Communication failure in the prehospital response to major terrorist attacks: lessons learned and future directions.

INTRODUCTION: Communication is key in efficient disaster management. However, in many major incidents, prehospital communication failure led to insufficient upscaling, safety concerns for the emergency responders, logistical problems and inefficient disaster management. METHODS: A review of medical reports and news articles of mass-casualty terrorist attacks was performed using PubMed-archived and (non-)governmental reports. The terrorist attacks in Tokyo 1995, Oklahoma 1995, Omagh 1998, New York 2001, Myyr-manni 2002, Istanbul 2003, Madrid 2004, London 2005, Oslo/Utøya 2011, Boston 2013, Paris 2015, Berlin 2016, Brussels 2016, Wuerzburg 2016, Manchester 2017, London 2017 were included. RESULTS: In all mass-casualty terrorist attacks, communication failure was reported. Some failures had significant impact on casualty numbers. Outdated communication equipment, overwhelmed communication services, failure due to damaged infrastructure by the terrorist attack itself, and lack of training were the major issues. Communication failures were most commonly observed in both attacks between 1995-2009 and 2011-2017. DISCUSSION: Communication failure was reported in all mass-casualty terrorist incidents. In several cases, communication between the different responding actors was poor or non-existing. Malfunctioning of (outdated) telecommunication services, inadequate training in the use of communication devices, unfortunate damage of telecommunication network infrastructure were also worrisome. CONCLUSION: Despite reports of lessons learned in previous EMS responses, communication failures were still reported in most recent terrorist attacks. Governments should provide sufficient resources to equip hospitals, emergency departments, and ambulance services with (back-up) communication systems and invest in training. A European registration system is warranted. We provide proposals for improvement.

Burnout, stress and Type D personality amongst hospital/emergency physicians.

INTRODUCTION: In previous studies, physicians have been identified as a high-risk group for burnout. Although the work environment has received more attention than specific determinants of personality traits, the latter might contribute to burnout. STUDY OBJECTIVE: We aimed to investigate the association of Type D personality, job and organizational determinants with burnout, stress and work engagement as outcome factors among emergency physicians and hospital physicians working in intensive care and surgery departments. We specifically focused on our group of emergency physicians. METHODS: In this cross-sectional study, self-report questionnaires were distributed via social media using a specific survey link to 531 Belgian hospital physicians working at the Emergency Department, Intensive Care, and Surgery Department between October 21, 2018, and April 11, 2019. The survey instrument included questions about sociodemographic characteristics, job characteristics, organizational factors, job satisfaction, social support by supervisors and colleagues (Leiden Quality of Work Questionnaire for Medical Doctors) and Type D personality (Distress Scale-14) and as outcomes burnout (Oldenburg Burnout Inventory) and work engagement (Utrecht Work Engagement Scale). A multiple regression analysis was used to examine the associations between the determinants and each of the outcomes with emergency physicians as the study population. RESULTS: Eligible data were available for 436 questionnaires and involved 212 emergency physicians, 162 other hospital physicians (Intensive Care and Surgery Department) and 62 residents concerning both groups of physicians. Type D personality ranged from 28.5 to 29.1% in emergency physicians and other hospital physicians. Additionally, even after correcting for job-related and organizational factors, emergency physicians with Type D personality were seven times more likely to have a high risk for burnout. CONCLUSION: As a result, this study offers a new perspective on the associations between burnout, stress and Type D personality. Type D personality might be a personality-related risk factor for burnout among emergency physicians. Therefore, we recommend enhanced prevention measures that take into account this individual factor in the further development of coaching programs. Improving the professional well-being of emergency physicians is necessary, especially in the scope of the recent COVID-19 pandemic, which has put a high demand on acute and emergency care departments.

Aural Myiasis: A Case Report on a Rare Entity.

Myiasis is the infestation of live vertebrates with dipterous larvae. It is a rare entity in the otolaryngology and is more common to occur in patients with mental or physical disabilities. There are only few cases reported in the literature, and most cases are seen in tropical and rural areas. In this case report, we present a 65-year-old patient, with a history of parotid malignancy, who presented with aural myiasis with extension to the mastoid. We discuss the clinical presentation, the further examinations, and the treatment for early- and late-stage infection.

A rare cause of severe epigastric pain, emesis and increased lipase.

INTRODUCTION: Gastric volvulus is an uncommon, but severe pathology requiring early diagnosis and urgent treatment. Its atypical symptoms and rarity make it difficult to diagnose, possibly leading to delayed treatment and fatal complications. PATIENTS AND METHODS: We present a case of a 73-year-old patient with Parkinson's disease with complaints of severe epigastric pain, emesis and an increased lipase. RESULTS: Diagnosis of an organo-axial gastric volvulus was made. Treatment consisted of reduction of the volvulus by decompression via nasogastric tube. The underlying cause was a para-esophageal hernia that was repaired by Nissen-fundoplication later on. CONCLUSIONS: We describe symptomatology, diagnostic and therapeutic options of gastric volvulus.

Non-traumatic vertebral artery dissection presenting with unilateral cervical pain, hemilateral vision problems and headache.

Spontaneous vertebral artery dissection is a rare condition, mainly affecting young adults with non-specific symptoms, which are often considered not severe. We report a case of a non-traumatic vertebral artery dissection in a 30-year-old woman. Our patient presented with unilateral right-sided neck pain and frontal headache during 3 weeks and recently developed right-sided vision problems. History and clinical findings were non-specific. Neurovascular imaging showed a right-sided vertebral artery dissection from C2 to C6 with an intima flap at C5-C6. The patient was observed in the stroke unit for 1 week and antithrombotics were given during 3 months. There was a complete revascularization of the vertebral artery after 3 months. A review of literature is given concerning predisposing factors, clinical symptoms, neurovascular imaging and treatment options.

Increased ß-adrenergic inotropy in ventricular myocardium from Trpm4-/- mice.

RATIONALE: The Trpm4 gene has recently been associated with several disorders, including cardiac conduction diseases and Brugada syndrome. Transient receptor potential member 4 (TRPM4) proteins constitute Ca2+ -activated, but Ca2+ -impermeable, nonselective cation channels and are expressed both in atrial and in ventricular cardiomyocytes. The physiological function of TRPM4 in the heart remains, however, incompletely understood. OBJECTIVE: To establish the role of TRPM4 in cardiac muscle function. METHODS AND RESULTS: We used TRPM4 knockout mice and performed patch-clamp experiments, membrane potential measurements, microfluorometry, contractility measurements, and in vivo pressure-volume loop analysis. We demonstrate that TRPM4 proteins are functionally present in mouse ventricular myocytes and are activated on Ca2+ -induced Ca2+ release. In Trpm4(-/-) mice, cardiac muscle displays an increased ß-adrenergic inotropic response both in vitro and in vivo. Measurements of action potential duration show a significantly decreased time for 50% and 90% repolarization in Trpm4(-/-) ventricular myocytes. We provide evidence that this change in action potential shape leads to an increased driving force for the L-type Ca2+ current during the action potential, which explains the altered contractility of the heart muscle. CONCLUSIONS: Our results show that functional TRPM4 proteins are novel determinants of the inotropic effect of ß-adrenergic stimulation on the ventricular heart muscle.

NO-dependent endothelial dysfunction in type II diabetes is aggravated by dyslipidemia and hypertension, but can be restored by angiotensin-converting enzyme inhibition and weight loss.

AIMS: Insulin resistance, dyslipidemia and hypertension are independent mediators of endothelial dysfunction. It is incompletely defined whether dyslipidemia and hypertension in addition to diabetes mellitus type II (DMII), as seen in the metabolic syndrome (MS), worsen diabetes-induced endothelial dysfunction. Furthermore, it is unclear whether treatment influences endothelial dysfunction similarly in MS and DMII. Therefore, we studied vascular reactivity and the effect of in vivo treatment with angiotensin-converting enzyme inhibition (ACE-I) or hypocaloric diet in LDL receptor- and leptin-deficient (ob/ob), double knockout mice (DKO), featuring MS and in ob/ob mice with DMII. METHODS AND RESULTS: Vascular reactivity was studied in isolated aortic ring segments. Maximum vasorelaxant response to acetylcholine (Ach) was more depressed in DKO than in ob/ob mice, whereas response to bradykinin (BK) was equally attenuated in both genotypes (52 ± 3 and 23 ± 9% reversal of preconstriction induced by 10(-7) M phenylephrine in DKO vs. 76 ± 3 and 23 ± 8% reversal of preconstriction in ob/ob mice, respectively). ACE-I and hypocaloric diet improved ACh-induced vasorelaxation significantly (89 ± 2 and 59 ± 2% reversal of preconstriction in DKO vs. 80 ± 3 and 84 ± 4% in ob/ob mice, respectively), but not the response to BK. CONCLUSION: These results indicate a differential impact of DMII and MS on endothelial function. ACE-I and hypocaloric diet improved ACh-, but not BK-induced vasorelaxation in these mouse models of DMII and MS.

ACE-inhibition, but not weight reduction restores cardiomyocyte response to ß-adrenergic stimulation in the metabolic syndrome.

BACKGROUND: Diabetic cardiomyopathy is characterized by systolic and early diastolic ventricular dysfunction. In the metabolic syndrome (MS), ventricular stiffness is additionally increased in a later stage. It is unknown whether this is related to intrinsic cardiomyocyte dysfunction, extrinsic factors influencing cardiomyocyte contractility and/or cardiac function, or a combination of both. A first aim was to study cardiomyocyte contractility and Ca2+ handling in vitro in a mouse model of MS. A second aim was to investigate whether in vivo hypocaloric diet or ACE-inhibition (ACE-I) improved cardiomyocyte contractility in vitro, contractile reserve and Ca2+ handling. METHODS: This study was performed in LDL-receptor (LDLR-/-) and leptin-deficient (ob/ob), double knock-out mice (DKO), featuring obesity, type II diabetes, atherogenic dyslipidemia and hypertension. Single knock-out LDLR-/-, ob/ob and wild type mice were used as controls. Cellular contractility, Ca2+ handling and their response to in vivo treatment with diet or ACE-I were studied in isolated cardiomyocytes at baseline, during ß-adrenergic stimulation or increased extracellular Ca2+, using field stimulation and patch-clamp. RESULTS: In untreated conditions, prolongation of contraction-relaxation cycle and altered Ca2+ handling are observed in MS. Response to increased extracellular Ca2+ and ß-adrenergic stimulation is impaired and could not be rescued by weight loss. ACE-I restored impaired response to ß-adrenergic stimulation in MS, but not the decreased response to increased extracellular Ca2+. CONCLUSIONS: Cardiomyocyte contractility and ß-adrenergic response are impaired in MS, due to alterations in cellular Ca2+ handling. ACE-I, but not weight loss, is able to restore cardiomyocyte response to ß-adrenergic stimulation in MS.

Angiotensin-converting enzyme inhibition and food restriction restore delayed preconditioning in diabetic mice.

BACKGROUND: Classical and delayed preconditioning are powerful endogenous protection mechanisms against ischemia-reperfusion damage. However, it is still uncertain whether delayed preconditioning can effectively salvage myocardium in patients with co-morbidities, such as diabetes and the metabolic syndrome. We investigated delayed preconditioning in mice models of type II diabetes and the metabolic syndrome and investigated interventions to optimize the preconditioning potential. METHODS: Hypoxic preconditioning was induced in C57Bl6-mice (WT), leptin deficient ob/ob (model for type II diabetes) and double knock-out (DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome). Twenty-four hours later, 30 min of regional ischemia was followed by 60 min reperfusion. Left ventricular contractility and infarct size were studied. The effect of 12 weeks food restriction or angiotensin-converting enzyme inhibition (ACE-I) on this was investigated. Differences between groups were analyzed for statistical significance by student's t-test or one-way ANOVA followed by a Fisher's LSD post hoc test. Factorial ANOVA was used to determine the interaction term between preconditioning and treatments, followed by a Fisher's LSD post hoc test. Two-way ANOVA was used to determine the relationship between infarct size and contractility (PRSW). A value of p<0.05 was considered significant. RESULTS: Left ventricular contractility is reduced in ob/ob compared with WT and even further reduced in DKO. ACE-I improved contractility in ob/ob and DKO mice. After ischemia/reperfusion without preconditioning, infarct size was larger in DKO and ob/ob versus WT. Hypoxic preconditioning induced a strong protection in WT and a partial protection in ob/ob mice. The preconditioning potential was lost in DKO. Twelve weeks of food restriction or ACE-I restored the preconditioning potential in DKO and improved it in ob/ob. CONCLUSION: Delayed preconditioning is restored by food restriction and ACE-I in case of type II diabetes and the metabolic syndrome.

Angiotensin-converting enzyme inhibition and food restriction in diabetic mice do not correct the increased sensitivity for ischemia-reperfusion injury.

BACKGROUND: The number of patients with diabetes or the metabolic syndrome reaches epidemic proportions. On top of their diabetic cardiomyopathy, these patients experience frequent and severe cardiac ischemia-reperfusion (IR) insults, which further aggravate their degree of heart failure. Food restriction and angiotensin-converting enzyme inhibition (ACE-I) are standard therapies in these patients but the effects on cardiac IR injury have never been investigated. In this study, we tested the hypothesis that 1° food restriction and 2° ACE-I reduce infarct size and preserve cardiac contractility after IR injury in mouse models of diabetes and the metabolic syndrome. METHODS: C57Bl6/J wild type (WT) mice, leptin deficient ob/ob (model for type II diabetes) and double knock-out (LDLR-/-;ob/ob, further called DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome) were used. The effects of 12 weeks food restriction or ACE-I on infarct size and load-independent left ventricular contractility after 30 min regional cardiac ischemia were investigated. Differences between groups were analyzed for statistical significance by Student's t-test or factorial ANOVA followed by a Fisher's LSD post hoc test. RESULTS: Infarct size was larger in ob/ob and DKO versus WT. Twelve weeks of ACE-I improved pre-ischemic left ventricular contractility in ob/ob and DKO. Twelve weeks of food restriction, with a weight reduction of 35-40%, or ACE-I did not reduce the effect of IR. CONCLUSION: ACE-I and food restriction do not correct the increased sensitivity for cardiac IR-injury in mouse models of type II diabetes and the metabolic syndrome.

Surgical angioplasty and unroofing technique for intramural coronary anomaly.

A malign intramural course of the left main coronary artery is a rare anatomical anomaly. Surgical repair is mandatory since the condition is associated with myocardial ischemic syndromes and sudden death. Unroofing the intramural part and reconstructing a neo-ostium is challenging if the neo-ostium is immediately adjacent to the intercoronary commissure as there is a risk of narrowing the newly created ostium. We report a case in which we performed a surgical angioplasty of the left main coronary artery in combination with unroofing of the intramural section and resuspension of the intercoronary commissure.

Effect of sutureless implantation of the Perceval S aortic valve bioprosthesis on intraoperative and early postoperative outcomes.

OBJECTIVE: Prolonged aortic crossclamping can increase mortality and morbidity after aortic valve replacement in elderly and high-risk patients. Sutureless implantation of the prosthesis has the potential to shorten aortic crossclamp time. METHODS: The Perceval S valve (Sorin Biomedica Cardio Srl, Sallugia, Italy), a sutureless implantable aortic bioprosthesis, was used in 32 patients (median age, 78 years; median logistic euroSCORE, 9.99) requiring aortic valve replacement with or without concomitant coronary artery bypass grafting. Hemodynamic parameters and clinical outcome were obtained at discharge, at 6 months, and up to 1 year postoperatively. RESULTS: Aortic crossclamp time needed for aortic valve replacement was 18 ± 6 minutes. Hemodynamics at discharge showed good function of all Perceval S valves with low transvalvular pressure gradients (mean, 12 ± 5 mm Hg and peak, 23 ± 9 mm Hg) and low incidence of paravalvular or valvular leakage. Operative mortality was 0%. Follow-up at 1 year showed 3 non-valve-related deaths. Survivors showed good clinical outcome and stable hemodynamic function of the valve prosthesis, except for 1 patient in whom endocarditis developed. Despite a moderate decrease in platelet counts persisting up to 12 months, freedom of bleeding and thromboembolic events was 100%. CONCLUSIONS: It is possible to implant a well-functioning sutureless stent-mounted valve in the aortic position in less than 20 minutes of aortic crossclamping. This is associated with excellent early clinical and hemodynamic outcome in high-risk patients. Moderate changes in hematologic parameters persisted but were not related to clinical events.

Increased catecholamine secretion contributes to hypertension in TRPM4-deficient mice.

Hypertension is an underlying risk factor for cardiovascular disease. Despite this, its pathogenesis remains unknown in most cases. Recently, the transient receptor potential (TRP) channel family was associated with the development of several cardiovascular diseases linked to hypertension. The melastatin TRP channels TRPM4 and TRPM5 have distinct properties within the TRP channel family: they form nonselective cation channels activated by intracellular calcium ions. Here we report the identification of TRPM4 proteins in endothelial cells, heart, kidney, and chromaffin cells from the adrenal gland, suggesting that they have a role in the cardiovascular system. Consistent with this hypothesis, Trpm4 gene deletion in mice altered long-term regulation of blood pressure toward hypertensive levels. No changes in locomotor activity, renin-angiotensin system function, electrolyte and fluid balance, vascular contractility, and cardiac contractility under basal conditions were observed. By contrast, inhibition of ganglionic transmission with either hexamethonium or prazosin abolished the difference in blood pressure between Trpm4-/- and wild-type mice. Strikingly, plasma epinephrine concentration as well as urinary excretion of catecholamine metabolites were substantially elevated in Trpm4-/- mice. In freshly isolated chromaffin cells, lack of TRPM4 was shown to cause markedly more acetylcholine-induced exocytotic release events, while neither cytosolic calcium concentration, size, nor density of vesicles were different. We therefore conclude that TRPM4 proteins limit catecholamine release from chromaffin cells and that this contributes to increased sympathetic tone and hypertension.

Long-term blinded placebo-controlled study of SNT-MC17/idebenone in the dystrophin deficient mdx mouse: cardiac protection and improved exercise performance.

AIMS: Duchenne muscular dystrophy (DMD) is a severe and still incurable disease, with heart failure as a leading cause of death. The identification of a disease-modifying therapy may require early-initiated and long-term administration, but such type of therapeutic trial is not evident in humans. We have performed such a trial of SNT-MC17/idebenone in the mdx mouse model of DMD, based on the drug's potential to improve mitochondrial respiratory chain function and reduce oxidative stress. METHODS AND RESULTS: In this study, 200 mg/kg bodyweight of either SNT-MC17/idebenone or placebo was given from age 4 weeks until 10 months in mdx and wild-type mice. All evaluators were blinded to mouse type and treatment groups. Idebenone treatment significantly corrected cardiac diastolic dysfunction and prevented mortality from cardiac pump failure induced by dobutamine stress testing in vivo, significantly reduced cardiac inflammation and fibrosis, and significantly improved voluntary running performance in mdx mice. CONCLUSION: We have identified a novel potential therapeutic strategy for human DMD, as SNT-MC17/idebenone was cardioprotective and improved exercise performance in the dystrophin-deficient mdx mouse. Our data also illustrate that the mdx mouse provides unique opportunities for long-term controlled prehuman therapeutic studies.

Pericardial synovial sarcoma: 14-year survival with multimodality therapy.

We report a case of recurrent primary synovial sarcoma of the pericardium. Reverse transcriptase-polymerase chain reaction analysis for t(X,18) demonstrated the presence of the chimeric transcript SYT/SSX. Because of the rarity of this entity, optimal therapy is unknown. The prognosis of this tumor is very poor in previous reports. In this report, we present a case with five recurrences treated by a combination of surgery, chemotherapy, and radiotherapy. The patient survives now for more than 14 years, the longest reported survival of a primary synovial sarcoma of the pericardium.