RESUMEN
BACKGROUND The incidence of lung diseases in premature newborns is significantly higher than in full-term newborns due to their underdeveloped lungs. Ultrasound and X-ray are commonly-used bedside examinations in neonatology. This study primarily compares the efficacy of chest X-ray (CXR) and lung ultrasound (LUS) images in evaluating lung consolidation and edema in premature newborns at Neonatal Intensive Care Units (NICU). MATERIAL AND METHODS A retrospective analysis was conducted on LUS and CXR examination results, along with clinical records of premature newborns admitted to our hospital's NICU from November 1, 2019, to December 31, 2021. CXR and LUS scans were performed on the same newborn within a day. We evaluated the consolidations and edema by interpreting the CXR and LUS images, then compared the findings. RESULTS Out of 75 cases, 34 showed lung consolidations on LUS (45%), while only 14 exhibited consolidations on CXR (19%). The detection rate of consolidations by LUS was significantly higher compared to CXR (34/75 vs 14/75, P<0.001). Differences were observed between the 2 bedside examinations in identifying consolidations, with some cases seen only on LUS. CXR struggled to accurately assess the severity of lung edema visible on LUS, showing significant disparity in detecting interstitial edema (53/75 vs 21/75, P<0.001). CONCLUSIONS LUS outperforms chest CXR for bedside assessment of lung consolidation and edema in premature newborns.
Asunto(s)
Recien Nacido Prematuro , Unidades de Cuidado Intensivo Neonatal , Pulmón , Radiografía Torácica , Ultrasonografía , Humanos , Recién Nacido , Ultrasonografía/métodos , Masculino , Femenino , Pulmón/diagnóstico por imagen , Estudios Retrospectivos , Radiografía Torácica/métodos , Edema Pulmonar/diagnóstico por imagen , Edema/diagnóstico por imagen , Enfermedades Pulmonares/diagnóstico por imagenAsunto(s)
Estenosis de la Válvula Aórtica , Edema Pulmonar , Humanos , Estenosis de la Válvula Aórtica/diagnóstico por imagen , Estenosis de la Válvula Aórtica/cirugía , Estenosis de la Válvula Aórtica/fisiopatología , Estenosis de la Válvula Aórtica/complicaciones , Resultado del Tratamiento , Edema Pulmonar/etiología , Edema Pulmonar/diagnóstico por imagen , Edema Pulmonar/terapia , Hemodinámica , Factores de RiesgoRESUMEN
INTRODUÇÃO Cardiomiopatia (CMP) induzida por estresse, como a cardiomiopatia de Takotsubo, pode ter características clínicas semelhantes à isquemia miocárdica, como elevação de troponinas, alterações no Eletrocardiograma (ECG), mas sem obstrução coronariana ou lesões isquêmicas. Semelhante, a CMP induzida por Feocromocitoma possui sintomas também semelhantes a CMP hipertrófica, hipertensão e edema pulmonar devido a fatores cardiogênicos ou não cardiogênicos. Ambas supracitadas podem ter associação com excesso de catecolaminas, mas raramente estão associadas. RELATO DO CASO Paciente masculino, 46 anos, diabético, com história de estresse por situações familiares importantes, recentemente. Chega no serviço de emergência, com queixas de dispnéia, náuseas e êmese, iniciados há 1 dia, associado a retenção urinária e parestesia em mãos e paraparesia de membros inferiores. Refere também tratamento com Amoxicilina + Clavulanato há um mês por Colecistite Aguda. Na chegada, paciente se encontrava taquicárdico, taquipneico e saturando 98% em uso de óculos nasal a 2l/min, além de acidose metabólica. Realizou-se uma tomografia computadorizada de abdome, que evidenciou uma massa em Adrenal, sugestivo de Feocromocitoma, bem como metanefrinas urinárias e catecolaminas positivas. Ainda na emergência, evoluiu com insuficiência respiratória aguda por edema agudo de pulmão, necessitando de manejo com Nitroglicerina e 03 ampolas de Furosemida e uso de máscara não reinalante a 10l/min. Foi encaminhado para Unidade de Terapia Intensiva, onde foi realizado um ECG com alterações primárias da repolarização, seguido de alterações nos valores de Troponina e alterações no Ecocardiograma (ECO) de acinesia apical, hipocinesia de todos os segmentos médios e contratilidade preservada em segmentos basais. Cateterismo cardíaco com achados semelhantes ao ECO e presença de balonamento na ventriculografia, além de ausência de lesões obstrutivas em coronárias. CONCLUSÃO A excepcionalidade desse caso diz respeito ao quadro de síndrome coronariana aguda com dois motivos plausíveis e evidenciados na condução do caso, sendo eles: CMP de Takotsubo e a induzida por Feocromocitoma. Fica evidente, pela evolução do quadro, a gravidade do mesmo e a importância de considerar diagnósticos diferenciais, inclusive os menos comuns.
Asunto(s)
Humanos , Masculino , Persona de Mediana Edad , Feocromocitoma , Cardiomiopatía de Takotsubo , Edema Pulmonar , Insuficiencia Respiratoria , Cateterismo Cardíaco , Catecolaminas , Colecistitis Aguda , Disnea , ElectrocardiografíaRESUMEN
RATIONALE: Anaphylactic shock, a severe and rapid systemic allergic reaction, poses significant treatment challenges. Epinephrine, the first-line treatment, effectively reverses symptoms but can complicate the clinical picture by elevating lactate levels, blurring the distinction between shock-induced hypoperfusion and drug-induced metabolic effects. PATIENT CONCERNS: A 26-year-old female presented with anaphylactic shock following an antibiotic infusion, experiencing chest tightness, hypotension, and pulmonary edema, without significant past medical history apart from a noted allergy to fish and shrimp. DIAGNOSES: Anaphylaxis was diagnosed based on clinical presentation and supported by imaging that revealed pulmonary edema, despite normal troponin levels and electrocardiogram. INTERVENTIONS: Treatment included 0.5 mg of intramuscular epinephrine and 5 mg of intravenous dexamethasone, with subsequent intubation and mechanical ventilation in the intensive care unit. An intravenous epinephrine infusion was also administered for hemodynamic support. OUTCOMES: While epinephrine resolved the pulmonary edema and stabilized circulation, it led to a significant, albeit transient, increase in lactate levels, which normalized following discontinuation of epinephrine, indicating the metabolic effect of the drug rather than ongoing tissue hypoperfusion. LESSONS: This case illustrates the importance of recognizing epinephrine-induced lactate elevation in anaphylactic shock, necessitating a nuanced interpretation of lactate dynamics. Clinicians must differentiate between lactate elevations due to tissue hypoperfusion and those arising from epinephrine's pharmacologic effects to optimize patient care.
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Anafilaxia , Epinefrina , Ácido Láctico , Humanos , Anafilaxia/tratamiento farmacológico , Anafilaxia/sangre , Femenino , Adulto , Epinefrina/administración & dosificación , Ácido Láctico/sangre , Dexametasona/uso terapéutico , Dexametasona/administración & dosificación , Edema Pulmonar/inducido químicamente , Edema Pulmonar/tratamiento farmacológico , Antibacterianos/efectos adversos , Antibacterianos/administración & dosificaciónRESUMEN
The foramen ovale plays a vital role in sustaining life in-utero; however, a patent foramen ovale (PFO) after birth has been associated with pathologic sequelae in the systemic circulation including stroke/transient ischemic attack (TIA), migraine, high altitude pulmonary edema, decompression illness, platypnea-orthodeoxia syndrome (POS) and worsened severity of obstructive sleep apnea. Importantly, each of these conditions is most commonly observed among specific age groups: migraine in the 20 to 40s, stroke/TIA in the 30-50s and POS in patients >50 years of age. The common and central pathophysiologic mechanism in each of these conditions is PFO-mediated shunting of blood and its contents from the right to the left atrium. PFO-associated pathologies can therefore be divided into (1) paradoxical systemic embolization and (2) right to left shunting (RLS) of blood through the PFO. Missing in the extensive literature on these clinical syndromes are mechanistic explanations for the occurrence of RLS, including timing and the volume of blood shunted, the impact of age on RLS, and the specific anatomical pathway that blood takes from the venous system to the left atrium. Visualization of the flow pattern graphically illustrates the underlying RLS and provides a greater understanding of the critical flow dynamics that determine the frequency, volume, and pathway of flow. In the present review, we describe the important role of foramen ovale in in-utero physiology, flow visualization in patients with PFO, as well as contributing factors that work in concert with PFO to result in the diverse pathophysiological sequelae.
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Foramen Oval Permeable , Humanos , Foramen Oval Permeable/fisiopatología , Foramen Oval Permeable/complicaciones , Trastornos Migrañosos/fisiopatología , Trastornos Migrañosos/etiología , Ataque Isquémico Transitorio/fisiopatología , Ataque Isquémico Transitorio/etiología , Apnea Obstructiva del Sueño/fisiopatología , Apnea Obstructiva del Sueño/complicaciones , Accidente Cerebrovascular/etiología , Accidente Cerebrovascular/fisiopatología , Enfermedad de Descompresión/fisiopatología , Enfermedad de Descompresión/complicaciones , Edema Pulmonar/etiología , Edema Pulmonar/fisiopatología , Embolia Paradójica/fisiopatología , Embolia Paradójica/etiologíaRESUMEN
ABSTRACT: Venovenous (VV) ECMO is rarely used during decompensated circulatory states. Although VA ECMO is the routine option, VV ECMO may be an option in selected patients. We present a case of pulmonary edema due to acute heart failure in a patient 4- and 12-year post-lung transplantation who received VV ECMO. Using a thoughtful cannulation strategy, VV ECMO, and aggressive ultrafiltration, the patient was successfully decannulated, extubated, and discharged from the hospital. In cardiogenic pulmonary edema, VV ECMO represents an additional, and likely under-utilized tool, especially in patients who are at high risk for ventilator-associated lung injury. Cannula location and size should be given additional consideration to potentially transition to V-AV ECMO configuration if necessary.
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Oxigenación por Membrana Extracorpórea , Insuficiencia Cardíaca , Trasplante de Pulmón , Humanos , Oxigenación por Membrana Extracorpórea/métodos , Insuficiencia Cardíaca/cirugía , Insuficiencia Cardíaca/terapia , Insuficiencia Cardíaca/complicaciones , Masculino , Edema Pulmonar/etiología , Edema Pulmonar/terapia , Persona de Mediana Edad , Enfermedad Aguda , Enfermedad Crónica , Complicaciones Posoperatorias/terapia , Complicaciones Posoperatorias/etiologíaRESUMEN
Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e' ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema.
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Altitud , Contencion de la Respiración , Buceo , Ecocardiografía Doppler , Hipoxia , Pulmón , Humanos , Masculino , Buceo/fisiología , Buceo/efectos adversos , Adulto , Adulto Joven , Hipoxia/fisiopatología , Persona de Mediana Edad , Adolescente , Pulmón/fisiopatología , Pulmón/diagnóstico por imagen , Pulmón/irrigación sanguínea , Edema Pulmonar/etiología , Edema Pulmonar/fisiopatología , Edema Pulmonar/diagnóstico por imagen , Presión Arterial/fisiología , Saturación de Oxígeno/fisiología , Óxido Nítrico/metabolismo , Presión Sanguínea/fisiología , Hemoglobinas/análisisRESUMEN
Millions of people visit high-altitude regions annually and more than 80 million live permanently above 2,500 m. Acute high-altitude exposure can trigger high-altitude illnesses (HAIs), including acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE). Chronic mountain sickness (CMS) can affect high-altitude resident populations worldwide. The prevalence of acute HAIs varies according to acclimatization status, rate of ascent and individual susceptibility. AMS, characterized by headache, nausea, dizziness and fatigue, is usually benign and self-limiting, and has been linked to hypoxia-induced cerebral blood volume increases, inflammation and related trigeminovascular system activation. Disruption of the blood-brain barrier leads to HACE, characterized by altered mental status and ataxia, and increased pulmonary capillary pressure, and related stress failure induces HAPE, characterized by dyspnoea, cough and exercise intolerance. Both conditions are progressive and life-threatening, requiring immediate medical intervention. Treatment includes supplemental oxygen and descent with appropriate pharmacological therapy. Preventive measures include slow ascent, pre-acclimatization and, in some instances, medications. CMS is characterized by excessive erythrocytosis and related clinical symptoms. In severe CMS, temporary or permanent relocation to low altitude is recommended. Future research should focus on more objective diagnostic tools to enable prompt treatment, improved identification of individual susceptibilities and effective acclimatization and prevention options.
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Mal de Altura , Altitud , Humanos , Mal de Altura/fisiopatología , Mal de Altura/epidemiología , Mal de Altura/complicaciones , Aclimatación/fisiología , Edema Encefálico/fisiopatología , Edema Encefálico/etiología , Edema Encefálico/epidemiología , Edema Pulmonar/fisiopatología , Edema Pulmonar/etiología , Edema Pulmonar/epidemiología , Hipertensión Pulmonar/fisiopatología , Hipertensión Pulmonar/epidemiología , Hipertensión Pulmonar/etiología , Hipoxia/fisiopatología , Hipoxia/complicaciones , Hipoxia/etiologíaRESUMEN
INTRODUCTION: Intravenous loop diuretics have been a key component in treating pulmonary oedema since the 1960s and have a Class 1 recommendation in the 2021 guidelines for acute heart failure (AHF). While the diuretic effect of loop diuretics is well established, it remains unclear how furosemide influences pulmonary congestion and cardiac filling pressures in the hyperacute phase before significant diuresis occurs. METHODS: This was a prospective study of adult patients with AHF and objective signs of pulmonary congestion admitted to the cardiac ward. Remote dielectric sensing (ReDS) will directly measure lung fluid content, and cardiac filling pressures will be assessed by echocardiography with Doppler and strain analysis. CONCLUSIONS: This study will examine if furosemide leads to a hyperacute reduction in pulmonary congestion assessed by ReDS independent of diuretic effects in patients with AHF. We hypothesise that the haemodynamic effect of furosemide shown on pulmonary congestion may explain the subjective instant relief in patients with AHF receiving furosemide. FUNDING: Dr. Grand's salary during this project is supported by a research grant from the Danish Cardiovascular Academy funded by Novo Nordisk Foundation grant number NNF20SA0067242 and by the Danish Heart Foundation. TRIAL REGISTRATION: This protocol was approved by the Scientific Ethical Committee, H-23029822, and the Danish Data Protection Agency P-2013-14703. The protocol was registered with ClinicalTrial.org on 29 August 2023 (Identifier: NCT06024889).
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Furosemida , Insuficiencia Cardíaca , Edema Pulmonar , Furosemida/uso terapéutico , Furosemida/administración & dosificación , Humanos , Insuficiencia Cardíaca/tratamiento farmacológico , Insuficiencia Cardíaca/fisiopatología , Estudios Prospectivos , Edema Pulmonar/tratamiento farmacológico , Diuréticos/uso terapéutico , Enfermedad Aguda , Tecnología de Sensores Remotos/métodos , Femenino , Masculino , Inhibidores del Simportador de Cloruro Sódico y Cloruro Potásico/uso terapéuticoRESUMEN
INTRODUCTION: Pulmonary edema is a rare complication occurring after naloxone administration, but the causal relationship remains insufficiently investigated. We aimed to determine the likelihood of naloxone as the causative agent in published cases of pulmonary edema. METHODS: A literature search was conducted across multiple databases, utilizing database-specific search terms such as "pulmonary edema/chemically induced" and "naloxone/adverse effects." Each case report was evaluated using the Naranjo scale, a standardized causality assessment algorithm. RESULTS: We identified 49 published case reports of pulmonary edema following naloxone administration. The median total dose of naloxone was 0.2 mg for patients presenting following a surgical procedure and 4 mg for out-of-hospital opioid overdoses. Based on the Naranjo scale, the majority of cases were classified as "possible" (n = 38) or "probable" (n = 11) adverse reactions, while no "definite" cases of naloxone-induced pulmonary edema were identified. Many patients were classified as "possible" due to limited patient information or other potential risks, such as fluid administration or airway obstruction. Forty-six of 49 patients survived (94 percent). DISCUSSION: Pulmonary edema may occur after both low and high doses of naloxone; however, low doses were primarily reported in the surgical population. Despite this complication, the majority of patients survived. Furthermore, no case report in our analysis was classified as a "definite" case of naloxone-induced pulmonary edema which limits the establishment of causality. Future studies should explore patient risk factors, including surgical versus outpatient setting and opioid-naïve versus opioid-tolerant for developing pulmonary edema and employ a causality assessment algorithm. CONCLUSIONS: These case reports suggest pulmonary edema can occur following naloxone administration, irrespective of dose. According to the Naranjo scale, there were no definite cases of naloxone-induced pulmonary edema. Overall, we suggest the benefits of naloxone administration outweigh the risks. Naloxone should be administered to treat opioid overdoses while monitoring for the development of pulmonary edema.
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Naloxona , Antagonistas de Narcóticos , Edema Pulmonar , Naloxona/uso terapéutico , Naloxona/administración & dosificación , Edema Pulmonar/inducido químicamente , Humanos , Antagonistas de Narcóticos/uso terapéutico , Antagonistas de Narcóticos/administración & dosificación , Analgésicos Opioides/efectos adversos , Sobredosis de Opiáceos , Sobredosis de DrogaRESUMEN
PURPOSE: To determine the safety and efficacy associated with drainage volumes greater than 1,500 mL in a single, unilateral thoracentesis without pleural manometry measurements. MATERIALS AND METHODS: This retrospective, single-institution study included 872 patients (18 years and older) who underwent ultrasound-guided thoracentesis. Patient and procedures data were collected including demographics, number of and laterality of thoracenteses, volume and consistency of fluid removed, and whether clinical or radiologic evidence of re-expansion pulmonary edema (REPE) developed within 24 h of thoracentesis. Fisher's exact test was used to test the significance of the relationship between volume of fluid removed and evidence of REPE. RESULTS: A total of 1376 thoracenteses were performed among the patients included in the study. The mean volume of fluid removed among all procedures was 901.1 mL (SD = 641.7 mL), with 194 (14.1%) procedures involving the removal of ≥ 1,500 mL of fluid. In total, six (0.7%) patients developed signs of REPE following thoracentesis, five of which were a first-time thoracentesis. No statistically significant difference in incidence of REPE was observed between those with ≥ 1,500 mL of fluid removed compared to those with < 1,500 mL of fluid removed (p-value = 0.599). CONCLUSIONS: Large-volume thoracentesis may safely improve patients' symptoms while preventing the need for repeat procedures.
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Edema Pulmonar , Toracocentesis , Ultrasonografía Intervencional , Humanos , Toracocentesis/métodos , Estudios Retrospectivos , Edema Pulmonar/epidemiología , Edema Pulmonar/diagnóstico por imagen , Edema Pulmonar/etiología , Femenino , Masculino , Anciano , Persona de Mediana Edad , Incidencia , Anciano de 80 o más Años , Drenaje/métodos , Adulto , Derrame Pleural/epidemiología , Derrame Pleural/diagnóstico por imagenRESUMEN
High-altitude pulmonary edema (HAPE) is a deadly form of altitude sickness, and there is no effective treatment for HAPE. Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cell isolated from dental pulp tissues and possess various functions, such as anti-inflammatory and anti-oxidative stress. DPSCs have been used to treat a variety of diseases, but there are no studies on treating HAPE. In this study, Sprague-Dawley rats were exposed to acute low-pressure hypoxia to establish the HAPE model, and SOD1-modified DPSCs (DPSCsHiSOD1) were administered through the tail vein. Pulmonary arterial pressure, lung water content (LWC), total lung protein content of bronchoalveolar lavage fluid (BALF) and lung homogenates, oxidative stress, and inflammatory indicators were detected to evaluate the effects of DPSCsHiSOD1 on HAPE. Rat type II alveolar epithelial cells (RLE-6TN) were used to investigate the effects and mechanism of DPSCsHiSOD1 on hypoxia injury. We found that DPSCs could treat HAPE, and the effect was better than that of dexamethasone treatment. SOD1 modification could enhance the function of DPSCs in improving the structure of lung tissue, decreasing pulmonary arterial pressure and LWC, and reducing the total lung protein content of BALF and lung homogenates, through anti-oxidative stress and anti-inflammatory effects. Furthermore, we found that DPSCsHiSOD1 could protect RLE-6TN from hypoxic injury by reducing the accumulation of reactive oxygen species (ROS) and activating the Nrf2/HO-1 pathway. Our findings confirm that SOD1 modification could enhance the anti-oxidative stress ability of DPSCs through the Nrf2/HO-1 signalling pathway. DPSCs, especially DPSCsHiSOD1, could be a potential treatment for HAPE. Schematic diagram of the antioxidant stress mechanism of DPSCs in the treatment of high-altitude pulmonary edema. DPSCs can alleviate oxidative stress by releasing superoxide dismutase 1, thereby reducing ROS production and activating the Nrf2/HO-1 signalling pathway to ameliorate lung cell injury in HAPE.
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Mal de Altura , Pulpa Dental , Factor 2 Relacionado con NF-E2 , Estrés Oxidativo , Ratas Sprague-Dawley , Superóxido Dismutasa-1 , Animales , Pulpa Dental/citología , Pulpa Dental/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , Ratas , Superóxido Dismutasa-1/metabolismo , Superóxido Dismutasa-1/genética , Mal de Altura/terapia , Mal de Altura/metabolismo , Masculino , Células Madre/metabolismo , Modelos Animales de Enfermedad , Transducción de Señal , Edema Pulmonar/metabolismo , Edema Pulmonar/terapia , Hipertensión Pulmonar/terapia , Hipertensión Pulmonar/metabolismo , Humanos , Hemo Oxigenasa (Desciclizante)/metabolismo , Hemo-Oxigenasa 1/metabolismo , Hemo-Oxigenasa 1/genéticaRESUMEN
OBJECTIVE: While the association between metabolic dysfunction-associated steatotic liver disease (MASLD) and long-term cardiovascular risks has been studied, the impact of MASLD on cardiovascular events during delivery hospitalizations remains relatively unexplored. This study aims to examine the prevalence of cardiovascular diseases (CVDs) and cardiac arrhythmias in pregnant patients with MASLD and identify potential risk factors. METHODS: A retrospective analysis of hospital discharge records from the National Inpatient Sample database between 2009 and 2019 was conducted to assess maternal cardiovascular outcomes. Multivariable logistic regression models were employed, and adjusted odds ratios (AOR) were calculated to evaluate the association between MASLD and cardiovascular outcomes during pregnancy. RESULTS: The study sample included 17â 593 pregnancies with MASLD and 41â 171â 211 pregnancies without this condition. Women with MASLD exhibited an increased risk of congestive heart failure [AOR 3.45, 95% confidence interval (CI) 1.04-11.43], cardiac arrhythmia (AOR 2.60, 95% CI 1.94-3.49), and gestational hypertensive complications (AOR 3.30, 95% CI 2.93-3.72). Pregnancies with MASLD were also associated with a higher rate of pulmonary edema (AOR 3.30, 95% CI 1.60-6.81). CONCLUSION: MASLD is an independent risk factor for cardiovascular complications during delivery hospitalizations, emphasizing the necessity for prepregnancy screening and targeted prevention strategies to manage CVD risks in expectant patients with MASLD.
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Arritmias Cardíacas , Hospitalización , Enfermedad del Hígado Graso no Alcohólico , Complicaciones del Embarazo , Humanos , Embarazo , Femenino , Adulto , Estudios Retrospectivos , Enfermedad del Hígado Graso no Alcohólico/epidemiología , Enfermedad del Hígado Graso no Alcohólico/complicaciones , Hospitalización/estadística & datos numéricos , Factores de Riesgo , Complicaciones del Embarazo/epidemiología , Arritmias Cardíacas/epidemiología , Arritmias Cardíacas/etiología , Prevalencia , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/etiología , Parto Obstétrico/estadística & datos numéricos , Edema Pulmonar/epidemiología , Edema Pulmonar/etiología , Hipertensión Inducida en el Embarazo/epidemiología , Estados Unidos/epidemiología , Adulto Joven , Insuficiencia Cardíaca/epidemiología , Insuficiencia Cardíaca/etiología , Complicaciones Cardiovasculares del Embarazo/epidemiologíaRESUMEN
AIMS: Patients with structural heart disease (SHD) undergoing catheter ablation (CA) for ventricular tachycardia (VT) are at considerable risk of periprocedural complications, including acute haemodynamic decompensation (AHD). The PAINESD score was proposed to predict the risk of AHD. The goal of this study was to validate the PAINESD score using the retrospective analysis of data from a large-volume heart centre. METHODS AND RESULTS: Patients who had their first radiofrequency CA for SHD-related VT between August 2006 and December 2020 were included in the study. Procedures were mainly performed under conscious sedation. Substrate mapping/ablation was performed primarily during spontaneous rhythm or right ventricular pacing. A purposely established institutional registry for complications of invasive procedures was used to collect all periprocedural complications that were subsequently adjudicated using the source medical records. Acute haemodynamic decompensation triggered by CA procedure was defined as intraprocedural or early post-procedural (<12â h) development of acute pulmonary oedema or refractory hypotension requiring urgent intervention. The study cohort consisted of 1124 patients (age, 63 ± 13 years; males, 87%; ischaemic cardiomyopathy, 67%; electrical storm, 25%; New York Heart Association Class, 2.0 ± 1.0; left ventricular ejection fraction, 34 ± 12%; diabetes mellitus, 31%; chronic obstructive pulmonary disease, 12%). Their PAINESD score was 11.4 ± 6.6 (median, 12; interquartile range, 6-17). Acute haemodynamic decompensation complicated the CA procedure in 13/1124 = 1.2% patients and was not predicted by PAINESD score with AHD rates of 0.3, 1.8, and 1.1% in subgroups by previously published PAINESD terciles (<9, 9-14, and >14). However, the PAINESD score strongly predicted mortality during the follow-up. CONCLUSION: Primarily substrate-based CA of SHD-related VT performed under conscious sedation is associated with a substantially lower rate of AHD than previously reported. The PAINESD score did not predict these events. The application of the PAINESD score to the selection of patients for pre-emptive mechanical circulatory support should be reconsidered.
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Ablación por Catéter , Hemodinámica , Taquicardia Ventricular , Humanos , Taquicardia Ventricular/cirugía , Taquicardia Ventricular/fisiopatología , Taquicardia Ventricular/etiología , Taquicardia Ventricular/diagnóstico , Masculino , Femenino , Persona de Mediana Edad , Ablación por Catéter/efectos adversos , Estudios Retrospectivos , Cicatriz/fisiopatología , Anciano , Hipotensión/etiología , Hipotensión/fisiopatología , Hipotensión/diagnóstico , Edema Pulmonar/etiología , Edema Pulmonar/diagnóstico , Edema Pulmonar/fisiopatología , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/diagnóstico , Factores de RiesgoRESUMEN
BACKGROUND: A syndrome of acute non-cardiogenic pulmonary edema associated with hunting is prevalent in the drever breed, but etiology of this syndrome is currently unknown. Alveolar surfactant has a critical role in preventing alveolar collapse and edema formation. The aim of this study was to investigate, whether the predisposition to hunting associated pulmonary edema in drever dogs is associated with impaired biophysical properties of alveolar surfactant. Seven privately owned drever dogs with recurrent hunting associated pulmonary edema and seven healthy control dogs of other breeds were included in the study. All affected dogs underwent thorough clinical examinations including echocardiography, laryngeal evaluation, bronchoscopy, and bronchoalveolar lavage (BAL) as well as head, neck and thoracic computed tomography imaging to rule out other cardiorespiratory diseases potentially causing the clinical signs. Alveolar surfactant was isolated from frozen, cell-free supernatants of BAL fluid and biophysical analysis of the samples was completed using a constrained sessile drop surfactometer. Statistical comparisons over consecutive compression expansion cycles were performed using repeated measures ANOVA and comparisons of single values between groups were analyzed using T-test. RESULTS: There were no significant differences between groups in any of the biophysical outcomes of surfactant analysis. The critical function of surfactant, reducing the surface tension to low values upon compression, was similar between healthy dogs and affected drevers. CONCLUSIONS: The etiology of hunting associated pulmonary edema in drever dogs is not due to an underlying surfactant dysfunction.
Asunto(s)
Enfermedades de los Perros , Edema Pulmonar , Surfactantes Pulmonares , Animales , Perros , Edema Pulmonar/veterinaria , Edema Pulmonar/etiología , Masculino , Femenino , Líquido del Lavado Bronquioalveolar/química , Estudios de Casos y ControlesRESUMEN
El síndrome de dificultad respiratoria aguda (SDRA), inicialmente descrito en 1967, se caracteriza por insuficiencia respiratoria aguda con hipoxemia profunda, disminución de la distensibilidad pulmonar e infiltrados bilaterales en la Rx de tórax. En 2012 la definición de Berlín estableció tres categorías con base en la hipoxemia (SDRA leve, moderado y grave), precisando aspectos temporales y permitiendo el diagnóstico con ventilación no invasiva. La pandemia de COVID-19 llevó a reconsiderar la definición, enfocándose en el monitoreo continuo de la oxigenación y la oxigenoterapia de alto flujo. En 2021 se propuso una nueva definición global de SDRA, basada en la definición de Berlín, pero incluyendo una categoría para pacientes no intubados, permitiendo el uso de saturación periférica de oxígeno medida con oximetría de pulso/fracción inspirada de oxígeno (SpO2/FiO2) y la ecografía pulmonar para el diagnóstico, y sin ningún requerimiento de soporte especial de la oxigenación en regiones con recursos limitados. Aunque persisten debates, la evolución continua busca adaptarse a las necesidades clínicas y epidemiológicas, y personalizar tratamientos. (AU)
Acute respiratory distress syndrome (ARDS), first described in 1967, is characterized by acute respiratory failure causing profound hypoxemia, decreased pulmonary compliance, and bilateral CXR infiltrates. After several descriptions, the Berlin definition was adopted in 2012, which established three categories of severity according to hypoxemia (mild, moderate and severe), specified temporal aspects for diagnosis, and incorporated the use of non-invasive ventilation. The COVID-19 pandemic led to changes in ARDS management, focusing on continuous monitoring of oxygenation and on utilization of high-flow oxygen therapy and lung ultrasound. In 2021, a New Global Definition based on the Berlin definition of ARDS was proposed, which included a category for non-intubated patients, considered the use of SpO2, and established no particular requirement for oxygenation support in regions with limited resources. Although debates persist, the continuous evolution seeks to adapt to clinical and epidemiological needs, and to the search of personalized treatments. (AU)