Search

Background:. Variations among methods to measure glenoid version have created uncertainty regarding which method provides the most consistent measurements of morphology. Greater deformity may also make accurate depiction of the native morphology more challenging. This study examined 4 current methods (Friedman, corrected Friedman, Ganapathi-Iannotti, and Matsumura) and an experimental scapular border-derived coordinate system method, to compare measurement inconsistencies between methods and reference systems and assess the impact of glenoid deformity on measured glenoid version. Methods:. Three-dimensional scapulae were created from computed tomography (CT) scans of 74 shoulders that had undergone arthroplasty (28 A2, 22 B2, 10 B3, and 14 C glenoids) and 34 shoulders that had not undergone arthroplasty. Glenoid version measurements were made in Mimics using the 4 methods. For the experimental method, scapulae were reconstructed, and 3 orthogonal global coordinate planes (GCPs) were derived from the medial and lateral borders. Version was measured as the angle between the sagittal reference plane and an anterior-posterior glenoid vector. The intraclass correlation coefficient (ICC) was calculated for the Friedman and corrected Friedman methods. Inconsistencies were assessed for all methods using the interquartile range, mean and standard deviation, and repeated-measures analysis of variance. Concordance correlation coefficients (CCCs) were calculated to assess agreement among the methods. Results:. Scapular plane-based methods (experimental, Friedman, and corrected Friedman) yielded an average version between −10° and −12°, with average measurement differences among these methods of 12° when compared with each other. Scapular plane-based methods maintained consistency with increasing deformity. Conclusions:. The other methods of version measurement using the scapular planes as the reference were highly comparable with the corrected Friedman method. However, when the reference plane was the glenoid vault, version measurements were inconsistent with scapular plane-based methods, which is attributed to differences in the reference systems. In surgical planning, the coordinate system utilized will impact version measurements, which can result in variations in the planned surgical solutions. Additionally, as glenoid deformity increases, this variation resulting from the utilization of different coordinate systems is magnified.

OBJECTIVE: We sought to define the characteristics that distinguish Kawasaki disease shock syndrome from hemodynamically normal Kawasaki disease. METHODS: We collected data prospectively for all patients with Kawasaki disease who were treated at a single institution during a 4-year period. We defined Kawasaki disease shock syndrome on the basis of systolic hypotension for age, a sustained decrease in systolic blood pressure from baseline of > or =20%, or clinical signs of poor perfusion. We compared clinical and laboratory features, coronary artery measurements, and responses to therapy and analyzed indices of ventricular systolic and diastolic function during acute and convalescent Kawasaki disease. RESULTS: Of 187 consecutive patients with Kawasaki disease, 13 (7%) met the definition for Kawasaki disease shock syndrome. All received fluid resuscitation, and 7 (54%) required vasoactive infusions. Compared with patients without shock, patients with Kawasaki disease shock syndrome were more often female and had larger proportions of bands, higher C-reactive protein concentrations, and lower hemoglobin concentrations and platelet counts. Evidence of consumptive coagulopathy was common in the Kawasaki disease shock syndrome group. Patients with Kawasaki disease shock syndrome more often had impaired left ventricular systolic function (ejection fraction of <54%: 4 of 13 patients [31%] vs 2 of 86 patients [4%]), mitral regurgitation (5 of 13 patients [39%] vs 2 of 83 patients [2%]), coronary artery abnormalities (8 of 13 patients [62%] vs 20 of 86 patients [23%]), and intravenous immunoglobulin resistance (6 of 13 patients [46%] vs 32 of 174 patients [18%]). Impairment of ventricular relaxation and compliance persisted among patients with Kawasaki disease shock syndrome after the resolution of other hemodynamic disturbances. CONCLUSIONS: Kawasaki disease shock syndrome is associated with more-severe laboratory markers of inflammation and greater risk of coronary artery abnormalities, mitral regurgitation, and prolonged myocardial dysfunction. These patients may be resistant to immunoglobulin therapy and require additional antiinflammatory treatment. [ABSTRACT FROM AUTHOR]

Patient blood management is a patient-centered evidence-based approach to improve patient outcomes by harnessing the patient's own hematopoietic system to optimize blood health while promoting patient safety and empowerment. Perioperative patient blood management is a standard of care in adult medicine, yet it is not commonly accepted in pediatrics. Raising awareness may be the first step in improving perioperative care for the anemic and/or bleeding child. This article highlights five preventable perioperative blood conservation error traps for children. The goal is to provide practical clinical guidance to improve preoperative diagnosis and treatment of anemia, facilitate recognition and treatment of massive hemorrhage, reduce unnecessary allogeneic blood transfusions, and decrease associated complications of anemia and blood component transfusions utilizing a patient/family-centered informed consent and shared decision-making approach., (© 2023 John Wiley & Sons Ltd.)

Background: Epidermolysis bullosa (EB) is a group of rare epithelial disorders caused by abnormal or absent structural proteins at the epidermal-dermal junction. As a result, patients experience blisters and wounds from mild shearing forces. Some forms of EB are complicated by resultant scarring and contractures. The perioperative anesthetic management of patients with EB is complex and requires a systems-based approach to limit harm. We reviewed our experience with providing general anesthesia to patients at our tertiary EB referral center, including adverse events related to anesthetic care, outcomes in the immediate perioperative period, and details of anesthetic management., Methods: We retrospectively reviewed the charts of all patients with EB anesthetized at the Children's Hospital Colorado between January 2011 and December 2016. A subset of pediatric anesthesiologists cared for all patients using a standardized clinical care pathway. Patient demographics, detailed anesthetic methods, immediate perioperative outcomes, and adverse events were characterized., Results: Over a 6-year period, 37 patients underwent 202 general anesthetics. Most patients (75.7%) had dystrophic EB (DEB). Female patients comprised 48.6%. The majority (56.7%) traveled >50 miles to receive care, and many (35.1%) traveled >150 miles for their care. Common adaptations to care included avoidance of electrocardiogram leads (88.6%) and temperature probes (91.6%). Nasal fiberoptic intubation (n = 160) was performed, or natural airway/mask (n = 27) was maintained for most patients. Supraglottic devices were not used for airway management during any of the anesthetics. Anesthesia preparation time was longer (average 25.8 minutes [standard deviation {SD} = 12.7]) than our average institutional time (14 minutes). Succinylcholine was never used, and nondepolarizing muscle relaxants were used in only 1.5% of patient encounters. Blood was transfused in 16.3% of cases and iron infused in 24.8%. Average length of stay in the postanesthesia care unit was comparable to our institutional average (average 40.1 [SD = 28.6] vs 39 minutes). New skin or mucosal injury occurred in 8 encounters (4%), and desaturation occurred in 43 cases (21.3%). There were no major adverse events., Conclusions: By using a specialized team and a standardized clinical care pathway, our institution was able to minimize adverse events caused by the anesthetic and surgical care of patients with EB. We recommend natural airway or nasal fiberoptic airway management, meticulous avoidance of shear stress on the skin, and a multidisciplinary approach to care. Supportive therapy such as perioperative blood transfusions and iron infusions are feasible for the treatment of chronic anemia in this population., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2021 International Anesthesia Research Society.)

Background: A diagnosis of Kawasaki syndrome is based on clinical criteria with nonspecific laboratory findings, and there is a substantial risk of coronary artery aneurysms if treatment with intravenous immunoglobulin is delayed. In this study, we examined the contributions of sociodemographic factors and parent and physician behavior to the development of coronary artery aneurysms in children with Kawasaki syndrome., Methods: We performed a retrospective, case-control chart review of Kawasaki syndrome patients treated at our institution during an 11-year period (1991-2002). Of 324 patients, 21 patients had coronary artery aneurysms and were matched with 81 Kawasaki syndrome control patients without coronary artery aneurysms., Results: Patients who developed coronary artery aneurysms were more likely to have had their diagnosis established after 10 days of fever as a result of a delay in physician recognition of Kawasaki syndrome. In addition, these patients were also more likely to have been hospitalized at an outside facility with an erroneous diagnosis, to have had a greater number of healthcare visits before diagnosis, to have sought medical care in Mexico, to lack medical insurance and to speak Spanish as a primary language. Independent predictors of delayed diagnosis included incomplete clinical signs of Kawasaki syndrome, seeking health care in Mexico, and being hospitalized at an outside facility with a different diagnosis., Conclusions: Increased risk of coronary artery aneurysms is associated with a delay in diagnosis by physicians and not with a delay in seeking medical consultation by parents. Sociodemographic factors influence the likelihood that patients will have a delayed diagnosis.

Prior analyses of the impact of stringent, preablative low-iodine diets (LIDs) on ablation in patients with differentiated thyroid cancer postthyroidectomy are dated. We retrospectively reviewed first-time, short-term ablation rates for 44 LID patients and 50 patients following a regular diet (RD) who were verbally instructed to avoid salt, seafood, and multivitamins containing iodine. Patients who had undergone ablation were given between 100 and 200 mCi of 131I, depending on the presence of metastases. We found a 68.2% ablation rate for LID patients, compared to a 62.0% rate for RD patients, a nonsignificant difference (p = 0.53). We observed a dose-response relationship for both patient groups, with higher ablation rates corresponding to higher doses of radioiodine administered. We also measured iodine levels in spot urine samples from 7 matched LID patients and 7 matched RD adherents (healthy volunteers) prediet and postdiet as well as 39 healthy volunteers. LID patients had a lower mean urinary iodine level postdiet (173.9 microg/L; range, 45-1,217 microg/L; standard deviation [SD] = 127.7) than the RD patients (mean, 381.4 microg/L; range, 140-630 microg/L; SD = 196.3) or the 39 normal controls (444.0 microg/L; range, 50-1,690 microg/L; SD = 413.4). Whereas the LID lowered urinary iodine levels by 69.4% from prediet values, the RD reduced urinary iodine by 23.6%. Although differences in the reduction of urinary iodine levels between the LID and the RD were substantial, both groups experienced equivalent outcomes. The level of iodine in the American diet has progressively decreased, and may be much lower now than when prior LID studies were conducted. We suggest that prescribing a refined, less stringent diet that avoids high-iodine-containing foods would offer equivalent outcomes with increased patient convenience.

Previous reports from this laboratory have revealed that macrophages obtained from 7-day Listeria-immune mice elicited 15 h before harvest with heat-killed homologous microorganisms were able to kill Listeria monocytogenes while resident or elicited cells were not [14, 16]. In the present study, experiments were conducted to determine if phagocytosis-associated oxidative metabolic activity participates in the enhanced destruction of Listeria by activated macrophages. Investigations into production of oxygen radicals by zymosan-stimulated macrophages revealed that Listeria-immune antigen-elicited (LIAE) cells produced significantly more superoxide and hydrogen peroxide than did resident, thioglycolate, or Listeria antigen-elicited macrophages. Additionally, the percentage of nitroblue tetrazolium (NBT) dye positive cells following exposure to zymosan was maximal in the immune-elicited population. Utilizing a luminol-dependent assay, a short-term chemiluminescent (CL) burst was noted in phagocytizing macrophages. This response was greatest in the LIAE population that exhibited a tenfold increase in peak chemiluminescence over other cell types. Prolonged in vitro culture of these cells diminishes their capacity to generate oxygen radicals. Additionally, LIAE macrophages cultured in excess of 38 h exhibited a significant decrease in zymosan-stimulated hydrogen peroxide release while the decline in superoxide generation was minimal. A substantial diminution in the Listeria-stimulated CL response was also noted during this time period. However, phagocytosis of Listeria by LIAE cells failed to induce the level of oxygen metabolites seen when zymosan was used as the particulate stimulant. In addition, scavengers of oxygen radicals were found to be relatively ineffective in reducing the killing of L monocytogenes by immunologically activated macrophages in culture. It therefore appears that toxic oxygen species do not play a major role in the heightened killing of Listeria by activated macrophages.

Listeria monocytogenes strains differing in virulence were examined for production of oxygen species. Virulent strains A4413 and JH-H exhibited maximal generation of hydrogen peroxide and superoxide, whereas the avirulent strain 9037-7R was least active. The virulence was confirmed by the in vitro assessment of the intracellular fate of the microorganisms in resident macrophages.

Macrophage functions, including phagocytosis and bactericidal and oxidative activities, were measured in highly susceptible Listeria monocytogenes-sensitive HRS/J homozygous and heterozygous mice. Phagocytic studies with both caseinate-elicited and L. monocytogenes-immune macrophages revealed comparable engulfment of latex particles, zymosan, and bacteria by mononuclear phagocytes obtained from all experimental mouse strains. Elicited macrophages cultivated from mutant hairless and heterozygous littermates exhibited a reduced capacity to control Listeria infection compared with cells derived from CD-1 mice. However, intracellular killing of the microorganisms by immune macrophages was comparable to that observed with the outbred controls. Studies on oxidative metabolic activities associated with the respiratory burst indicate that while intracellular nitroblue tetrazolium reduction was comparable for macrophages cultivated from all mouse strains, the liberation of superoxide anion and chemiluminescence responses were significantly diminished in caseinate-elicited HRS/J cells. Moreover, immune elicited hr/hr and hr/+ macrophages generated oxidative species at levels comparable to that observed with cells derived from resistant animals. Thus, immunologically elicited HRS/J mice are capable of responding to sublethal Listeria infection with heightened antibacterial and oxidative activities.

Peritoneal macrophages derived from CD-1 and C57BL/6 mice were separated into distinct groups based on their buoyant densities on discontinuous gradients of Percoll and assayed for antibacterial activity against Listeria monocytogenes. Subpopulations of peritoneal macrophages derived from Listeria-immune mice present a wide variation in their ability to control intracellular infection. Distinct subsets were found which exhibited bacteriostatic and listericidal activity. The fractionation procedure yielded a population of peroxidase-positive macrophages which were devoid of antilisterial action. Subpopulations of resident and elicited macrophages were also functionally heterogeneous in their ability to restrict intracellular growth of bacterial. In some experiments, subclasses were examined for secretion of plasminogen activator and phagocytosis of latex particles. These activities varied considerably with the status of activation of the macrophages, but failed to correlate with antimicrobial activity within given subpopulations.

Experiments were performed to examine the interaction of tuberculin with platelets and complement. Hemolytic complement titrations show that tuberculin consumes complement in human, rabbit, and guinea pig serum. Evidence in support of classical pathway activation was provided by observation of C1 consumption and failure to detect significant conversion of alternative pathway factor B to B by immunoelectrophoresis. Platelets in plasma from guinea pigs deficient in the fourth component of complement were not affected by tuberculin. However, studies on platelet aggregation in plasma chelated with ethyleneglycolbis(beta-aminoethyl ether)-N,N-tetraacetic acid indicated that tuberculin may initiate sluggish activation of the alternative pathway. That the reaction between tuberculin and platelets is a lytic one was evidenced by observing the release of the cytoplasmic enzyme lactic dehydrogenase and efflux of rubidium-86. Studies with C6-deficient rabbits indicated that platelet release of exogenously supplied tritiated serotonin is caused by platelet lysis.

Congenitally hairless HRS/J homozygous (hr/hr) mice as well as phenotypically normal littermates (hr/+) were found to exhibit unusual susceptibility to infection with Listeria monocytogenes with 50% of the animals dying within a 10-day period (LD50) at an infecting inoculum approaching 200 microorganisms. In marked contrast to the outbred CD-1 strain as well as other Listeria-susceptible mice, HRS/J hosts are virtually incapable of limiting infection with virulent Listeria. The dynamics of infection reveal early uncontrolled bacterial growth within the peritoneal cavity, followed by a sharp increase of bacterial load in the spleen of both HRS/J homozygotes and heterozygous littermates. Spleen indices obtained for mutant mice indicate substantial splenomegaly which parallels the onset of infection in that organ. Assessment of the exudate population within the peritoneal cavity during infection indicates that HRS/J mice produce an early sustained influx of polymorphonuclear leukocytes while exhibiting a diminished macrophage inflammatory response. Additionally, it was shown that the mutant strain expresses significant increases in the total number of recoverable peritoneal leukocytes in response to other phlogistic stimuli.

A sensitive and highly reproducible assay was utilized to study in vitro interactions of Listeria monocytogenes with resident and activated macrophages. The technique is not compromised by extracellular events and can readily differentiate between the efficiency of ingestion and the postphagocytic fate of bacteria. Heat-labile factors in human or homologous serum markedly enhanced the phagocytosis of Listeria without noticeably affecting the intracellular fate of the microorganisms. The behavior of Listeria within macrophages cultivated from C57BL/6 and BALB/c mouse strains corresponded to previous reports of in vivo growth patterns in inbred mice. Thioglycolate- or caseinate-elicited macrophages, although highly phagocytic, were unable to prevent the proliferation of Listeria. A bactericidal macrophage population was derived from from C57BL/6 mice which had been immunized intraperitoneally with a sublethal dose of L. monocytogenes and subsequently boosted with heat-killed homologous organisms. Elicitation of immune animals produced an increase in the percentage of peroxidase-positive macrophages, but this activity could not be correlated with restriction of intracellular bacterial growth.

Murine peritoneal macrophages were rapidly rendered listericidal after exposure to lymphokine-rich supernatants (LRSs) derived from antigen-pulsed Listeria monocytogenes-immune spleen cells. A 6-h incubation period with LRSs was sufficient to induce microbicidal activity in resident macrophages. In vitro induction of macrophage listericidal activity by constant exposure to LRSs persisted for 18 h, after which time spleen cell factors were no longer capable of modifying intracellular inactivation of Listeria. Results obtained by utilizing a short assay indicated that the killing kinetics is extremely rapid, with large numbers of bacteria destroyed during the first 15 min of infection. Intracellular killing at this time appeared to be greatly dependent upon the stage of growth from which the microorganisms were harvested. Induction of bactericidal macrophages by infection of mice with a sublethal dose of virulent Listeria cells and subsequent intraperitoneal elicitation with heat-killed homologous bacteria was similarly a transient event. Macrophages harvested 18 h after antigenic challenge displayed dramatic antibacterial activity during the first 22 h in culture. After 22 h, activity was lost, and stasis was observed during the ensuing 23 h. At 68 h, macrophages were devoid of antilisterial action. Activity, however, could be recalled after incubation with LRSs.

Our studies reveal that normal rabbit blood contains a potent bactericidin active against Listeria monocytogenes. The factor is present in greatest amounts in fresh undiluted serum but is absent in platelet extracts. A correlation was observed between the virulence of Listeria strains and their relative ability to survive in serum. The bactericidal titers obtained for plasma and plasma serum indicate that clotting must occur for optimum expression of antilisterial activity. The lethal action is not elevated after immunization with viable Listeria nor does it appear to depend on heat-labile components of complement. The active factor was removed from serum by filtration through a cellulose asbestos filter pad and further purified by carboxymethyl cellulose chromatography. Iron significantly diminishes serum lethality and completely abolishes the action of the purified component. The listericidal factor resembles beta-lysin but may be a distinct part of a multiple system of similar bactericidins.

Several physiological and biochemical changes which occur in CD-1 pathogen-free mice during the course of infection with Listeria monocytogenes strain A4413 have been examined. Mice injected with 10(4) to 10(6) organisms by the intraperitoneal route displayed a significant depression in weight gain. In contrast, at 24 hr after infection an increment in total liver weight averaging 0.1 g was observed. The ratios of liver to body weight increased throughout the observation period. As the severity of the infection increased, food intake, as well as total liver protein and nitrogen, showed a corresponding decrease, with the diminution being most evident immediately prior to the death of the animals. Blood urea nitrogen remained relatively constant for 24 hr and then increased continuously as the infection progressed to the acute stage. Total liver lipid increased until the death of the animals. At 72 hr postinfection, a significant decrease in oxidative phosphorylation was observed. Xanthine dehydrogenase activity increased, with maximal values obtained 72 hr after infection. Uric acid levels remained constant for 24 hr, diminished at 48 hr, and then increased until the death of the animals. After 24 hr, uricase activity showed a slight increase. This activity returned to within normal ranges at 48 hr and decreased as the infection progressed to the acute stage at 72 hr. The results support the hypothesis that at least a part of the cause of death is a derangement in hepatic purine and carbohydrate metabolism. The data are also consistent with the possibility of changes in iron transport in the infected mice.

Rabbit platelets enhance the bactericidal capability of cultured mouse peritoneal macrophages against Listeria monocytogenes.

Viability of Listeria monocytogenes suspended in either normal rabbit serum or listericidal factor is significantly reduced before cell lysis. In normal serum Listeria populations are initially reduced by clumping of viable bacteria, and the cells within these clumps are morphologically altered and killed by the listericidal factor in serum. This clumping is complement independent and does not occur after suspension in purified listericidal factor. In electron micrographs, densely stained amorphous material was seen surrounding clumped cells suspended in serum. Initial damage to Listeria suspended in either serum or listericidal factor appears to be confined to plasma and mesosomal membranes. The mesosomes are rapidly disorganized, and the plasma membrane becomes crenated and separates from the cell wall. Subsequently, the fibrillar organization of the nuclear region disrupts, and the cytoplasm increases in granularity. Studies utilizing Listeria protoplasts provided evidence in support of the plasma membrane as the site of listericidal action. Cell death may be related to loss in enzyme function after crenation of the plasma membrane and mesosomal dissolution.

Several enzymes and metabolites concerned with carbohydrate metabolism were examined in mice infected with Listeria monocytogenes. Liver glycogen and glucose decreased parallel to severity of infection. The concentration of glucose in the blood fell to abnormally low levels with a hypoglycemia being most evident at 72 hr. There was a significant decrease in the activity of hepatic uridine diphosphate glucose-glycogen transglucosylase. This decrease in enzymatic activity correlated with the rate of glycogen depletion. Phosphorylase activity declined in a similar fashion, contraindicating enhanced glycogenolysis as the mechanism responsible for glycogen depletion. Although glucose-6-phosphatase decreased throughout the infection period, it did not appear to be the major metabolic defect causing hypoglycemia in Listeria-infected mice. Further distortion of carbohydrate metabolism was indicated by findings of increased levels of pyruvate and lactate in the blood of infected animals.

The interaction between smooth and rough Listeria monocytogenes and mouse peritoneal macrophages in culture was investigated. Initially, antibiotics were deleted from the culture medium, and no attempt other than the removal of unphagocytized bacteria by extensive washings was made to control extracellular growth. Under these conditions the monolayers were rapidly destroyed within an 8-h period, and this was associated with increases in the intracellular population of both strains. Extracellular viability counts revealed that washings failed to reduce the bacteria in the medium to less than 10% of the original inoculum. Continuous phagocytosis of Listeria which grew logarithmically in the maintenance media appears to account for the observed changes in the number of intracellular bacteria. The data also indicate that it is primarily the free bacteria in the culture medium which are responsible for the cytotoxic effects. In other experiments streptomycin-penicillin solutions were added to the maintenance media after an initial period of phagocytosis. In the presence of antibiotics, the total number of macrophages per field remained relatively constant, and no morphological alterations in the leukocyte cultures were observable. Extensive intracellular multiplication of either strain was not evident in fixed and stained cover slips. Viable intracellular counts reveal that after 24 h there is almost total killing of the rough variant, whereas the smooth strain tended towards complete survival.