Borgess Medical Center

BACKGROUND: Obstructive sleep apnea is associated with considerable health risks. Although continuous positive airway pressure (CPAP) can mitigate these risks, effectiveness can be reduced by inadequate adherence to treatment. We evaluated the clinical safety and effectiveness of upper-airway stimulation at 12 months for the treatment of moderate-to-severe obstructive sleep apnea. METHODS: Using a multicenter, prospective, single-group, cohort design, we surgically implanted an upper-airway stimulation device in patients with obstructive sleep apnea who had difficulty either accepting or adhering to CPAP therapy. The primary outcome measures were the apnea-hypopnea index (AHI; the number of apnea or hypopnea events per hour, with a score of ≥15 indicating moderate-to-severe apnea) and the oxygen desaturation index (ODI; the number of times per hour of sleep that the blood oxygen level drops by ≥4 percentage points from baseline). Secondary outcome measures were the Epworth Sleepiness Scale, the Functional Outcomes of Sleep Questionnaire (FOSQ), and the percentage of sleep time with the oxygen saturation less than 90%. Consecutive participants with a response were included in a randomized, controlled therapy-withdrawal trial. RESULTS: The study included 126 participants; 83% were men. The mean age was 54.5 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 28.4. The median AHI score at 12 months decreased 68%, from 29.3 events per hour to 9.0 events per hour (P<0.001); the ODI score decreased 70%, from 25.4 events per hour to 7.4 events per hour (P<0.001). Secondary outcome measures showed a reduction in the effects of sleep apnea and improved quality of life. In the randomized phase, the mean AHI score did not differ significantly from the 12-month score in the nonrandomized phase among the 23 participants in the therapy-maintenance group (8.9 and 7.2 events per hour, respectively); the AHI score was significantly higher (indicating more severe apnea) among the 23 participants in the therapy-withdrawal group (25.8 vs. 7.6 events per hour, P<0.001). The ODI results followed a similar pattern. The rate of procedure-related serious adverse events was less than 2%. CONCLUSIONS: In this uncontrolled cohort study, upper-airway stimulation led to significant improvements in objective and subjective measurements of the severity of obstructive sleep apnea. (Funded by Inspire Medical Systems; STAR ClinicalTrials.gov number, NCT01161420.).

To examine the role of neutrophils, their presence and the degree of infiltration, as important determinants of ischemia and reperfusion injury of the liver, male Sprague-Dawley rats were subjected to 60 and 90 min of total-liver ischemia. The presence of neutrophils, assessed by the measurement of liver tissue myeloperoxidase (MPO), and the degree of neutrophil liver infiltration, determined by the naphthol AS-D chloroacetate esterase technique, correlated well with animal survival and response to FK506 and cyclosporine administration. Lipid peroxidation, measured by the malondialdehyde (MDA) test in liver tissue, was another factor closely linked with liver function and survival. Pretreatment with FK506 (0.3 mg/kg) and CsA (5 mg/kg) was given at 4 hr and 1 hr before ischemia and at the time of reperfusion. Control ischemic animals showed increased neutrophil liver infiltration, high MPO and MDA liver levels, and diminished overall survival. FK506 and CsA-treated animals had better survival and diminished neutrophil liver infiltration, as well as MPO and MDA levels. The mechanism by which FK506 and CsA protected the animals from severe liver ischemic injury is unknown. Our data indicated that the presence and the degree of infiltration of neutrophils were important components of liver ischemia/reperfusion injury in the rat. So it is possible that one of the fundamental effects of the FK506 and CsA might be through the inhibition of the presence and infiltration of neutrophils in liver tissue.

BACKGROUND: This study evaluated a large group of patients enrolled in a double-blind randomized trial of the sirolimus-eluting stent to document whether the initial clinical improvement seen in previous smaller series is maintained out to 12 months and to study the potential treatment effect in patient subsets known to be at increased risk of restenosis. METHODS AND RESULTS: A total of 1058 patients with de novo native coronary stenosis undergoing clinically indicated percutaneous coronary intervention were randomly assigned to sirolimus-eluting stent (533) or control bare stent (525). Procedural success and in-hospital outcomes were excellent and did not differ between the 2 groups. At 9 months, clinical restenosis, defined as target-lesion revascularization, was 4.1% in the sirolimus limb versus 16.6% in the control limb (P<0.001). At 12 months, the absolute difference in target-lesion revascularization continued to increase and was 4.9% versus 20% (P<0.001). There were no differences in death or myocardial infarction rates. In high-risk patient subsets, defined by vessel size, lesion length, and presence of diabetes mellitus, there was a 70% to 80% reduction in clinical restenosis at 1 year. CONCLUSIONS: Placement of the sirolimus-eluting stent results in continued clinical improvement at 1 year after initial implantation, with significant reduction in clinical restenosis as defined by target-lesion revascularization. Between 9 and 12 months, the absolute reduction of clinical restenosis continues to increase. Even in high-risk subsets of patients, there is a 70% to 80% relative reduction in clinical restenosis at 12 months with this drug-eluting stent.

Strollo, Patrick J. JR*; Soose, Ryan J.†; Maurer, Joachim T.‡; de Vries, Nico§; Cornelius, Jason‖; Froymovich, Oleg¶; Hanson, Ronald D.#; Padhya, Tapan A.**; Steward, David L.††; Boyd Gillespie, M.‡‡; Woodson, Tucker§§; Van de Heyning, Paul H.‖‖; Goetting, Mark G.¶¶; Vanderveken, Oliver M.‖‖; Feldman, Neil##; Knaack, Lennart***; STROHL, Kingman P.††† for the STAR (Stimulation Therapy for Apnea Reduction) Trial Group Author Information

With use of data culled from twenty studies, members of the Prevalence and Natural History Committee of the Scoliosis Research Society conducted a meta-analysis of 1910 patients who had been managed with bracing (1459 patients), lateral electrical surface stimulation (322 patients), or observation (129 patients) because of idiopathic scoliosis. Three variables - the type of treatment, the level of maturity, and the criterion for failure - were analyzed to determine which had the greatest impact on the outcome. We also examined the effect of the type of brace that was used and the duration of bracing on the success of treatment. The number of failures of treatment in each study was determined by calculating the total number of patients who had unacceptable progression of the curve (as defined in the study), who could not comply with or tolerate treatment, or who had an operation. The percentage of patients who completed a given course of treatment without failure, adjusted for the sample sizes of the studies in which that treatment was used, yielded the weighted mean proportion of success for that treatment. The weighted mean proportion of success was 0.39 for lateral electrical surface stimulation, 0.49 for observation only, 0.60 for bracing for eight hours per day, 0.62 for bracing for sixteen hours per day, and 0.93 for bracing for twenty-three hours per day. The twenty-three-hour regimens were significantly more successful than any other treatment (p < 0.0001). The difference between the eight and sixteen-hour regimens was not significant, with the numbers available. Although lateral electrical surface stimulation was associated with a lower weighted mean proportion of success than observation only, the difference was not significant, with the numbers available. This meta-analysis demonstrates the effectiveness of bracing for the treatment of idiopathic scoliosis. The weighted mean proportion of success for the six types of braces included in this review was 0.92, with the highest proportion (0.99) achieved with the Milwaukee brace. We found that use of the Milwaukee brace or another thoracolumbosacral orthosis for twenty-three hours per day effectively halted progression of the curve. Bracing for eight or sixteen hours per day was found to be significantly less effective than bracing for twenty-three hours per day (p < 0.0001).

Infections have represented for a long time the leading cause of death in humans. During the 19th century, pneumonia, tuberculosis, diarrhea and diphtheria were considered the main causes of death in children and adults. Only in the late 19th century did it become possible to correlate the existence of microscopic pathogens with the development of various diseases. Within a few years the introduction of antiseptic procedures had begun to reduce mortality due to postsurgical infections. Sanitation and hygiene played a significant role in the reduction of the mortality due to several infectious diseases. The introduction of the first compounds with antimicrobial activity succeeded in conquering many diseases. In this review we analyzed, from a historical perspective, the development of antibiotics and the circumstances that led to their discovery. The first compound with antimicrobial activity was introduced in 1911 by Erlich. He focused his research activity on the discovery of a "magic bullet" to treat syphilis. Afterwards, Foley and colleagues brought penicillin to the forefront. Streptomycin represents the first drug discovered for the treatment of tuberculosis, and its development included the first use of clinical trials. Finally, with the development of cephalosporins, the introduction of new antimicrobial compounds with broad activity against gram-positive and also some gram-negative bacteria began.

BACKGROUND: Few studies have reported the outcomes of surgical treatment of an acute grade-III posterolateral knee injury. Our purpose was to report the objective stability and subjective outcomes for a prospective series of patients with an acute grade-III posterolateral knee injury treated with anatomic repair and/or reconstruction of all injured structures. METHODS: A prospective study of all patients with a grade-III posterolateral knee injury treated with an anatomic repair and/or reconstruction within six weeks of injury was initiated in May 2005. International Knee Documentation Committee (IKDC) objective scores and bilateral varus stress radiographs were obtained at each visit, including preoperatively and at the final follow-up visit. In addition, all patients completed Cincinnati and IKDC subjective evaluations. All associated cruciate ligament tears were reconstructed concurrently. RESULTS: Twenty-nine patients (twenty-four men and five women with a mean age of twenty-seven years) (thirty knees) were enrolled in the study. Eight knees had an isolated posterolateral corner injury, ten also had an anterior cruciate ligament tear, four also had a posterior cruciate ligament tear, and eight also had tears of both cruciate ligaments. Four patients were lost to follow-up prior to two years, resulting in a final study cohort of twenty-five patients (twenty-six knees). All five IKDC objective subscores had improved significantly at the time of the final follow-up evaluation at an average of 2.4 years postoperatively. Varus stress radiographs demonstrated a significant improvement in the side-to-side difference in the lateral compartment gap, from 6.2 mm preoperatively to 0.1 mm at the time of the final follow-up. The mean Cincinnati and IKDC subjective outcomes scores improved from 21.9 to 81.4 points and from 29.1 to 81.5 points, respectively. CONCLUSIONS: Treatment of grade-III posterolateral knee injuries with acute repair of avulsed structures, reconstruction of midsubstance tears, and concurrent reconstruction of any cruciate ligament tears resulted in significantly improved objective stability.

Evolution of plaque that is prone to rupture is characterized by inflammation and physical changes. Accumulation of low-density lipoprotein in the sub-intima provides esterified cholesterol (ESC) to macrophages and smooth muscle cells that convert it into free cholesterol (FRC) by cholesteryl ester hydrolases (CEHs). Membrane-bound cholesterol carriers transport FRC to high-density lipoprotein (HDL). Impaired HDL transport function and altered composition can lead to extracellular accumulation of FRC, whereas impaired membrane carrier activity can lead to intracellular FRC accumulation. Saturation of FRC can result in cholesterol crystallization with cell death and intimal injury. Disequilibrium between ESC and FRC can impact foam cell and cholesterol crystal (CC) formation. Cholesterol crystals initiate inflammation via NLRP3 inflammasome leading to interleukin-1β (IL-1β) production inducing C-reactive protein. Eventually, crystals growing from within the plaque and associated inflammation destabilize the plaque. Thus, inhibition of inflammation by antagonists to IL-1β or agents that dissolve or prevent CC formation may stabilize vulnerable plaques.

BACKGROUND AND PURPOSE: Medical treatment of symptomatic intracranial stenosis carries a high risk of stroke. This study was done to evaluate the clinical and angiographic outcomes after intracranial angioplasty for this disease. METHODS: A total of 120 patients with 124 intracranial stenoses were treated by primary angioplasty. All patients had neurologic symptoms (stroke or transient ischemic attack) attributable to intracranial stenoses > or =50%. Angiograms were evaluated before and after angioplasty for the degree of stenosis. RESULTS: Pretreatment stenoses varied from 50% to 95% (mean 82.2+/-10.2). Post-treatment stenoses varied from 0% to 90% (mean 36.0+/-20.1). There were 3 strokes and 4 deaths (all neurological) within 30 days of the procedure, giving a combined periprocedural stroke and death rate of 5.8%. A total of 116 patients (96.7%) were available for a mean follow-up time of 42.3 months. There were 6 patients who had a stroke in the territory of treatment and 5 additional patients with stroke in other territories. Ten deaths occurred during the follow-up period, none of which were neurological. Including the periprocedural stroke and deaths, this yielded an annual stroke rate of 3.2% in the territory of treatment and a 4.4% annual rate for all strokes. CONCLUSIONS: Intracranial angioplasty can be performed with a high degree of technical success and a low risk of complications. Long-term clinical follow-up of intracranial angioplasty patients demonstrates a risk of future strokes that compares favorably to patients receiving medical therapy.

This study reviews the current understanding of the mechanisms that mediate the complex processes involved in apoptosis secondary to ischemia and reperfusion (I/R) and is not intended as a complete literature review of apoptosis. Several biochemical reactions trigger a cascade of events, which activate caspases. These caspases exert their effect through downstream proteolysis until the final effector caspases mediate the nuclear features characteristic of apoptosis, DNA fragmentation and condensation. Within the context of ischemia, the hypoxic environment initiates the expression of several genes involved in inflammation, the immune response, and apoptosis. Many of these same genes are activated during reperfusion injury in response to radical oxygen species generation. It is plausible that inhibition of specific apoptotic pathways via inactivation or downregulation of those genes responsible for the initiation of inflammation, immune response, and apoptosis may provide promising molecular targets for ameliorating reperfusion injury in I/R-related processes. Such inhibitory mechanisms are discussed in this review. Important targets in I/R-related pathologies include the brain during stroke, the heart during myocardial infarction, and the organs during harvesting and/or storage for transplantation. In addition, we present data from our ongoing research of specific signal transduction-related elements and their role in ischemia/reperfusion injury. These data address the potential therapeutic application of anti-inflammatory and anti-ischemic compounds in the prevention of I/R damage.

Diffuse idiopathic skeletal hyperostosis (DISH) is a common disorder of unknown etiology that is characterized by back pain and spinal stiffness. There may be mild pain if ankylosis has occurred. The condition is recognized radiographically by the presence of "flowing" ossification along the anterolateral margins of at least four contiguous vertebrae and the absence of changes of spondyloarthropathy or degenerative spondylosis. Even in patients who present with either lumbar or cervical complaints, radiographic findings are almost universally seen on the right side of the thoracic spine. Thus, radiographic examination of this area is critical when attempting to establish a diagnosis of DISH. The potential sequelae of hyperostosis in the cervical and lumbar spine include lumbar stenosis, dysphagia, cervical myelopathy, and dense spinal cord injury resulting from even minor trauma. There may be a delay in diagnosis of spinal fractures in a patient with DISH because the patient often has a baseline level of spinal pain and because the injury may be relatively trivial. The incidence of delayed neurologic injury due to such fractures is high as a result of unrecognized instability and subsequent deterioration. Extraspinal manifestations are also numerous and include an increased risk of heterotopic ossification after total hip arthroplasty. Prophylaxis to prevent heterotopic ossification may be indicated for these patients.

Injury due to ischemia and reperfusion (I/R) causes an inflammatory response due to oxidative damage, which triggers stress signaling processes that eventually result in cell apoptosis and death. There are a number of chemical mediators and pathways involved in the I/R response. Thus from a therapeutic point of view, it would be most efficient to focus on the most important active mediators of inflammation and apoptosis and manipulate these to improve cell function and survival. Over the last few years, the Akt pathway has become such a target due to its role as a signaling pathway where modulation of substrates prevents apoptosis. The involvement of Akt in the cell survival pathway is a complex process that requires an extensive machinery of intracellular events. The aim of this review is to organize these findings to better understand Akt's mechanism of protection and how it modulates specific substrates in the heart, liver, and brain affected by I/R. Akt functions as a survival kinase by phosphorylating a number of apoptosis-regulatory molecules such as BAD, forkhead transcription factors, caspase 9, and IkappaB kinase to influence NF-kappaB and GSK-3beta. Akt's broad scope places it at the center of multiple critical steps, allowing it to play a protective role in various organs affected by I/R injury. From a practical and clinical application point of view, the upregulation of Akt could potentially be used alone or in combination with other therapeutic strategies to treat I/R injury and thus to improve cell and organ function. The means by which Akt manipulation should occur is not well defined, and it is possible that pharmacologically, such as in the case of selectin inhibitors in our experience or through well-orchestrated gene therapy, this important molecule can be better upregulated and therefore can offer effective protection. The short- and long-term effects with Akt upregulation have not been well studied so far. Early concerns about cancer or cardiac damage potential are inconclusive. Thus, more experiments are required in this particular area of research.

BACKGROUND: Receptor for advanced-glycation end products (RAGE) and its ligands AGEs and S100/calgranulins have been implicated in a range of disorders. However, the role of RAGE/ligand interaction in neointimal hyperplasia after vascular injury remains unclear. METHODS AND RESULTS: We examined the expression of RAGE and its ligands after balloon injury of the carotid artery in both Zucker diabetic and nondiabetic rats. Using a soluble portion of the extracellular domain of RAGE, we determined the effects of suppressing RAGE/ligand interaction on vascular smooth muscle cell (VSMC) proliferation and neointimal formation after arterial injury. We demonstrate a significantly increased accumulation of AGE and immunoreactivities of RAGE and S100/calgranulins in response to balloon injury in diabetic compared with nondiabetic rats. Blockade of RAGE/ligand interaction significantly decreased S100-stimulated VSMC proliferation in vitro and bromodeoxyuridine (BrdU)-labeled proliferating VSMC in vivo, and suppressed neointimal formation and increased luminal area in both Zucker diabetic and nondiabetic rats. CONCLUSIONS: These findings indicate that RAGE/ligand interaction plays a key role in neointimal formation after vascular injury irrespective of diabetes status and suggest a novel target to minimize neointimal hyperplasia.

BACKGROUND AND PURPOSE: The volume of ischemic stroke on CT scans has been studied in a standardized fashion in acute stroke therapy trials with median volumes between 10.5 to 55 cm(3). The volume of first-ever ischemic stroke in the population is not known. METHODS: The first phase of the population-based Greater Cincinnati/Northern Kentucky Stroke Study identified all ischemic strokes occurring in blacks in the greater Cincinnati region between January and June of 1993. The patients in this phase of the study who had a first-ever ischemic clinical stroke were identified, and the volume of ischemic stroke was measured. RESULTS: There were 257 verified clinical cases of ischemic stroke, of which 181 had a first-ever ischemic infarct. Imaging was available for 150 of these patients, and 79 had an infarct on the CT or MRI study that was definitely or possibly related to the clinical symptoms. For these patients, volumetric measurements were performed by means of the modified ellipsoid method. The median volume of first-ever ischemic stroke for the 79 patients was 2.5 cm(3) (interquartile range, 0.5 to 8.8 cm(3)). There was a significant relation between location of lesion and infarct size (P<0.001) and between volume and mechanism of stroke (P=0.001). CONCLUSIONS: The volume of first-ever ischemic stroke among blacks in our population-based study is smaller than has been previously reported in acute stroke therapy trials. The large proportion of small, mild strokes in blacks may be an important reason for the low percentage of patients who meet the inclusion criteria for tissue plasminogen activator. Further study is necessary to see if these results are generalizable to a multiracial population.

We evaluated the in vitro activity of the new echinocandin antifungal micafungin against Candida spp. using microdilution and time-kill methods. Additionally, we examined the postantifungal effect (PAFE) of micafungin. Finally, we evaluated the effect of the addition of serum and plasma on the MIC of micafungin. Four Candida albicans isolates and two isolates of each Candida glabrata, Candida krusei, and Candida tropicalis were selected for testing. The MICs of micafungin were determined in RPMI 1640 medium buffered with morpholinepropanesulfonic acid alone and with the addition of 10, 20, and 50% human serum and plasma. MICs were determined by using two endpoints: a prominent reduction in growth (the MIC at which 80% of isolates are inhibited [MIC(80)]) and complete visual inhibition of growth (MIC(100)). The minimum fungicidal concentration (MFC) of micafungin for each isolate was also determined. Time-kill curves were determined for each isolate in RPMI 1640 medium with micafungin at concentrations ranging from 0.125 to 16 times the MIC(80) to assess the correlation between MIC(80) and fungicidal activity. PAFE studies were conducted with each isolate by using concentrations ranging between 0.25 and 4 times the MIC(80). The MIC(80)s for the test isolates ranged from 0.0039 to 0.25 micro g/ml. Overall, the addition of serum or plasma increased the MIC 6 to 7 doubling dilutions for C. albicans and 3 to 4 doubling dilutions for C. krusei and C. tropicalis. Micafungin time-kill studies demonstrated fungicidal activity at concentrations ranging from 4 to 16 times the MIC(80). Micafungin is very potent agent against a variety of Candida spp., producing fungicidal activity against 7 of 10 isolates tested. A PAFE was observed against all isolates. The PAFE was influenced by the drug concentration, with the highest concentration resulting in the longest observed PAFE in each case. The highest concentration tested, four times the MIC, resulted in a PAFE of more than 9.8 h for 5 of 10 isolates tested (range, 0.9 to > or =20.1 h).

The harvesting of an autogenous iliac bone graft is a frequently performed orthopedic procedure. Although often regarded as the simple or routine part of bone graft requiring surgery, complications are not necessarily uncommon. Documented donor-site complications include nerve, arterial, or urethral injury; chronic donor-site pain; cosmetic deformity; herniation of abdominal contents; sacroiliac joint instability; pelvic fractures; gait disturbances; hematoma; infection; peritoneal perforation; and hip subluxation. Most of these complications are avoidable when the surgeon is aware of their possibility and is familiar with the involved anatomy and preferred surgical approaches.

OBJECTIVE: To determine the stability of improvement in polysomnographic measures of sleep disordered breathing, patient reported outcomes, the durability of hypoglossal nerve recruitment and safety at 18 months in the Stimulation Treatment for Apnea Reduction (STAR) trial participants. DESIGN: Prospective multicenter single group trial with participants serving as their own controls. SETTING: Twenty-two community and academic sleep medicine and otolaryngology practices. MEASUREMENTS: Primary outcome measures were the apnea-hypopnea index (AHI) and the 4% oxygen desaturation index (ODI). Secondary outcome measures were the Epworth Sleepiness Scale (ESS), the Functional Outcomes of Sleep Questionnaire (FOSQ), and oxygen saturation percent time < 90% during sleep. Stimulation level for each participant was collected at three predefined thresholds during awake testing. Procedure- and/or device-related adverse events were reviewed and coded by the Clinical Events Committee. RESULTS: The median AHI was reduced by 67.4% from the baseline of 29.3 to 9.7/h at 18 mo. The median ODI was reduced by 67.5% from 25.4 to 8.6/h at 18 mo. The FOSQ and ESS improved significantly at 18 mo compared to baseline values. The functional threshold was unchanged from baseline at 18 mo. Two participants experienced a serious device-related adverse event requiring neurostimulator repositioning and fixation. No tongue weakness reported at 18 mo. CONCLUSION: Upper airway stimulation via the hypoglossal nerve maintained a durable effect of improving airway stability during sleep and improved patient reported outcomes (Epworth Sleepiness Scale and Functional Outcomes of Sleep Questionnaire) without an increase of the stimulation thresholds or tongue injury at 18 mo of follow-up.

OBJECTIVE: To determine the efficacy of CT scan in mapping the superior and inferior epigastric vessels, relative to landmarks apparent at laparoscopy. SUMMARY BACKGROUND DATA: Trauma to abdominal wall blood vessels occurs in 0.2% to 2% of laparoscopic procedures. Both superficial and deep abdominal wall vessels are at risk. The superficial vessels may be located by transillumination; however, the deep epigastric vessels cannot be effectively located by transillumination and, thus, other techniques should be used to minimize the risk of injury to these vessels. METHODS: Abdominal and pelvic CT images of 100 patients were studied. The location of the superior and inferior epigastric vessels from the midline were determined at five levels, correlated with each other and with the patient age, body mass index, and history of midline laparotomy using Pearson's correlation coefficient and multivariate analysis. RESULTS: CT scan was successful in mapping the epigastric vessels in 95% of patients. At the xiphoid process level, the superior epigastric vessels (SEA) were 4.41 +/- 0.13 cm from the midline on the right and 4.53 +/- 0.14 cm on the left. Midway between xiphoid and umbilicus, the SEA were 5.50 +/- 0.16 cm on the right of the midline and 5.36 +/- 0.16 cm on the left. At the umbilicus, the epigastric vessels were 5.88 +/- 0.14 cm on the right and 5.55 +/- 0.13 on the left of the midline. Midway between the umbilicus and symphysis pubis, the inferior epigastric (IEA) were 5.32 +/- 0.12 cm on right and 5.25 +/- 0.11 cm on the left. At the symphysis pubis, the IEA were 7.47 +/- 0.10 cm on the right and 7.49 +/- 0.09 cm away from the midline on the left side. CONCLUSIONS: Epigastric vessels are usually located in the area between 4 and 8 cm from the midline. Staying away from this area will determine the safe zone of entry of the anterior abdominal wall.

OBJECTIVES: Systematic evaluation of prehospital provider performance during actual resuscitations is difficult. Although prior studies reported pediatric drug-dosing mistakes and other types of management errors, the underlying causes of those errors were not investigated. The objective of this study was to identify causes of errors during a simulated, prehospital pediatric emergency. METHODS: Two-person emergency medical services (EMS) crews from five geographically diverse agencies participated in a validated simulation of an infant with altered mental status, seizures, and respiratory arrest using their own equipment and drugs. A scoring protocol was used to identify errors. A debriefing conducted by a trained facilitator immediately after the simulated event elicited root causes of active and latent errors, which were analyzed by thematic qualitative assessment methods. RESULTS: Forty-five crews completed the study. Clinically important themes that emerged from the data included oxygen delivery, equipment organization and use, glucose measurement, drug administration, and inappropriate cardiopulmonary resuscitation. Delay in delivery of supplemental oxygen resulted from two different automaticity errors and a 54% failure rate in using an oropharyngeal airway (OPA). Most crews struggled to locate essential pediatric equipment. Three found broken or inoperable bag/valve/masks (BVMs), resulting in delayed ventilation. Some mistrusted their intraosseous (IO) injection gun device; others used it incorrectly. Only 51% of crews measured blood glucose; some discovered that glucometers were not stored in their sealed pediatric bags. The error rate for diazepam dosing was 47%; for midazolam, it was 60%. Underlying causes of dosing errors were found in four domains (cognitive, procedural, affective, and teamwork), and they included incorrect estimates of weight, incorrect use of the Broselow pediatric emergency tape, faulty recollection of doses, difficulty with calculations under stress, mg/kg to mg to mL conversion errors, inaccurate measurement of volumes, use of the wrong end of prefilled syringes, and failure to crosscheck doses with partners. CONCLUSIONS: Simulation, followed immediately by facilitated debriefing, uncovered underlying causes of active cognitive, procedural, affective, and teamwork errors, latent errors, and error-producing conditions in EMS pediatric care.

Contrary to the literature about drug removal during hemodialysis, data regarding drug removal during plasmapheresis are sparse. Over the last 40 years, approximately 70 publications-mostly case reports of overdoses-have described the effects of plasmapheresis on pharmaceutical agents. Important issues are drug extraction during plasma exchange with chemotherapy, as well as drug classes such as antiinfectives, anticoagulants, antiepileptics, cardiovascular agents, and immunosuppressants. Other considerations are the merits and pitfalls of the different methods used in published reports and recommendations for future pharmacokinetic studies in this field.