Hospital Costs Associated With Laparoscopic and Open Inguinal Herniorrhaphy

Purpose:

The purpose of this study was to compare the total hospital costs associated with elective laparoscopic and open inguinal herniorrhaphy.

Methods:

A prospectively maintained database was used to identify patients who underwent elective inguinal herniorrhaphy from April 2009 to March 2011. A retrospective review of electronic patient records was performed along with a standardized case-costing analysis using data from the Ontario Case Costing Initiative. The main outcomes were operating room (OR) and total hospital costs.

Results:

Two hundred eleven patients underwent elective unilateral inguinal herniorrhaphy (117 open and 94 laparoscopic), and 33 patients underwent elective bilateral inguinal herniorrhaphy (9 open and 24 laparoscopic). OR and total hospital costs for open unilateral inguinal hernia repair were significantly lower than for the laparoscopic approach (median total cost, $3207.15 vs $3723.66; P < .001). OR and total hospital costs for repair of elective bilateral inguinal hernias were similar between the open and laparoscopic approaches (median total cost, $4574.02 vs $4662.89; P = .827).

Conclusions:

In the setting of a Canadian academic hospital, when considering the repair of an elective unilateral inguinal hernia, the OR and total hospital costs of open surgery were significantly lower than for the laparoscopic techniques. There was no statistical difference between OR and total hospital costs when comparing open surgery and laparoscopic techniques for the repair of bilateral inguinal hernias. Given the perioperative benefits of laparoscopy, further studies incorporating hernia-specific outcomes are necessary to determine the cost-effectiveness of each approach and to define the optimal treatment strategy.     

Tumor Size Predicts Vascular Invasion and Histologic Grade Among Patients Undergoing Resection of Intrahepatic Cholangiocarcinoma

The association between tumor size and survival in patients with intrahepatic cholangiocarcinoma (ICC) undergoing surgical resection is controversial. We sought to define the incidence of major and microscopic vascular invasion relative to ICC tumor size, and identify predictors of microscopic vascular invasion in patients with ICC ≥5 cm. A total of 443 patients undergoing surgical resection for ICC between 1973 and 2011 at one of 11 participating institutions were identified. Clinical and pathologic data were evaluated using uni- and multivariate analyses. As tumor sized increased, the incidence of microscopic vascular invasion increased: <3 cm, 3.6 %; 3–5 cm, 24.7 %; 5–7 cm, 38.3 %; 7–15 cm, 32.9 %, ≥15 cm, 55.6 %; (p?<?0.001). Increasing tumor size was also found to be associated with worsening tumor grade. The incidence of poorly differentiated tumors increased with increasing ICC tumor size: <3 cm, 9.7 %; 3–5 cm, 19.8 %; 5–7 cm, 24.2 %; 7–15 cm, 21.1 %; >15 cm, 31.6 % (p?=?0.04). The presence of perineural invasion (odds ratio [OR]?=?2.98) and regional lymph node metastasis (OR?=?4.43) were independently associated with an increased risk of microscopic vascular invasion in tumors ≥5 cm (both p?<?0.05). Risk of microscopic vascular invasion and worse tumor grade increased with tumor size. Large tumors likely harbor worse pathologic features; this information should be considered when determining therapy and prognosis of patients with large ICC.     

Campylobacter fetus Bacteremia in an Immunocompetent Traveler

Campylobacter fetus bacteremia is a rare human infection that occurs almost exclusively in the setting of advanced age, immunosuppression, human immunodeficiency virus infection, alcoholism, or recent gastrointestinal surgery. This report of C. fetus bacteremia in a 39-year-old immunocompetent traveler who ate raw beef identifies C. fetus as a potential emerging pathogen in normal hosts.Campylobacter fetus is a common pathogen of cattle, sheep, and other ungulates. Human C. fetus infection is associated with consumption of raw or undercooked meat, unpasteurized milk, and other uncooked foods.¹ Although the Campylobacter genus is a common cause of gastrointestinal symptoms in humans, C. fetus bacteremia is very rare, occurring almost exclusively in the setting of advanced age, immunosuppression, human immunodeficiency virus (HIV) infection, alcoholism, or recent gastrointestinal surgery.² We report a case of C. fetus bacteremia in an immunocompetent patient after travel to Ethiopia.A 39-year-old Ethiopian male presented with fever, hypotension, tachycardia, watery diarrhea, lower back and hip pain, nausea, and vomiting. His symptoms began 2 days after returning from a trip to Addis Ababa, Ethiopia, where he stayed within the city for 3 months to visit his family. He reported eating uncooked beef and raw honey during his trip. He did not take malarial prophylaxis because of the high elevation of the area. He reported consuming two to three alcoholic beverages a week, and his medical history was significant only for mild hepatic steatosis, treated latent tuberculosis infection 15 years before, and obstructive sleep apnea. His initial hospital treatment included intravenous fluid resuscitation as well as intravenous vancomycin and piperacillin/tazobactam. An abdominal computed tomography scan without contrast revealed a diffusely distended colon with multiple air–fluid levels. The patient was transitioned to oral ciprofloxacin and metronidazole as he clinically improved. Blood cultures were positive for C. fetus on day 3 of hospitalization. Because fluoroquinolone resistance in C. fetus can exceed 30%,³ antibiotic therapy was empirically changed to azithromycin, and the patient was discharged to complete a 14-day total antibiotic course. Other laboratory testing revealed three negative malaria smears, normal immunoglobulin levels, a negative serum HIV enzyme-linked immunosorbent assay, negative anti-Hepatitis C virus antibodies, and positive Hepatitis B surface antibodies.Reports on the incidence of C. fetus bacteremia vary. Of 183 episodes of Campylobacter bacteremia in 23 French hospitals between 2000 and 2004, 53% were caused by C. fetus.³ Other investigators have identified C. fetus less frequently; 19% of 71 Campylobacter bacteremia episodes were C. fetus in one Spanish teaching hospital over 23 years, and 8.6% of 394 Campylobacter bacteremia cases were C. fetus in an English report spanning 11 years.^4,5 Although the Centers for Disease Control and Prevention Foodborne Outbreak Online Database (FOOD) reported only one confirmed case of C. fetus infection from 1998 to 2011, US cases may be underreported.⁶ Cases of C. fetus bacteremia are more likely to occur in patients with advanced age, comorbid illness, or immunodeficiency.³ Our case shows that systemic infection from this organism can occur in immunocompetent individuals and highlights the importance of pre-travel education on sanitary food practices.     

Myeloid cell microsomal prostaglandin E synthase-1 fosters atherogenesis in mice

Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vascular cells differentially regulates the response to vascular injury, reflecting distinct effects of mPGES-1–derived PGE₂ in these cell types on discrete cellular components of the vasculature. The cell selective roles of mPGES-1 in atherogenesis are unknown. Mice lacking mPGES-1 conditionally in myeloid cells (Mac-mPGES-1-KOs), vascular smooth muscle cells (VSMC-mPGES-1-KOs), or endothelial cells (EC-mPGES-1-KOs) were crossed into hyperlipidemic low-density lipoprotein receptor-deficient animals. En face aortic lesion analysis revealed markedly reduced atherogenesis in Mac-mPGES-1-KOs, which was concomitant with a reduction in oxidative stress, reflective of reduced macrophage infiltration, less lesional expression of inducible nitric oxide synthase (iNOS), and lower aortic expression of NADPH oxidases and proinflammatory cytokines. Reduced oxidative stress was reflected systemically by a decline in urinary 8,12-iso-iPF_2α-VI. In contrast to exaggeration of the response to vascular injury, deletion of mPGES-1 in VSMCs, ECs, or both had no detectable phenotypic impact on atherogenesis. Macrophage foam cell formation and cholesterol efflux, together with plasma cholesterol and triglycerides, were unchanged as a function of genotype. In conclusion, myeloid cell mPGES-1 promotes atherogenesis in hyperlipidemic mice, coincident with iNOS-mediated oxidative stress. By contrast, mPGES-1 in vascular cells does not detectably influence atherogenesis in mice. This strengthens the therapeutic rationale for targeting macrophage mPGES-1 in inflammatory cardiovascular diseases.Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce pain and inflammation by suppressing the formation of proinflammatory prostaglandins (PGs), particularly prostaglandin E₂ (PGE₂) formed by cyclooxygenase-2 (COX-2) (1). However, the development of NSAIDs specific for inhibition of COX-2 revealed a cardiovascular hazard attributable to suppression of cardioprotective PGs, especially prostacyclin (PGI₂) (2). This risk appears to extend to some of the older NSAIDs, like diclofenac, that also inhibit specifically COX-2 (3, 4). These developments prompted interest in microsomal PGE synthase (mPGES)-1 as a downstream alternative drug target to COX-2 (5): it is the dominant source among PGES enzymes in the biosynthesis of PGE₂ (6). Unlike NSAIDs, inhibitors of mPGES-1 would spare PGI₂ from suppression. Indeed, blockade or deletion of mPGES-1 results in accumulation of its PGH₂ substrate, rendering it available for metabolism by other PG synthases, including PGI₂ synthase (PGIS) (7).Consistent with these observations, we have found that whereas deletion of COX-2 in endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) renders mice susceptible to thrombosis and hypertension (2), deletion of mPGES-1 in vascular cells has no such effect (8). Indeed, global deficiency of mPGES-1 restrains atherogenesis (9), the proliferative response to vascular injury (10) and angiotensin-induced aortic aneurysm formation (11) in mice.Despite this attractive cardiovascular profile, mPGES-1 is a complex drug target. The dominant prostanoid products of substrate rediversion differ among cell types. For example, whereas PGI₂ might be augmented in vascular cells, the consequence of mPGES-1 blockade in other cells might be an increase in thromboxane (Tx)A₂, a PG that promotes platelet activation, vasoconstriction, and atherogenesis (9). Even if an increase in PGI₂ afforded a desirable cardiovascular profile, it might undermine the analgesic efficacy of mPGES-1 inhibitors. Although the impacts of global deletion of mPGES-1 and COX-2 in many mouse models of analgesia are indistinguishable (12, 13), in some, PGI₂ rather than PGE₂ predominates (14) and thus may be the dominant mediator in certain subtypes of human pain. Finally, the consequences of PGE₂ suppression might differ between cell types. PGE₂ activates four E prostanoid (EP) receptors with contrasting intracellular signaling and consequent biology (15, 16). Indeed, the contrasting effect of mPGES-1 deletion in myeloid vs. vascular cells on the proliferative response to vascular injury reflects the differential consequences of EP activation rather than substrate rediversion (8).A potentially discriminating feature among inhibitors of COX-2 and mPGES-1 is their effect on atherosclerosis. Global postnatal deletion of COX-2 accelerates atherogenesis in hyperlipidemic mice (17), an observation that accords with a similar effect of deleting the PGI₂ receptor (the IP) (18, 19) and with the delayed detection of a cardiovascular hazard in randomized trials of COX-2 inhibitors in patients initially selected for being at low cardiovascular risk (20). By contrast, global deletion of mPGES-1 restrains atherogenesis in mice; in this case suppression of PGE₂ coincides with an increase in biosynthesis of PGI₂ (9). Here, we wished to segregate the effects on atherosclerosis of mPGES-1 depletion in myeloid from vascular cells. Our results strengthen the rationale for targeting macrophage mPGES-1 in the treatment of inflammatory cardiovascular disease.     

Form,function, and evolution of living organisms

Despite the vast diversity of sizes and shapes of living organisms, life’s organization across scales exhibits remarkable commonalities, most notably through the approximate validity of Kleiber’s law, the power law scaling of metabolic rates with the mass of an organism. Here, we present a derivation of Kleiber’s law that is independent of the specificity of the myriads of organism species. Specifically, we account for the distinct geometries of trees and mammals as well as deviations from the pure power law behavior of Kleiber’s law, and predict the possibility of life forms with geometries intermediate between trees and mammals. We also make several predictions in excellent accord with empirical data. Our theory relates the separate evolutionary histories of plants and animals through the fundamental physics underlying their distinct overall forms and physiologies.Understanding the origin and evolution of the geometries of living forms is a formidable challenge (1, 2). The geometry of an object can be characterized by its surface−volume relationship—the surface area S of an object of volume V can scale at most as and at least as (3). These geometries have been used by nature in space-filling trees and animals, respectively. Here, our principal goal is to explore how it is that both geometries of life coexist on Earth, whether intermediate geometries are possible, and what all this implies for evolution of life on Earth.Living organisms span an impressive range of body mass, shapes, and scales. They are inherently complex, they have been shaped by history through evolution and natural section, and they continually extract, transform, and use energy from their environment. The most prevalent large multicellular organisms on Earth, namely plants and animals, exhibit distinct shapes, as determined by the distribution of mass over the volume. Animals are able to move and are approximately homogeneous in their mass distribution—yet they have beautiful fractal transportation networks. Plants are rooted organisms with a heterogeneous self-similar (fractal) geometry—the mass of the tree is more concentrated in the stem and branches than in the leaves.The approximate power law dependence of the metabolic rate, the rate at which an organism burns energy, on organism mass has been carefully studied for nearly two centuries and is known as allometric scaling (4–32). From the power law behavior, with an exponent around 3/4, one can deduce the scaling of characteristic quantities with mass and, through dimensional analysis, obtain wide-ranging predictions often in accord with empirical data. However, what underlies this ubiquitous quarter-power scaling, and with a dominant exponent of 3/4?In an influential series of papers, West and coworkers (11, 12, 14–16) suggested that fractality was at the heart of allometric scaling. Inspired by these papers, a contrasting view was presented (13), which argued that, although fractal circulatory networks may have advantages, quarter-power scaling came built in with the directed transport of nutrients. However, this latter paper was necessarily incomplete because it did not address the distinct geometries of animals and trees. More recently, members of both groups joined together to construct explicit models for animals, which showed (24) that “quarter-power scaling can arise even when there is no underlying fractality.” Here, we take a fresh look at the problem and derive quarter-power scaling quite generally for all living organisms. We then turn to a consideration of the sharp differences in the geometries of animals and trees and argue that the evolution of organismal forms follows from a rich interplay of geometry, evolutionary history, developmental symmetry, and efficient nutrient acquisition.Despite their independent evolution and different metabolisms, vascular plants and bilaterian animals share major design features, namely, an internal mass comprising organized cells capable of metabolic and bioenergetic activities, a transport mechanism for distributing molecules and energy within itself, and a surface capable of exchanging matter and energy with the environment. Regardless of the shape differences observed between these two groups, the physics associated with the transformation, transport, and exchange of matter and energy must unavoidably impose physical constraints on their designs. An organism is akin to an engine—part of the energy obtained from nourishment is used for organism function, growth, reproduction, while the rest is dissipated through its surface. We consider the hypothesis of the survival of the fittest in terms of energy metabolism and postulate that an organism with a higher energy intake would have a competitive advantage over another organism of similar mass performing energetically suboptimally, and explore its consequences.Consider an isotropic 3D organism of spatial extent h whose volume V scales as . Generalization to organisms with distinct scaling along the three different directions is straightforward. We make the simplifying assumption that the consumption and metabolic activity is distributed uniformly in space and in time or suitable averaging is used. We denote the basal metabolic rate of the organism by B and its mass by M. B is a measure of the energy being delivered to the organism per unit time and ought to be proportional to the energy dissipated through its surface. There is no evidence of size selection in empirical data, and this lends support to the assumption that the efficiency of the engine is independent of the organism’s size. We will derive Kleiber’s law based on energy intake considerations and study the role of geometry, as captured in the surface−volume relationship, on considering the expelled energy.Our goal is to understand the ideal dependence of B on M in the scaling regime. The characteristic time scale associated with the organism is known to scale as —it is a measure of how long it would take for energy proportional to M to be dissipated at a rate of B. Henceforth, proportionality constants, which serve to fix the correct units of various quantities related through scaling relations, will be omitted for the sake of simplicity.The number of metabolites, N, consumed in the organism per unit time is proportional to B. Let us define , so that a single metabolite is consumed per unit time in the local region surrounding each site of an grid. Each of these sites can be thought of as being within a service volume, in which one metabolite is consumed per unit time, of linear spatial extent . At the local level, the metabolites need to be transported this distance over unit time, and one immediately finds (24) that the transport velocity . Another measure of the transport velocity is obtained by noting that it is a characteristic length scale of the organism divided by the corresponding characteristic time scale and therefore scales as . Setting the two measures to be proportional to each other, one obtains Kleiber’s law .An alternative way of deriving the same result in a more rigorous manner is through the consideration of the properties of efficient transportation networks. The goal is to determine the minimum number of metabolites in transit, a measure of the organism mass, to ensure that metabolites are delivered in unit time within the organism volume. One can prove that the mass scales at least as with the optimality arising for efficient directed networks with no large-scale backtracking (13). This again leads to Kleiber’s law.Remarkably, the idealized metabolic rate−mass relationship is predicted to be algebraic with a exponent independent of the geometry of the organism. Such competitive equivalence explains the coexistence of animals with a homogeneous tissue density and fractal plants on Earth. The mass-specific metabolic rate, , scales as , whereas the transit time scales as . Indeed, characteristic biological rates (such as the heart beat and mutation rates) and characteristic biological times (such as circulation times or lifetimes) scale as and , respectively (6, 7, 9–12, 14–16).     

A case report and review of the locked metacarpophalangeal joint

A 59-year-old female with metacarpal joint locking is presented. The successful closed manipulation is described with a review of the literature.     

Penetrating injuries of the laryngotracheal area.

Penetrating injuries of the laryngotracheal area require immediate maintenance of an adequate airway and prompt surgical exploration and repair. Two basic principles are illustrated by case reports: repairing major vessels before doing the laryngotracheal repair and using adjacent tissues to repair traumatic defects. We suggest a team approach at operation.