Social determinants and pre-arrest care patterns associated with cardiac arrest and mortality.

BACKGROUND: Understanding the impact of social determinants of health (SDOH) on CA, including access to care pre-cardiac arrest (CA) can improve outcomes. Large databases, such as Epic Cosmos, can help identify trends in patient demographics and SDOH that identify gaps in care. The purpose of this study was to determine the incidence of CA and subsequent mortality in a large national database across patient demographics and social determinants and characterize pre-arrest care patterns. METHODS: This was a retrospective cohort study using a large national deidentified electronic health database (Epic Cosmos) with 227 million patients. Inclusion criteria was ED encounter for CA (ICD-10-CM: I46). Patient demographics and social determinants included age, sex, race, ethnicity, social vulnerability index (SVI, a composite measure with greater SVI representing more vulnerability). The primary outcome was difference in CA incidence between groups, reported as odds ratios (ORs). The secondary outcomes were 1) incidence of pre-arrest care within 30 days and 2) post-arrest mortality at 7,30, and 180 days. Statistical analysis was performed using Chi-squared analysis (unadjusted OR) and aggregated logistic procedure (adjusted OR). RESULTS: There were 201,846 ED visits for CA between April 20, 2020, and April 19, 2023 (0.11% incidence). For all ages, males had a higher incidence of CA (OR 1.76, p < 0.0001). Black, Native Hawaiian or Pacific Islander, and American Indian or Alaska Native had a higher OR of CA while Asian patients were less likely than White patients (adjusted OR 1.85, 1.44,1.51, and 0.81 respectively, all p < 0.0001). Hispanic/Latino patients had a lower OR of CA (adjusted OR 0.72, p < 0.0001). CA was more common in the highest SVI quartile compared to the lowest (adjusted OR 1.71, p < 0.0001). Significant heterogeneities were identified in pre-arrest care across patient demographics and social determinants, where ED visits were more common than office visits among male patients, patients in the highest SVI, Hispanic/Latino, and minority patients, except for Asian patients. Post-arrest mortality after 30 days was highest in females, Black patients, and patients in the highest SVI. CONCLUSIONS: SDOH have a significant impact on the risk of CA, pre-arrest care patterns, and post-arrest mortality. Determining the impact that SDOH have on the CA care continuum provides can provide actionable targets to prevent CA and subsequent mortality.

Beneficial Effect of Calcium Treatment for Hyperkalemia Is Not Due to "Membrane Stabilization".

OBJECTIVES: Hyperkalemia is a common life-threatening condition causing severe electrophysiologic derangements and arrhythmias. The beneficial effects of calcium (Ca2+) treatment for hyperkalemia have been attributed to "membrane stabilization," by restoration of resting membrane potential (RMP). However, the underlying mechanisms remain poorly understood. Our objective was to investigate the mechanisms underlying adverse electrophysiologic effects of hyperkalemia and the therapeutic effects of Ca2+ treatment. DESIGN: Controlled experimental trial. SETTING: Laboratory investigation. SUBJECTS: Canine myocytes and tissue preparations. INTERVENTIONS AND MEASUREMENTS: Optical action potentials and volume averaged electrocardiograms were recorded from the transmural wall of ventricular wedge preparations (n = 7) at baseline (4 mM potassium), hyperkalemia (8-12 mM), and hyperkalemia + Ca2+ (3.6 mM). Isolated myocytes were studied during hyperkalemia (8 mM) and after Ca2+ treatment (6 mM) to determine cellular RMP. MAIN RESULTS: Hyperkalemia markedly slowed conduction velocity (CV, by 67% ± 7%; p < 0.001) and homogeneously shortened action potential duration (APD, by 20% ± 10%; p < 0.002). In all preparations, this resulted in QRS widening and the "sine wave" pattern observed in severe hyperkalemia. Ca2+ treatment restored CV (increase by 44% ± 18%; p < 0.02), resulting in narrowing of the QRS and normalization of the electrocardiogram, but did not restore APD. RMP was significantly elevated by hyperkalemia; however, it was not restored with Ca2+ treatment suggesting a mechanism unrelated to "membrane stabilization." In addition, the effect of Ca2+ was attenuated during L-type Ca2+ channel blockade, suggesting a mechanism related to Ca2+-dependent (rather than normally sodium-dependent) conduction. CONCLUSIONS: These data suggest that Ca2+ treatment for hyperkalemia restores conduction through Ca2+-dependent propagation, rather than restoration of membrane potential or "membrane stabilization." Our findings provide a mechanistic rationale for Ca2+ treatment when hyperkalemia produces abnormalities of conduction (i.e., QRS prolongation).

Post-ROSC Atrial fibrillation is not associated with rearrest but is associated with stroke and mortality following out of hospital cardiac arrest.

BACKGROUND: Atrial fibrillation (AF) in patients resuscitated from cardiac arrest (CA) is associated with increased short-term mortality. However, whether this is because AF adversely affects early resuscitation success, causes post-resuscitation morbidity, or because it is a marker for patient co-morbidities, remains unclear. We aimed to determine the prevalence of AF in patients with ROSC to test the hypothesis that AF is associated with increased risk of rearrest and to determine its impact on mortality and stroke risk. METHODS: We performed a retrospective study of emergency medical services patients with OHCA and ROSC. To examine long-term morbidity and mortality due to AF, an additional observational cohort analysis was performed using a large electronic health record (EHR) database. RESULTS: One hundred nineteen patients with ROSC prior to ED arrival were identified. AF was observed in 39 (33%) of patients. Rearrest was not different between AF and no AF groups (44% vs. 41%, p = 0.94). In the EHR analysis, mortality at one year in patients who developed AF was 59% vs. 39% in no AF patients. Odds of stroke was 5x greater in AF patients (p < 0.001), with the majority not anticoagulated (93%, p < 0.001) and comorbidities were greater p < 0.001). CONCLUSIONS: AF was common following ROSC and not associated with rearrest. AF after CA was associated with increased mortality and stroke risk. These data suggest rhythm control for AF in the immediate post-ROSC period is not warranted; however, vigilance is required for patients who develop persistent AF, particularly with regards to stroke risk and prevention.

Pantarsal arthrodesis stabilized with circular external skeletal fixators in 8 dogs (2010-2022).

OBJECTIVE: To report the surgical technique, complications, and outcomes of 8 dogs that underwent a unilateral pantarsal arthrodesis stabilized using a circular external skeletal fixator (CESF) construct for the treatment of uni- or multilevel tarsal instability. ANIMALS: 8 dogs. CLINICAL PRESENTATION: Medical records from 2010 to 2023 from 2 small animal hospitals were retrospectively reviewed for dogs undergoing pantarsal arthrodeses stabilized with CESF. Data collected for each dog included signalment, injury etiology, construct configuration, radiographic imaging, antimicrobial use, complications, length of time until construct removal, and outcome based on clinical evaluation by the owner and veterinary surgeon. RESULTS: 8 dogs met the requirements of inclusion for the study. Dogs had a mean age of 5.5 years (range, 0.42 to 13 years) and weight of 15.1 kg (range, 2.5 to 26.4 kg). Angulated 3- and 4-ring constructs were used in 5 and 3 dogs, respectively, with or without hybridization. Tarsi were stabilized with a mean angle of extension of 124.8° (range, 111.5° to 136.5°). Fixator removal was performed at a mean time of 11.3 weeks (range, 6 to 16 weeks). Complications developed in 4 dogs, 2 of which had poor clinical outcomes despite additional interventions, including recurrent digit trauma and poor limb use postoperatively. Six dogs had excellent outcomes. CLINICAL RELEVANCE: A CESF may be considered as an alternative to plate stabilization when performing a pantarsal arthrodesis. This fixation requires rigorous postoperative care but obviates the need for supplemental postoperative coaptation.

Spontaneous Repolarization Alternans Causes VT/VF Rearrest That Is Suppressed by Preserving Gap Junctions.

BACKGROUND: Ventricular tachycardia (VT)/ventricular fibrillation (VF) rearrest after successful resuscitation is common, and survival is poor. A mechanism of VT/VF, as demonstrated in ex vivo studies, is when repolarization alternans becomes spatially discordant (DIS ALT), which can be enhanced by impaired gap junctions (GJs). However, in vivo spontaneous DIS ALT-induced VT/VF has never been demonstrated, and the effects of GJ on DIS ALT and VT/VF rearrest are unknown. OBJECTIVES: This study aimed to determine whether spontaneous VT/VF rearrest induced by DIS ALT occurs in vivo, and if it can be suppressed by preserving Cx43-mediated GJ coupling and/or connectivity. METHODS: We used an in vivo porcine model of resuscitation from ischemia-induced cardiac arrest combined with ex vivo optical mapping in porcine left ventricular wedge preparations. RESULTS: In vivo, DIS ALT frequently preceded VT/VF and paralleled its incidence at normal (37°C, n = 9) and mild hypothermia (33°C, n = 8) temperatures. Maintaining GJs in vivo with rotigaptide (n = 10) reduced DIS ALT and VT/VF incidence, especially during mild hypothermia, by 90% and 60%, respectively (P < 0.001; P < 0.013). Ex vivo, both rotigaptide (n = 5) and αCT11 (n = 7), a Cx43 mimetic peptide that promotes GJ connectivity, significantly reduced DIS ALT by 60% and 100%, respectively (P < 0.05; P < 0.005), and this reduction was associated with reduced intrinsic heterogeneities of action potential duration rather than changes in conduction velocity restitution. CONCLUSIONS: These results provide the strongest in vivo evidence to date suggesting a causal relationship between spontaneous DIS ALT and VT/VF in a clinically realistic scenario. Furthermore, our results suggest that preserving GJs during resuscitation can suppress VT/VF rearrest.

Caudoventral hip luxation in 160 dogs (2003-2023): A multicenter retrospective case series.

OBJECTIVE: To describe patient characteristics, etiology, treatment outcomes and complications of caudoventral hip luxation (CvHL) in a large cohort of dogs and investigate factors associated with nonsurgical treatment outcomes. STUDY DESIGN: Multicenter retrospective case series. ANIMAL POPULATION: A total of 160 client-owned dogs (170 limbs). METHODS: Medical records from 2003 to 2023 were reviewed for signalment, history, treatment outcomes and complications. Logistic regression was performed to investigate factors associated with nonsurgical treatment outcome. RESULTS: Low-trauma accidents accounted for 82.9% of cases. Over-represented breeds included poodles (38.1%) and poodle crosses (11.3%). On a per-treatment basis, success rates of closed reduction alone, closed reduction/Ehmer sling, closed reduction/hobbles were 9.1%, 15.2% and 48.8%, respectively. When accounting for repeated attempts using closed reduction alone, Ehmer sling, or hobbles, eventual success rate increased to 10.3%, 18.5% and 61.8%, respectively. Success rate for toggle rod stabilization was 88.2%. Complication rate of hobbles was 31.9% versus 60.6% for Ehmer slings. Use of hobbles (OR:7.62, p = .001, CI:2.23-26.05), treatment by specialist surgeons (OR:2.68, p = .047, CI: 1.01-7.08) and increasing age (OR:1.15, p < .005, CI: 1.08-1.23) were associated with successful nonsurgical treatments. CONCLUSION: Low-trauma etiology, and poodles and their crosses were over-represented in cases of CvHL. Success rate of nonsurgical treatments was lower than previously reported. Hobbles were 7.6 times more likely to be successful when compared to dogs treated without hobbles and remains a viable noninvasive first-line treatment. CLINICAL SIGNIFICANCE/IMPACT: Hobbles are recommended as a low-morbidity first-line treatment for CvHL. An Ehmer sling is not recommended. Toggle rod stabilization is an effective surgical treatment for CvHL.

Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation.

Background Amiodarone is administered during resuscitation, but its antiarrhythmic effects during targeted temperature management are unknown. The purpose of this study was to determine the effect of both therapeutic hypothermia and amiodarone on arrhythmia substrates during resuscitation from cardiac arrest. Methods and Results We utilized 2 complementary models: (1) In vitro no-flow global ischemia canine left ventricular transmural wedge preparation. Wedges at different temperatures (36°C or 32°C) were given 5 µmol/L amiodarone (36-Amio or 32-Amio, each n=8) and subsequently underwent ischemia and reperfusion. Results were compared with previous controls. Optical mapping was used to measure action potential duration, dispersion of repolarization (DOR), and conduction velocity (CV). (2) In vivo pig model of resuscitation. Pigs (control or targeted temperature management, 32-34°C) underwent ischemic cardiac arrest and were administered amiodarone (or not) after 8 minutes of ventricular fibrillation. In vitro: therapeutic hypothermia but not amiodarone prolonged action potential duration. During ischemia, DOR increased in the 32-Amio group versus 32-Alone (84±7 ms versus 40±7 ms, P<0.05) while CV slowed in the 32-Amio group. Amiodarone did not affect CV, DOR, or action potential duration during ischemia at 36°C. Conduction block was only observed at 36°C (5/8 36-Amio versus 6/7 36-Alone, 0/8 32-Amio, versus 0/7 32-Alone). In vivo: QTc decreased upon reperfusion from ischemia that was ameliorated by targeted temperature management. Amiodarone did not worsen DOR or CV. Amiodarone suppressed rearrest caused by ventricular fibrillation (7/8 without amiodarone, 2/7 with amiodarone, P=0.041), but not pulseless electrical activity (2/8 without amiodarone, 5/7 with amiodarone, P=0.13). Conclusions Although amiodarone abolishes a beneficial effect of therapeutic hypothermia on ischemia-induced DOR and CV, it did not worsen susceptibility to ventricular tachycardia/ventricular fibrillation during resuscitation.

Translational Models of Arrhythmia Mechanisms and Susceptibility: Success and Challenges of Modeling Human Disease.

We discuss large animal translational models of arrhythmia susceptibility and sudden cardiac death, focusing on important considerations when interpreting the data derived before applying them to human trials. The utility of large animal models of arrhythmia and the pros and cons of specific translational large animals used will be discussed, including the necessary tradeoffs between models designed to derive mechanisms vs. those to test therapies. Recent technical advancements which can be applied to large animal models of arrhythmias to better elucidate mechanistic insights will be introduced. Finally, some specific examples of past successes and challenges in translating the results of large animal models of arrhythmias to clinical trials and practice will be examined, and common themes regarding the success and failure of translating studies to therapy in man will be discussed.

Arrhythmogenic cardiac alternans in heart failure is suppressed by late sodium current blockade by ranolazine.

BACKGROUND: Cardiac alternans is promoted by heart failure (HF)-induced calcium (Ca2+) cycling abnormalities. Late sodium current (INa,L) is enhanced in HF and promotes Ca2+ overload; however, mechanisms underlying an antiarrhythmic effect of INa,L blockade in HF remain unclear. OBJECTIVE: The purpose of this study was to determine whether ranolazine suppresses cardiac alternans in HF by normalizing Ca2+ cycling. METHODS: Transmural dual optical mapping of Ca2+ transients and action potentials was performed in wedge preparations from 8 HF and 8 control (normal) dogs. Susceptibility to action potential duration alternans (APD-ALT) and Ca2+ transient alternans (Ca-ALT) was compared at baseline and with ranolazine (5-10 µM). RESULTS: HF increased APD- and Ca-ALT compared to normal (both P <.05), and ranolazine suppressed APD- and Ca-ALT in both groups (P <.05). The incidence of spatially discordant alternans (DIS-ALT) was increased by HF (8/8) compared to normal (4/8; P <.05), and ranolazine decreased DIS-ALT in HF (4/8; P <.05).Not only did ranolazine mitigate HF-induced Ca2+ overload, it also attenuated APD-ALT to Ca-ALT gain (amount of APD-ALT produced by Ca-ALT). In HF, APD-ALT to Ca-ALT gain was significantly increased (0.55 ± 0.02) compared to normal (0.44 ± 0.02; P <.05) and was normalized by ranolazine (0.36 ± 0.05; P <.05), representing a complementary mechanism by which INa,L blockade suppressed cardiac alternans. CONCLUSION: Ranolazine attenuated arrhythmogenic cardiac alternans in HF, both by suppressing Ca-ALT and decreasing the coupling gain of APD-ALT to Ca-ALT. Blockade of INa,L may reverse impaired Ca2+ cycling to mitigate cardiac alternans, representing a mechanism underlying the antiarrhythmic benefit of INa,L blockade in HF.

Hypothermia Modulates Arrhythmia Substrates During Different Phases of Resuscitation From Ischemic Cardiac Arrest.

BACKGROUND: We designed an innovative porcine model of ischemia-induced arrest to determine dynamic arrhythmia substrates during focal infarct, global ischemia from ventricular tachycardia or fibrillation (VT/VF) and then reperfusion to determine the effect of therapeutic hypothermia (TH) on dynamic arrhythmia substrates and resuscitation outcomes. METHODS AND RESULTS: Anesthetized adult pigs underwent thoracotomy and regional plunge electrode placement in the left ventricle. Subjects were then maintained at either control (CT; 37°C, n=9) or TH (33°C, n=8). The left anterior descending artery (LAD) was occluded and ventricular fibrillation occurred spontaneously or was induced after 30 minutes. Advanced cardiac life support was started after 8 minutes, and LAD reperfusion occurred 60 minutes after occlusion. Incidences of VF/VT and survival were compared with ventricular ectopy, cardiac alternans, global dispersion of repolarization during LAD occlusion, and LAD reperfusion. There was no difference in incidence of VT/VF between groups during LAD occlusion (44% in CT versus 50% in TH; P=1s). During LAD occlusion, ectopy was increased in CT and suppressed in TH (33±11 ventricular ectopic beats/min versus 4±6 ventricular ectopic beats/min; P=0.009). Global dispersion of repolarization and cardiac alternans were similar between groups. During LAD reperfusion, TH doubled the incidence of cardiac alternans compared with CT, with a marked increase in VF/VT (100% in TH versus 17% in CT; P=0.004). Ectopy and global dispersion of repolarization were similar between groups during LAD reperfusion. CONCLUSIONS: TH alters arrhythmia substrates in a porcine translational model of resuscitation from ischemic cardiac arrest during the complex phases of resuscitation. TH worsens cardiac alternans, which was associated with an increase in spontaneous VT/VF during reperfusion.

Standardized anthropological measurement of postcranial bones using three-dimensional models in CAD software.

This study introduces a standardized protocol for conducting linear measurements of postcranial skeletal elements using three-dimensional (3D) models constructed from post-mortem computed tomography (PMCT) scans. Using femoral DICOM datasets, reference planes were generated and plane-to-plane measurements were conducted on 3D surface rendered models. Bicondylar length, epicondylar breadth, anterior-posterior (AP) diameter, medial-lateral (ML) diameter and cortical area at the midshaft were measured by four observers to test the measurement error variance and observer agreement of the protocol (n=6). Intra-observer error resulted in a mean relative technical error of measurement (%TEM) of 0.11 and an intraclass correlation coefficient (ICC) of 0.999 (CI=0.998-1.000); inter-observer error resulted in a mean %TEM of 0.54 and ICC of 0.996 (CI=0.979-1.000) for bicondylar length. Epicondylar breadth, AP diameter, ML diameter and cortical area also yielded minimal error. Precision testing demonstrated that the approach is highly repeatable and is recommended for implementation in anthropological investigation and research. This study exploits the benefits of virtual anthropology, introducing an innovative, standardized alternative to dry bone osteometric measurements.

Arrhythmogenic Delayed Afterdepolarizations Are Promoted by Severe Hypothermia But Not Therapeutic Hypothermia.

BACKGROUND: Severe hypothermia (SH) is known to be arrhythmogenic, but the effect of therapeutic hypothermia (TH) on arrhythmias is unclear. It is hypothesized that susceptibility to Ca-mediated arrhythmia triggers would be increased only by SH.Methods and Results:Spontaneous Ca release (SCR) and resultant delayed afterdepolarizations (DADs) were evaluated by optical mapping in canine wedge preparations during normothermia (N, 36℃), TH (32℃) or SH (28℃; n=8 each). The slope (amplitude/rise time) of multicellular SCR (mSCR) events, a determinant of triggered activity, was suppressed in TH (24.4±3.4%/s vs. N: 41.5±6.0%/s), but significantly higher in SH (96.3±8.1%/s) producing higher amplitude DADs in SH (35.7±1.6%) and smaller in TH (5.3±1.0% vs. N: 10.0±1.1%, all P<0.05). Triggered activity was only observed in SH. In isolated myocytes, sarcoplasmic reticulum (SR) Ca release kinetics slowed in a temperature-dependent manner, prolonging Ca transient rise time [33±3 (N) vs. 50±6 (TH) vs. 88±12 ms (SH), P<0.05], which can explain the decreased mSCR slope and DAD amplitude in TH. Although the SR Ca content was similar in TH and SH, Ca spark frequency was markedly increased only in SH, suggesting that increased ryanodine receptor open probability could explain the increased triggered activity during SH. CONCLUSIONS: Temperature dependence of Ca release can explain susceptibility to Ca-mediated arrhythmia triggers in SH. This may therefore explain the increased risk of lethal arrhythmia in SH, but not during TH.

Mild hypothermia preserves myocardial conduction during ischemia by maintaining gap junction intracellular communication and Na+ channel function.

Acute cardiac ischemia induces conduction velocity (CV) slowing and conduction block, promoting reentrant arrhythmias leading to sudden cardiac arrest. Previously, we found that mild hypothermia (MH; 32°C) attenuates ischemia-induced conduction block and CV slowing in a canine model of early global ischemia. Acute ischemia impairs cellular excitability and the gap junction (GJ) protein connexin (Cx)43. We hypothesized that MH prevented ischemia-induced conduction block and CV slowing by preserving GJ expression and localization. Canine left ventricular preparations at control (36°C) or MH (32°C) were subjected to no-flow prolonged (30 min) ischemia. Optical action potentials were recorded from the transmural left ventricular wall, and CV was measured throughout ischemia. Cx43 and Na+ channel (NaCh) remodeling was assessed using both confocal immunofluorescence (IF) and/or Western blot analysis. Cellular excitability was determined by microelectrode recordings of action potential upstroke velocity (dV/dtmax) and resting membrane potential (RMP). NaCh current was measured in isolated canine myocytes at 36 and 32°C. As expected, MH prevented conduction block and mitigated ischemia-induced CV slowing during 30 min of ischemia. MH maintained Cx43 at the intercalated disk (ID) and attenuated ischemia-induced Cx43 degradation by both IF and Western blot analysis. MH also preserved dV/dtmax and NaCh function without affecting RMP. No difference in NaCh expression was seen at the ID by IF or Western blot analysis. In conclusion, MH preserves myocardial conduction during prolonged ischemia by maintaining Cx43 expression at the ID and maintaining NaCh function. Hypothermic preservation of GJ coupling and NaCh may be novel antiarrhythmic strategies during resuscitation.NEW & NOTEWORTHY Therapeutic hypothermia is now a class I recommendation for resuscitation from cardiac arrest. This study determined that hypothermia preserves gap junction coupling as well as Na+ channel function during acute cardiac ischemia, attenuating conduction slowing and preventing conduction block, suggesting that induced hypothermia may be a novel antiarrhythmic strategy in resuscitation.

Does cutting a plaster window weaken its strength?

INTRODUCTION: A plaster window is usually created over a pressure area, or in some cases a wound or suture line. This can relieve pressure at the site, and provide an opportunity to change dressings, check on drainage, and inspect a wound or ulcer. There is concern that this can have an effect on its function to provide fracture stability, and weakens the plaster. The biomechanical effects of windowing on plaster strength were therefore investigated, as it has not previously been reported. METHOD: A laboratory study was undertaken to compare the bending, kinking and torsion loads withstood by standardised Plaster of Paris (POP), Softcast and Fibreglass casts compared to those with a 60×40mm window fabricated in the centre at clinically defined endpoints using an Instron machine. RESULTS: The addition of a window significantly weakened the load to failure of POP; Fibreglass, and Softcast by 23.1% (473.1N); 25.9% (401.8N), and 29% (146.6N) respectively, during the 4-point bending tests. During the 3-point kinking tests, load to failure was reduced by 38.5% (297.8N); 35.3% (146.9N), and 51.5% (103.8N) respectively. All tests were checked for consistency and carried out in a single orthogonal plane for ease of comparison. DISCUSSION: The addition of a 60×40mm window to a cast made up of POP, Fibreglass or Softcast weakens the cast load to failure by up to 51% against a 3-point loading force. Though windowing of casts is necessary in certain situations, we advise precautions such as adding further layers of plaster to the window site, keeping the window as small as possible, and advising the patient of the increased risk of weakening and failure of the plaster so that they can take more care.

Amidation of Polyesters Is Slow in Nonaqueous Solvents: Efficient Amidation of Poly(ethylene terephthalate) with 3-Aminopropyltriethoxysilane in Water for Generating Multifunctional Surfaces.

This paper describes surface functionalization of poly(ethylene terephthalate) (PET) films by transamidation of the ester groups with primary amines. The use of water as a solvent improves tremendously the reaction rate and yield compared to conventionally used alcohols. In this study, PET films were exposed to an aqueous solution of 3-aminopropyltriethoxysilane (APTES), which resulted in ester-to-amide reactions on the surface of the film. Hydrolysis of the resulting ethoxy moieties in APTES creates hydroxyl groups that can be used as anchoring points for further modification of PET films. This scheme offers an alternative approach to modify polyesters using water as the solvent.

Is softcast (3M) strong enough for potentially unstable paediatric forearm fractures?

INTRODUCTION: The majority of paediatric forearm fractures are treated using a circumferential splint, with prior manipulation as necessary. Plaster of Paris is often chosen for its ease of application, cost and proven reliability. Softcast is an alternative, providing a comfortable and water-resistant splint that can be removed without a plaster saw, and is in widespread use for immobilising buckle fractures. Softcast has not been recommended for acute unstable fractures. We established whether a Softcast splint could provide sufficient mechanical stability to control an unstable paediatric forearm fracture. METHODS: A laboratory study was undertaken to compare the 3 point (kinking) and 4 point bending, and torsion loads to defined clinical failure points withstood by standardised 4-wrap POP compared to Softcast splints with 6-wrap, 4 wrap and reinforced 4-wrap configurations. RESULTS: The load at clinically relevant failure of a 6-wrap Softcast forearm splint was 504N in 4 point bending, 202N in 3 point bending (kinking), and 11Nm in torsion (equalling 30.4%, 26% and 42.2% of the equivalent values for a circumferential 4-wrap POP). The 6-wrap Softcast was however stronger in all modes than a fibreglass-reinforced Softcast splint (previously recommended for acute fractures). Furthermore, the load to failure in all modes exceeds that which can be exerted by body weight in many paediatric patients. Softcast demonstrated complete recovery of its original shape on unloading, whereas POP was permanently deformed. 6-wrap Softcast splints were 4% lighter than POP. CONCLUSION: A 6-wrap Softcast splint provides adequate mechanical stability and protection for paediatric patients up to approximately 20kg, avoiding high-risk activities. The primary risk is not of fracture angulation and loss of position, but temporary indentation of the splint, causing discomfort or pain. Considering its ease of removal, Softcast may be preferable for younger paediatric patients. Its cost may be offset by reducing the number and duration of hospital visits.

Effects of ethanol on systemic hemodynamics in a porcine model of accidental hypothermia.

OBJECTIVES: Accidental hypothermia is frequently associated with ethanol intoxication. Each has independent effects on systemic hemodynamics, but their combined effects are poorly understood. We aimed to describe the hemodynamic effects of ethanol intoxication in a model of severe hypothermia and rewarming. METHODS: Anesthetized pigs was assigned to control (n=8) or ethanol groups (ETOH) (n=7, 3 mg/kg of ethanol via an orogastric tube). Subjects were cooled to 25°C using ice packs and then warmed to baseline core temperature with passive external and active core rewarming. RESULTS: In the ETOH group, peak serum ethanol concentration was 202 mg/dL at 25°C. Ethanol had no effect on time of cooling or rewarming. In both the control and ETOH, there were similar maximal decreases in mean arterial pressure (from 94±24 to 50±15 mm Hg and 100±27 to 31±12 mm Hg, respectively), ventricular contractility (rate of maximal left ventricular pressure rise from 5731±1462 to 2610±596 mm Hg/s and 6832±1384 to 1937±437 mm Hg/s, respectively), and cardiac output (from 2.14±0.8 to 0.53±0.3 L/min and 2.93±0.9, to 0.44±0.2 L/min, respectively; all P<.001). After rewarming, only in the ETOH group were persistent decreases in mean arterial pressure (59±14 mm Hg), contractility (3982±1573 mm Hg/s), and cardiac output (1.6±0.9 L/min, all P<.03) observed. CONCLUSIONS: Hypothermia caused significant adverse effects on cardiac function and systemic hemodynamics, which returned to baseline with rewarming. Ethanol intoxication had no additional effects on systemic hemodynamics during cooling; however, it caused more prolonged depression of cardiac function and adverse effects on systemic hemodynamics during rewarming. These data may have implications for resuscitation of ethanol-intoxicated victims of accidental hypothermia.