For whom the bell tolls: assessing the incremental costs associated with failure to rescue after elective colorectal surgery.

BACKGROUND: Failure to rescue after elective surgery is associated with increased healthcare costs. These costs are poorly understood and have not been reported for colorectal surgery. This study aimed to assess the incremental costs of failure to rescue after elective colorectal surgery. METHODS: This was a retrospective study of adult patients identified in the National Inpatient Sample from 2016 to 2019 who underwent an elective colectomy or proctectomy. Patients were stratified into 4 groups: uneventful recovery, successfully rescued, failure to rescue, and died without rescue attempts. "Rescue" was defined as admissions with ≥1 procedure code ≥1 day after the initial procedure. The primary outcome was total admission costs. RESULTS: Of 451,490 admissions for elective colorectal resection, 94.6% had an uneventful recovery, 4.8% were successfully rescued, 0.4% were failure to rescue, and 0.3% died without rescue attempts. The median total hospital cost for the uneventful recovery cohort was $16,751 (IQR, $12,611-$23,116), for the successfully rescued cohort was $42,295 (IQR, $27,959-$67,077), for the failure-to-rescue cohort was $53,182 (IQR, $30,852-$95,615), and for the died without attempted rescue cohort was $29,296 (IQR, $19,812-$45,919). When comparing cost quantiles by regression analysis, failure-to-rescue patients had significantly higher costs than the successfully rescued patients for the last 3 quantiles (fifth quantile [90th percentile], $163,963 vs $106,521; P < .001). CONCLUSION: Across a nationally representative cohort, the median total hospital costs for patients who failed to be rescued were $10,887 more than for those who were successfully rescued. These findings emphasize the importance of shared decision making and medical futility and highlight opportunities for resource optimization after postoperative complications.

Management of Colonic Emergencies.

The etiology of colonic emergencies includes a wide-ranging and diverse set of pathologic conditions. Fortunately, for the surgeon treating a patient with one of these emergencies, the surgical management of these various causes is limited to choosing among proximal diversion, segmental colectomy with or without proximal diversion, or a total abdominal colectomy with end ileostomy (or rarely, an ileorectal anastomosis). The nuanced complexity in these situations usually revolves around the nonsurgical and/or endoscopic options and deciding when to proceed to the operating room.

Sexually transmitted infections of the anus and rectum.

Sexually transmitted infections (STIs) represent a significant public health concern. Several STIs, once thought to be on the verge of extinction, have recently reemerged. This change is thought to be partially related to an increase in STIs of the anus and rectum. Importantly, the global human immunodeficiency virus and acquired immunodeficiency syndrome (HIV/AIDS) epidemic has contributed to the emergence of particular anorectal lesions that require specialized approaches. In this report, we review common anorectal STIs that are frequently referred to colorectal surgeons in the United States. Epidemiology, clinical presentation, and management are summarized, including the latest treatment recommendations. The particularity of anorectal diseases in HIV/AIDS is addressed, along with recent trends in anal cytology and human papillomavirus vaccination.

The burden of diverticular disease on patients and healthcare systems.

Diverticulitis is a debilitating complication of diverticular disease that affects approximately 2.5 million individuals in the United States. Compared to many other gastrointestinal conditions, diverticular disease is poorly understood in terms of its burden on patients and healthcare systems. This review examines the existing literature and discusses the current knowledge of the burden of diverticular disease. Literature confirmed that bothersome symptoms (such as abdominal pain and bloating) and potentially serious, disease-related complications (such as diverticulitis and diverticular bleeding) place a significant burden on patients. Broad-spectrum antibiotic therapy and surgery are the generally accepted mainstays of treatment for acute complications of diverticular disease. Despite these options, patients frequently experience substantially reduced quality of life (particularly in terms of social and emotional functioning) and increased mortality (predominantly due to disease-related complications) compared to healthy controls. Furthermore, diverticular disease accounted for 254,179 inpatient discharges and 1,493,865 outpatient clinic visits in the United States in 2002, at an estimated cost per hospitalization of $9,742-$11,729. Enhancing the quality of life of patients with diverticular disease and reducing disease exacerbations and complications will substantially benefit patients and healthcare systems. However, long-established treatment algorithms fall short of these therapeutic goals. Research into new treatment options for patients with diverticular disease should therefore be pursued.

Asymptomatic ileal adenocarcinoma in the setting of undiagnosed Crohn's disease.

A 53-year old previously healthy male underwent a screening colonoscopy for detection of a potential colorectal neoplasm. The terminal ileum was intubated and a mass was noted. Examination of the colon was normal. The biopsy of the ileal mass was consistent with an adenocarcinoma arising from the terminal ileum. His father who had never been previously ill from gastrointestinal disease died of natural causes, but was found to have Crohn's disease postmortem. The patient underwent exploratory laparotomy and a right hemicolectomy with a 30 cm section of terminal ileum in continuity. Findings were consistent with ileal adenocarcinoma in the setting of Crohn's disease. The patient made an uneventful recovery. The pathology was stage 1 adenocarcinoma. This is a unique case in that on a screening colonoscopy, a favorable ileal adenocarcinoma was discovered in the setting of asymptomatic, undiagnosed ileal Crohn's disease in a patient whose father had Crohn's disease diagnosed postmortem.

Decreased endothelin binding and [Ca2+]i signaling in microvessels of DOCA-salt hypertensive rats.

OBJECTIVES AND DESIGN: The deoxycorticosterone acetate (DOCA)-salt model of hypertension is characterized by elevated vascular endothelin-1 (ET-1) and by reduced contraction to ET-1 in isolated mesenteric small arteries. The decreased contraction to ET-1 may be a compensatory mechanism caused by elevations in ET-1 and arterial pressure. The present study was designed to determine whether down-regulation of endothelin receptors or altered Ca2+ signaling contribute to the decreased contraction to ET-1. METHODS AND RESULTS: Contraction to ET-1 (10 to 10 mol/l) was significantly reduced in isolated mesenteric small arteries (87-286 microm intraluminal diameter) from DOCA-salt rats compared with placebo rats. Membrane protein was obtained for measurement of [125I]ET-1 receptor binding and ET receptor expression. Maximum binding was significantly reduced in vascular membranes from DOCA-salt rats (670 +/- 71 fmol/mg protein) compared with placebo rats (1165 +/- 75 fmol/mg protein), but binding affinity was unchanged. Conversely, ETA receptor protein was increased in DOCA-salt rat vessels. To assess Ca2+ signaling, freshly dissociated mesenteric small artery smooth muscle cells were loaded with fura-2 for measurement of the average myoplasmic free Ca2+ concentration ([Ca2+ ] ). The ET-1 (10 mol/l) induced increase in [Ca2+ ] was significantly less in cells from DOCA-salt rats compared with from placebo rats. This effect was not due to a loss of L-type Ca2+ channels since expression was increased in membrane protein from DOCA-salt rats compared with placebo rats, as measured by Western blot analysis. CONCLUSIONS: These findings indicate that decreases in receptor binding and Ca2+ signaling contribute to the impaired contraction to ET-1 in DOCA-salt hypertensive rats. However, these changes are not due to reduced expression of ETA receptors or L-type Ca2+ channels.

Role of ET-1 receptor binding and [Ca(2+)](i) in contraction of coronary arteries from DOCA-salt hypertensive rats.

Hypertension is associated with an increase in coronary artery disease, but little is known about the regulation of coronary vascular tone by endothelin-1 (ET-1) in hypertension. The present study evaluated the mechanisms mediating altered contraction to ET-1 in coronary small arteries from deoxycorticosterone acetate (DOCA)-salt hypertensive rats. DOCA-salt rats exhibited an increase in systolic blood pressure and plasma ET-1 levels compared with placebo rats. Contraction to ET-1 (1 x 10(-11) to 3 x 10(-8) M), measured in isolated coronary small arteries maintained at a constant intraluminal pressure of 40 mmHg, was largely reduced in vessels from DOCA-salt rats compared with placebo rats. To determine the role of endothelin receptor binding in the impaired contraction to ET-1, (125)I-labeled ET-1 receptor binding was measured in membranes isolated from coronary small arteries. Maximum binding (fmol/mg protein) and binding affinity were similar in coronary membranes from DOCA-salt rats compared with placebo rats. Changes in intracellular Ca(2+) concentration ([Ca(2+)](i)) were measured in freshly dissociated coronary small artery smooth muscle cells loaded with fura 2. ET-1 (10(-9) M) produced a 30 +/- 9% increase in [Ca(2+)](i) in smooth muscle cells from placebo rats, but had no effect on cells from DOCA-salt rats (2 +/- 2%). In summary, the ET-1-induced coronary artery contraction and increase in [Ca(2+)](i) are impaired in DOCA-salt hypertensive rats, whereas endothelin receptor binding is not altered. These results suggest endothelin receptor uncoupling from signaling mechanisms and indicate that impaired [Ca(2+)](i) signaling contributes to the decrease in ET-1-induced contraction of coronary small arteries in DOCA-salt hypertensive rats.