Pulmonary edema

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

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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

Histopathology


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

Non-cardiogenic

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

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

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

HEENT

  • Nasal flaring

Lungs

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

Cardiovascular

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

Pulmonary edema
Pulmonary edema

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

Echocardiography is useful in confirming a cardiac or no-cardiac cause of pulmonary edema. Among cardiac causes, echocardiography can identify if systolic or diastolic dysfunction is present. Echocardiography is useful in identify if focal segment wall motion abnormalities are present which would suggest ischemia or myocardial infarction as an underlying cause. If there is a global impairment of left ventricular function, then this suggests a cardiomyopathy may be present. Echocardiography may identify the presence and severity of valvular causes of pulmonary edema including aortic stenosis, aortic insufficiency, mitral stenosis. mitral insufficiency, and hypertrophic cardiomyopathy.

Cardiac Catheterization

Insertion of a pulmonary arterial catheter Swan-Ganz catheter may be required to distinguish between the two main forms of pulmonary edema and to help guide management[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

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



References

  1. 1.0 1.1 1.2 1.3 1.4 Ware LB, Matthay MA. Acute pulmonary edema. N Engl J Med 2005;353:2788-96. PMID 16382065.
  2. M Bates. "High altitude pulmonary edema". Apex (Altitude Physiology Expeditions). Retrieved 2007-03-06.
  3. M Bates. "High altitude pulmonary edema". Apex (Altitude Physiology Expeditions). Retrieved 2007-03-06.
  4. M Bates. "High altitude pulmonary edema". Apex (Altitude Physiology Expeditions). Retrieved 2007-03-06.
  5. Kramer K, Kirkman P, Kitzman D, Little WC. Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization. Am Heart J. 2000 Sep;140(3):451-5. PMID 10966547.
  6. Pickering TG, Herman L, Devereux RB, Sotelo JE, James GD, Sos TA, Silane MF, Laragh JH. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet 1988;2(8610):551-2. PMID 2900930.
  7. Masip J, Roque M, Sanchez B, Fernandez R, Subirana M, Exposito JA. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA 2005;294:3124-30. PMID 16380593.
  8. Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet 2006;367(9517):1155-63. PMID 16616558.

See also

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