Effect of rhubarb on extravascular lung water in patients with acute respiratory distress syndrome

Summary Objective: The aim of this study was to evaluate the effect of rhubarb on extravascular lung water (EVLW) in patients with acute respiratory distress syndrome (ARDS). Method: A total of 80 patients with ARDS were randomly divided into a treatment group (40 cases) and control group (40 cases). Patients in the treatment group received rhubarb (30.0 g/d) and patients in the control group received conventional therapy for seven consecutive days. Extravascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI) were determined using pulse contour cardiac output (PiCCO) technology, and the oxygenation index was measured by blood gas analysis at baseline and on days 3, 5 and 7 after treatment. Results: The oxygenation index was higher and the levels of EVLWI and PVPI were lower after treatment in the two groups; however, these indexes showed significant differences on the 5th and 7th days after rhubarb treatment compared with the results in the control group (p<0.05). Conclusion: Rhubarb can decrease EVLWI and PVPI, and improve oxygenation in patients with ARDS.

P2L2A0 Emergency Lower Segment Caesarean Section (LSCS) with Atrial Septal Defect (ASD) with severe Pulmonary Arterial Hypertension (PAH) with Bidirectional flow with Pulmonary Edema with Sepsis.

Severe pulmonary Arterial Hypertension with Pulmonary Edema with Sepsis in a postnatal mother with Atrial Septal Defect (ASD) followed by LSCS is uncommon. Atrial Septal Defect (ASD) is the commonest adult congenital heart defect (CHD). 15 % of these patients will eventually develop pulmonary hypertension if left untreated. ASD closure is not recommended when pulmonary hypertension is irreversible. Congenital heart disease should be considered in the evaluation of dyspnoea in a young adult. The management of ASD with associated pulmonary hypertension is difficult. It is pertinent that a detailed hemodynamic assessment be undertaken. The present case report focusses on a patient with severe ASD with pulmonary hypertension with pulmonary edema and sepsis who was with 35 weeks of gestation and the control of symptoms during Caesarean section.

Cyclophosphamide dose: how much is needed to win the war against paraquat poisoning?

No abstract available.

Injuria pulmonar aguda en la intoxicación por ácido acetilsalicílico: Caso clínico y revisión bibliográfica / Acute lung injury due to acetylsalicylic acid poisoning: Case report and review

La intoxicación por salicilatos frecuentemente no es tenida en cuenta como causa de edema pulmonar no cardiogénico y de alteración del sensorio en pacientes adultos. Se describe el caso de una mujer de 52 años de edad, la cual presentó dos episodios de edema pulmonar no cardiogénico habiendo requerido para su manejo, asistencia ventilatoria mecánica. La presentación clínica de la intoxicación fue reconocida al ingreso al servicio de urgencias y llevó al diagnóstico correcto. Se le realizó hemodiálisis y alcalinización urinaria llevando a una rápida resolución del edema pulmonar. Varios aspectos de la presentación clínica sugirieron que la paciente tenía una intoxicación crónica, una condición que a menudo no es diagnosticada oportunamente, lo que contribuye al aumento de la morbi-mortalidad en estos pacientes. Frente a un caso de edema pulmonar agudo no cardiogénico debe considerarse la posibilidad de intoxicación con salicilatos, porque la institución rápida de una terapia apropiada, incluyendo la hemodiálisis, una vez establecido el diagnóstico, es un factor determinante de los resultados en esta grave intoxicación.

Salicylate intoxication is frequently overlooked as a cause of noncardiogenic pulmonary edema and altered mental status in adult patients. We described the case of a 52 years-old woman who presented two episodes of recurrent non-cardiogenic pulmonary edema requiring intubation. On admission, recognition of the clinical syndrome in the emergency department led to the correct diagnosis of salicylate intoxication. The patient was successfully treated with hemodialysis and urinary alkalinization, leading to rapid resolution of pulmonary edema and extubation. Several aspects of the clinical presentation suggest that the patient suffered from chronic salicylism, a condition often misdiagnosed or diagnosed late in the course of disease, contributing to substantial morbidity and mortality in these patients. This poisoning should be considered in the differential diagnosis of acute pulmonary edema not cardiogenic and altered sensorium because rapid institution of appropriate therapy, including hemodialysis, once the diagnosis is established is an important determinant of outcome in this serious disorder.

Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy

OBJECTIVE: The objective of this study was to evaluate the involvement of peripheral nitric oxide (NO) in vagotomy-induced pulmonary edema by verifying whether the nitric oxide synthases (NOS), constitutive (cNOS) and inducible (iNOS), participate in this mechanism. INTRODUCTION: It has been proposed that vagotomy induces neurogenic pulmonary edema or intensifies the edema of other etiologies. METHODS: Control and vagotomized rats were pretreated with 0.3 mg/kg, 3.0 mg/kg or 39.0 mg/kg of L-NAME, or with 5.0 mg/kg, 10.0 mg/kg or 20.0 mg/kg of aminoguanidine. All animals were observed for 120 minutes. After the animals' death, the trachea was catheterized in order to observe tracheal fluid and to classify the severity of pulmonary edema. The lungs were removed and weighed to evaluate pulmonary weight gain and edema index. RESULTS: Vagotomy promoted pulmonary edema as edema was significantly higher than in the control. This effect was modified by treatment with L-NAME. The highest dose, 39.0 mg/kg, reduced the edema and prolonged the survival of the animals, while at the lowest dose, 0.3 mg/kg, the edema and reduced survival rates were maintained. Aminoguanidine, regardless of the dose inhibited the development of the edema. Its effect was similar to that observed when the highest dose of L-NAME was administered. It may be that the non-selective blockade of cNOS by the highest dose of L-NAME also inhibited the iNOS pathway. CONCLUSION: Our data suggest that iNOS could be directly involved in pulmonary edema induced by vagotomy and cNOS appears to participate as a protector mechanism.

Effectiveness of Human Atrial Natriuretic Peptide Supplementation in Pulmonary Edema Patients Using the Pulse Contour Cardiac Output System

PURPOSE: Atrial natriuretic peptide (ANP) has a variety of pharmacologic effects, including natriuresis, diuresis, vasodilatation, and suppression of the renin-angiotensin system. A recent study showed that ANP infusion improved hypoxemia and pulmonary hypertension in a lung injury model. On the other hand, the pulse contour cardiac output (PiCCO(TM)) system (Pulsion Medical Systems, Munich, Germany) allows monitoring of the intravascular volume status and may be used to guide volume therapy in severe sepsis and critically ill patients. MATERIALS AND METHODS: We treated 10 pulmonary edema patients without heart disease with human ANP (HANP). The patients were divided into two groups: a group with normal Intrathoracic Blood Volume (ITBV) (900-1100 mL/m2) (n = 6), and a group with abnormal ITBV (n = 4), as measured by the PiCCOtrade mark device; the extravascular lung water (EVLW) and pulmonary vascular permeability index (PVPI) in the two groups were compared. RESULTS: The average patient age was 63.9 +/- 14.4 years. The normal ITBV group showed significant improvement of the EVLW (before, 16.7 +/- 2.7 mL/kg; after, 10.5 +/- 3.6 mL/kg; p = 0.0020) and PVPI (before, 3.2 +/- 0.3; after, 2.1 +/- 0.7; p = 0.0214) after the treatment. The abnormal ITBV group showed no significant improvement of either the EVLW (before, 16.3 +/- 8.9 mL/kg; after, 18.8 +/- 9.6 mL/kg; p = 0.8387) or PVPI (before, 2.3 +/- 0.8; after, 2.7 +/- 1.3; p = 0.2782) after the treatment. In both groups, the EVLW and PVPI were strongly correlated with the chest X-ray findings. CONCLUSION: We conclude that HANP supplementation may improve the EVLW and PVPI in pulmonary edema patients without heart disease with a normal ITBV. The PiCCO(TM) system seems to be a useful device for the management of pulmonary edema.

Asymmetric pulmonary edema after scorpion sting: a case report / Edema pulmonar assimétrico após picada de escorpião: relato de caso

A 12-year-old boy was referred with acute asymmetric pulmonary edema (APE) four-hour after scorpion sting to Emergency department. On admission, the main clinical manifestations were: dyspnea, tachypnea, and tachycardia. Chest x-ray revealed APE predominantly on the right hemithorax. The patient was treated with oxygen, intravenous frusemide and digoxin and discharged on the sixth hospital day in a good condition. This case report emphasizes the occurrence of asymmetric pulmonary edema after severe scorpion envenomation within few hours immediately after the sting.

Menino de 12 anos foi internado no Pronto Socorro, com edema pulmonar assimétrico agudo (APE), quatro horas após picada de escorpião. À admissão, as principais manifestações clínicas foram: dispnéa, taquipnéa e taquicardia. Raio X do pulmão revelou APE predominantemente no hemitórax direito. O paciente foi tratado com oxigênio, frusemida intravenosa e digoxina e teve alta no sexto dia de internação, em boas condições. Este relato de caso enfatiza a ocorrência de edema pulmonar assimétrico algumas horas após a picada.

Edema pulmonar de altura: Modelo de estudio de la fisiopatología del edema pulmonar y de la hipertensión pulmonar hipóxica en humanos / High altitude pulmonary edema. An experiment of Nature to study the underlying mechanisms of hypoxic pulmonary hypertension and pulmonary edema in humans

La altura, fascinante laboratorio natural de investigación médica, provee resultados con importantes implicancias para la comprensión de enfermedades que afectan a millones de personas que viven en ella, asi como para el tratamiento de enfermedades ligadas a la hipoxemia en pacientes que viven en baja altitud. El edema pulmonar de altura (EPA) es una entidad que pone en peligro la vida y que ocurre en sujetos predispuestos pero sanos. Esto permite estudiar los mecanismos subyacentes del edema pulmonar en humanos, sin la presencia de factores que presten a la confusión como enfermedades concomitantes. El EPA resulta de la conjunción de dos defectos mayores: acumulación de líquido en el espacio alveolar debido a una hipertensión pulmonar hipóxica exagerada, y alteración en la eliminación del mismo por un defecto en el transporte transepitelial alveolar de sodio. En esta revisión, describimos brevemente las características clínicas y revisaremos este novedoso concepto. Proveemos evidencia experimental de como la síntesis alterada de óxido nítrico y/o la disminución de su biodisponibilidad representan el defecto central que predispone a la vasoconstricción pulmonar hipóxica exagerada y a la acumulación de líquido en el espacio alveolar. Mostramos que la hipertensión pulmonar hipóxica exagerada, per se, no es suficiente para producir un EPA, y que una alteración en la eliminación del fluido del espacio alveolar representa un segundo mecanismo fisiopatológico importante. Finalmente, describimos cómo los nuevos aportes obtenidos de los estudios del EPA pueden ser trasladados al manejo de otros estados patológicos ligados a la hipoxemia.

High altitude constitutes an exciting natural laboratory for medical research. Over the past decade, it has become clear that the results of high-altitude research may have important implications not only for the understanding of diseases in the millions of people living permanently at high altitude, but also for the treatment of hypoxemia-related disease states in patients living at low altitude. High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed, but otherwise healthy subjects, and, therefore, allows to study underlying mechanisms of pulmonary edema in humans, in the absence of confounding factors. Over the past decade, evidence has accumulated that HAPE results from the conjunction of two major defects, augmented alveolar fluid flooding resulting from exaggerated hypoxic pulmonary hypertension, and impaired alveolar fluid clearance related to defective respiratory transepithelial sodium transport. Here, after a brief presentation of the clinical features of HAPE, we review this novel concept. We provide experimental evidence for the novel concept that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent the central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction and alveolar fluid flooding. We demonstrate that exaggerated pulmonary hypertension, while possibly a condition sine qua non, may not be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we outline how this insight gained from studies in HAPE may be translated into the management of hypoxemia related disease states in general.

Cocaine-induced myocardial infarction associated with severe reversible systolic dysfunction and pulmonary edema

Myocardial infarction (MI) associated to cocaine use was originally reported in 1982 and cases are being encountered more frequently in our milieu. The literature regarding this diagnosis has included mostly cases of cocaine associated chest pain and MI without serious sequelae. A lesser number of reports however focus on the clinical presentation of severe myocardial dysfunction and severe pulmonary edema, with the mechanism for pulmonary edema still being debated. Although previously described individually, these manifestations are thought to be an uncommon complication of cocaine ingestion. In this article the subject is reviewed and we report our experience with two patients that presented to our care with severe pulmonary edema and concomitant severe left ventricular systolic dysfunction that resolved spontaneously with supportive therapy. It is felt that this clinical picture after cocaine use may be more common than expected. In this article we discuss the possible mechanisms associated to this presentation as well as review the literature regarding this subject.

High altitude pulmonary oedema

High altitude pulmonary edema [HAPE] is a common problem at high altitude that generally occurs above 2500 meters in un-acclimatized persons, due to hypoxemia. Variable incidence of HAPE has been reported in literature ranging from 2-15%. Recent studies have established beyond doubt,that RAPE is caused by high pulmonary artery pressures due to patchy hypoxic vasoconstriction that leads to high permeability changes in remaining patent capillaries in lung that results in protein rich oedema. The development of an inflammatory process could then occur after the initiation of the early capillary leak in alveoli. Inflammatory markers such as neutrophils, leukotriene B4, cytokines and the complement fragment C5a are frequently seen in the lungs lavage in RAPE. In addition Endothelin-1, nitric oxide, oxidative stress and genetic factors may play a role in the pathogenesis. The common clinical features include dyspnoea, cough, tachypnoea, fatigue, chest tightness, tachycardia and rales upon systemic examination of chest. Even susceptible individuals can avoid HAPE when they ascend slowly. Currently oxygen therapy, nifedipine, and nitric oxide can be used in the treatment of HAPE. This review provides latest developments in understanding pathogenesis leading to early diagnosis and better management of RAPE at high altitude that are necessary in view of the development of our troops and increasing frequency of persons going for recreation to high altitude in northern areas of Pakistan

Crisis de esclerodermia renal: rol de la vasculopatía esclerodérmica en la inducción de fibrosis cutáneo-visceral en dos casos / Renal scleroderma crisis: role of sclerodermic vasculopathy in the induction of cutaneous and visceral fibrosis: report of 2 cases

Although fibrosis and vasculopathy coexist in most patients with progressive systemic sclerosis, it is not clear if these events are the result of an unique etiologic factor or if one is consequence of the other. We report two cases of progressive systemic sclerosis that evolved to a renal scleroderma crisis. A 36 years old female presented with a Sjögren syndrome and painful subcutaneous nodules whose biopsy showed perivascular lymphocytic infiltration, perivascular thickening and normal skin. The ESR was 100 mm/h. She developed an hypertensive crisis and progressive renal failure, followed by a rapidly evolving progressive systemic sclerosis. The patient died in the course of this crisis. A 32 years old female with a progressive systemic sclerosis refractory to D-penicillamine treatment, receiving cyclosporin, presented a renal scleroderma crisis, that was successfully treated, with complete recovery of renal function. We highlight the different evolution of these cases, probably due to an early diagnosis and a better experience in the management of this condition

Edema agudo pulmonar em um lactente com síndrome hemolítico-urêmica / Acute pulmonary edema in an infant with hemolytic uremic syndrome

Descrevemos um caso de edema agudo (EAP) devido a uma insuficiência renal (IRA) ocorrendo na evolução de uma Síndrome Hemolítico-Urêmica (SHU)em um lactente. Enfatizamos a apresentação e evolução atípicas da SHU neste caso, os prováveis fatores responsáveis e a conduta terapêutica adotada

Mecanismos de aclaramiento del edema pulmonar mediado por agonistas ß-adrenérgicos / Mechanisms of pulmonary edema clearance mediated by ß-adrenergic agonists

El edema pulmonar es causa frecuente de deterioro del intercambio gaseoso y aumento del trabajo respiratorio en el paciente crítico. La formación del edema pulmonar depende de cambios en la presión hidrostática y/u oncótica en el lecho vascular pulmonar o aumento de la permeabilidad de la membrana alvéolo-capilar. El aclaramiento del edema pulmonar depende principalmente de gradientes osmóticos generados por el transporte activo de Na+ en el epitelio alveolar ocurre predominantemente a través de los canales de Na+ localizados en la región apical y la bomba Na, K-ATPasa ubicada en la superficie basolateral de las células alveolares. El movimiento de agua transepitelial es pasivo y sigue el gradiente osmótico generado por el transporte iónico hacia fuera del alvéolo. Estudios fisiológicos en pulmón aislado, animales in vitro y en cultivos de células alveolares tipo II han demostrado que los agonistas ß-adrenérgicos aumentan la expresión y función de los canales de sodio y la bomba Na, K-ATPasa en las células alveolares, activando la enzima adenil-ciclasa que cataliza la síntesis de AMPc intracelular y la vía de la proteína kinasa A. De este modo, el aumento del transporte activo de Na+ mediado por los agonistas ß-adrenérgicos podría acelerar la resolución del edema pulmonar y mejorar el pronóstico de los enfermos con insuficiencia respiratoria aguda

Emergências cardiovasculares: Parte 5. Edema pulmonar agudo / Cardiovasculary emergencies: pulmonary acute edema

O EAP representa forma clínica da insuficiência cardíaca sistólica ou diastólica, podendo também ser decorrente de causas näo cardiológicas. Na fisiopatologia destacamos o aumento da pressäo hidrostática e a diminuiçäo da pressäo oncótica. O EAP pode ser unilateral como na embolia pulmonar e no pneumotórax. Clinicamente, chama a atençäo a dispnéia acompanhada da sensaçäo de morte iminente. Os diuréticos, a morfina e os inotrópicos, bem como os vasodilatadores consituem-se nas drogas de eleiçäo. O tratamento do EAP näo cardiogênico baseia-se na causa do mesmo. As vezes, é difícil o diagnóstico diferencial entre EAP näo cardiogênico com EAP por insuficiência cardíaca diastólica e o EAP clássico por disfunçäo sistólica

Non-cardiac pulmonary oedema in scorpion bite.

A 30 year old male presented with non-cardiac pulmonary oedema after scorpion bite. Clinical features, X-ray chest and ECG findings after bite and recovery are discussed.