Neurogenic Pulmonary Edema in Fatal and Nonfatal Head Injuries

Rogers, Frederick B.; Shackford, Steven R.; Trevisani, Gino T.; Davis, James W.; Mackersie, Robert C.; Hoyt, David B.

doi:10.1097/00005373-199511000-00009

Cited by 127 publications

(73 citation statements)

References 38 publications

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“…The Division of Transplantation of the Health Resources and Services Administration, part of the Department of Health and Human Services, is beginning to address these issues (3). Unfortunately, there are even fewer suitable lungs than other solid organs among deceased donors because of lung injury from a combination of the high incidence of aspiration (4), neurogenic pulmonary edema (5), nosocomial infection, lung contusion, and acute respiratory distress syndrome/acute inflammation in trauma patients who become donors. Because each of these factors may adversely affect the outcome of lung transplantation, there is reluctance among lung transplant surgeons to use grafts from donors that may function poorly.…”

Section: Inadequate Number Of Lungs For Transplantmentioning

confidence: 99%

Lung Transplantation: Opportunities for Research and Clinical Advancement

Wilkes¹

2006

Am J Respir Crit Care Med

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Lung transplantation is the only definitive therapy for many forms of end-stage lung diseases. However, the success of lung transplantation is limited by many factors: (1 ) Too few lungs available for transplantation due to limited donors or injury to the donor lung; (2 ) current methods of preservation of excised lungs do not allow extended periods of time between procurement and implantation; (3 ) acute graft failure is more common with lungs than other solid organs, thus contributing to poorer short-term survival after lung transplant compared with that for recipients of other organs; (4 ) lung transplant recipients are particularly vulnerable to pulmonary infections; and (5 ) chronic allograft dysfunction, manifest by bronchiolitis obliterans syndrome, is frequent and limits long-term survival. Scientific advances may provide significant improvements in the outcome of lung transplantation. The National Heart, Lung, and Blood Institute convened a working group of investigators on June 14-15, 2004, in Bethesda, Maryland, to identify opportunities for scientific advancement in lung transplantation, including basic and clinical research. This workshop provides a framework to identify critical issues related to clinical lung transplantation, and to delineate important areas for productive scientific investigation. Keywords: allograft dysfunction; infection; ischemia-reperfusion injury; lung transplantation; obliterative bronchiolitis; rejectionThe transplantation of organs offers the promise of life-saving and life-enhancing therapy for a variety of ailments. Lung transplantation (LTx) has become an acceptable therapy to palliate patients with a variety of end-stage lung diseases. However, lung transplantation has not turned out to be a panacea for chronic lung disease because of significant limitations in the entire transplant process (Figure 1). First, there are not nearly enough suitable donor lungs to meet the needs of all patients with end-stage lung disease. As a result, more patients die waiting for transplants than from mortality associated with a lung transplant. Second, early graft survival after LTx is worse than for other types of organs transplanted (1). Finally, late survival after successful LTx is hampered by the development of chronic allograft dysfunction and by the life-limiting complications associated with conventional immunosuppressive medications. Two factors impede progress to address these problems: (1 ) lung transplant centers lack the infrastructure to facilitate prospective, multicenter clinical studies of sufficient power to address clinical questions and (2 ) there are too few investigators studying the biology of lung transplantation.The NHLBI convened a workshop on June 14-15, 2004, to better understand these complex problems and to identify strategies to address these and prioritize them. The topics addressed by participants were wide-ranging. They included the following: lung use rates from conventional brain-dead organ donors; safe limits for donor lung function; consideration o...

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Section: Inadequate Number Of Lungs For Transplantmentioning

confidence: 99%

Lung Transplantation: Opportunities for Research and Clinical Advancement

Wilkes¹

2006

Am J Respir Crit Care Med

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“…7 Furthermore, severe hypoxia causes cerebral edema and elevation in intracranial pressure (ICP). Elevated ICP levels correlate with increased levels of extravascular lung water (EVLW) playing an important role in the pathogenesis of neurogenic pulmonary edema (NPE).…”

Section: Discussionmentioning

confidence: 99%

Survivor by asphyxiation due to helium inhalation

Etteri¹,

Bellone²,

Vella³

et al. 2016

Emerg Care J

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In this rare case report we describe a 27-year-old white man survived to suicide by asphyxiation using the so-called suicide bag (or exit bag) filled with helium supplied through a plastic tube. He had no previous psychiatric or organic illnesses. At the time of presentation to our Emergency Department he was awake and reported severe dyspnea with a clinical pattern of acute respiratory failure. Imaging studies showed pulmonary edema and the patient was treated with non-invasive ventilation in Intensive Care Unit. After 15 days the patient was discharged from hospital in optimal conditions. These rare cases of survivor might suggest the possible causes of death from inhaling helium. Case ReportA 27-year-old male student was rescued at home by his father: he was found to be uncounscious with so-called suicide bag (or exit bag) filled with helium supplied through a plastic tube. Immediately he removed the bag (not really narrow neck) from the head and called the emergency number.When the ambulance arrived he was found with prompt resumption of breathing and slow recovery of consciousness with peripheral cyanosis, pulse rate was 130/minute and blood pressure 160/90 mmHg. On arrival at the Emergency Department he was conscious with hemodynamic stability, the respiratory rate was 35/min, pheripheral pulse oxymetry revealed SpO2 of 80% in air. Past medical history was negative.Thoracic fine crepitations were auscultated on both sides. Heart sound was normal. Hemogasanalysis showed a severe respiratory failure with PaO2/FiO2 value of 120. Electrocardiogram revealed non-abnormalities except sinus tachycardia. We performed a chest X-ray and a bedside lung ultrasound with convex probe 5 MHz that revealed a bilateral Bpattern typical of interstitial syndrome, mainly due to acute pulmonary edema. Inferior vena cava and heart contractility were normal (studied with a cardiac phased array probe 2.5 MHz). Moreover it was performed a thoracic CT scan which confirmed the diagnosis of bilateral pulmonary edema that was bilateral, symmetric, ground-glass like, and not involving the anterior areas of the chest.A non-invasive ventilation (NIV) with fullface mask was applied. Ventilatory settings were as follows: FiO2 50%, PEEP 10 cm of H2O, PS 5 cm of H2O. Blood test was normal except for a slight increase of troponins.He was transferred to the Intensive Care Unit. On the three day of hospitalization patient was successfully weaned off the non invasive ventilator: pulse rate was 80/minute and blood pressure 120/70 mm of Hg, the respiratory rate was 15/min, SpO2 of 98%. Then he was transferred to the pulmonology ward.The patient remained asymptomatic over the next 10 days. Blood test was normal. Chest was clinically clear. After being subjected to a psychiatric evaluation, he was discharged from the hospital. DiscussionHelium is one of inert gases causing physical asphyxiation, whose excess content in the breathing atmosphere reduces the partial pressure of oxygen and may be fatal after short-term exposure. When breathing a m...

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“…Neurogenic pulmonary edema (NPE) is defined as an increase in pulmonary interstitial and alveolar fluid (132)(133)(134)(135) developing after an acute injury to the brain or brainstem in patients with intracranial pathology, including subarachnoid haemorrhage, cerebral emboli, cerebral tumours, status epilepticus, and raised intracranial pressure (ICP). The increased intracranial pressure is thought to precipitate an increased central sympathetic nerve activity transmitted via peripheral alpha and beta-adrenergic receptors.…”

Section: Neurogenic Pulmonary Oedemamentioning

confidence: 99%