Dorsal motor vagal neurons can elicit bradycardia and reduce anxiety-like behavior.

Cardiovagal neurons (CVNs) innervate cardiac ganglia through the vagus nerve to control cardiac function. Although the cardioinhibitory role of CVNs in nucleus ambiguus (CVNNA) is well established, the nature and functionality of CVNs in dorsal motor nucleus of the vagus (CVNDMV) is less clear. We therefore aimed to characterize CVNDMV anatomically, physiologically, and functionally. Optogenetically activating cholinergic DMV neurons resulted in robust bradycardia through peripheral muscarinic (parasympathetic) and nicotinic (ganglionic) acetylcholine receptors, but not beta-1-adrenergic (sympathetic) receptors. Retrograde tracing from the cardiac fat pad labeled CVNNA and CVNDMV through the vagus nerve. Using whole-cell patch-clamp, CVNDMV demonstrated greater hyperexcitability and spontaneous action potential firing ex vivo despite similar resting membrane potentials, compared to CVNNA. Chemogenetically activating DMV also caused significant bradycardia with a correlated reduction in anxiety-like behavior. Thus, DMV contains uniquely hyperexcitable CVNs and is capable of cardioinhibition and robust anxiolysis.

A comprehensive review of the medical and cosmetic applications of exosomes in dermatology.

BACKGROUND: Exosomes are a subset of extracellular vesicles that are released by all cell types and are theorized to play a crucial role in intercellular communication. Ranging from 40 to 160 nm in diameter, exosomes contain a variety of genetic materials including DNA, RNA, mRNA, metabolites, proteins, and lipids depending on their cellular origin. AIM: Given that intercellular communication is abetted by the exchange of cellular components via exosomes, their applied use can have important implications for disease pathology and exosome-based therapeutics. We provide a comprehensive review of the current application of exosomes in medical (and skin) diseases and in cutaneous medical aesthetics. METHODS: A literature search was conducted on PubMed reviewing exosomes and their application in medical and aesthetic fields. RESULTS: While the therapeutic use of exosomes in the treatment of medical and cosmetic dermatological procedures is promising, it is also important to note that most studies implementing exosomes as therapeutic agents have been conducted in preclinical models, thus highlighting the need for additional studies and clinical trials. One more important note in the aesthetic world associated with exosomes is that in the United States, at the time of this writing, exosomes may only be topically applied and not injected into the skin, as is done in many countries worldwide. CONCLUSION: There is a need for additional studies and clinical trials to evaluate the safety and therapeutic effect and safety of exosomes in medical and aesthetic fields.

Dorsal Motor Vagal Neurons Can Elicit Bradycardia and Reduce Anxiety-Like Behavior.

Cardiovagal neurons (CVNs) innervate cardiac ganglia through the vagus nerve to control cardiac function. Although the cardioinhibitory role of CVNs in nucleus ambiguus (CVNNA) is well established, the nature and functionality of CVNs in dorsal motor nucleus of the vagus (CVNDMV) is less clear. We therefore aimed to characterize CVNDMV anatomically, physiologically, and functionally. Optogenetically activating cholinergic DMV neurons resulted in robust bradycardia through peripheral muscarinic (parasympathetic) and nicotinic (ganglionic) acetylcholine receptors, but not beta-1-adrenergic (sympathetic) receptors. Retrograde tracing from the cardiac fat pad labeled CVNNA and CVNDMV through the vagus nerve. Using whole cell patch clamp, CVNDMV demonstrated greater hyperexcitability and spontaneous action potential firing ex vivo despite similar resting membrane potentials, compared to CVNNA. Chemogenetically activating DMV also caused significant bradycardia with a correlated reduction in anxiety-like behavior. Thus, DMV contains uniquely hyperexcitable CVNs capable of cardioinhibition and robust anxiolysis.

Early central cardiovagal dysfunction after high fat diet in a murine model.

High fat diet (HFD) promotes cardiovascular disease and blunted cardiac vagal regulation. Temporal onset of loss of cardiac vagal control and its underlying mechanism are presently unclear. We tested our hypothesis that reduced central vagal regulation occurs early after HFD and contributes to poor cardiac regulation using cardiovascular testing paired with pharmacology in mice, molecular biology, and a novel bi-transgenic mouse line. Results show HFD, compared to normal fat diet (NFD), significantly blunted cardio/pulmonary chemoreflex bradycardic responses after 15 days, extending as far as tested (> 30 days). HFD produced resting tachycardia by day 3, reflected significant loss of parasympathetic tone. No differences in bradycardic responses to graded electrical stimulation of the distal cut end of the cervical vagus indicated diet-induced differences in vagal activity were centrally mediated. In nucleus ambiguus (NA), surface expression of δ-subunit containing type A gamma-aminobutyric acid receptors (GABAA(δ)R) increased at day 15 of HFD. Novel mice lacking δ-subunit expression in vagal motor neurons (ChAT-δnull) failed to exhibit blunted reflex bradycardia or resting tachycardia after two weeks of HFD. Thus, reduced parasympathetic output contributes to early HFD-induced HR dysregulation, likely through increased GABAA(δ)Rs. Results underscore need for research on mechanisms of early onset increases in GABAA(δ)R expression and parasympathetic dysfunction after HFD.

Neuroprotective Roles of the Adenosine A3 Receptor Agonist AST-004 in Mouse Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) remains one of the greatest public health concerns with increasing morbidity and mortality rates worldwide. Our group reported that stimulation of astrocyte mitochondrial metabolism by P2Y1 receptor agonists significantly reduced cerebral edema and reactive gliosis in a TBI model. Subsequent data on the pharmacokinetics (PK) and rapid metabolism of these compounds suggested that neuroprotection was likely mediated by a metabolite, AST-004, which binding data indicated was an adenosine A3 receptor (A3R) agonist. The neuroprotective efficacy of AST-004 was tested in a control closed cortical injury (CCCI) model of TBI in mice. Twenty-four (24) hours post-injury, mice subjected to CCCI and treated with AST-004 (0.22 mg/kg, injected 30 min post-trauma) exhibited significantly less secondary brain injury. These effects were quantified with less cell death (PSVue794 fluorescence) and loss of blood brain barrier breakdown (Evans blue extravasation assay), compared to vehicle-treated TBI mice. TBI-treated mice also exhibited significantly reduced neuroinflammatory markers, glial-fibrillary acidic protein (GFAP, astrogliosis) and ionized Ca2+-binding adaptor molecule 1 (Iba1, microgliosis), both at the mRNA (qRT-PCR) and protein (Western blot and immunofluorescence) levels, respectively. Four (4) weeks post-injury, both male and female TBI mice presented a significant reduction in freezing behavior during contextual fear conditioning (after foot shock). AST-004 treatment prevented this TBI-induced impairment in male mice, but did not significantly affect impairment in female mice. Impairment of spatial memory, assessed 24 and 48 h after the initial fear conditioning, was also reduced in AST-004-treated TBI-male mice. Female TBI mice did not exhibit memory impairment 24 and 48 h after contextual fear conditioning and similarly, AST-004-treated female TBI mice were comparable to sham mice. Finally, AST-004 treatments were found to increase in vivo ATP production in astrocytes (GFAP-targeted luciferase activity), consistent with the proposed mechanism of action. These data reveal AST-004 as a novel A3R agonist that increases astrocyte energy production and enhances their neuroprotective efficacy after brain injury.

Functional, cognitive, and nutritional decline in 435 elderly nursing home residents after the first wave of the COVID-19 Pandemic.

PURPOSE: Many institutionalized older people have died during the first wave of COVID-19. Other related consequences have not yet been described objectively. The aim of this study was to compare functional, cognitive, and nutritional status before and after the first wave among nursing home residents, in both COVID-19 and non-COVID-19 patients. METHODS: Older adults institutionalized in four nursing homes were assessed from May to June 2020, by a geriatric multidisciplinary team in collaboration with the nursing homes staff. Comprehensive geriatric assessment was performed including functional, cognitive, and nutritional variables before and after the first wave of the pandemic. Data from residents with positive results for microbiological testing for SARS-CoV-2 were compared with those who did not. RESULTS: 435 nursing home residents were included. The median age was 86.77 ± 8.5 years, 78.4% were women. 190 (43.9%) tested positive for coronavirus. Functional decline after the first wave was detected in 20.2% according to the Barthel Index and in 18.5% according to functional ambulation categories, p < 0.001. Cognitive status worsened by 22 and 25.9% according to the global deterioration scale (p < 0.001) and Lobo's Mini-Examen Cognoscitivo (p 0.01), respectively. Onset of depressive symptoms was found in 48% (p < 0.001). The prevalence of malnutrition increased by 36.8 and 38.4% lost weight. When comparing the functional, cognitive, and nutritional decline between COVID-19 and non-COVID-19 patients no clinical or statistically significant differences were found except for the presence of prior malnutrition, higher in the COVID-19 group. CONCLUSION: We observed a significative functional, cognitive, and nutritional decline in institutionalized elderly after the first wave of COVID-19. These results may be caused by the lockdown itself, since no differences have been found between COVID-19 and non-COVID-19 patients. According to these results, interventions are necessary during social isolation or confinement to prevent systemic decline in the elderly.

Interplay Between Systemic Metabolic Cues and Autonomic Output: Connecting Cardiometabolic Function and Parasympathetic Circuits.

There is consensus that the heart is innervated by both the parasympathetic and sympathetic nervous system. However, the role of the parasympathetic nervous system in controlling cardiac function has received significantly less attention than the sympathetic nervous system. New neuromodulatory strategies have renewed interest in the potential of parasympathetic (or vagal) motor output to treat cardiovascular disease and poor cardiac function. This renewed interest emphasizes a critical need to better understand how vagal motor output is generated and regulated. With clear clinical links between cardiovascular and metabolic diseases, addressing this gap in knowledge is undeniably critical to our understanding of the interaction between metabolic cues and vagal motor output, notwithstanding the classical role of the parasympathetic nervous system in regulating gastrointestinal function and energy homeostasis. For this reason, this review focuses on the central, vagal circuits involved in sensing metabolic state(s) and enacting vagal motor output to influence cardiac function. It will review our current understanding of brainstem vagal circuits and their unique position to integrate metabolic signaling into cardiac activity. This will include an overview of not only how metabolic cues alter vagal brainstem circuits, but also how vagal motor output might influence overall systemic concentrations of metabolic cues known to act on the cardiac tissue. Overall, this review proposes that the vagal brainstem circuits provide an integrative network capable of regulating and responding to metabolic cues to control cardiac function.

Neuroprotective effect of immunomodulatory peptides in rats with traumatic spinal cord injury.

Several therapies have shown obvious effects on structural conservation contributing to motor functional recovery after spinal cord injury (SCI). Nevertheless, neither strategy has achieved a convincing effect. We purposed a combined therapy of immunomodulatory peptides that individually have shown significant effects on motor functional recovery in rats with SCI. The objective of this study was to investigate the effects of the combined therapy of monocyte locomotion inhibitor factor (MLIF), A91 peptide, and glutathione monoethyl ester (GSH-MEE) on chronic-stage spinal cord injury. Female Sprague-Dawley rats underwent a laminectomy of the T9 vertebra and a moderate contusion. Six groups were included: sham, PBS, MLIF + A91, MLIF + GSH-MEE, A91 + GSH-MEE, and MLIF + A91 + GSH-MEE. Two months after injury, motor functional recovery was evaluated using the open field test. Parenchyma and white matter preservation was evaluated using hematoxylin & eosin staining and Luxol Fast Blue staining, respectively. The number of motoneurons in the ventral horn and the number of axonal fibers were determined using hematoxylin & eosin staining and immunohistochemistry, respectively. Collagen deposition was evaluated using Masson's trichrome staining. The combined therapy of MLIF, A91, and GSH-MEE greatly contributed to motor functional recovery and preservation of the medullary parenchyma, white matter, motoneurons, and axonal fibres, and reduced the deposition of collagen in the lesioned area. The combined therapy of MLIF, A91, and GSH-MEE preserved spinal cord tissue integrity and promoted motor functional recovery of rats after SCI. This study was approved by the National Commission for Scientific Research on Bioethics and Biosafety of the Instituto Mexicano del Seguro Social under registration number R-2015-785-116 (approval date November 30, 2015) and R-2017-3603-33 (approval date June 5, 2017).

Diabetes, and its treatment, as an effector of autonomic nervous system circuits and its functions.

Diabetes increases the risk of cardiovascular complications, including heart failure, hypertension, and stroke. There is a strong involvement of autonomic dysfunction in individuals with diabetes that exhibit clinical manifestations of cardiovascular diseases (CVD). Still, the mechanisms by which diabetes and its treatments alter autonomic function and subsequently affect cardiovascular complications remain elusive. For this reason, understanding the brainstem circuits involved in sensing metabolic state(s) and enacting autonomic control of the cardiovascular system are important to develop more comprehensive therapies for individuals with diabetes at increased risk for CVD. We review how autonomic nervous system circuits change during these disease states and discuss their potential role in current pharmacotherapies that target diabetic states. Overall, this review proposes that the brainstem circuits provide an integrative sensorimotor network capable of responding to metabolic cues to regulate cardiovascular function and this network is modified by, and in turn affects, diabetes-induced CVD and its treatment.

GABAA receptor currents in the dorsal motor nucleus of the vagus in females: influence of ovarian cycle and 5α-reductase inhibition.

The dorsal motor nucleus of the vagus (DMV) contains the preganglionic motor neurons important in the regulation of glucose homeostasis and gastrointestinal function. Despite the role of sex in the regulation of these processes, few studies examine the role of sex and/or ovarian cycle in the regulation of synaptic neurotransmission to the DMV. Since GABAergic neurotransmission is critical to normal DMV function, the present study used in vitro whole cell patch-clamping to investigate whether sex differences exist in GABAergic neurotransmission to DMV neurons. It additionally investigated whether the ovarian cycle plays a role in those sex differences. The frequency of phasic GABAA receptor-mediated inhibitory postsynaptic currents in DMV neurons from females was lower compared with males, and this effect was TTX sensitive and abolished by ovariectomy (OVX). Amplitudes of GABAergic currents (both phasic and tonic) were not different. However, females demonstrated significantly more variability in the amplitude of both phasic and tonic GABAA receptor currents. This difference was eliminated by OVX in females, suggesting that these differences were related to reproductive hormone levels. This was confirmed for GABAergic tonic currents by comparing females in two ovarian stages, estrus versus diestrus. Female mice in diestrus had larger tonic current amplitudes compared with those in estrus, and this increase was abolished after administration of a 5α-reductase inhibitor but not modulation of estrogen. Taken together, these findings demonstrate that DMV neurons undergo GABAA receptor activity plasticity as a function of sex and/or sex steroids.NEW & NOTEWORTHY Results show that GABAergic signaling in dorsal vagal motor neurons (DMV) demonstrates sex differences and fluctuates across the ovarian cycle in females. These findings are the first to demonstrate that female GABAA receptor activity in this brain region is modulated by 5α-reductase-dependent hormones. Since DMV activity is critical to both glucose and gastrointestinal homeostasis, these results suggest that sex hormones, including those synthesized by 5α-reductase, contribute to visceral, autonomic function related to these physiological processes.

The Severity of Spinal Cord Injury Determines the Inflammatory Gene Expression Pattern after Immunization with Neural-Derived Peptides.

Previous studies revealed that the intensity of spinal cord injury (SCI) plays a key role in the therapeutic effects induced by immunizing with neural-derived peptides (INDP), as severe injuries abolish the beneficial effects induced by INDP. In the present study, we analyzed the expression of some inflammation-related genes (IL6, IL12, IL-1ß, IFNÉ£, TNFα, IL-10, IL-4, and IGF-1) by quantitative PCR in rats subjected to SCI and INDP. We investigated the expression of these genes after a moderate or severe contusion. In addition, we evaluated the effect of INDP by utilizing two different peptides: A91 and Cop-1. After moderate injury, both A91 and Cop-1 elicited a pattern of genes characterized by a significant reduction of IL6, IL1ß, and TNFα but an increase in IL10, IL4, and IGF-1 expression. There was no effect on IL-12 and INFÉ£. In contrast, the opposite pattern was observed when rats were subjected to a severe spinal cord contusion. Immunization with either peptide caused a significant increase in the expression of IL-12, IL-1ß, IFNÉ£ (pro-inflammatory genes), and IGF-1. There was no effect on IL-4 and IL-10 compared to controls. After a moderate SCI, INDP reduced pro-inflammatory gene expression and generated a microenvironment prone to neuroprotection. Nevertheless, severe injury elicits the expression of pro-inflammatory genes that could be aggravated by INDP. These findings correlate with our previous results demonstrating that severe injury inhibits the beneficial effects of protective autoimmunity.

Vß T cell receptor (TCR) genes in circulating cells of patients with systemic lupus erythematosus and their healthy relatives / Genes del receptor variable beta de células T en células circulantes de pacientes con lupus eritematoso generalizado y sus familiares sanos.

Objective: We investigated the proportion of Vß T cell receptor (TCR) gene expression in peripheral CD3+ lymphocytes in familial and non-familial systemic lupus erythematosus (SLE) patients. Method: The Vß TCR repertoire was studied in 14 families in which several members had SLE. The Vß TCR usage in SLE patients (n = 27) was compared with that in healthy members of these multiplex families (n = 47), in 37 sporadic SLE patients who had no relatives with SLE, and in 15 healthy unrelated controls. Vß TCR repertoire expression was studied by multiparameter flow cytometry with the use of an array of 24 different Vß TCR gene family-specific monoclonal antibodies. Results: We found the same Vß TCR expression profile in the comparisons between sporadic SLE and familial SLE cases and healthy relatives, which included increased expression of Vß 5.2, Vß 11 and Vß 16, and lower expression of Vß 3, Vß 4, Vß 7.1 and Vß 17. Interestingly, solely Vß 17 was differentially expressed among sporadic and familial SLE. Also, increased expression of Vß 9 was the hallmark among familial SLE (casesand h ealthy relatives) in comparison to controls. Conclusion: These results highlight the notion that the final profile of the Vß TCR repertoire seen in familial and non-familial SLE seems to arise from the interaction of genetic, environmental, and immunoregulatory factors. Furthermore, it may contribute to the immunologic abnormalities affecting relatives of SLE patients.

Objetivo: Se investigó la proporción de la expresión génica del receptor variable beta de células T (Vß TCR) en linfocitos periféricos CD3+ en pacientes con lupus eritematoso generalizado (LEG) familiar y no familiar. Método: El repertorio de Vß TCR se estudió en 14 familias que presentaban más de un miembro con LEG. El uso de Vß TCR en pacientes con LEG (n = 27) se comparó con el de los miembros sanos de estas familias (n = 47), con 37 pacientes con LEG esporádico y con 15 controles sanos. La expresión del repertorio de Vß TCR se estudió por citometría de flujo multiparamétrica utilizando un arreglo de 24 diferentes anticuerpos monoclonales específicos de genes familiares para Vß TCR. Resultados: Se encontró el mismo perfil de expresión en las comparaciones entre los casos de LEG esporádico y familiar, así como en los consanguíneos sanos de las familias multicasos, que incluía una expresión incrementada de Vß 5.2, Vß 11 y Vß 16, y una menor expresión de Vß 3, Vß4, Vß 7.1 y Vß 7. De manera interesante, solo Vß 17 se expresó de modo diferente entre casos familiares y esporádicos de LEG. Igualmente, la expresión incrementada de Vß 9 fue el distintivo entre los casos de LEG familiar (casos y consanguíneos sanos) y los controles sanos. Conclusiones: Estos resultados refuerzan la noción de que el perfil final del repertorio Vß TCR observado en LEG familiar y no familiar parece surgir de la interacción de factores genéticos, ambientales e inmunorreguladores, además de que pueden explicar las alteraciones inmunitarias que se observan en los consanguíneos sanos de pacientes con LEG.

Hyponatraemia diagnosis and treatment clinical practice guidelines. / Guía de práctica clínica sobre el diagnóstico y tratamiento de la hiponatremia.

Hyponatremia, defined as a serum sodium concentration <135mmol/l, is the most common water-electrolyte imbalance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from mild to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay. Despite this, the management of hyponatremia patients remains problematic. The prevalence of hyponatremia in a wide variety of conditions and the fact that hyponatremia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and specialty-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association-European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed clinical practice guidelines on the diagnostic approach and treatment of hyponatremia as a joint venture of 3societies representing specialists with a natural interest in hyponatremia. In addition to a rigorous approach to the methodology and evaluation of the evidence, the document focuses on patient-positive outcomes and on providing a useful tool for clinicians involved in everyday practice. In this article, we present an abridged version of the recommendations and suggestions for the diagnosis and treatment of hyponatremia extracted from the full guide.

Immunization with neural derived peptides plus scar removal induces a permissive microenvironment, and improves locomotor recovery after chronic spinal cord injury.

BACKGROUND: Immunization with neural derived peptides (INDP) as well as scar removal-separately-have shown to induce morphological and functional improvement after spinal cord injury (SCI). In the present study, we compared the effect of INDP alone versus INDP with scar removal on motor recovery, regeneration-associated and cytokine gene expression, and axonal regeneration after chronic SCI. Scar removal was conducted through a single incision with a double-bladed scalpel along the stump, and scar renewal was halted by adding α,α'-dipyridyl. RESULTS: During the chronic injury stage, two experiments were undertaken. The first experiment was aimed at testing the therapeutic effect of INDP combined with scar removal. Sixty days after therapeutic intervention, the expression of genes encoding for TNFα, IFNγ, IL4, TGFß, BDNF, IGF1, and GAP43 was evaluated at the site of injury. Tyrosine hydroxylase and 5-hydroxytryptamine positive fibers were also studied. Locomotor evaluations showed a significant recovery in the group treated with scar removal + INDP. Moreover; this group presented a significant increase in IL4, TGFß, BDNF, IGF1, and GAP43 expression, but a decrease of TNFα and IFNγ. Also, the spinal cord of animals receiving both treatments presented a significant increase of serotonergic and catecholaminergic fibers as compared to other the groups. The second experiment compared the results of the combined approach versus INDP alone. Rats receiving INDP likewise showed improved motor recovery, although on a lesser scale than those who received the combined treatment. An increase in inflammation and regeneration-associated gene expression, as well as in the percentage of serotonergic and catecholaminergic fibers was observed in INDP-treated rats to a lesser degree than those in the combined therapy group. CONCLUSIONS: These findings suggest that INDP, both alone and in combination with scar removal, could modify the non-permissive microenvironment prevailing at the chronic phase of SCI, providing the opportunity of improving motor recovery.

Agudeza visual en alumnos de medicina en una universidad privada de Puebla, México / Visual acuity in students of medicine at a private university of Puebla, Mexico

Introducción. La agudeza visual se considera como un parámetro visualhabitual que se emplea para evaluar la salud ocular y sirve para detectaralteraciones a bajo costo y reducir la ceguera prevenible o curable. Objetivo.Identificar las alteraciones de la agudeza visual normal, discapacidad moderada o severa y ceguera en los estudiantes de medicina que se encuentran a la mitad de la carrera a través de la toma de agudeza visual. Método. Se utilizó un diseño no experimental, descriptivo, observacional, transversal prospectivo. La muestra se conformó por 308 alumnos de la Universidad Popular Autónoma del Estado de Puebla de la carrera de Medicina que cumplían con los criterios de inclusión. Se aplicó un cuestionario el cual incluía antecedentes personales oftalmológicos y sintomatología oftálmica y se realizó la prueba de agudeza visual con la cartilla de snellen. Resultados. El 88.31 porciento tuvieron una agudeza visual normal, 11.68 porciento de los alumnos presentó déficit de la agudeza visual delos cuales la discapacidad visual moderada se presentó en un 10.71 porciento en el ojo derecho y en un 11.03 porciento en el ojo izquierdo, la categoría de discapacidad severa el porcentaje presentado fue menor al 1% en ambos ojos. Conclusión. En esta universidad la mayoría de los alumnos se encuentran visualmente normales, pero existe la necesidad de establecer programas continuos que permitan ir identificando a aquellos alumnos que han disminuido su agudeza visual para evitar que no se reduzca el aprendizaje y desarrollo de destrezas propias de la carrera de Medicina.

Hematoma paravesical espontáneo posterior a dosis única profiláctica de enoxaparina en cirugía ortopédica. Presentación de un caso / Spontaneous paravesical hematoma at a single prophylactic doses of enoxaparin in Orthopedic surgery. Case report

El hematoma paravesical espontáneo es una complicación infrecuente, con pocos casos reportados en la literatura. Aproximadamente el 2 % de los pacientes que se traten con enoxaparina profiláctica tendrán complicaciones hemorrágicas, de las cuales el 20 % son hematomas retroperitoneales o intracraneales, en dependencia de los factores de riesgo. Por tales razones se presenta el caso de un paciente de 35 años de edad, previamente sano, que fue sometido a una sutura de tendón de Aquiles después de sufrir un trauma, al que se le administró profilácticamente una sola dosis de enoxaparina en el posoperatorio inmediato y 24 horas después comenzó a quejarse de dolor en fosa iliaca derecha y disuria. El ultrasonido abdominal demostró un hematoma paravesical, que fue confirmado por topografía. Se manejó conservadoramente con sonda intravesical por diez días. Se realizó seguimiento del paciente, sin que se encontraran secuelas. Los autores infieren que el sangrado fue secundario a una sobredistensión vesical secundaria a la anestesia que provocó el sangrado de la pared de la vejiga. Este reporte demuestra que la enoxaparina profiláctica puede causar hematomas paravesicales espontáneos asociados a la sobredistención vesical. Sin embargo son necesarios otros reportes similares para confirmar lo anteriormente planteado.

Spontaneous paravesical hematoma is an infrequent complication, with a few reported cases in literature. Approximately 2 % of the patients treated with prophylactic enoxoparin will have hemorrhagic complications, from which 2 0% are retroperitoneal or intracranial hematomas depending on the risk factors. For such reasons it is presented a 35 year old patient, previously healthy, who was performed to a suture of the Achilles tendon after suffering a trauma. He was administered prophylactically a single doses of enoxoparin in the immediate post surgery and 24 hours later he started to complain of pain in the right lower quadrant and dysuria. Abdominal ultrasound showed a paravesical hematoma secondary to anesthesia which caused bleeding of the vesicle walls. This report shows prophylactic exoparin may produce spontaneous paravesical hematomas associated to vesical overdistention. However it is necessary other similar reports to confirm the previous statement.

Calidad de vida en pacientes bajo hemodiálisis en un hospital público de Puebla, México / Quality of life in patients on hemodialysis in a public hospital of Puebla, Mexico

Fundamento: la evaluación de la calidad de vida relacionada con la salud, ha adquirido cada vez más importancia en la práctica de la medicina como indicador reflejo de la calidad de los diferentes tratamientos y sus resultados. En pacientes con enfermedad renal crónica terminal, la hemodiálisis como terapia de reemplazo renal mejora la sobrevida, pero no lo que la persona considera como calidad de vida. Objetivo: establecer el nivel de calidad de vida en pacientes con enfermedad renal crónica bajo hemodiálisis y el área (salud física, psicológica, relaciones sociales, ambiente) en la que presenta niveles bajos. Métodos: se utilizó un diseño no experimental, transversal, descriptivo. Se realizó un muestreo no probabilístico por conveniencia, que incluyó a 67 pacientes con enfermedad crónica terminal, inscritos en la unidad de hemodiálisis de un hospital público de la ciudad de Puebla. Se les aplicó el instrumento Whoqol-bref, para luego ordenar la información en Excel, se recurrió al programa SPSS para realizar pruebas estadísticas. Resultados: la calidad de vida de los pacientes bajo tratamiento de reemplazo renal con hemodiálisis tuvo una calidad baja (23, 88 %) y media (76, 12 %). El dominio menos afectado es el psicológico con 67, 01 puntos y el mayor es el físico con 60, 76. El dominio relacionado con la calidad de vida fue las relaciones sociales (p=0.000). Conclusiones: los pacientes en hemodiálisis presentan una calidad de vida media-baja y el área más afectada es la física, pero existe mayor correlación con las relaciones sociales, a mejor relación social mejor calidad de vida percibe el paciente.

Introduction: the evaluation of the quality of life related to health has assumed importance in the practice of medicine, as an indicator of the different treatments’ qualities and their results. In patients with end-stage chronic kidney disease, hemodialysis as a kidney replacement therapy improves survival, but not necessarily what the person thinks about quality of life. Objective: to establish the level of quality of life in patients with chronic kidney disease on hemodialysis and the area (physical, psychological health, social relations, the environment) in which low levels are presented. Methods: a non-experimental, transversal, and descriptive design was used. A non-probabilistic sample of convenience was carried out. The study was composed of 67 patients with end-stage chronic kidney disease, admitted in a hemodialysis unit of a public hospital in Puebla. Whogol-bref instrument was applied to them. Information was ordered in Excel and SPSS program was used to do statistical tests. Results: patients with kidney replacement treatment on hemodialysis had a low quality of life 23, 88 % and a medium 76, 12 %. The less affected domain was the psychological with 67, 01 points and the most affected one was the physical with 60, 76 %. The domain strongly related to quality of life was social relations (p=0, 000). Conclusion: patients on hemodialysis have a middle-low quality of life and the most affected area is physical. However, there is more correlation with social relations. The better social relation is, the better quality of life the patient gains.

Síndrome de fragilidad en el adulto mayor en una comunidad rural de Puebla, México / Syndrome of frailty in the older adult in a rural community in Puebla, Mexico

El síndrome de fragilidad en el adulto mayor implica presentar eventos adversos, mayor necesidad de cuidados, mayor riesgo de evolucionar hacia la discapacidad, dependencia y muerte. El objetivo de la investigación fue determinar el número de adultos mayores que presentan síndrome de fragilidad y el factor más determinante, en una población rural del estado de Puebla, México. Se realizó un estudio descriptivo, observacional, transversal, prospectivo. La muestra estuvo conformada por 200 pacientes mayores de 65 años de edad, registrados en el centro de salud de la comunidad en estudio. Los datos fueron recolectados a través de la aplicación de la escala geriátrica y se aplicaron los criterios cubanos de fragilidad. De los adultos mayores incluidos 52.5% fueron femeninos y 47.5 masculinos. La prevalencia del síndrome de fragilidad fue del 45%, siendo mayor en mujeres. Como factor asociado se encontraron las alteraciones en la movilidad y el equilibrio con un 26.5%. Se concluye que existe una alta prevalencia de adultos mayores frágiles en una comunidad rural de Puebla, México; las alteraciones en la movilidad y el equilibrio son el principal factor detonante, debido a las actividades cotidianas que predominan en las zonas rurales latinoamericanas.

Syndrome of frailty in the elderly, involves presenting adverse events, most in need of care, increased risk of progression to disability, dependency and death. The objective of the research was to determine the number of older adults presenting fragility syndrome and the most determining factor in a rural population of the State of Puebla, Mexico. A descriptive, observational, cross-sectional, prospective study was conducted. The sample was composed of 200 patients over 65 years of age, registered in the study community health center. Data was collected through the application of the geriatric scale and fragility of Cuban criteria were applied. Including older adults 52.5% were female and 47.5 male. The prevalence of fragility Syndrome was 45%, being higher in women. As associated factor found alterations in mobility and balance with a 26.5%. It is concluded that there is a high prevalence of fragile seniors in a rural community in Puebla, Mexico; alterations in mobility and balance are the main detonating factor, due to activities of daily living that predominate in Latin American rural areas.

2012 ERA-EDTA Registry Annual Report: cautious optimism on outcomes, concern about persistent inequalities and data black-outs.

The 2012 ERA-EDTA Registry Annual Report contains both good news and bad news. On the bright side, the 2-year survival of patients starting renal replacement therapy (RRT) for chronic kidney disease (CKD), on dialysis or receiving a living-related kidney transplantation, has progressively increased to 82.2, 79.7 and 98.3%, respectively, whereas for cadaveric kidney transplantation it remains stable (96.0-96.1%). On the dark side, inequalities persist between European citizens in access to renal transplantation and in incidence and prevalence of RRT. Living in Greece, Belgium (French- or Dutch-speaking) or Portugal (the GBP countries) is associated with higher chances of initiating RRT than living in other European countries. The adjusted RRT incidence for GBP countries was 188, 201-174 and 220* (* unadjusted) pmp in 2012, respectively (versus 122, 114 and 97 pmp in the Netherlands or two Spanish regions bordering Portugal). In lower income countries, a low RRT incidence may represent lack of access to needed healthcare (e.g. Montenegro 26 pmp). However, how can the high incidence and prevalence of RRT in the GBP countries be explained? Do GBP citizens have access to RRT that is denied, rejected or considered unnecessary in other high income countries? Does the GBP healthcare system fail to prevent progression of CKD? Do local genetic or environmental factors favour CKD progression? Unravelling the underlying reasons is an urgent research need: only an understanding of the causes will allow correction of the problem. Unavailability of data from some large countries (e.g. Germany and Italy) is not helpful.