Causes Of Noncardiogenic Pulmonary Edema Research Articles

BUPRENORPHINE-NALOXONE-INDUCED NONCARDIOGENIC PULMONARY EDEMA

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Buprenorphine-naloxone is used to treat chronic pain and opioid use disorder. Each medication in this combination has been associated with noncardiogenic pulmonary edema. Here we report the case of a 56-year-old woman treated for chronic pain with buprenorphine-naloxone, and a history of multiple hospitalizations for pulmonary edema. Her buprenorphine-naloxone was held on admission and her symptoms improved gradually with supportive care. CASE PRESENTATION: A 56-year-old woman with past history significant for congestive heart failure, chronic obstructive pulmonary disease, and chronic pain treated with buprenorphine-naloxone presented to the emergency department via ambulance for altered mental status and worsening dyspnea for 3 days. Upon arrival to the ED she was tachypneic with a SpO2 of 50% on room air and required non-invasive ventilation. Physical exam revealed diminished breath sounds bilaterally and no peripheral edema. Laboratory data was significant for an elevated D-dimer and BNP. Covid-19 screening was negative. Chest x-ray showed diffuse hazy opacities. CTA chest was negative for pulmonary embolism, but did show extensive parenchymal opacities and diffuse ground glass densities bilaterally. Steroids and antibiotics were initiated, and buprenorphine-naloxone was discontinued.She described several similar prior hospitalizations, but denied ever receiving a diagnosis. Echocardiogram showed a normal ejection fraction and grade II diastolic dysfunction. Infectious and vasculitis etiologies were ruled out. The patient declined bronchoscopy. Records from prior hospitalizations revealed non-diagnostic bronchoalveolar lavage and wedge biopsies. Environmental exposure was ruled out via a peer reviewed questionnaire and negative allergen testing. With no clear etiology, the patient's hypoxia improved. We propose that the patient's presentation was secondary to noncardiogenic pulmonary edema induced by buprenorphine-naloxone. DISCUSSION: Non-cardiogenic pulmonary edema is an acute process resulting in hypoxia secondary to an increase in capillary permeability. Major causes include ARDS, pulmonary embolism, TRALI, and opioid overdose, but many other etiologies have been implicated. Buprenorphine, like other opioids, is a known cause of pulmonary edema (1). Naloxone induced pulmonary edema, while rare, has also been described (2). A review of the literature was not able to find buprenorphine-naloxone combination as a cause of non-cardiogenic pulmonary edema. We believe this patient's pulmonary edema may have been secondary to this medication's opioid effects, naloxone effects, or possibly an allergic reaction. Given the wide use of this medication physicians should be made aware of this possible complication. CONCLUSIONS: Non-cardiogenic pulmonary edema is a potential complication of buprenorphine-naloxone. REFERENCE #1: Thammakumpee G, Sumpatanukule P. Noncardiogenic Pulmonary Edema Induced by Sublingual Buprenorphine. Chest. 1994;106(1):306-308. REFERENCE #2: Bansal S, Khan R, Tietjen P. Naloxone-Induced Pulmonary Edema [abstract]. Chest. 2007;132(4):692A. DISCLOSURES: No relevant relationships by Muhammad Aboudan, source=Web Response No relevant relationships by Brandon Govan, source=Web Response No relevant relationships by Abi Waqas, source=Web Response

Uncommon causes of noncardiogenic pulmonary edema.

Although acute respiratory distress syndrome is the most common cause of noncardiogenic pulmonary edema, NPs also should be familiar with several other less common causes, including transfusion-related acute lung injury, neurogenic pulmonary edema, preeclampsia/eclampsia, opioid overdose, high-altitude pulmonary edema, and pulmonary embolism. This article addresses the pathophysiology, clinical presentation, diagnostics, treatment, and nursing considerations associated with each uncommon cause of noncardiogenic pulmonary edema.

Uncommon causes of noncardiogenic pulmonary edema

Uncommon causes of noncardiogenic pulmonary edema

Uncommon causes of noncardiogenic pulmonary edema

In Brief Although acute respiratory distress syndrome is the most common cause of noncardiogenic pulmonary edema, critical care nurses also should be familiar with several other less common causes, including transfusion-related acute lung injury, neurogenic pulmonary edema, preeclampsia/eclampsia, opioid overdose, high-altitude pulmonary edema, and pulmonary embolism. This article addresses the pathophysiology, clinical presentation, diagnostics, treatment, and nursing considerations associated with each uncommon cause of noncardiogenic pulmonary edema. This article reviews the pathophysiology, clinical presentation, diagnostics, treatment, and nursing considerations associated with several uncommon causes of noncardiogenic pulmonary edema, including transfusion-related acute lung injury, neurogenic pulmonary edema, preeclampsia/eclampsia, opioid overdose, high altitude pulmonary edema, and pulmonary embolism.

RADIOGRAPHIC APPEARANCE OF PRESUMED NONCARDIOGENIC PULMONARY EDEMA AND CORRELATION WITH THE UNDERLYING CAUSE IN DOGS AND CATS.

Noncardiogenic pulmonary edema is an important cause of respiratory disease in dogs and cats but few reports describe its radiographic appearance. The purpose of this retrospective case series study was to describe radiographic findings in a large cohort of dogs and cats with presumed noncardiogenic pulmonary edema and to test associations among radiographic findings versus cause of edema. Medical records were retrieved for dogs and cats with presumed noncardiogenic edema based on history, radiographic findings, and outcome. Radiographs were reviewed to assess lung pattern and distribution of the edema. Correlation with the cause of noncardiogenic pulmonary edema was evaluated with a Fisher's exact test. A total of 49 dogs and 11 cats were included. Causes for the noncardiogenic edema were airway obstruction (n = 23), direct pulmonary injury (n = 13), severe neurologic stimulation (n = 12), systemic disease (n = 6), near-drowning (n = 3), anaphylaxis (n = 2) and blood transfusion (n = 1). Mixed, symmetric, peripheral, multifocal, bilateral, and dorsal lung patterns were observed in 44 (73.3%), 46 (76.7%), 55 (91.7%), 46 (76.7%), 46 (76.7%), and 34 (57.6%) of 60 animals, respectively. When the distribution was unilateral, pulmonary infiltration involved mainly the right lung lobes (12 of 14, 85.7%). Increased pulmonary opacity was more often asymmetric, unilateral, and dorsal for postobstructive pulmonary edema compared to other types of noncardiogenic pulmonary edema, but no other significant correlations could be identified. In conclusion, noncardiogenic pulmonary edema may present with a quite variable radiographic appearance in dogs and cats.

Understanding negative pressure pulmonary edema.

Understanding negative pressure pulmonary edema.

Negative Pressure Pulmonary Edema Following Bronchospasm

Negative pressure pulmonary edema (NPPE) is an important cause of noncardiogenic pulmonary edema but is rarely reported in the setting of bronchospasm. A 43-year-old woman with severe reactive airway disease suffered an episode of severe bronchospasm after endotracheal extubation following an otherwise uneventful general anesthetic. Subsequently, she developed clinical and radiographic signs of pulmonary edema in the absence of other symptoms of acute left-sided heart failure, leading to the diagnosis of noncardiogenic pulmonary edema. She received noninvasive positive pressure ventilation for a few hours, after which her clinical and radiologic signs and symptoms of pulmonary edema were greatly improved. This clinical scenario strongly suggests NPPE. We submit that it is possible to create NPPE by generating highly negative intrathoracic pressures in the setting of severe bronchospasm.

Hydrochlorothiazide-Induced Noncardiogenic Pulmonary Edema: BAL Fluid Analysis

Hydrochlorothiazide (HCTZ)-induced pulmonary disease has been described as either an allergic interstitial pneumonitis or a cause of noncardiogenic pulmonary edema. The mechanism of this rare life-threatening side effect is largely unknown. Many patients show peripheral leukopenia and extensive immunologic studies reveal decreased levels of serum immunoglobulins. However, evaluation of the peripheral blood may not reflect local lung changes. Literature reports of bronchoalveolar differentials on such patients are scarce. Bronchoscopy was performed on our patient, and the lavage revealed a significant percentage of neutrophils (70%) and no eosinophils.

Anti-thymocyte globulin induced non-cardiogenic pulmonary edema during renal transplantation

Non-cardiogenic pulmonary edema (NCPE) is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest radiograph, without evidence of left atrial hypertension/congestive heart failure/fluid overload. The diagnosis of drugrelated NCPE relies upon documented exclusion of other causes of NCPE like gastric aspiration, sepsis, trauma, negative pressure pulmonary edema. We describe a 28year-old, 50 kg male with ASA risk III posted for laparoscopic renal transplantation, who developed NCPE after 4 hours of administration of rabbit anti-human thymocyte immunoglobulin (ATG). He was successfully treated with mechanical ventilatory support and adjuvant therapy. This report emphasizes that this fatal complication may occur with use of ATG.

Noncardiogenic pulmonary edema following accidental near-hanging

A 79 year-old woman was admitted to our institution unconscious with pulmonary edema. She had been trapped by the neck in the electric sliding gate of her own home garage. A pulmonary artery catheter was inserted through the right internal jugular vein and her hemodynamic profile and chest x ray revealed a non cardiogenic pulmonary edema. Intensive care management consisted of assisted/controlled ventilatory support with low grade of PEEP (6 cm H2O) and loop diuretics. Three days later, the chest x-ray showed resolution of the pulmonary edema and she made a full recovery. Near-hanging due to neck compression can be a life-threatening cause of non-cardiogenic pulmonary edema, and should be included in the differential diagnosis of pulmonary edema.

Collapsing glomerulopathy: A cause of noncardiogenic pulmonary edema

Collapsing glomerulopathy is a pathologic diagnosis characterized by obliteration of glomerular capillary lumina, seen most commonly as a primary glomerular disease in young black men. A secondary form with almost identical pathologic features is described in association with human immunodeficiency virus infection. The disease is characterized by heavy proteinuria with variable renal insufficiency at the onset followed by rapid progression to end-stage renal disease with no documented effective therapy. We describe a patient who presented with systemic manifestations, including fever, acute renal failure with massive proteinuria, and noncardiogenic pulmonary edema. Renal biopsy showed classic collapsing glomerulopathy. All known causes of noncardiogenic pulmonary edema were ruled out. The pulmonary syndrome resolved, but the renal disease progressed to end-stage renal disease. We propose consideration of collapsing glomerulopathy in the differential diagnosis of any patient presenting with a multisystem disease including acute renal failure and pulmonary edema. © 2002 by the National Kidney Foundation, Inc.

Chronic salicylism resulting in noncardiogenic pulmonary edema requiring hemodialysis

Salicylate intoxication is frequently overlooked as a cause of noncardiogenic pulmonary edema and altered mental status in adult patients. We describe a 42-year-old woman who presented with two episodes of recurrent noncardiogenic pulmonary edema requiring intubation. The first admission to hospital triggered an extensive initial workup that did not indicate a cause for the pulmonary edema. At the second presentation, 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 suffers from chronic salicylism, probably complicated by episodic superimposed acute intoxication, a condition often misdiagnosed or diagnosed late in the course of disease, contributing to substantial morbidity and mortality in these patients. Maintenance of a high index of suspicion and rapid institution of appropriate therapy including hemodialysis once the diagnosis is established is an important determinant of outcome in this serious but underdiagnosed disorder.