULTS: Ninety-five patients fitting the criteria were identified. Twenty patients completed all aspects of the study. Ten of the respondents had undergone parathyroidectomy, and 10 had not. The surgical patients scored more favorably in all 8 of the measured parameters than patients treated medically. The differences in 3 domains, physical functioning, pain, and social functioning, were statistically significant. CONCLUSIONS: Our findings suggest that surgical therapy confers a better quality of life and is superior to medical therapy in the treatment of primary hyperparathyroidism, even in patients having a negative sestamibi scan.

Has the pendulum swung too far in postoperative pain control?

BACKGROUND: The Joint Commission on Accreditation of Health Care Organizations declared pain level to be the "fifth vital sign." This has led to increased efforts to reduce patients' pain scores. Current postoperative analgesic modalities may not be entirely safe. We prospectively studied pain and sedation scores to determine whether postoperative patients were reaching sedation levels similar to patients undergoing "conscious sedation" (eg, colonoscopy cases). "Conscious sedation" patients have been shown to achieve states of sedation, which at time result in oxygen desaturation. METHODS: Fifty-three patients within three groups were compared in an observational study. Group 1 included "conscious sedation" patients undergoing colonoscopy. Group 2 included postoperative patients using patient-controlled analgesia (PCA). Group 3 included postoperative patients under nurse-controlled analgesia (NCA). Levels of sedation were monitored using the 6-point Ramsay sedation scale. Pain and oxygen saturation were monitored using an 11-point verbal scale and finger pulse oximetry, respectively. Patients were monitored for up to 12 hours in the postoperative period or for the length of their colonoscopy procedure. RESULTS: Patients in groups 1 and 2 reached similar sedation levels. CONCLUSIONS: Patients may reach dangerous levels of sedation during the first 24 hours postoperatively. Patients using PCA devices warrant close observation during this time period.

Does a new surgical residency program increase operating room times?

BACKGROUND: Our country faces a shortage of surgeons; hence, we may anticipate the development of new surgery residencies. Therefore, the question of the effect of a new program on operating room times (ORT) is important. Our primary aim was to compare ORT of 3 common procedures done by attendings alone vs ORT of cases with residents. METHODS: We queried records of 1458 patients from the JFK Medical Center database for laparoscopic cholecystectomy, open inguinal hernia repair, and laparoscopic appendectomy from July 2010 to July 2012. We divided the sample into 2 groups: "attending alone" (2010-2011) and "with residents" (2011-2012). The ORT was calculated by "Cut time" and "Close time," as recorded in the OR. ORT for both groups was calculated using the unpaired t test. RESULTS: Of the total number of patients, 778 underwent laparoscopic cholecystectomy, 407 underwent open inguinal hernia repair, and 273 underwent laparoscopic appendectomy; of these, 620, 315, and 211 procedures, respectively, were done by the attending alone and 158, 92, and 62, respectively, were done with residents. Differences in ORT for the 3 types of surgery were statistically significant (p < 0.001). There was no statistical significance when comparing the first half with the second half of the academic year for residents' ORT. CONCLUSIONS: Resident involvement increases ORT. Cost analysis considering OR time and anesthesia time vs federal funding for Graduate Medical Education is complicated. The benefit of new programs in diminishing the shortage of surgeons cannot be underestimated.