NON-CARDIOGENIC PULMONARY OEDEMA

PATHOGENESIS

changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult

elevated intravascular pressure and pulmonary capillary leak

Blast Theory

An initial and rapid increase in pulmonary vascular pressure due to pulmonary vasoconstriction or pulmonary blood flow can lead to pulmonary microvascular injury. An increase in vascular permeability consequently results in edema formation, as suggested by the frequent observation of pulmonary hemorrhage in NPE

Causes

ARDS Neurogenic pulmonary edema Pulmonary edema in renal failure and/or fluid overload Negative-pressure pulmonary edema Pulmonary edema in marathon runners Decompression sickness Heroin and naloxone overdose NPE associated with cytotoxic chemotherapy Pulmonary complications of pregnancy Drowning NPE induced by a molecular adsorbent recirculating system Transfusion-related pulmonary edema between mother and child NPE after lung transplantation NPE in children with nonaccidental injury

Adult respiratory distress syndrome

presence of bilateral pulmonary infiltrates on chest radiograph, impaired oxygenation resulting in a PaO2 -to–fraction of inspired oxygen (FIO2) ratio of less than 200, and absence of elevated pulmonary arterial occlusion pressure (PAOP) or left atrial pressure.

originates from a number of insults involving damage to the alveolocapillary membrane with subsequent fluid accumulation in the airspaces of the lung.

Neurogenic pulmonary edema

increased intracranial pressure,stimulate the hypothalamus and the

vasomotor centers of the medulla.Pulmonary venoconstriction occurs with

sympathetic stimulationdramatic change in Starling forces, govern

the movement of fluid between capillaries and the interstitium

Pulmonary edema in renal failure/fluid overload

Impaired salt and/or water excretion leads to plasma volume expansion.

along with decreased plasma oncotic pressure and an increase in capillary permeability

Negative-pressure pulmonary edema

associated with upper airway obstructionMost cases are croup or epiglottitis in the

pediatric and adults requiring emergent airway intervention for laryngospasm or upper airway tumors

Negative intrapleural pressure is the primary pathologic event

increasing venous return to the right heart and by decreasing the output of the left ventricle,

increasing pulmonary blood volume and microvascular pressures.

Pulmonary edema in marathon runners

Hyponatremia, cerebral edema, and NPE can occur in healthy marathon runners.

often associated with hyponatremic encephalopathy

Decompression sickness

type 2 decompression sicknessoccurs within 6 hours of a dive.

High-Altitude Pulmonary Edema

prolonged exposure to an environment with a lower partial oxygen atmospheric pressure.

occurs most frequently in young males 24–48 hours after they have made a rapid ascent to heights greater than 3,000 meters and have remained in that environment (52-54)

Heroin and naloxone overdose

Pathogenesis is unknownclinically apparent immediately after or

within 2 hours following drug use.Signs include rales; significant hypoxia; pink,

frothy sputum; and bilateral, fluffy infiltrates on chest radiography

Drug-Related NPE

reported following the accidental intra-arterial injection of benzathine penicillin in the gluteal region

reported on a patient in whom pulmonary edema was associated with low left ventricular filling pressures and hypotension, which developed soon after the person ingested 12.5 mg of hydrochlorothiazide.

life-threatening NPE has been reported following an idiosyncratic reaction after clopidogrel use

NPE associated with cytotoxic chemotherapy

said to occur in 20% of patients receiving cytotoxic chemotherapy.

clinical and imaging findings are similar to those of NPE due to other causes.

Pulmonary complications of pregnancy

Physiologic changesdiaphragm is elevated by as much as 4 cm

because of displacement of the abdominal organs by the gravid uterus, decreasing lung volumes.

Maternal blood volume and cardiac output increase approximately 45% by midpregnancy.

Cardiac output can increase as much as 80% during vaginal delivery and up to 50% with cesarean delivery

Drowning

extent and severity of the edema depends on the amount of water aspirated and the degree of hypoxia

injury of the alveolar septa, increased permeability of the pulmonary vascular endothelium, pulmonary microvascular platelet aggregation, and intra-alveolar edema

Whether the water is fresh or salt makes no difference

NPE induced by a molecular adsorbent recirculating system

related, among others, to blood or blood-product transfusion, intravenous contrast injection, air embolism, and drug ingestion.

possibly by means of an immune-mediated mechanism.

Transfusion-related pulmonary edema between mother and

child(TRALI)

underdiagnosed and serious complication of blood transfusion

presence of anti–human leukocyte antigen (anti-HLA) and/or antigranulocyte antibodies in the plasma of donors is implicated in the pathogenesis of TRALI.

Designated blood transfusion between multiparous mothers and their children might add an additional transfusion-related risk owing to the increased likelihood of the HLA antibody-antigen specificity between mother and child.

NPE after lung transplantation

Complications of lung transplantation include the reimplantation response, acute rejection, pleural effusion, lymphoproliferative disorders, bronchiolitis obliterans, infection, and airway stenosis or dehiscence.

reimplantation response is a form of NPE that begins soon after surgery and resolves in days to weeks.

NPE in children with nonaccidental injury

NPE in children may occur after head injury, prolonged seizure, acute airway obstruction, or ingestion or inhalation of toxic drugs or chemicals. Rarely, NPE may be associated with child abuse or maltreatment.

RADIOLOGICAL FEATURE

Heart size may be normal in lung injury and NPE

nephrogenic pulmonary edema are classically described as having a bat-wing distribution

those in lung injury tend to be more peripherally finding, diffuse variety is seen with equal frequency, presence of air bronchograms

ARDS may resemble cardiac pulmonary edema. However, over the course of 24-48 hours following the onset of tachypnea, dyspnea, and hypoxia, ARDS becomes more widespread and uniform

characteristic for differentiating cardiac pulmonary edema from NPE, as well as from pneumonia and other widespread exudates, is the amount of time it takes for the edema to develop and to vanish.

The reimplantation response (NPE due to ischemia, trauma, denervation, and lymphatic interruption) occurred in 12 patients and usually consisted of bilateral perihilar and basal consolidation

ARDS associated with DAD in a 20-year-old man involved in a motor vehicle accident who underwent massive bronchoaspiration during tracheal intubation. bilateral diffuse airspace consolidations with a marked anteroposterior gradient. In addition, bilateral peripheral

areas of hyperlucency representing trapped air are seen. Kerley lines are notably absent, and pleural effusions are minor compared with

the extent of the airspace lesions.

 Neurogenic pulmonary edema in a 54-year-old woman who was admitted for intracranial hemorrhage due to arterial

hypertension. Chest x-ray shows airspace consolidations predominantly at the apices. There are no pleural effusions or

Kerley lines, and heart size is normal.

High-altitude pulmonary edema in an experienced 30-year-old female at an altitude of 4,500 meters demonstrate numerous small, confluent airspace consolidations that spare the apices

and most of the lung cortex. No Kerley lines or pleural effusions are seen. The heterogeneity of the airspace disease may reflect

the heterogeneity of the pulmonary vascular constriction.

 Heroin-induced pulmonary edema in a 19-year-old male addict with ARDS. Chest radiograph reveals massive diffuse pulmonary

edema.

Heroin-induced pulmonary edema in a 19-year-old male addict with ARDS obtained 27 hours later reveals substantial resolution of the pulmonary edema, which is only possible in the absence of

DAD

Heroin-induced pulmonary edema in a 24-year-old male addict who was admitted with a Glasgow coma score of 3. (a) Chest radiograph obtained at the time of admission demonstrates

confluent right pulmonary edema due to the right lateral decubitus position the patient had maintained for the previous

24 hours

Pulmonary edema following administration of a cytokine in a 37-year-old woman with malignant melanoma. obtained 48 hours after

treatment demonstrates bilateral diffuse pulmonary edema with peribronchial cuffing (arrow), enlarged hila, ill-defined vessels, and pleural effusions. Note the absence of alveolar areas of increased

opacity. The infiltrates disappeared within 5 days.

Pulmonary edema in a 34-year-old man who had undergone bilateral lung transplantation for end-stage cystic fibrosis.

radiograph obtained 48 hours after transplantation demonstrates diffuse, confluent alveolar areas of increased opacity.

Chest radiograph, before blood transfusion, of a patient with transfusion-related acute lung injury

(TRALI)

Chest radiograph after blood transfusion, of a patient with transfusion-related acute lung injury (TRALI). Bilateral

pulmonary infiltrates consistent with pulmonary oedema are an essential criterion for the clinical diagnosis of TRALI. Radiographs may be patchy in the first hours following

transfusion, with progression of the alveolar and interstitial infiltrates such that there can be a ‘whiteout’ of the entire lung.

Pulmonary edema in a 34-year-old man who had undergone bilateral lung transplantation for end-stage cystic fibrosis. obtained

2 days later, the areas of increased opacity have decreased markedly. The heart and vascular axes are normal in size.

The radiologic distinction of cardiogenic and noncardiogenic edema ,EN Milne, M Pistolesi, M Miniati, and C Giuntini American Journal of Roentgenology, Vol 144, Issue 5, 879-894Copyright © 1985 by American Roentgen Ray Society

Clinical and Radiologic Features of Pulmonary Edema, Thomas Gluecker, MD , Patrizio Capasso, MD , Pierre Schnyder, MD , François Gudinchet, MD , Marie-Denise Schaller, MD , Jean-Pierre Revelly, MD , René Chiolero, MD , Peter Vock, MD and Stéphan Wicky, MD (http://radiographics.rsna.org/content/19/6/1507.ful )

Pulmonary Edema, NoncardiogenicAuthor: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, Consultant Radiologist and Honorary Professor, North Manchester General Hospital Pennine Acute NHS Trust, UK Coauthor(s): Klaus L Irion, MD, PhD, Consulting Staff, The Cardiothoracic Centre Liverpool NHS Trust, The Royal Liverpool University Hospital, UK; Ram Sundar Kasthuri, MBBS, Specialist Registrar, Department of Radiology, North Manchester General Hospital; Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular InstituteContributor Information and Disclosures(http://emedicine.medscape.com/article/360932-overview )