Acute Coronary Syndrome at Altitude: Diagnostic Dilemma on Aconcagua Using Point-of-Care Ultrasound.

At the Plaza de Mulas medical tent, located at 4300 m (14,100 ft) along the Normal Route to the 6960 m (22,837 ft) summit of Aconcagua in Argentina, a Korean male in his 50s with no known medical conditions presented with lightheadedness and shortness of breath. He had taken sildenafil and acetazolamide that morning without improvement. Vital signs on arrival were notable for oxygen saturations in the high 60s with basilar crackles on lung auscultation, concerning for high altitude pulmonary edema. The patient was started on oxygen via nasal cannula and given dexamethasone. History was limited secondary to language barriers, but on review of systems the patient noted mild chest pressure. Bedside cardiac echocardiogram was performed, which revealed a septal wall motion abnormality. The patient was therefore given aspirin and clopidogrel and was flown to a lower trailhead, where he was met by local Emergency Medical Services. A 12-lead electrocardiogram revealed an anterior ST-elevation myocardial infarction, and the patient was taken emergently to the catheterization lab in Mendoza and underwent stent placement with a full recovery.

Successful management of pulmonary edema secondary to accidental electrocution in a young dog.

BACKGROUND: Human records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes. CASE PRESENTATION: A 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide ≤ 40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H2O) and positive end-expiratory pressure (3 to 10 cm H2O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation ≥ 96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits. CONCLUSIONS: We present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine.

Caracterización de los pacientes con edema agudo del pulmón en el servicio de urgencias / Characterization of patients in the emergency services with acute pulmonary edema

Introducción: El edema agudo del pulmón es una enfermedad frecuente en los pacientes que se presentan en los servicios de urgencias. Objetivo: Caracterizar a los pacientes con edema agudo del pulmón en el servicio de urgencias. Método: Se realizó un estudio descriptivo y transversal en 37 pacientes con edema agudo del pulmón, que asistieron al cuerpo de guardia del Hospital Clinicoquirúrgico Docente Dr. Joaquín Castillo Duany de Santiago de Cuba, desde enero a noviembre de 2019. Las variables estudiadas fueron edad, sexo, estado al egreso y uso de la ventilación no invasiva. Resultados: No hubo diferencias entre ambos sexos, predominaron los mayores de 60 años, que padecían de hipertensión arterial. Se comprobó el poco uso de la ventilación no invasiva o invasiva. Conclusiones: El edema agudo del pulmón es más frecuente en pacientes mayores de 60 años, sin distinción de sexo. La mayoría lo presenta relacionado con la hipertensión arterial y existe un escaso uso de la ventilación no invasiva en estos casos.

Introduction: Acute pulmonary edema is a frequent disease among patients in emergency services. Objective: To characterize patients with acute pulmonary edema who attended the emergency services. Methods: A descriptive and cross-sectional study of 37 patients with acute pulmonary edema who attended the emergency services of Dr. Joaquín Castillo Duany Teaching Clinical Surgical Hospital in Santiago de Cuba was carried out, from January to November 2019. The studied variables were age, sex, alive or dead when discharged, noninvasive ventilation usage. Results: There were no differences between the sexes; there was a prevalence of patients older than 60 years of age, who suffered from hypertension. It was demonstrated low noninvasive or invasive ventilation usage. Conclusions: Acute pulmonary edema is more frequent among patients older than 60 years of age in both sexes. Most of the patients suffered from hypertension and there was a deficit in the implementation of noninvasive ventilation in these cases.

[Circulatory support with venovenous ECMO in a patient with reperfusion pulmonary edema after pulmonary artery thromboendarterectomy]. / Soporte circulatorio con ECMO venovenoso en paciente con síndrome de reperfusión pulmonar secundario a tromboendarterectomía arterial pulmonar.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a subtype of pulmonary hypertension characterized by the obstruction of pulmonary arteries secondary to chronic thromboembolism. Pulmonary thromboendarterectomy surgery (PTE) is the main treatment for patients with CTEPH, as it removes the chronic thrombi from the pulmonary arteries. Pulmonary reperfusion syndrome is a common complication of the surgery, which involves the development of pulmonary edema in the area where blood perfusion improves after the surgery. The incidence of this syndrome varies from 8 to 91% depending on the criteria used for diagnosis, and it is one of the most serious complications of pulmonary thromboendarterectomy. In such cases, circulatory support with extracorporeal membrane oxygenation (ECMO) has become a valuable therapeutic modality. We present the case of a 60-year-old woman with a history of acute pulmonary embolism due to deep vein thrombosis of the right pelvic limb who was diagnosed later with CTEPH who was admitted for scheduled surgical treatment involving bilateral PTE. However, during the immediate postoperative period, she developed cardiogenic shock and refractory hypoxemia secondary to pulmonary reperfusion syndrome following the surgical procedure. As a result, she required veno-venous ECMO circulatory support for 6 days, leading to resolution of the pulmonary condition and clinical improvement.

La hipertensión pulmonar tromboembólica crónica (HPTEC) es un subtipo de hipertensión pulmonar caracterizada por la obstrucción de las arterias pulmonares secundaria a tromboembolias crónicas. La cirugía de tromboendarterectomía pulmonar (TEAP) es el tratamiento principal para los pacientes con HPTEC, elimina los trombos crónicos de las arterias pulmonares. El síndrome de reperfusión pulmonar es una complicación común de la cirugía, se trata del desarrollo de edema pulmonar en el área en la que la perfusión sanguínea mejora después de la cirugía. La incidencia del síndrome varía del 8 al 91% según los criterios utilizados para diagnosticarlo y es una de las complicaciones más graves de la tromboendarterectomía pulmonar. En tales casos, el soporte circulatorio con oxigenación por membrana extracorpórea (ECMO) se ha convertido en una valiosa modalidad terapéutica. Presentamos el caso de una paciente de 60 años de edad con antecedente de tromboembolia pulmonar aguda secundaria a trombosis venosa profunda de miembro pélvico derecho a quien durante el seguimiento se realizó el diagnóstico de HPTEC e ingresó de manera programada para tratamiento quirúrgico con realización de TEAP bilateral, sin embargo durante el posquirúrgico inmediato presentó choque cardiogénico e hipoxemia refractaria secundarios a síndrome de reperfusión pulmonar, por lo cual requirió soporte circulatorio con ECMO venovenosa durante seis días, con resolución del cuadro pulmonar y mejoría clínica.

Edema pulmonar por reexpansión. Reporte de Caso / Pulmonary edema due to re-expansion. Case Report

Introducción. El edema pulmonar por reexpansión es una complicación poco frecuente, secundaria a una rápida reexpansión pulmonar posterior al drenaje por toracentesis o toracostomía cerrada. Al día de hoy, se ha descrito una incidencia menor al 1 % tras toracostomía cerrada, con mayor prevalencia en la segunda y tercera década de la vida. Su mecanismo fisiopatológico exacto es desconocido; se ha planteado un proceso multifactorial de daño intersticial pulmonar asociado con un desequilibrio de las fuerzas hidrostáticas. Caso clínico. Presentamos el caso de un paciente que desarrolló edema pulmonar por reexpansión posterior a toracostomía cerrada. Se hizo una revisión de la literatura sobre esta complicación. Resultados. Aunque la clínica sugiere el diagnóstico, la secuencia de imágenes desempeña un papel fundamental. En la mayoría de los casos suele ser autolimitado, por lo que su manejo es principalmente de soporte; sin embargo, se han reportado tasas de mortalidad que alcanzan hasta el 20 %, por tanto, es importante conocer los factores de riesgo y las medidas preventivas. Conclusión. El edema pulmonar de reexpansión posterior a toracostomía es una complicación rara en los casos con neumotórax, aunque es una complicación que se puede presentar en la práctica diaria, por lo cual debe tenerse en mente para poder hacer el diagnóstico y un manejo adecuado.

Introduction. Re-expansion pulmonary edema is a rare complication secondary to rapid pulmonary re-expansion after drainage by thoracentesis and/or closed thoracostomy. As of today, an incidence of less than 1% has been described after closed thoracostomy, with a higher prevalence in the second and third decades of life. Its exact pathophysiological mechanism is unknown; a multifactorial process of lung interstitial damage associated with an imbalance of hydrostatic forces has been proposed. Clinical case. We present the case of a patient who developed pulmonary edema due to re-expansion after closed thoracostomy, conducting a review of the literature on this complication. Results. Although the clinic suggests the diagnosis, the sequence of images plays a fundamental role. In most cases, it tends to be a self-limited disease, so its management is mainly supportive. However, mortality rates of up to 20% have been recorded. Therefore, it is important to identify patients with major risk factors and initiate preventive measures in these patients. Conclusions. Re-expansion pulmonary edema after thoracostomy is a rare complication in cases with pneumothorax; however, it is a complication that can occur in daily practice. Therefore, it must be kept in mind to be able to make the diagnosis and an adequate management.

Pulmonary involvement from animal toxins: the cellular mechanisms.

Venomous animals and their venom have always been of human interest because, despite species differences, coevolution has made them capable of targeting key physiological components of our bodies. Respiratory failure from lung injury is one of the serious consequences of envenomation, and the underlying mechanisms are rarely discussed. This review aims to demonstrate how toxins affect the pulmonary system through various biological pathways. Herein, we propose the common underlying cellular mechanisms of toxin-induced lung injury: interference with normal cell function and integrity, disruption of normal vascular function, and provocation of excessive inflammation. Viperid snakebites are the leading cause of envenomation-induced lung injury, followed by other terrestrial venomous animals such as scorpions, spiders, and centipedes. Marine species, particularly jellyfish, can also inflict such injury. Common pulmonary manifestations include pulmonary edema, pulmonary hemorrhage, and exudative infiltration. Severe envenomation can result in acute respiratory distress syndrome. Pulmonary involvement suggests severe envenomation, thus recognizing these mechanisms and manifestations can aid physicians in providing appropriate treatment.

High altitude pulmonary edema at 2640 m altitude associated with an acute Rhinovirus infection. First case in the literature.

High altitude pulmonary edema (HAPE) is a multifactorial condition that may occur after ascent of high altitudes, especially in genetic predisposed individuals. Diagnosis is challenging and could lead to potentially lethal complications such as acute respiratory distress syndrome (ARDS). We present one of the few reported cases of HAPE below 3000 m of altitude, and the first to our knowledge to present with a concomitant acute Rhinovirus infection, precipitating and complicating the diagnosis and clinical course. Clinical manifestations, treatment, and outcomes are shown below.

High altitude pulmonary edema in children: A systematic review.

INTRODUCTION: High altitude pulmonary edema (HAPE) is a form of acute noncardiogenic pulmonary edema caused by altitude-related hypoxia seen in children as well as in adults. In this systematic review we focus in HAPE occurring in children and adolescents. METHODS: A systematic review was conducted including publications in children 0-18 years of age from three databases up to June 2022. RESULTS: Thirty-five studies representing 210 cases were found. The mean age was 9.8 ± 3.6 years with a male/female ratio of 2.6. The peak age incidence was seen in children between 6 and 10 years old. Only two children (0.9%) were ≤2 years old. The mean altitude in 166 cases was 2861 masl. Only 17 cases (8.1%) occurred at altitudes below 2500 masl. Regarding the different HAPE subtypes there was a predominance of re-entry HAPE (R-HAPE) with 58%, followed by classic HAPE (C-HAPE) with 37.6%. The mean time between arrival and onset of symptoms was 16.5 h. The mortality rate was 1.4%. In 10/28 (36%) of C-HAPE cases there was a structural cardiac/pulmonary anomaly compared to 1/19 (5%) in R-HAPE (p < 0.01). HAPE recurrence was found in 46 cases (21.9%). The involvement in the chest X-rays was seen predominantly in the apices and in the right lung. CONCLUSIONS: R-HAPE was the most common HAPE subtype; HAPE peak age was found between 6 and 10 years of age; HAPE was more frequent in males and was rare in children under 2 years old; associated HAPE structural abnormalities were more common in C-HAPE than in R-HAPE.

Fisiología respiratoria. Neumología de altura: saturación de oxígeno, edema pulmonar y pruebas de función pulmonar / Respiratory physiology - High -altitude pneumology: oxygen saturation, pulmonary edema and pulmonary function tests

En las alturas, sobre todo a 2500 metros sobre el nivel del mar, la cantidad absoluta de oxígeno va decreciendo y por lo tanto la cantidad disponible para el intercambio gaseoso disminuye, produciéndose una vasoconstricción hipóxica pulmonar (VHP). La VHP asociada a la hipoxia hipobárica de la altura produce un aumento de la presión pulmonar que es mayor en los lactantes y a mayores alturas. No hay valores únicos de saturación de oxígeno (SatO2) en la altura, porque ésta va disminuyendo según el mayor nivel de altura, aumenta con la edad, y la brecha entre la vigilia y sueño es grande (sobre todo en los primeros meses de vida). El 25% de los niños sanos que viven en altura tienen valores de SatO2 significativamente menores que el 75% restante. Los valores normales de los índices de apnea/hipopnea son distintos a los de nivel del mar. El edema pulmonar de las alturas es una patología frecuente, que se produce por un incremento desproporcionado en la VHP reflejando una hiperactividad del lecho vascular pulmonar ante la exposición aguda a la hipoxia hipobárica. Tiene cuatro fenotipos, es infrecuente en menores de 5 años y rara vez es mortal, la sospecha clínica y el manejo oportuno con oxigeno es la clave. Finalmente, en la altura los valores normales de la función pulmonar de la espirometría, oscilometría de impulso y capacidad de difusión son distintos que a nivel del mar.

At high altitude, especially > 2,500 meters above sea level, the absolute amount of oxygen decreases and therefore the amount available for gas exchange decreases, producing hypoxic pulmonary vasoconstriction (VHP). VHP associated with high-altitude hypobaric hypoxia produces an increase in pulmonary pressure that is greater in infants and at higher altitudes. There are no single values of oxygen saturation (SatO2) at altitude, because it decreases with the highest level of altitude, increases with age, and the gap between wakefulness and sleep is large (especially in the first months of life). Around 25% of healthy children living at altitude have SatO2 values significantly lower than the remaining 75%. The normal values of the apnea/hypopnea indices are different from those at sea level. High altitude pulmonary edema is a frequent pathology that is produced by a disproportionate increase in VHP reflecting hyperactivity of the pulmonary vascular bed in the face of acute exposure to hypobaric hypoxia, it has four phenotypes, it is uncommon in children under 5 years of age, and it is rarely fatal, the clinical suspicion and timely management with oxygen is the key. Finally, at high altitude, the normal values of lung function from spirometry, impulse oscillometry, and diffusing capacity are different from those at sea level.

Pulmonary involvement from animal toxins: the cellular mechanisms

Venomous animals and their venom have always been of human interest because, despite species differences, coevolution has made them capable of targeting key physiological components of our bodies. Respiratory failure from lung injury is one of the serious consequences of envenomation, and the underlying mechanisms are rarely discussed. This review aims to demonstrate how toxins affect the pulmonary system through various biological pathways. Herein, we propose the common underlying cellular mechanisms of toxin-induced lung injury: interference with normal cell function and integrity, disruption of normal vascular function, and provocation of excessive inflammation. Viperid snakebites are the leading cause of envenomation-induced lung injury, followed by other terrestrial venomous animals such as scorpions, spiders, and centipedes. Marine species, particularly jellyfish, can also inflict such injury. Common pulmonary manifestations include pulmonary edema, pulmonary hemorrhage, and exudative infiltration. Severe envenomation can result in acute respiratory distress syndrome. Pulmonary involvement suggests severe envenomation, thus recognizing these mechanisms and manifestations can aid physicians in providing appropriate treatment.(AU)

Clinical cases of infectious endocarditis in cats.

Infectious endocarditis (IE) is a contagious polyposis ulcerative inflammation of the endocardium, accompanied by lesions of the heart valve apparatus and endothelium by various pathogenic and opportunistic pathogens. Mainly mitral and aortic valves are affected, less often - tricuspid valve. The purpose of this study was to report two cases of IE in cats. Due to the low prevalence of the disease in cats, there is no clear diagnostic algorithm, so the diagnostic search is complicated. In both cases, autonomic lesions of the heart valve apparatus were observed. In the first clinical case, we could hardly diagnose the disease because of its rapid progression: initial echocardiogram result was normal, but after 48 hours, the cat's condition became much worse, and 18 hours later, it died. In the second case, histopathological examination confirmed an infectious inflammatory process of the endocardium and myocardium of unclear genesis. However, the presence of lower respiratory tract infection and the absence of additional laboratory tests, such as bacterial blood culture and PCR diagnosis, limited us in proposing a hypothesis about the origin and etiology of IE.

A endocardite infecciosa (EI) é uma polipose contagiosa inflamação ulcerativa do endocárdio, acompanhada de lesões do aparelho valvar cardíaco e do endotélio por diversos agentes patogênicos e oportunistas. Principalmente as válvulas mitral e aórtica são afetadas, com menos frequência a válvula tricúspide. O objetivo deste estudo foi relatar dois casos de EI em gatos. Devido à baixa prevalência da doença em gatos, não existe um algoritmo diagnóstico claro, por isso a busca diagnóstica é complicada. Em ambos os casos foram observadas lesões autonômicas do aparelho valvar cardíaco. No primeiro caso clínico, dificilmente conseguimos diagnosticar a doença devido à sua rápida progressão: o resultado inicial do ecocardiograma foi normal, mas após 48 horas o estado do gato piorou muito e, 18 horas depois, veio a óbito. No segundo caso, o exame histopatológico confirmou processo inflamatório infeccioso do endocárdio e miocárdio de gênese incerta. No entanto, a presença de infecção do trato respiratório inferior e a ausência de exames complementares de laboratório, como hemocultura bacteriana e diagnóstico por PCR, nos limitaram a propor uma hipótese sobre a origem e etiologia da EI.

Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure.

Exposure to high altitudes generates a decrease in the partial pressure of oxygen, triggering a hypobaric hypoxic condition. This condition produces pathophysiologic alterations in an organism. In the lung, one of the principal responses to hypoxia is the development of hypoxic pulmonary vasoconstriction (HPV), which improves gas exchange. However, when HPV is exacerbated, it induces high-altitude pulmonary hypertension (HAPH). Another important illness in hypobaric hypoxia is high-altitude pulmonary edema (HAPE), which occurs under acute exposure. Several studies have shown that inflammatory processes are activated in high-altitude illnesses, highlighting the importance of the crosstalk between hypoxia and inflammation. The aim of this review is to determine the inflammatory pathways involved in hypobaric hypoxia, to investigate the key role of inflammation in lung pathologies, such as HAPH and HAPE, and to summarize different anti-inflammatory treatment approaches for these high-altitude illnesses. In conclusion, both HAPE and HAPH show an increase in inflammatory cell infiltration (macrophages and neutrophils), cytokine levels (IL-6, TNF-α and IL-1ß), chemokine levels (MCP-1), and cell adhesion molecule levels (ICAM-1 and VCAM-1), and anti-inflammatory treatments (decreasing all inflammatory components mentioned above) seem to be promising mitigation strategies for treating lung pathologies associated with high-altitude exposure.

Impact of Moderate Altitude on Lung Diseases and Risk of High Altitude Illnesses

ABSTRACT A large world population resides at moderate altitudes. In the Valley of Mexico (2240 m above sea level) and for patients with respiratory diseases implies more hypoxemia and clinical deterioration, unless supplementary oxygen is prescribed or patients move to sea level. A group of individuals residing at 2500 or more meters above sea level may develop acute or chronic mountain disease but those conditions may develop at moderate altitudes although less frequently and in predisposed individuals. In the valley of México, at 2200 m above sea level, re-entry pulmonary edema has been reported. The frequency of other altitude-related diseases at moderate altitude, described in skiing resorts, remains to be known in visitors to Mexico City and other cities at similar or higher altitudes. Residents of moderate altitudes inhale deeply the city's air with all pollutants and require more often supplementary oxygen.

Impact of moderate altitude on lung diseases and risk of high altitude illnesses.

A large world population resides at moderate altitudes. In the Valley of Mexico (2240 m above sea level) and for patients with respiratory diseases implies more hypoxemia and clinical deterioration, unless supplementary oxygen is prescribed or patients move to sea level. A group of individuals residing at 2500 or more meters above sea level may develop acute or chronic mountain disease but those conditions may develop at moderate altitudes although less frequently and in predisposed individuals. In the valley of México, at 2200 m above sea level, re-entry pulmonary edema has been reported. The frequency of other altituderelated diseases at moderate altitude, described in skiing resorts, remains to be known in visitors to Mexico City and other cities at similar or higher altitudes. Residents of moderate altitudes inhale deeply the city's air with all pollutants and require more often supplementary oxygen.

Edema agudo de pulmón asociado al mal de altitud agudo en Huaraz: estudio transversal analítico / Acute high-altitude pulmonary edema in Huaraz: an analytical cross-sectional study

RESUMEN Objetivo: Describir algunas características epidemiológicas y clínicas del edema agudo de pulmón por mal de altitud (EAP) observadas en un hospital de Áncash (3052 m s. n. m.). Materiales y métodos: Estudio observacional descriptivo de 57 pacientes, quienes se presentaron en el Servicio de Emergencia del Hospital Víctor Ramos Guardia Huaraz entre enero de 1997 y enero del 2020. Todos cumplieron con los criterios diagnósticos de Lake Louise y una radiografía del tórax. La información se analizó mediante los usos de mediana y rango. Resultados: El 91,20 % de casos fueron del sexo masculino; 38,61% hicieron EAP de ascenso; 61,40 %, EAP de reascenso. El 21,10 % tuvo antecedente de EAP; 19,33 % desarrolló infección respiratoria previa; 10,53 %, un proceso patológico concomitante; 40,42 % hizo EAP durante el primer trimestre del año, y 45 % estuvo 10 días o menos a baja altitud. La presentación clínica incluyó disnea de reposo, crepitantes pulmonares, taquipnea, taquicardia y radiografía del tórax anormal en 100 % de los casos; tos productiva (96,52 %), dolor torácico (92,95 %), cefalea (56,11 %), cianosis (68,41 %), esputo rosado (42,13 %), fiebre (21,13 %) y leucocitosis (60,82 %). La mediana para la edad fue 20 años, frecuencia respiratoria 36/min, frecuencia cardiaca 124/min, PAS 100 mmHg, PAD 60 mmHg, temperatura 37,2 ºC, Hb 17,3 g/dl, Hto 53 %, recuento de leucocitos 12,500/mm3, resolución radiográfica del edema a las 48 horas. No hubo fallecidos. Conclusiones: Los factores que influyen en el EAP y sus determinantes son altura alcanzada, velocidad de ascenso, factores genéticos y antecedentes de EAP.

ABSTRACT Objective: To describe some epidemiological and clinical characteristics of acute high-altitude pulmonary edema (HAPE) observed in a hospital of the highlands of Ancash, located at 3,052 m a.s.l. Materials and methods: A descriptive observational study conducted with 57 patients who attended the emergency service of Hospital Víctor Ramos Guardia - Huaraz between January 1997 and January 2020. All patients fulfilled Lake Louise Criteria and had a chest X-ray. Median and range were used to analyze the information. Results: Male sex accounted for 91.20 %, ascent HAPE 38.61 % and re-ascent HAPE 61.40 %. Out of all patients, 21.10 % had a history of HAPE, 19.33 % developed a previous respiratory infection, 10.53 % had a concomitant disease, 40.42 % had HAPE during the first quarter of the year and 45 % had been 10 days or less at low altitude. Patients' clinical presentation included dyspnea at rest, pulmonary crackles, tachypnea, tachycardia and abnormal X-ray in 100 %; productive cough in 96.52 %; chest pain in 92.95 %; headache in 56.11 %; cyanosis in 68.41 %; pink sputum in 42.13 %; fever in 21.13 % and leukocytosis in 60.82 %. The median age was 20 years, respiratory rate 36/min, heart rate 124/min, SBP 100 mmHg, DBP 60 mmHg, temperature 37.2 °C, HGB 17.3 g/dl, HCT 53 %, WBC 12,500/mm3, radiographic resolution of the edema in 48 hours. There were no deaths. Conclusions: The factors that influence HAPE and its determinants are altitude, rate of ascent, genetic factors and history of HAPE.

Sudden death of an egg donor during oocyte retrieval due to ovarian hyperstimulation syndrome.

Ovarian Hyperstimulation Syndrome (OHSS) is uncommon among oocyte donors during in vitro fertilization (IVF) procedure and is rarely associated with death. We report a case of a 23-year-old oocyte donor who suddenly died on the operation table during oocyte retrieval. She had no risk factors in her menstrual history, laboratory, or clinical parameters. The antagonist cycle, triggered with the GnRH agonist protocol, was carried out. The cause of death at autopsy was attributed to respiratory failure due to acute massive pulmonary edema, which developed due to the complication of OHSS. Only a few autopsy cases associated with OHSS have been published, but, as far as we know, no clinical or autopsy cases of sudden death caused by OHSS have been reported.

High Altitude Pulmonary Edema in a Chronic Kidney Disease Patient-Is Peritoneal Dialysis A Risk Factor?

Vizcarra-Vizcarra, Cristhian A. and Angélica L. Alcos-Mamani. High-altitude pulmonary edema in a chronic kidney disease patient-Is peritoneal dialysis a risk factor? High Alt Med Biol. 23:96-99, 2022.-High-altitude pulmonary edema is a cause of acute respiratory failure secondary to hypobaric hypoxia, which occurs after ascent above 2,500 m (8,202 feet), in susceptible people or without prior acclimatization. We present the case of a 20-year-old man with chronic kidney disease (CKD) on peritoneal dialysis (PD), living at sea (Mollendo, Peru) who presented with dyspnea and pulmonary congestion, after ascending to a high-altitude city (Juliaca, Peru at 3,827 m or 12,555 feet). The patient required diuretics, nifedipine, PD, tracheal intubation, and mechanical ventilation, but recovered and was discharged without complications. We think that CKD and PD could be risk factors for the development of high-altitude pulmonary edema, secondary to pulmonary hypertension and fluid overload, so this diagnosis should be considered in this group of patients when they ascend to high altitude.

Lesión Pulmonar Aguda Relacionada a Transfusión (TRALI) y dos diagnósticos diferenciales para tener en cuenta: Reporte de caso y revisión de la literatura / Transfusion-Related Acute Lung Injury (TRALI) and Two Differential Diagnoses to Consider: Case Report and Literature Review

Resumen Las complicaciones pulmonares asociadas a la transfusión de hemoderivados son reacciones adversas graves y potencialmente mor tales. La Lesión Pulmonar Aguda Relacionada a Transfusión (TRALI), es una de las más frecuentes y con mayor mortalidad asociada. Es una entidad infradiagnosticada debido a su sintomatología inespecífica, a la ausencia de biomarcadores séricos específicos para su diagnóstico y a que aún la evidencia acerca de sus causas es heterogénea. El objetivo del presente artículo es documentar un caso clínico de TRALI y posteriormente, basados en la literatura actual, consolidar los aspectos fundamentales para la identificación oportuna de esta entidad y de dos diagnósticos diferenciales en el contexto de transfusión de hemoderivados y trauma: la Sobrecarga Circulatoria Asociada a Transfusión (TACO) y el Embolismo graso (EG). Así pues, se expone el caso clínico de una paciente adulto joven quien en el contexto de un politraumatismo requiere transfusión de hemoderivados, desarrollo de cuadro clínico compatible con TRALI; de esta manera, la discusión incluye aspectos epidemiológicos, fisiopatología, hallazgos imagenológicos y diagnóstico. Se logra concluir que es preciso poner a disposición de los profesionales del área de la salud literatura científica que favorezca la identificación de estas patologías con base en criterios clínicos, paraclínicos e imagenológicos, para así mismo, disminuir el riesgo de presentación y la mortalidad asociada.

Abstract Pulmonary complications associated with the transfusion of blood products are severe, potentially mortal adverse reactions. The transfusion-related acute lung injury (TRALI) is one of the most common and with higher associated mortality. It is an underdiagnosed entity due to its unspecified symptoms, the absence of diagnosis-specific serum biomarkers and the fact that the evidence about its causes is still heterogeneous. The objective of this article is to document a clinical case of TRALI and then, basing on the current literature, consolidate key aspects for the timely identification of this disease and of two differential diagnoses within the context of transfusion of blood products and trauma: the transfusion-associated circulatory overload (TACO) and fat embolism (FE). So, we pres ent the clinical case of a female young adult patient requiring a transfusion of blood products due to a polytraumatism whose clinical condition is compatible with TRALI; thus, the discussion includes epidemiological aspects, physiopathology, imaging findings and diagnosis. We conclude that it is necessary to provide healthcare professionals with scientific literature that favors the identification of these diseases basing on clinical, paraclinical and imaging criteria so as to reduce the risk of presentation and associated mortality.

Brain-lung interaction: a vicious cycle in traumatic brain injury.

The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the "blast injury" theory or "double hit" model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.

Asociación entre el tiempo de inicio de la ventilación no invasiva y la mortalidad en el edema pulmonar cardiogénico / Relationship between timing of initiation of non-invasive ventilation and mortality in cardiogenic pulmonary edema

Resumen Introducción: La ventilación no invasiva reduce la necesidad de intubación y la estancia en la unidad de cuidados intensivos en los pacientes con edema pulmonar cardiogénico. Objetivo: Evaluar la posible asociación entre el inicio de la ventilación no invasiva desde el ingreso a urgencias con la mortalidad y el requerimiento de intubación en pacientes con edema pulmonar cardiogénico. Método: Estudio analítico de cohorte retrospectiva, en el que se revisaron las historias clínicas de pacientes mayores de 18 años hospitalizados en una institución de Medellín, Colombia. Resultados: 70 pacientes cumplieron los criterios de inclusión y se compararon según el estado vital al alta. Sobrevivientes (49): la edad promedio fue de 63 años, el 34.7% fueron mujeres, el 57.1% tuvieron historia de neumopatía crónica y el 89% eran hipertensos; el promedio para recibir la intervención fue de 10 horas y el 20% requirieron intubación orotraqueal. No sobrevivientes (21): la edad promedio fue de 74 años, el 57.1% fueron mujeres, el 57.1% tuvieron historia de neumopatía crónica y el 90% eran hipertensos; el promedio para recibir la intervención fue de 7 horas y el 62% requirieron intubación. Tiempo de inicio en relación con la mortalidad en el análisis multivariado: odds ratio (OR) 1,05, intervalo de confianza del 95% (IC95%) 0.89-1.24, p = 0.499; y por variable instrumental: 7% de diferencia de medias. En cuanto al tiempo de inicio y su asociación con la necesidad de intubación: OR 0.93, IC95% 0,86-1,01. Conclusiones: Este estudio sugiere que el inicio tardío de la ventilación no invasiva es un factor de riesgo; sin embargo, no se halló asociación estadísticamente significativa, por lo que se requieren estudios adicionales para confirmar este hallazgo.

Abstract Introduction: Non-invasive ventilation reduces the need for intubation and intensive care stay in cardiogenic pulmonary edema. Objective: To evaluate the possible relationship between the initiation of non-invasive ventilation on admission to the emergency room and mortality and the need for intubation in patients with cardiogenic pulmonary edema. Method: A retrospective analytical cohort study. A chart review of patients over the age of 18 hospitalized at an institution in Medellín, Colombia. Results: 70 patients met the inclusion criteria and were compared by vital status at discharge. Survivors (49): the average age was 63 years, 34.7% were women, 57.1% had a history of chronic pulmonary disease, 89% had hypertension, 10 hours was the average for receiving the intervention, and 20% required orotracheal intubation. Non-survivors (21): the average age was 74 years, 57.1% were women, 57.1% had a history of chronic pulmonary disease, 90% had hypertension; 7 hours was the average for receiving the intervention, and 62% required intubation. Timing of initiation related to mortality on the multivariate analysis: odds ratio (OR) 1.05, 95% confidence interval (95%CI) 0.89-1.24, p = 0.499; and by instrumental variable: 7% difference in means. With regard to timing of initiation and its association with the need for intubation: OR 0.93, 95%CI 0.86-1.01. Conclusions: This study suggests that late initiation of non-invasive ventilation is a risk factor; however, no statistically significant association was found. Therefore, further studies are needed to confirm this finding.