The Value of History and Physical Examination to Optimize Outcomes of Cataract Surgery: A Systematic Review.

This systematic review was conducted to examine the value of the preoperative history and physical (H&P) examination and preoperative care prior to cataract extraction and the resulting outcomes of adverse events, patient experience, and cost. Four databases were searched using appropriate keywords from 2012 to 2022. Observational studies, randomized controlled trials, and quality improvement studies with data on the precataract H&P were included. Outcome measures were adverse events, cost, and patient experience. Of the 4,170 studies screened, 12 studies were included. Risk stratification of patients into a high-risk group with an H&P and a low-risk group without an H&P resulted in an increased incidence of minor adverse events in the low-risk group but did not increase the incidence of major adverse events or surgical adverse events. A short-term cost savings was reported, and patient experience was unchanged. In 2020, the Centers for Medicare and Medicaid Services removed the requirement for the precataract H&P within 30 days prior to ambulatory surgery, which has implications for surgery center policy. More research on the role of the preoperative H&P on patient experience, adverse events, cost, and outcomes should be conducted, given the methodological heterogeneity of this review.

The Tissue Response to Hypoxia: How Therapeutic Carbon Dioxide Moves the Response toward Homeostasis and Away from Instability.

Sustained tissue hypoxia is associated with many pathophysiological conditions, including chronic inflammation, chronic wounds, slow-healing fractures, microvascular complications of diabetes, and metastatic spread of tumors. This extended deficiency of oxygen (O2) in the tissue sets creates a microenvironment that supports inflammation and initiates cell survival paradigms. Elevating tissue carbon dioxide levels (CO2) pushes the tissue environment toward "thrive mode," bringing increased blood flow, added O2, reduced inflammation, and enhanced angiogenesis. This review presents the science supporting the clinical benefits observed with the administration of therapeutic CO2. It also presents the current knowledge regarding the cellular and molecular mechanisms responsible for the biological effects of CO2 therapy. The most notable findings of the review include (a) CO2 activates angiogenesis not mediated by hypoxia-inducible factor 1a, (b) CO2 is strongly anti-inflammatory, (c) CO2 inhibits tumor growth and metastasis, and (d) CO2 can stimulate the same pathways as exercise and thereby, acts as a critical mediator in the biological response of skeletal muscle to tissue hypoxia.

Compliance with Surgical Care Improvement Project for Body Temperature Management (SCIP Inf-10) Is Associated with Improved Clinical Outcomes.

BACKGROUND: In an effort to measure and improve the quality of perioperative care, the Surgical Care Improvement Project (SCIP) was introduced in 2003. The SCIP guidelines are evidence-based process measures designed to reduce preventable morbidity, but it remains to be determined whether SCIP-measure compliance is associated with improved outcomes. METHODS: The authors retrospectively analyzed the electronic medical record data from 45,304 inpatients at a single institution to assess whether compliance with SCIP Inf-10 (body temperature management) was associated with a reduced incidence of morbidity and mortality. The primary outcomes were hospital-acquired infection and ischemic cardiovascular events. Secondary outcomes were mortality and hospital length of stay. RESULTS: Body temperature on admission to the postoperative care unit was higher in the SCIP-compliant group (36.6° ± 0.5°C; n = 44,064) compared with the SCIP-noncompliant group (35.5° ± 0.5°C; n = 1,240) (P < 0.0001). SCIP compliance was associated with improved outcomes in both nonadjusted and risk-adjusted analyses. SCIP compliance was associated with a reduced incidence of hospital-acquired infection (3,312 [7.5%] vs.160 [12.9%] events; risk-adjusted odds ratio [OR], 0.68; 95% CI, 0.54 to 0.85), ischemic cardiovascular events (602 [1.4%] vs. 38 [3.1%] events; risk-adjusted OR, 0.60; 95% CI, 0.41 to 0.92), and mortality (617 [1.4%] vs. 60 [4.8%] events; risk-adjusted OR, 0.41; 95% CI, 0.29 to 0.58). Median (interquartile range) hospital length of stay was also decreased: 4 (2 to 8) versus 5 (2 to 14) days; P < 0.0001. CONCLUSION: Compliance with SCIP Inf-10 body temperature management guidelines during surgery is associated with improved clinical outcomes and can be used as a quality measure.

Development of a risk-adjusted blood utilization metric.

BACKGROUND: Blood utilization has become an important outcome measure for surgical patients because of the recognized risks and costs associated with transfusion. However, comparisons of blood utilization between providers or institutions are difficult, because there is no standard method for risk adjustment when assessing surgical blood requirements. We examined whether accepted diagnosis-related group (DRG) case mix indexes can be used for this purpose. STUDY DESIGN AND METHODS: We retrospectively analyzed electronic medical record data from 37,403 surgical inpatients to assess the relationship between intraoperative blood component transfusion requirements and the case mix indexes: weighted Medicare severity DRG and weighted all-patient refined DRG. Thirty-one surgeons from the general surgery service were compared to determine correlations between blood component utilization and case mix index in both a risk unadjusted and an adjusted fashion. RESULTS: Case mix indexes and transfusion requirements were directly correlated for red blood cells (RBCs), plasma, and platelet (PLT) transfusions (p < 0.0001 for all three blood components, for both indexes). Surgeons with greater case mix index values had greater transfusion requirements, and adjustment for case mix index resulted in less variation among surgeons (p < 0.0001, p = 0.0003, and p < 0.0001 for unadjusted vs. adjusted utilization of RBCs, plasma, and PLTs, respectively). CONCLUSIONS: The standard DRG-based case mix indexes used to determine hospital reimbursement were strongly correlated with intraoperative transfusion requirements. We propose that these methods can be used as a risk-adjusted blood utilization metric for surgical patients.

Cataract surgery in patients with left ventricular assist device support.

UNLABELLED: Left ventricular assist devices (LVADs) have been increasingly used for 20 years in terminally ill patients with advanced heart failure or awaiting cardiac transplantation. Despite improvement in morbidity and mortality from use of these devices, quality of life may be limited by cataract. Access to cataract surgery in this predominantly elderly population is essential but limited by unfamiliarity with these devices. We describe phacoemulsification and intraocular lens implantation in 2 patients with LVADs. The patients had extensive preoperative cardiology evaluations and were instructed to continue warfarin through the day of surgery. Monitored sedation was used with fentanyl and midazolam. Both patients experienced significant improvement in visual acuity and quality of life. Neither experienced intraoperative hemodynamic instability. Cataract surgery may be safely performed in patients with LVAD support when adequate monitoring resources are available. FINANCIAL DISCLOSURE: No author has a financial or proprietary interest in any material or method mentioned.

Optimizing preoperative blood ordering with data acquired from an anesthesia information management system.

BACKGROUND: The maximum surgical blood order schedule (MSBOS) is used to determine preoperative blood orders for specific surgical procedures. Because the list was developed in the late 1970s, many new surgical procedures have been introduced and others improved upon, making the original MSBOS obsolete. The authors describe methods to create an updated, institution-specific MSBOS to guide preoperative blood ordering. METHODS: Blood utilization data for 53,526 patients undergoing 1,632 different surgical procedures were gathered from an anesthesia information management system. A novel algorithm based on previously defined criteria was used to create an MSBOS for each surgical specialty. The economic implications were calculated based on the number of blood orders placed, but not indicated, according to the MSBOS. RESULTS: Among 27,825 surgical cases that did not require preoperative blood orders as determined by the MSBOS, 9,099 (32.7%) had a type and screen, and 2,643 (9.5%) had a crossmatch ordered. Of 4,644 cases determined to require only a type and screen, 1,509 (32.5%) had a type and crossmatch ordered. By using the MSBOS to eliminate unnecessary blood orders, the authors calculated a potential reduction in hospital charges and actual costs of $211,448 and $43,135 per year, respectively, or $8.89 and $1.81 per surgical patient, respectively. CONCLUSIONS: An institution-specific MSBOS can be created, using blood utilization data extracted from an anesthesia information management system along with our proposed algorithm. Using these methods to optimize the process of preoperative blood ordering can potentially improve operating room efficiency, increase patient safety, and decrease costs.

Variability in blood and blood component utilization as assessed by an anesthesia information management system.

BACKGROUND: Data can be collected for various purposes with anesthesia information management systems. The authors describe methods for using data acquired from an anesthesia information management system to assess intraoperative utilization of blood and blood components. METHODS: Over an 18-month period, data were collected on 48,086 surgical patients at a tertiary care academic medical center. All data were acquired with an automated anesthesia recordkeeping system. Detailed reports were generated for blood and blood component utilization according to surgical service and surgical procedure, and for individual surgeons and anesthesiologists. Transfusion hemoglobin trigger and target concentrations were compared among surgical services and procedures, and between individual medical providers. RESULTS: For all patients given erythrocytes, the mean transfusion hemoglobin trigger was 8.4 ± 1.5, and the target was 10.2 ± 1.5 g/dl. Variation was significant among surgical services (trigger range: 7.5 ± 1.2-9.5 ± 1.1, P = 0.0001; target range: 9.1 ± 1.2-11.3 ± 1.4 g/dl, P = 0.002), surgeons (trigger range: 7.2 ± 0.7-9.8 ± 1.0, P = 0.001; target range: 8.8 ± 0.9-11.8 ± 1.3 g/dl, P = 0.001), and anesthesiologists (trigger range: 7.2 ± 0.8-9.6 ± 1.2, P = 0.001; target range: 9.0 ± 0.9-11.7 ± 1.3 g/dl, P = 0.0004). The use of erythrocyte salvage, fresh frozen plasma, and platelets varied threefold to fourfold among individual surgeons compared with their peers performing the same surgical procedure. CONCLUSIONS: The use of data acquired from an anesthesia information management system allowed a detailed analysis of blood component utilization, which revealed significant variation among surgical services and surgical procedures, and among individual anesthesiologists and surgeons compared with their peers. Incorporating these methods of data acquisition and analysis into a blood management program could reduce unnecessary transfusions, an outcome that may increase patient safety and reduce costs.

Multiple receptor subtypes and multiple mechanisms of dilation are involved in vascular network dilation caused by adenosine.

We previously demonstrated a vascular network response initiated by elevated tissue concentrations of adenosine that is distinct from the dilation caused when adenosine is applied directly to the arteriole. The purpose of this study was to elucidate the potential mechanism(s) for the different responses. In the cheek pouch of anesthetized hamster, arteriolar responses were measured when adenosine (10(-4)M) was applied with micropipette into the tissue 500 microm from the arteriole (n=67, baseline diameter 22+/-0.6 microm) or onto the arteriole itself. Application of adenosine to the vessel or into the tissue caused arteriolar dilation with similar concentration profiles. In stark contrast, the concentration profiles were significantly different for vessel and tissue initiated dilation when either sodium nitroprusside or methacholine was tested. Arteriolar dilation was not enhanced when adenosine was simultaneously applied with two pipettes at along a single arteriole; however, the dilation doubled when adenosine was applied simultaneously at arteriole and tissue. Control dilations caused by tissue adenosine (5+/-0.4 microm) were not altered by superfusion of the A(1) receptor antagonist DPCPX (10(-6)M; 4.6+/-0.3 microm), A(2B) receptor antagonist alloxazine (10(-6)M; 6+/-0.8 microm), or A(3) receptor antagonist MRS1220 (5 x 10(-9)M; 6+/-0.8 microm) but were abolished by the selective A(2A) receptor antagonist ZM241385 (10(-7)M; 1+/-0.2 microm), suggesting that activation of A(2A) receptors mediates these network responses. Disruption of arteriolar endothelium and direct arteriolar application of ZM241385 (10(-7)M; 5+/-0.4 microm) did not alter the dilation caused by tissue adenosine. However, local application of ZM241385 into the tissue inhibited adenosine-induced network responses (2+/-0.3 microm). Furthermore, application into the tissue of A(2A) receptor agonist CGS21680 (10(-5)M), but not A(1) (CPA; 10(-4)M), A2b (NECA, 10(-4)M) or A3 (IB-MECA; 10(-4)M) receptor agonists mimicked the adenosine network response. These data demonstrate dual, complimentary, yet distinct pathways for network dilations induced by increases in tissue adenosine.

The involvement of CGRP, adrenomedullin, and sensory nerves in remote vasomotor responses within the hamster cheek pouch microcirculation.

Previous work from our laboratory demonstrated a role for sensory nerves in remote dilations to microapplied methacholine by blocking the response with CGRP8-37 and concluded CGRP was the neurotransmitter. Recently, a more specific CGRP receptor antagonist, BIBN4096BS, was developed. The goals of the present study are to characterize the effects of BIBN4096BS on vasomotor responses in the hamster cheek pouch microcirculation, and to verify the role of CGRP in remote dilations to capsaicin and methacholine and to test adrenomedullin as an alternative neurotransmitter. BIBN4096BS pretreatment inhibits dilation to CGRP while having no significant effect on baseline diameter, it shifts the EC(50) to superfused CGRP from 1.5+/-0.3 pM to 2.5+/-0.6 nM and it shifts the apparent EC(50) to capsaicin from 31.5 nM to 171 nM. Local and remote dilations caused by the microapplication of methacholine are not inhibited by 300 nM BIBN4096BS (Local: 9.7+/-1.2 versus 9.7+/-1.5; 500:5.5+/-0.4 versus 5.7+/-0.5; 1000:4.4+/-0.6 versus 4.8+/-0.5). Remote dilations to methacholine were significantly inhibited however when adrenomedullin receptor antagonist adrenomedullin-(26-52) was microapplied to the remote site. Perivascular neurons containing adrenomedullin can be detected with immunohistochemistry. The results, combined with previous work, suggest that adrenomedullin, and not CGRP, is involved in remote dilations to methacholine.

Mechanisms initiating integrin-stimulated flow recruitment in arteriolar networks.

Our purpose was to investigate the local mechanisms involved in network-wide flow and diameter changes observed with localized downstream vitronectin receptor ligation; we tested specific K or Cl channels known to be involved in either dilation or elevated permeability following vitronectin receptor activation and tested integrin-linked pathway elements of tyrosine phosphorylation and protein kinase C (PKC). Arteriolar networks were observed in the cheek pouch tissue of anesthetized (pentobarbital sodium, 70 mg/kg) hamsters (n=86) using intravital microscopy. Terminal arteriolar branches of the networks were stimulated with micropipette LM609 (0.5-10 microg/ml, 60 s) alone or with inhibitors (separate micropipette). Hemodynamic changes (diameter, red blood cell flux, velocity) were observed at the upstream entrance to the network. LM609 alone stimulated first an increase in wall shear stress (WSS), followed by a dilation that recovered WSS to baseline or below. K channel inhibition (glybenclamide, 4-AP) had no effect on the initial peak in WSS, but decreased remote vasodilation. Cl channel inhibition (DIDS, IAA-94, niflumic acid) or inhibition of PKC (chelerythrine) prevented the initial peak in WSS and decreased remote vasodilation. Inhibition of tyrosine phosphorylation (genistein) prevented both. With the use of nitro-arginine at the observation site, the initial peak in WSS was not affected, but remote vasodilation was decreased. We conclude the remote response consists of an initial peak in WSS that relies on both PKC activity and depolarization downstream, leading to an upstream flow mediated dilation and a secondary remote dilation that relies on hyperpolarization downstream at the stimulus site; both components require tyrosine phosphorylation downstream.

Remote arteriolar dilations caused by methacholine: a role for CGRP sensory nerves?

Remote vasodilation caused by arteriolar microapplication of acetylcholine cannot be completely attributed to passive cell-cell communication of a hyperpolarizing signal. The present study was undertaken to ascertain whether a neural component may be involved in the remote response. In the cheek pouch of anesthetized hamsters, methacholine (100 microM) was applied to the arteriole by micropipette for 5 s, and the arteriolar responses were measured at the site of application and at remote locations: 500 and 1,000 microm upstream from the application site. Superfusion with the local anesthetic bupivacaine attenuated a local dilatory response and abolished the conducted dilation response to methacholine. Localized micropipette application of bupivacaine 300 microm from the methacholine application site also attenuated the remote dilation but did not inhibit the local dilation. Blockade of neuromuscular transmission with botulinum neurotoxin A (1 U, 3 days), micropipette application of calcitonin gene-related peptide (CGRP) receptor inhibitor CGRP-(8-37) (10 microM) 300 microm upstream from the methacholine application site, and denervation of the CGRP sensory nerve by 2 days of capsaicin treatment reduced the conducted dilation response to methacholine but did not affect the local dilatory response. Together, these data support involvement of a TTX-insensitive nerve, specifically the CGRP containing nerve, in vascular communication. Understanding the effect of regulation of a novel neural network system on the vascular network may lead to a new insight into regulation of blood flow and intraorgan blood distribution.

Arteriolar occlusion causes independent cellular responses in endothelium and smooth muscle.

OBJECTIVES: To test the hypothesis that arteriolar occlusion causes different cellular changes in endothelial and smooth muscle cells. METHODS: Cheek pouch arterioles (resting diameter 41 +/- 2 microm) of anesthetized hamsters were occluded briefly (<60 seconds) either upstream or downstream from an observation site. Changes in membrane potential and intracellular calcium concentration ([Ca(2+)](i)) of the endothelial or smooth muscle cells were determined by using fluorescence microscopy (ratiometric analysis). RESULTS: The pressure in the occluded segment decreased by 17.4 +/- 2.6 cm H(2)O during upstream occlusion and increased by 16.8 +/- 6 cm H(2)O during downstream occlusion (n = 5). Upstream occlusion caused vasoconstriction of the occluded segment by 2.4 +/- 0.4 microm, whereas downstream occlusion produced brief vasodilatation by 1.1 +/- 0.2 microm. The endothelial cells hyperpolarized during upstream or downstream occlusion (ratio change: 2.26 +/- 0.24% and 2.39 +/- 0.42%, respectively; p < 0.01, n = 5). There were no changes in endothelial [Ca(2+)](i). The smooth muscle cells depolarized (ratio change: -2.08 +/- 0.14%, n = 5) with an increase in [Ca(2+)](i) (ratio change: 2.92 +/- 0.16%, n = 6) during downstream occlusion. However, there was no detectable change in membrane potential or [Ca(2+)](i) of smooth muscle cells during upstream occlusion. All the changes rapidly recovered when occlusion was released. Responses of an in-situ isolated segment on a side branch revealed conducted dilatory signals caused by the occlusions. CONCLUSIONS: Our results show that the endothelial and smooth muscle cells respond independently to arteriolar occlusion. The endothelial and smooth muscle cells do not effectively communicate in [Ca(2+)](i) or membrane potential during acute arteriolar occlusion. Hyperpolarizing signals in endothelium cause conducted dilation.