Pulmonary edema

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Pulmonary edema is fluid accumulation in the lungs. This fluid accumulation leads to impaired gas exchange and hypoxia.

Pulmonary edema was first described as a result of heart failure by Andreas Nerlich. In 1891 the first case of high altitude pulmonary edema was reported. In 1908, W. T. Shanahan noted acute pulmonary edema as an adverse effect of epileptic seizures.

Pulmonary edema can be classified on the basis of etiology into 2 subtypes, including cardiogenic pulmonary edema (left ventricular failure, myocardial infarction, left ventricle hypertrophy cardiomyopathy) and, noncardiogenic pulmonary edema (acute respiratory distress syndrome, pneumonia, pulmonary embolism, chest trauma).

Pulmonary edema is due to either failure of the heart to remove fluid from the lung circulation (“cardiogenic pulmonary edema”), or due to a direct injury to the lung parenchyma or increased permeability or leakiness of the capillaries (“noncardiogenic pulmonary edema”).

Common causes of cardiogenic pulmonary edema are cardiomyopathy, congestive heart failure, coronary heart disease, aortic regurgitation, aortic stenosis. Common causes of noncardiogenic pulmonary edema are acute respiratory distress syndrome, high altitude pulmonary edema, pulmonary embolism.

Pulmonary edema should be distinguished from other conditions that cause dyspnea, orthopnea, cough.

The prevalence of pulmonary edema was estimated to be 75000-83000 cases per 100,000 individuals among heart failure patients with reduced ejection fraction. Pulmonary edema commonly affects individuals older than 65 years of age. Males are more commonly affected by pulmonary edema than woman.

The risk factors in pulmonary edema refer to the risk factors for the underlying disease that cause pulmonary edema. Risk factors of cardinogenic pulmonary edema include high blood pressure, hyperlipidemia, atherosclerosis, diabetes mellitus, obesity. And risk factors for noncardiogenic pulmonary edema include sepsis, aspiration, pneumonia.

There is insufficient evidence to recommend routine screening for pulmonary edema.

Some patients may need to use a breathing machine for a long time, which may lead to damage to lung tissue.Kidney failure and damage to other major organs may occur if blood and oxygen flow are not restored promptly. If not treated, this condition can be fatal. If left untreated, acute pulmonary edema can lead to coma and even death, generally due to its main complication of hypoxia.

Pulmonary artery catheterization is the gold standard test for the diagnosis of pulmonary edema. Elevated pulmonary-artery pressure indicates cardiogenic pulmonary edema or pulmonary edema due to volume overload.

The history of a patient with pulmonary edema varies according to the underlying cause. The most common symptom of pulmonary edema is shortness of breath (dyspnea). Depending on the cause, it may occur acutely or have a gradual onset. When pulmonary edema is due to an acute myocardial infarction chest pain is common symptom.

Patients with pulmonary edema usually appear agitated. Physical examination of patients with pulmonary edema is usually remarkable for dyspnea, tachypnea. The presence of abnormal cardiac examination on physical examination is diagnostic of cardiogenic pulmonary edema. Patients with noncardiogenic pulmonary edema may have warm extremities, whereas patients with cardiogenic pulmonary edema may have cool extremities.

The diagnosis is confirmed on X-ray of the lungs, which shows increased fluid in the alveolar walls. Kerley B lines, increased vascular filling, pleural effusions, upper lobe diversion (increased blood flow to the higher parts of the lung) may be indicative of cardiogenic pulmonary edema, while patchy alveolar infiltrates with air bronchograms are more indicative of noncardiogenic edema

Although there is no diagnostic criteria of pulmonary edema on the EKG, there may be signs of the underlying cardiogenic cause of pulmonary edema.

Thoracic CT scan may be helpful in the diagnosis of pulmonary edema. Findings on CT scan diagnostic of hydrostatic pulmonary edema include cardiomegaly, vascular engorgment, pleural effusions.

There are no MRI findings associated with pulmonary edema.

Echocardiography is useful in confirming a cardiac or no-cardiac cause of pulmonary edema. Echocardiography may identify the presence and severity of valvular causes of pulmonary edema. Echocardiography is helpful in diagnosis of ischemia or myocardial infarction, cardiomyopathy as an underlying cause of pulmonary edema. Echocardiography is less sensitive in identifying diastolic dysfunction. Thus, a normal echocardiogram may not rule out cardiogenic pulmonary edema.

There are no additional imaging findings associated with pulmonary edema.

Pulmonary artery catheterization is the gold standard test for the diagnosis of pulmonary edema. Elevated pulmonary-artery pressure indicates cardiogenic pulmonary edema or pulmonary edema due to volume overload.

Pulmonary edema classified into cardiogenic and non-cardiogenic pulmonary edema, each requires different management and has a different prognosis. The main goal of a treatment are alleviate symptoms and improving hemodynamics. The initial management of patients is following the ABCs of resuscitation, that is, airway, breathing, and circulation. Medical treatment of cardiogenic pulmonary edema focuses on preload reduction, afterload reduction and inotropic support.

The mainstay of treatment for pulmonary edema is medical therapy. Surgery is usually reserved for patients who experienced cardiogenic shock following acute cardiogenic pulmonary edema.

Effective measures for the primary prevention of cardiogenic pulmonary edema include maintaining a healthy lifestyle, avoid tobacco, treat dyslipidemia, low salt diet, controlling hypertension, avoid cardiotoxic agents, controling diabetes. Effective measures for the primary prevention of high-altitude pulmonary edema include, encourage healthy lifestyle and exercise, gradual ascent, preacclimization, avoiding alcohol ingestion, high carbohydrate in diet, adequate hydration, vigorous exertion during the first few days at high altitude, oxygen enrichment.

The major complications of cardiogenic pulmonary edema are respiratory failure and sudden cardiac death secondary to cardiac arrhythmia. Prompt diagnosis and treatment are effective for secondary prevention in cardiogenic pulmonary edema.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Pulmonary edema was first described as a result of heart failure by Andreas Nerlich. In 1891 the first case of high altitude pulmonary edema was reported. In 1908, W. T. Shanahan noted acute pulmonary edema as an adverse effect of epileptic seizures.

• Pulmonary edema was first described as a result of heart failure by Andreas Nerlich, a pathologist from Munich, Germany.^[1]
• In 1891 the first case of high altitude pulmonary edema was reported.^[2]
• In 1913, TH Ravenhill suggested first diagnostic framework for high altitude pulmonary edema.^[2]
• In 1908, W. T. Shanahan noted acute pulmonary edema as an adverse effect of epileptic seizures.^[3][4]

• During WWI, francois Moutier noted the sudden onset of pulmonary edema among soldiers shot in the head.^[3][4]
• In the Vietnam War, alveolar edema and hemorrhage seen in the lungs of soldiers dying after isolated bullet head wounds.^[5]

• In 1953, intra-aortic balloon pumping (IABP) was described by Kantrowitz.^[6]
• In 1962, the modern intra-aortic counterpulsation device was described by Moulopoulos et al at the Cleveland Clinic.^[7]
• In 1969 intra-aortic balloon pumping (IABP) was first used clinically in a patient with cardiogenic shock.
• Since the 1980s, IABP has been increasingly used in stabilizing patient with cardiogenic pulmonary edema before definitive therapy.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Pulmonary edema can be classified on the basis of etiology into 2 subtypes, including cardiogenic pulmonary edema (left ventricular failure, myocardial infarction, left ventricle hypertrophy cardiomyopathy) and, noncardiogenic pulmonary edema (high altitude pulmonary edema, neurogenic pulmonary edema, reperfusion pulmonary edema, re-expansion pulmonary edema)

Pulmonary edema may be classified according to etiology into 2 groups:

• Cardiogenic pulmonary edema, which can be secondary to:^[1]
  • Left ventricular failure
  • Dysrhythmia
  • Left ventricular hypertrophy cardiomyopathy
  • Volume overload
  • Myocardial Infarction
  • Left ventricular outflow obstruction
• Non-cardiogenic pulmonary edema which can be secondary to:^[2]
  • Acute respiratory distress syndrome (ARDS)
  • High altitude pulmonary edema
  • Neurogenic pulmonary edema
  • Reperfusion pulmonary edema
  • Re-expansion pulmonary edema
  • Others(opioid overdose, salicylate toxicity, viral infections)

    Pulmonary edema

    Cardiogenic

    Non-cardiogenic

    LV failure

    Dysrhythmia

    LV hypertrophy and cardiomyopathy

    Volume overload

    Myocardial Infarction

    LV outflow obstruction

    Direct injury to lung

    Hematogenous injury to lung

    Lung injury plus elevated hydrostatic pressure

    Chest trauma,pulmonary contusion

    Aspiration

    Smoke inhalation

    Pneumonia

    Oxygen toxicity

    Pulmonary embolism,reperfusion

    High altitude pulmonary edema

    Neurogenic pulmonary edema

    Reexpansion pulmonary edema

    Sepsis

    Pancreatitis

    Nonthoracic trauma

    Multiple transfusions

    Intravenous drug use. e.g. heroin

    References

    1. ↑ Attias D, Mansencal N, Auvert B, Vieillard-Baron A, Delos A, Lacombe P, N’Guetta R, Jardin F, Dubourg O (2010). “Prevalence, characteristics, and outcomes of patients presenting with cardiogenic unilateral pulmonary edema”. Circulation. 122 (11): 1109–15. doi:10.1161/CIRCULATIONAHA.109.934950. PMID 20805429.
    2. ↑ Calenoff L, Kruglik GD, Woodruff A (1978). “Unilateral pulmonary edema”. Radiology. 126 (1): 19–24. doi:10.1148/126.1.19. PMID 619405.

    
    

    Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Pulmonary edema is due to either failure of the heart to remove fluid from the lung circulation (“cardiogenic pulmonary edema”), or due to a direct injury to the lung parenchyma or increased permeability or leakiness of the capillaries (“noncardiogenic pulmonary edema”).

It is understood that pulmonary edema is the abnormal increase in extravascular lung water (EVLW). This condition may be caused by the following underlying physiologic changes:^[1][2][3]

• Imbalance of staling force
• Altered valvular capillary membrane permeability
• Lymphatic insufficiency
• Other factors

These factors have been described bellow:

The flux of fluid across the capillary wall is controlled by a balance between hydrostatic pressure and osmotic pressure gradients between the capillaries and interstitial space that can be calculated via Starling equation:

JV = K.S.([Pmv-Ppmv]-σd[πmv-πpmv])

where:

JV = volume flow across the capillary bed

K = filtration coefficient of the capillary wall

S = surface area of the capillary bed

Pmv = microvascular hydrostatic pressure

Ppmv = perimicrovascular (interstitial) hydrostatic pressure

πmv = plasma colloid osmotic pressure

πpmv = perimicrovascular (interstitial) colloid osmotic pressure

σd = protein reflection coefficient

• Increase pulmonary capillary pressure
  • In cardiogenic pulmonary edema, the most common mechanism for a rise in transcapillary filtration is an increase in pulmonary capillary pressure.
    • Left ventricular failure
    • Left ventricular outflow obstruction
    • Mitral stenosis

• Increase negative interstitial pressure
  • Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema^[4]
    • It is understood that postobstructive pulmonary edema is caused by highly negative intrathoracic pressure that create by forceful attempts to inhale against an obstruction, this causes elevated venous return, declined cardiac output and fluid transudation into the alveolar space.

Following are a few important aspects about altered alveolar capillary membrane permeability leading to pulmonary edema:

• In noncardiogenic pulmonary edema, the most common mechanism for a rise in transcapillary filtration is an increase in capillary permeability.

• This increase in permeability damages the alveolar-capillary membrane, causing increased movement of water and proteins from the intravascular space to the interstitial space.

• In most cases of noncardiogenic pulmonary edema, the concentration of protein in the interstitium exceeds 60 percent of the plasma value, compared to less than 45 percent in cardiogenic pulmonary edema.

ARDS can be seen in a number of disorders:

• Sepsis
• Acute pulmonary infection
• Non-thoracic trauma
• Disseminated intravascular coagulation
• Aspiration

Lymphatic insufficiency may follow:

• Lymphangitic carcinomatosis
• Fibrosing lymphangitis

Various other factors contributing to the development of pulmonary edema include:

• High-altitude pulmonary edema
  • It is understood that high-altitude pulmonary edema is caused by hypoxic pulmonary vasoconstriction at altitudes above 12,000 to 13,000 feet (3600 to 3900 m).^[5]
• Neurogenic pulmonary edema
  • It is understood that neurogenic pulmonary edema is caused by sympathetic overreactivity with massive catecholamine surges that shifts blood from the systemic to the pulmonary circulation.^[6]
• Narcotic overdose
  • The exact pathogenesis of narcotic overdose pulmonary edema is not fully understood. Proposed mechanisms include combination of direct toxicity of the drug, hypoxia, and acidosis secondary to hypoventilation and/or cerebral edema.^[7]
• Pulmonary embolism 
  • It is understood that pulmonary embolism can cause pulmonary edema by damaging the pulmonary and nearby pleural systemic circulations, increasing hydrostatic pressures in pulmonary and/or systemic veins, and decreasing pleural pressure due to atelectasis.^[8]
• Re-expansion pulmonary edema
  • The exact pathogenesis of re-expansion pulmonary edema is not fully understood. Direct injury from surfactant dysfunction in chronic atelectatic lung, elevated transpleural pressures, or indirect injury from reperfusion has been proposed.^[9]

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Common causes of cardiogenic pulmonary edema are cardiomyopathy, congestive heart failure, coronary heart disease, aortic regurgitation, aortic stenosis. Common causes of noncardiogenic pulmonary edema are acute respiratory distress syndrome, high altitude pulmonary edema, pulmonary embolism.

• Congestive heart failure
• Coronary Heart Disease
• Aortic Regurgitation
• Aortic Stenosis
• Mitral Regurgitation
• Mitral Stenosis
• Myocarditis
• Pericardial Disease
• Infection
• Sepsis

• Severe arrhythmias (tachycardia/fast heartbeat or bradycardia/slow heartbeat)
• Arteriovenous malformation
• Anomalous pulmonary venous return
• Aortic Regurgitation
• Aortic Stenosis
• Arrhythmia
• Cardiomyopathy
• Congenita pulmonary venous stenosis
• Congestive heart failure
• Coronary Heart Disease
• Cytarabine
• Hypertensive crisis
• Left Heart Failure
• Left-to-Right Shunt
• Mitral Regurgitation
• Mitral Stenosis
• Myocarditis
• Pericardial Disease
• Pericardial effusion with tamponade
• ST elevation MI with left ventricular failure

This form is contiguous with ARDS (acute respiratory distress syndrome):

• Acute Bronchial Asthma
• Acute Renal Failure
• Bacterial toxins
• Blood Transfusions
• Burns
• Chronic mediastinitis
• Decompression sickness
• Disseminated Intravascular Coagulation
• Drowning
• Drugs– Cytomegalovirus immune globulin
• Fibrotic/inflammatory disease
• Fluid overload, e.g. from kidney failure
• Gastric content aspiration
• Goodpasture’s Syndrome
• High altitude sickness. Ascent to high altitude occasionally causes high altitude pulmonary edema (HAPE)^[3]
• Hyperhydration
• Hypoalbuminemia / Albumin deficiency
• Idiopathic Venoocclusive Disease
• Inhalation of toxic gases
• Infection
• Leukemia
• Malaria
• Miliary Tuberculosis
• Neurogenic, e.g. subarachnoid hemorrhage
• Oprelvekin
• Pheochromocytoma
• Pneumonia
• Pulmonary contusion, i.e. high-energy trauma
• Pulmonary Embolism
• Reexpansion, i.e. post pneumonectomy or large volume thoracentesis
• Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
• Sepsis
• Shock
• Toxic Shock Syndrome
• Multitrauma, e.g. motor vehicle accident
• Upper airway obstruction
• Uremia

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Pulmonary edema should be distinguished from other conditions that cause dyspnea, orthopnea, cough.

Pulmonary edema should be differentiated from other diseases presenting with dyspnea, orthopnea, cough.

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); DOE (dyspnea on exercise); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell);

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

The prevalence of pulmonary edema was estimated to be 75000-83000 cases per 100,000 individuals among heart failure patients with reduced ejection fraction. Pulmonary edema commonly affects individuals older than 65 years of age. Males are more commonly affected by pulmonary edema than woman.

• The incidence of neurogenic pulmonary edema is approximately 2000 to 42900 per 100,000 individuals in patients with subarachnoid hemorrhage.^[1][2]
• The incidence of neurogenic pulmonary edema is approximately 20000 per 100,000 individuals in patients with traumatic brain injury.^[3]

• The prevalence of pulmonary edema was estimated to be 75000-83000 cases per 100,000 individuals among heart failure patients with reduced ejection fraction.^[4]

• The mortality rate of pulmonary edema is approximately 12000 per 100000 among in-hospital patients.^[5]

• The median time from the pulmonary edema until death is approximately 10 days.
• Higher in-hospital mortality rate are associated with left ventricular myocardial function.

• Pulmonary edema commonly affects individuals older than 65 years of age.^[5]

• Blacks have the highest risk for heart failure as underlying cause of pulmonary edema.^[6]

• Males are more commonly affected by pulmonary edema than woman.^[5]

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

The risk factors in pulmonary edema refer to the risk factors for the underlying disease that cause pulmonary edema. Risk factors of cardinogenic pulmonary edema include high blood pressure, hyperlipidemia, atherosclerosis, diabetes mellitus, obesity. And risk factors for noncardiogenic pulmonary edema include sepsis, aspiration, pneumonia.

The risk factors in pulmonary edema refer to the risk factors for the underlying disease that cause pulmonary edema. Heart failure patients are the most at risk for pulmonary edema.^[1]

• High blood pressure

• Valvular disease

• Hyperlipidemia

• Atherosclerosis
• Acute myocardial infarction
• Unstable angina pectoris
• Rapid atrial fibrillation

• Diabetes mellitus

• Obesity

• Excessive alcohol intake

• Physical inactivity

• Dietary choices

• Smoking

• Sepsis
• Aspiration
• Pneumonia

• Trauma
• Inhaled toxins
• Disseminated intravascular coagulation 

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

Some patients may need to use a breathing machine for a long time, which may lead to damage to lung tissue. Kidney failure and damage to other major organs may occur if blood and oxygen flow are not restored promptly. If not treated, this condition can be fatal. If left untreated, acute pulmonary edema can lead to coma and even death, generally due to its main complication of hypoxia.

• If left untreated, acute pulmonary edema can lead to respiratory arrest, coma and death, generally due to its main complication of hypoxia^[1]

• Some patients may need to use a breathing machine for a long time, which may lead to damage to lung tissue

Common complications of pulmonary edema include:^[1]

• Respiratory arrest

• Leg swelling (edema)
• Abdominal swelling (ascites)
• Pleural effusion
• Congestion of liver
• Myocardial infarction (MI)
• Cardiogenic shock
• Arrhythmias
• Electrolyte disturbances
• Mesenteric insufficiency
• Protein enteropathy
• Death

Prognosis of non-cardiogenic pulmonary edema is generally good and responds well to treatment, while cardiogenic pulmonary edema has a variable mortality rate.

• In-hospital mortality rates in a high-acuity setting, are 15-20%.

The prognosis for patients with acute pulmonary edema depends on the:^[1]

• Underlying cause
• The patient’s age
• Comorbidities
• Prompt diagnosis
• Initiation of effective treatment

The following features are associated with a worse outcome:^[1]

• Advanced Age
• Wide QRS complex
• Hyponatremia
• Low Left Ventricular Ejection Fraction
• Hypotension
• Precipitated by ischaemia
• Previous hospitalisation for heart failure
• Marked BNP elevation
• Elevated troponin

Template:WikiDoc Sources