scholarly journals Acute Respiratory Distress Syndrome after Onyx Embolization of Arteriovenous Malformation

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Isaac Tawil ◽  
Andrew P. Carlson ◽  
Christopher L. Taylor
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Arteriovenous Malformation ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Ventilatory Support ◽  
Volume Overload ◽  
Embolization Procedure ◽  
Onyx Copolymer

Purpose. We report a case of a 60-year-old male who underwent sequential Onyx embolizations of a cerebral arteriovenous malformation (AVM) which we implicate as the most likely etiology of subsequent acute respiratory distress syndrome (ARDS).Methods. Case report and literature review.Results. Shortly after the second Onyx embolization procedure, the patient declined from respiratory failure secondary to pulmonary edema. Clinical entities typically responsible for pulmonary edema including cardiac failure, renal failure, iatrogenic volume overload, negative-pressure pulmonary edema, and infectious etiologies were evaluated and excluded. The patient required mechanical ventilatory support for several days, delaying operative resection. The patient met clinical and radiographic criteria for ARDS. After excluding other etiologies of ARDS, we postulate that ARDS developed as a result of Onyx administration. The Onyx copolymer is dissolved in dimethyl sulfoxide (DMSO), a solvent excreted through the lungs and has been implicated in transient pulmonary side effects. Additionally, a direct toxic effect of the Onyx copolymer is postulated.Conclusion. Onyx embolization and DMSO toxicity are implicated as the etiology of ARDS given the lack of other inciting factors and the close temporal relationship. A strong physiologic rationale provides further support. Clinicians should consider this uncommon but important complication.

Prone Positioning of Patients With Acute Respiratory Distress Syndrome

2015 ◽  
Vol 35 (6) ◽  
pp. 29-37 ◽  
Author(s):  
Dawn M. Drahnak ◽  
Nicole Custer
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Intensive Care ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Pulmonary Ventilation ◽  
Ventilatory Support ◽  
Positive Outcomes ◽  
Prone Positioning ◽  
Intensive Care Nurses

Effectively treating critically ill patients with acute respiratory distress syndrome (ARDS) is a challenge for many intensive care nurses. Multiple disease processes and injuries contribute to the complexity of ARDS and often complicate therapy. As a means of supportive care for ARDS, practitioners resort to rescue therapies to improve oxygenation and salvage the patient. The pathophysiology of ARDS and the use of prone positioning to improve pulmonary ventilation and oxygenation in ARDS patients are described. Educating nursing and medical staff on the use of prone positioning allows ease of patient placement with an emphasis on safety of both patients and staff. Scrupulous assessment of patients coupled with judicious timing of prone positioning expedites weaning from ventilatory support and contributes to positive outcomes for patients.

Acute Respiratory Distress Syndrome after Aprotinin Infusion

1997 ◽  
Vol 31 (4) ◽  
pp. 429-432 ◽  
Author(s):  
Zeljko Vucicevic ◽  
Tomislav Suskovic
Keyword(s):  
Adverse Reaction ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Anaphylactoid Reaction ◽  
Adverse Reactions ◽  
Distress Syndrome ◽  
Ventilatory Support ◽  
Allergic Reactions ◽  
Case Summary

Objective To report a case of acute respiratory distress syndrome (ARDS) following first exposure to aprotinin. Case Summary A 24-year-old previously healthy white man was treated with aprotinin infusion because of bleeding following tonsillectomy. The patient had never been treated with aprotinin before, including local application of different hemostatics containing the aprotinin component. Two hours later, hypotension and severe ARDS developed. A full recovery was noted after discontinuation of the drug and prolonged ventilatory support. Discussion To our knowledge, this is the first reported case of ARDS following first administration of aprotinin, although serious adverse effects at first exposure have been reported. We propose two possible mechanisms for this adverse reaction: a nonallergic or anaphylactoid reaction with direct degranulation of mast cells and basophils by aprotinin, and microthrombosis of the small pulmonary arterioles precipitated by aprotinin. Conclusions Most clinicians consider aprotinin to be a safe drug, especially if it has not been administered before. Reexposure carries a high risk of allergic reactions because of possible sensitization. Nonimmunologic, toxic, or idiosyncratic adverse reactions can be expected at first exposure to any drug, as well as to aprotinin.

scholarly journals Melkersson-Rosenthal Syndrome: A Rare Cause of Recurrent Facial Nerve Palsy and Acute Respiratory Distress Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Behiye Deniz Kosovali ◽  
Asiye Yavuz ◽  
Fatma Irem Yesiler ◽  
Mustafa Kemal Bayar
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Facial Nerve ◽  
Respiratory Distress ◽  
Facial Paralysis ◽  
Distress Syndrome ◽  
Facial Nerve Palsy ◽  
Ventilatory Support ◽  
Clinical Findings ◽  
Peripheral Facial Paralysis

Melkersson-Rosenthal Syndrome (MRS) is a rare disease characterized by persistent or recurrent orofacial oedema, relapsing peripheral facial paralysis, and furrowed tongue. Pathologically, granulomatosis is responsible for oedema of face, labia, oral cavity, and facial nerve. We present a patient with MRS admitted to our hospital with acute respiratory distress syndrome (ARDS). 45-year-old woman was admitted to an emergency department with dyspnea and swelling on her hands and face. She was intubated because of ARDS and accepted to intensive care unit (ICU). After weaning from ventilatory support, peripheral facial paralysis was diagnosed and steroid treatment was added to her therapy. On dermatologic examination, oedema on her face, pustular lesions on her skin, and fissure on her tongue were detected. The patient informed us about her recurrent and spontaneous facial paralysis in previous years. According to her history and clinical findings, MRS was diagnosed.

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

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