Acute Non-cardiogenic Pulmonary Edema Research Articles

Pulmonary veno-occlusive disease presenting with recurrent pulmonary oedema and the use of nitric oxide to predict response to sildenafil

Pulmonary veno-occlusive disease (PVOD) is a disorder which causes progressive pulmonary hypertension, usually presenting with worsening dyspnoea and right heart failure. Pulmonary oedema induced by pulmonary vasodilator therapy to reduce...

Noncardiogenic acute pulmonary edema due to severe hypoglycemia—an old but ignored cause

We present a rare case of noncardiogenic pulmonary edema (NCPE) associated with sudden coma due to severe hypoglycemia. We suggest that in every case of NCPE associated with coma, a rapid determination of glycemia should be provided because delays in diagnosis can lead to adverse outcome.

FIRST REPORT OF TRANSFUSION-RELATED ACUTE LUNG INJURY (TRALI)IN SLOVENIA

BACKGROUND Transfusion-related acute lung injury (TRALI) is a major cause of lethal side effects associated with transfusion of blood and blood components. TRALI is defined as a new acutenoncardiogenic pulmonary oedema as seen on the frontal radiography of lungs, manifested with the shortness of breath, hypoxemia, hypotension and fever, all occurring duringor within 6 h after transfusion.TRALI is rarely diagnosed and can be confused with other causes of acute respiratoryfailure. It occurs at the ratio of 1 in 1,120 to 1 in 5,000 transfusions of blood or bloodcomponents. The fatal incidence is 5 % to 25 % according to USA statistics. The data forSlovenia are not available as this is the first case reported ever.Case This article analyses a case of a female patient who had a hip replacement surgery, wastransfused with erythrocyte components, which was followed by TRALI. Radiographs andlaboratory analysis are presented. CONCLUSIONS The recognition of symptoms of TRALI on the part of clinicians could be crucial in preventing and treating this severe complication of blood transfusion

Acute paraplegia and pulmonary edema after benzathine penicillin injection

Accidental intra-arterial injection is a potentially devastating complication of the intragluteal injection of benzathine penicillin. A 35-year-old woman developed after intramuscular injection of benzathine penicillin G acute paraplegia and noncardiogenic pulmonary edema. Noninvasive positive pressure ventilation was initiated with furosemide and corticosteroids. A magnetic resonance imaging scan showed findings consistent with syringomyelia and spinal cord ischemia at T9 through T10. Vascular injury may be the result of microemboli of the injected crystals of the penicillin salts. The mechanism of noncardiogenic pulmonary edema is perhaps an immunogically mediated one. At 2-year follow-up, she had no improvement in neurologic status. The deficit is considered permanent.

Transfusion-Related Acute Lung Injury

Transfusion-related acute lung injury is a life-threatening clinical syndrome. In the last 3 years, it has become the leading cause of reported transfusion-related deaths in the United States. This syndrome is characterized by acute hypoxemia and noncardiogenic pulmonary edema directly linked in time to a blood transfusion. All types of blood products have been implicated in transfusion-related acute lung injury, but transfusion of plasma-containing products from multiparous women seems to carry the highest risk. The purpose of this article is to raise awareness of this syndrome for the critical care nurse. This article discusses the widely accepted clinical features of transfusion-related acute lung injury, its pathogenesis, differential diagnosis, and treatment.

Transfusion-Related Acute Lung Injury: An Update

Transfusion-associated acute lung injury (TRALI) has emerged as a leading cause of transfusion-related morbidity and mortality. TRALI is characterized by acute non-cardiogenic pulmonary edema and respiratory compromise in the setting of transfusion. The study of TRALI has been hampered by inadequate case definitions and an incomplete understanding of the pathologic mechanisms. Recent consensus conferences took an important first step by providing a framework for case definition. Recent advances in the understanding of the pathogenesis of TRALI have also occurred. TRALI has been primarily attributed to donor leukocyte antibodies that are thought to interact with recipient neutrophils, resulting in activation and aggregation in pulmonary capillaries, release of local biologic response modifiers causing capillary leak, and lung injury. An alternate mechanism termed the "two hit" or "neutrophil priming" hypothesis postulates that a pathway to neutrophil activation and aggregation can occur without leukocyte antibodies. A first event such as sepsis or trauma can induce pulmonary endothelial activation, release of cytokines, and priming of neutrophils. A subsequent second event such as exposure to lipids, cytokines or antibodies in a blood component would then cause activation of adherent neutrophils and a release of bioreactive molecules leading to lung injury. There are limited clinical and animal studies to support the "two hit" model. These proposed mechanisms are not mutually exclusive in that donor leukocyte antibody can be pathogenic in both models and have implications for new strategies to prevent TRALI.

Edema agudo de pulmón no cardiogénico secundario a hidroclorotiazida

Several commonly prescribed drugs can cause acute non-cardiogenic pulmonary edema. A cause-effect relationship is usually difficult to establish because symptoms are not specific. We report a case of pulmonary edema induced by a common diuretic, hydrochlorothiazide. This complication can occur after a first dose of the drug or in patients who have been taking it with no side effects. Edema is due to an idiosyncratic reaction rather than an immune response. The clinical course is usually favorable over the first 24 hours with treatment of blood pressure and respiratory support. Given that severity increases with recurrence, we underline the importance of diagnosis in the first episode.

Clinical Acute Lung Injury and Acute Respiratory Distress Syndrome.

This article provides a description of the clinical disorders associated with the development of acute noncardiogenic pulmonary edema, better known as clinical acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS). Much has been learned about the mechanisms by which the lung is injured in patients with sepsis, pneumonia, aspiration of gastric contents, and following major trauma. In the last 5 years, major progress has been made in the treatment of patients with ALI/ARDS. A lung protective ventilatory strategy with a low tidal volume (6 mL/kg/predicted body weight) in conjunction with a plateau pressure limit of 30 cm H(2)0 attenuated the severity of clinical lung injury and reduced mortality by 22%. Ironically, after years of searching for anti-inflammatory treatments for ALI/ARDS, it turns out that a lung protective ventilatory strategy has proven to be the most efficacious anti-inflammatory treatment ever discovered for ALI/ARDS. However, it is still possible that pharmacologic treatments also may enhance survival. For example, a recent report that activated protein C reduces mortality in patients with sepsis raises hope that the incidence and severity of sepsis-induced ALI/ARDS may be reduced by treatment with this agent that has both anti-inflammatory and anticoagulant properties. Also, therapy directed at hastening the resolution of lung injury by increasing the functional recovery of the alveolar epithelium may be of value, both in diminishing the fibroproliferative phase of ALI/ARDS as well as accelerating the resolution of alveolar edema.

Endothelial Selectins in Acute Mountain Sickness and High-Altitude Pulmonary Edema

Mechanical or inflammatory injury to pulmonary endothelial cells may cause impaired pulmonary gas exchange in acute mountain sickness (AMS) and noncardiogenic pulmonary edema in high-altitude pulmonary edema (HAPE). This study was designed to determine whether markers of endothelial cell activation or injury, plasma E- and P-selectin, were increased after ascent to high altitude, in AMS or in HAPE. We collected clinical data and plasma specimens in control subjects at sea level and after ascent to 4,200 m, and in climbers with AMS or HAPE at 4,200 m. Data analysis was performed using standard nonparametric statistical methods, and results reported as mean+/-SD. National Park Service medical camp at 4,200 m on Mt. McKinley (Denali), Alaska. Blood samples and clinical data were collected from 17 healthy climbers at sea level and again after ascent to 4,200 m, and from a different group of 13 climbers with AMS and 8 climbers with HAPE at 4,200 m. Climbers with AMS were divided into normoxic (n=7) and hypoxemic (n=6) groups. Using an enzyme immunoassay technique, plasma E-selectin concentrations were found to be increased in the 17 control subjects after ascent to 4,200 m (17.2+/-8.2 ng/mL) as compared to sea level (12.9+/-8.2 ng/mL) (p=0.001). Plasma E-selectin concentrations were also increased in subjects with hypoxemic AMS (30.6+/-13.4 ng/mL) and HAPE (23.3+/-9.1 ng/mL) compared to control subjects at sea level (p=0.009). Increased plasma E-selectin concentration significantly correlated with hypoxemia (p=0.006). Plasma P-selectin concentrations were unchanged after ascent to 4,200 m and in subjects with AMS and HAPE. Because E-selectin is produced only by endothelial cells, increased plasma E-selectin after ascent to high altitude and in hypoxemic climbers with AMS and HAPE provides evidence that endothelial cell activation or injury is a component of hypoxic altitude illness.

Pustular and Erythrodermic Psoriasis Complicated by Acute Respiratory Distress Syndrome

The pustular and erythrodermic types of psoriasis have been associated with a number of systemic complications, including congestive heart failure and pneumonia. Acute respiratory distress syndrome (ARDS) refers to acute noncardiogenic pulmonary edema with hypoxemia of various causes and has been attributed to pulmonary capillary leak. Recently, 4 cases of generalized pustular or erythrodermic psoriasis have been described associated with a pulmonary capillary leak syndrome. We describe 2 additional patients, 1 with pustular and erythrodermic psoriasis and 1 with erythrodermic psoriasis; who developed ARDS. Radiographic findings, pulmonary capillary wedge pressures, echocardiograms, and, in one case, an open lung biopsy specimen, were consistent with the diagnosis of ARDS. In neither case could we document any of the common causes of acute respiratory failure. Generalized pustular and erythrodermic psoriasis may be complicated by ARDS. The pathogenesis of this complication is unclear, but proinflammatory cytokines may be involved.

Acute pulmonary edema associated with transfusion of packed red blood cells

We experienced a patient who suffered noncardiogenic acute pulmonary edema after transfusion of packed red blood cells which contained antigranulocyte antibodies. The data suggested that complement activation and the release of polymorphonuclear protease were involved in the pathogenesis of the complication in the present patient. Furthermore, blood coagulative system was also activated after the transfusion. The underlying mechanisms of the complication are discussed.

Acral erythema and systemic toxicity related to CHA induction therapy in acute myeloid leukemia

Seventy-two adult patients with previously untreated acute myeloid leukemia received the CHA regimen as induction chemotherapy: CCNU 80 mg/m 2 on day 1, Adriamycin® 35 mg/m 2 i.v. on days 1, 2 and 3, and continuous infusion of cytarabine 100 mg/m 2/24 h from day 1 to 10. Forty-nine patients ( 68%) presented at least one of the following symptoms: acral erythema with dysesthesias in the palms and/or soles ( 39%); cholestatic hepatitis ( 39%); profuse sterile diarrhea associated with abdominal distention ( 33%); acute cerebellar dysfunction ( 32%) and non-cardiogenic pulmonary edema ( 21%). Most of these toxic symptoms appeared 8–20 days after the first dose. As these clinical features were absent or exceptional in patients treated with another regimen within a controlled trial, they are reported as toxic side-effects of the chemotherapy regimen. Acral erythema was found to be predictive of complete remission ( P < 0.01, odds ratio: 6.33); neurotoxicity was prognostic for death in aplasia ( P < 0.05); the absence of any of the five symptoms was associated with failure of the induction regimen ( P < 0.02).

Venovenous Extracorporeal Membrane Oxygenation for Noncardiogenic Pulmonary Edema After Coronary Bypass Surgery

A 71-year-old woman with noncardiogenic acute pulmonary edema early after having a coronary operation was treated with venovenous extracorporeal membrane oxygenation for uncontrollable hypoxia. Adequate oxygenation was achieved, the rapid deterioration of her condition was reversed, and ventilatory settings could be moderated. Two and a half days later, the patient was weaned from the system. At the time of this writing, the patient was in her sixth postoperative month and doing well. Details of this fairly simple but powerful technique are described.

ARDS due to Ingestion of Denatured Rapeseed Oil

Among the different etiologies of noncardiogenic acute pulmonary edema is found the administration or ingestion of various substances. We have studied two patients with ARDS secondary to the ingestion of toxic oil. Both patients presented similar roentgenographic findings characterized by interstitial and alveolar infiltration in "butterfly" distribution, pleural effusion, and a normal cardiac silhouette. The two cases also showed a pulmonary compliance either normal or slightly diminished. With the aid of artificial ventilation, they evolved favorably, gaseous exchange and chest x-ray films returning to normal 16 and 22 days after admission.