Pulmonary edema

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	Pulmonary edema;
	Chest x-ray showing pulmonary edema
ICD-10	J81
ICD-9	514
DiseasesDB	11017
MedlinePlus	000140

For patient information click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

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

Pathophysiology

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").^[1]

Gross Pathology Findings

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

This is a gross photograph of lungs that are distended and red. The reddish coloration of the tissue is due to congestion. Some normal pink lung tissue is seen at the edges of the lungs (arrows).
This is a gross photograph of lung demonstrating acute pulmonary congestion and edema. A frothy exudate fills the bronchus (arrow).
This gross photograph demonstrates the frothy exudate that is being extruded from the lung tissue.

Histopathology

This is a low-power photomicrograph of lung from this case. The lung section has a pale-red color indicating proteinaceous material within the lung.
This is a higher-power photomicrograph of lung. The edema fluid within the alveoli is visible at this higher magnification (arrows). The thickened pleura (1) is on the left.

This is a higher-power photomicrograph showing edema-filled alveoli in the right portion of this section (arrows).
This high-power photomicrograph illustrates the edema fluid within the alveoli (1) and the congestion (RBCs) in the alveolar capillaries (arrows).

Differential diagnosis of Underlying Causes of Pulmonary Edema

Pulmonary edema is either due to direct damage to the tissue or as a result of inadequate functioning of the heart or circulatory system.

Cardiogenic

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
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

Non-cardiogenic

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
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)^[2]
Hyperhydration
Hypoalbuminemia / Albumin deficiency
Idiopathic Venoocclusive Disease
Inhalation of toxic gases
Infection
Leukemia
Malaria
Miliary Tuberculosis
Neurogenic, e.g. subarachnoid hemorrhage
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

Complete Differential Diagnosis of the Causes of Pulmonary Edema

(By organ system)

Cardiovascular	Severe Arrhythmias (tachycardia/fast heartbeat or bradycardia/slow heartbeat),Arteriovenous malformation,Anomalous pulmonary venous return, Aortic Regurgitation, Aortic Stenosis, Arrhythmia, Cardiomyopathy, Congenital pulmonary vein stenosis, Congestive heart failure, Coronary Heart Disease, 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
Chemical / poisoning	Chemotherapy
Dermatologic
Drug Side Effect	A variety of Drugs, particularly Chemotherapeutic agents such as anthracyclines
Ear Nose Throat	Upper airway obstruction
Endocrine	Pheochromocytoma
Environmental	High altitude sickness. Ascent to high altitude occasionally causes high altitude pulmonary edema (HAPE)^[3], Inhalation of toxic gases such as amonia, Water intoxication
Gastroenterologic	Gastric content aspiration
Genetic
Hematologic	Blood Transfusions, Idiopathic Venoocclusive Disease, Disseminated Intravascular Coagulation, Leukemia
Iatrogenic	Hyperhydration, Blood Transfusions, High altitude sickness. Ascent to high altitude occasionally causes high altitude pulmonary edema (HAPE)^[4]
Infectious Disease	Bacterial toxins, Malaria, Miliary Tuberculosis, Sepsis, Toxic Shock Syndrome
Musculoskeletal / Ortho
Neurologic	Neurogenic, e.g. Subarachnoid hemorrhage
Nutritional / Metabolic	Hypoalbuminemia / Albumin deficiency, Water intoxication
Obstetric/Gynecologic	Toxic Shock Syndrome
Oncologic	Chemotherapy
Opthalmologic
Overdose / Toxicity	Chemotherapy, Water intoxication
Psychiatric	Psychogenic polydipsia with hyperhydration, Water intoxication
Pulmonary	Acute Bronchial Asthma, Drowning, Gastric content aspiration, Mediastinitis,Pneumonia, Pulmonary contusion, Pulmonary embolism, Reexpansion, i.e. post pneumonectomy or large volume thoracentesis, Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation, Upper airway obstruction
Renal / Electrolyte	Acute Renal Failure, Uremia
Rheum / Immune / Allergy	Goodpasture's Syndrome
Sexual
Trauma	Drowning, Burns, Inhalation of toxic gases, Pulmonary contusion, Trauma
Urologic	Acute Renal Failure, Uremia
Miscellaneous	Decompression sickness, Shock

Natural History, Complications and Prognosis

If left untreated, acute pulmonary edema can lead to coma and even death, generally due to its main complication of hypoxia.

Diagnosis

Symptoms

Acute Pulmonary Edema

Anxiety
Cough, particularly coughing up blood or bloody froth
Difficulty breathing
Excessive sweating or diaphoresis
Feeling of "air hunger" or "drowning" (if this occurs suddenly, awakening the patient from sleep and causing the patient to sit up and catch their breath, it's called "paroxysmal nocturnal dyspnea")
Grunting or gurgling sounds with breathing
Pale or blue skin
Blue or cyanotic lips
Restlessness
Shortness of breath
Shortness of breath when lying down (orthopnea)
Wheezing

Chronic Pulmonary Edema

If pulmonary edema has been developing gradually, symptoms of fluid overload may be elicited. These include nocturia (frequent urination at night), ankle edema (swelling of the legs, generally of the "pitting" variety, where the skin is slow to return to normal when pressed upon), orthopnea (inability to lie down flat due to breathlessness) and paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night).

Physical Examination

General Appearance of the Patient

Anxious
Decrease in level of alertness (consciousness)
Inability to speak in full sentences

HEENT

Nasal flaring

Lungs

End-inspiratory crackles (sounds heard at the end of a deep breath)

Cardiovascular

A third heart sound (S3) may be present^[1]

Laboratory Studies

Brain Natriuretic Peptide

B-type natriuretic peptide (BNP) is elevated in the patient with cardiogenic pulmonary edema. A low BNP (<100 pg/ml) makes a cardiac cause very unlikely and is associated with non-cardiogenic pulmonary edema.^[1]

Oxygen Saturation

Low oxygen saturation or hypoxia may be present on arterial blood gas readings.

Chest X Ray

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^[1]

Echocardiography

If urgent echocardiography is available, this may strengthen the diagnosis, as well as identify valvular heart disease.

Cardiac Catheterization

In rare occasions, insertion of a Swan-Ganz catheter may be required to distinguish between the two main forms of pulmonary edema.^[1]

Treatment

Depends on the cause, but focuses on maximizing respiratory function and removing the cause. When circulatory causes have led to pulmonary edema, treatment with intravenous nitrates (glyceryl trinitrate), and loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. These improve both preload and afterload, and aid in improving cardiac function.

There are no causal therapies for direct tissue damage; removal of the causes (e.g. treating an infection) is the most important measure.

Sometimes the development of pulmonary edema will be referred to as flash pulmonary edema (FPE). This referes to the rapid onset of pulmonary edema. It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be caused by aortic regurgitation, heart failure, or almost any cause of elevated left ventricular filling pressures.

Treatment of FPE should be directed at the underlying cause, but the mainstays are ensuring adequate oxygenation, diuresis, and decrease of pulmonary circulation pressures.

Reoccurrence of FPE is thought to be associated with hypertension^[5] and may signify renal artery stenosis.^[6] Prevention of reoccurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure.

Focus is initially on maintaining adequate oxygenation. This may happen with high-flow oxygen, noninvasive ventilation (either continuous positive airway pressure (CPAP) or variable positive airway pressure (VPAP)^[7]^[8]) or mechanical ventilation in extreme cases.

Pathology and Case Report

Clinical Summary

A 69-year-old male with well-controlled Type I diabetes mellitus (insulin-dependent) presented with upper abdominal and lower chest pain of four hours duration and accompanied by shortness of breath and diaphoresis.

An electrocardiogram revealed multiple premature ventricular contractions (PVCs).

The hospital course was characterized by recurrent pulmonary edema and oliguria.

The terminal event was cardiac arrest.

Autopsy Study

Significant findings at postmortem examination were old and recent myocardial infarctions and evidence of congestive heart failure.

The right and left lungs weighed 950 grams and 750 grams, respectively, and were reddish-brown.

Histopathological Findings