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Acute pulmonary edema secondary to a hidden hypertensive emergency.

ABSTRACT: Severe stenosis of the subclavian artery is a rare clinical finding, even more so for bilateral existence of the condition. Subclavian artery stenosis leads to erroneously normal or even low blood pressure values when measured at the brachial artery on the ipsilateral side. The poor control of blood pressure may cause cardiovascular complications such as heart failure and acute pulmonary edema without the patient having high blood pressure in the arms. Widespread clinical reliance on a sole brachial measurement of blood pressure, particularly in the emergency room setting, may result in inappropriate clinical management in patients with conditions that alter brachial blood pressure. We report a case of acute diastolic heart failure secondary to hypertensive emergency hidden due to bilateral stenosis of both subclavian arteries in a patient with severe atherosclerosis, cerebrovascular disease, and symptoms of subclavian steal syndrome.

SUBMITTER: Piqueras-Flores J

PROVIDER: S-EPMC6282879 | biostudies-other | 2016 Aug

REPOSITORIES: biostudies-other

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Acute pulmonary edema secondary to a hidden hypertensive emergency.

Piqueras-Flores Jesús J Jurado-Román Alfonso A López-Lluva María M Sánchez-Pérez Ignacio I Pinardo-Zabala Antonio A Lozano-Ruíz-Poveda Fernando F

Journal of cardiology cases 20160420 2

Severe stenosis of the subclavian artery is a rare clinical finding, even more so for bilateral existence of the condition. Subclavian artery stenosis leads to erroneously normal or even low blood pressure values when measured at the brachial artery on the ipsilateral side. The poor control of blood pressure may cause cardiovascular complications such as heart failure and acute pulmonary edema without the patient having high blood pressure in the arms. Widespread clinical reliance on a sole brac ...[more]

PMID: 30546664

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Project description:BackgroundAtosiban is commonly used to delay premature labor in pregnant women and is thought to have few side effects.ObjectivesTo report a case of acute pulmonary edema (APE) following administration of atosiban and conduct a systematic review to identify common characteristics and risk factors of atosiban-associated APE.MethodsSearches were performed in Pubmed, Embase, and Web of Science using the keyword "Atosiban" combined with the terms "Pulmonary edema" or "Dyspnea" or "Hypoxia" on 9th July 2022. Only case reports of atosiban-associated APE were included without language restrictions. Data were extracted from the reports, and median, range, and percentages were calculated as applicable. The risk of bias was assessed using the Joanna Briggs Institute critical appraisal checklist for case reports.ResultsSeven cases of atosiban-associated APE were included in the systematic review, including our case. APE occurred at a median gestational age of 32 + 6 weeks. Most patients were nulliparous (6/7, 85.7%) and were in multiple pregnancies (5/7, 71.4%). All patients were prescribed antenatal corticosteroids and tocolytics, with three (42.9%) receiving only atosiban and four (57.1%) receiving atosiban and other tocolytics. The median interval from starting atosiban administration to APE onset was about 40 h, and three patients (42.9%) showed symptoms 2-10 h after the end of atosiban treatment. Radiographic examinations (chest X-ray and/or computer tomography scan) confirmed APE in all patients and pleural effusion in four patients (57.1%). Five patients (71.4%) underwent emergency cesarean section, one patient (14.3%) with twin pregnancy had vaginal delivery with the help of suction cup and forceps, and another patient (14.3%) continued the pregnancy. All patients recovered well after administration of oxygen, diuresis, and other supportive therapy.ConclusionAtosiban may cause acute pulmonary edema in patients with underlying risk factors. This complication remains rare, but caution during tocolytic treatment using atosiban is recommended.

Project description:Secondary bacterial lung infection by Streptococcus pneumoniae (S. pneumoniae) poses a serious health concern, especially in developing countries. We posit that the emergence of multiantibiotic-resistant strains will jeopardize current treatments in these regions. Deaths arising from secondary infections are more often associated with acute lung injury, a common consequence of hypercytokinemia, than with the infection per se Given that secondary bacterial pneumonia often has a poor prognosis, newer approaches to improve treatment outcomes are urgently needed to reduce the high levels of morbidity and mortality. Using a sequential dual-infection mouse model of secondary bacterial lung infection, we show that host-directed therapy via immunoneutralization of the angiopoietin-like 4 c-isoform (cANGPTL4) reduced pulmonary edema and damage in infected mice. RNA sequencing analysis revealed that anti-cANGPTL4 treatment improved immune and coagulation functions and reduced internal bleeding and edema. Importantly, anti-cANGPTL4 antibody, when used concurrently with either conventional antibiotics or antipneumolysin antibody, prolonged the median survival of mice compared to monotherapy. Anti-cANGPTL4 treatment enhanced immune cell phagocytosis of bacteria while restricting excessive inflammation. This modification of immune responses improved the disease outcomes of secondary pneumococcal pneumonia. Taken together, our study emphasizes that host-directed therapeutic strategies are viable adjuncts to standard antimicrobial treatments.IMPORTANCE Despite extensive global efforts, secondary bacterial pneumonia still represents a major cause of death in developing countries and is an important cause of long-term functional disability arising from lung tissue damage. Newer approaches to improving treatment outcomes are needed to reduce the significant morbidity and mortality caused by infectious diseases. Our study, using an experimental mouse model of secondary S. pneumoniae infection, shows that a multimodal treatment that concurrently targets host and pathogen factors improved lung tissue integrity and extended the median survival time of infected mice. The immunoneutralization of host protein cANGPTL4 reduced the severity of pulmonary edema and damage. We show that host-directed therapeutic strategies as well as neutralizing antibodies against pathogen virulence factors are viable adjuncts to standard antimicrobial treatments such as antibiotics. In view of their different modes of action compared to antibiotics, concurrent immunotherapies using antibodies are potentially efficacious against secondary pneumococcal pneumonia caused by antibiotic-resistant pathogens.

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Acute pulmonary edema secondary to a hidden hypertensive emergency.

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Acute pulmonary edema secondary to a hidden hypertensive emergency.

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