Pulmonary edema

Pulmonary edema (British English: oedema), also known as pulmonary congestion, is excessive
fluid accumulation in the tissue or air spaces (usually alveoli) of the lungs.[1] This leads to
impaired gas exchange, most often leading to shortness of breath (dyspnea) which can progress
to hypoxemia and respiratory failure. Pulmonary edema has multiple causes and is traditionally
classified as cardiogenic (caused by the heart) or noncardiogenic (all other types not caused by
the heart).[2][3]

Various laboratory tests (CBC, troponin, BNP, etc.) and imaging studies (chest x-ray, CT scan,
ultrasound) are often used to diagnose and classify the cause of pulmonary edema.[4][5][6]
Treatment is focused on three aspects: improving respiratory function, treating the underlying
cause, and preventing further damage and allow full recovery to the lung. Pulmonary edema can
cause permanent organ damage, and when sudden (acute), can lead to respiratory failure or
cardiac arrest due to hypoxia.[7] The term edema is from the Greek οἴδημα (oidēma, "swelling"),
from οἰδέω (oidéō, "(I) swell").[8][9]

Pathophysiology

The amount of fluid in the lungs is governed by multiple forces and is visualized using the
Starling equation. There are two hydrostatic pressures and two oncotic (protein) pressures that
determine the fluid movement within the lung air spaces (alveoli). Of the forces that explain fluid
movement, only the pulmonary wedge pressure is obtainable via pulmonary artery
catheterization.[10] Due to the complication rate associated with pulmonary artery
catheterization, other imaging modalities and diagnostic methods have become more popular.[11]
Imbalance in any of these forces can cause fluid movement (or lack of movement) causing a
buildup of fluid where it should not normally be. Although rarely clinically measured, these forces
allow physicians to classify and subsequently treat the underlying cause of pulmonary edema.

Classification

Pulmonary edema has a multitude of causes, and is typically classified as cardiogenic or

noncardiogenic. Cardiogenic pulmonary edema is caused by increased hydrostatic pressure
causing increased fluid in the pulmonary interstitium and alveoli. Noncardiogenic causes are
associated with the oncotic pressure as discussed above causing malfunctioning barriers in the
lungs (increased microvascular permeability).[12]
Cardiogenic Pulmonary edema

Cardiogenic pulmonary edema is typically Other names Pulmonary oedema

caused by either volume overload or impaired
left ventricular function. As a result, pulmonary
pressures rises from the normal average of 15
mmHg.[13] As the pulmonary pressure rises,
these pressures overwhelm the barriers and
fluid enters the alveoli when the pressure is
above 25 mmHg.[14] Depending whether the
cause is acute or chronic determines how fast
Pulmonary edema with small pleural effusions
pulmonary edema develops and the severity of on both sides
symptoms.[12] Some of the common causes of
cardiogenic pulmonary edema include: Specialty Cardiology, critical
care medicine
Acute exacerbation of congestive heart pulmonology
failure which is due to the heart's inability to
Symptoms Progressive dyspnea,
pump the blood out of the pulmonary
cough, fever,
circulation at a sufficient rate resulting in
cyanosis, tachycardia
elevation in pulmonary wedge pressure and
edema. Complications ARDS, respiratory
failure
Pericardial tamponade as well as treating
pericardial tamponade via Causes Cardiogenic,
pericardiocentesis has shown to cause Noncardiogenic

pulmonary edema as a result of increased (pneumonia,

inhalation injury,
left-sided heart strain.[15]
sepsis, airway
Heart Valve Dysfunction such as mitral valve obstruction, high
regurgitation can cause increased pressure altitude)
and energy on the left side of the heart
Diagnostic method Medical imaging, lab
(increased pulmonary wedge pressure)
tests, ECG,
[16]
causing pulmonary edema. echocardiography

Hypertensive crisis can cause pulmonary

Treatment Supplemental
edema as the elevation in blood pressure oxygen, diuretics,
and increased afterload on the left ventricle treat underlying
hinders forward flow in blood vessels and disease process
causes the elevation in wedge pressure and
subsequent pulmonary edema. In a recent systematic review, it was found that pulmonary
edema was the second most common condition associated with hypertensive crisis after
ischemic stroke.[17]
Flash pulmonary edema

A particularly severe type of cardiogenic pulmonary edema is flash pulmonary edema (FPE).
Flash pulmonary edema is a clinical syndrome of acute heart failure that begins suddenly and
accelerates rapidly. Frequently the most noticeable abnormality is edema of the lungs.
Nevertheless it is a cardiovascular disease not a pulmonary disease. It is also known by other
appellations including sympathetic crashing acute pulmonary edema (SCAPE).[18] It is often
associated with severe hypertension[19] Typically, patients with the syndrome of flash pulmonary
edema do not have chest pain are often not recognized as having a cardiovascular disease.
Treatment of FPE should include reducing systemic vascular resistance with nitroglycerin,
providing supplemental oxygenation, and decreasing left ventricular filling pressure while FPE
stays.[20]

Recurrence of FPE is thought to be associated with hypertension[21] and may signify renal artery
stenosis.[22] Prevention of recurrence is based on managing or preventing hypertension, coronary
artery disease, renovascular hypertension, and heart failure.

Noncardiogenic

Noncardiogenic pulmonary edema is caused by increased microvascular permeability (increased

oncotic pressure) leading to increased fluid transfer into the alveolar spaces. The pulmonary
artery wedge pressure is typically normal as opposed to cardiogenic pulmonary edema where
the elevated pressure is causing the fluid transfer. There are multiple causes of noncardiogenic
edema with multiple subtypes within each cause. Acute respiratory distress syndrome (ARDS) is
a type of respiratory failure characterized by rapid onset of widespread inflammation in the
lungs. Although ARDS can present with pulmonary edema (fluid accumulation), it is a distinct
clinical syndrome that is not synonymous with pulmonary edema.

Direct lung injury

Acute lung injury may cause pulmonary edema directly through injury to the vasculature and
parenchyma of the lung, causes include:

Inhalation of hot or toxic gases[12] (including vaping-associated lung injury)

Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents)

Aspiration, e.g., gastric fluid

Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post

decortication, removal of endobronchial obstruction, effectively a form of negative pressure
pulmonary oedema.

Reperfusion injury, i.e., postpulmonary thromboendartectomy or lung transplantation

 Swimming induced pulmonary edema also known as immersion pulmonary edema[23][24][25]

Transfusion associated Acute Lung Injury is a specific type of blood-product transfusion injury
that occurs when the donors plasma contained antibodies against the recipient, such as anti-
HLA or anti-neutrophil antibodies.[26]
Negative pressure pulmonary edema[27] is when inspiration is attempted against some sort of
obstruction in the upper airway, most commonly happens as a result of laryngospasm in
adults. This negative pressure in the chest ruptures capillaries and floods the alveoli with
blood[28]

Pulmonary embolism[29]

Indirect lung injury

Neurogenic causes[30] (seizures, head trauma, strangulation, electrocution).

Transfusion Associated Circulatory Overload occurs when multiple blood transfusions or

blood-products (plasma, platelets, etc.) are transfused over a short period of time.[31]

It includes acute lung injury and acute respiratory distress syndrome.[32] (ALI-ARDS) cover
many of these causes, Sepsis- Severe infection or inflammation which may be local or
systemic. This is the classical form of acute lung injury-adult respiratory distress syndrome

Pancreatitis

Special causes

Some causes of pulmonary edema are less well characterized and arguably represent specific
instances of the broader classifications above.

Arteriovenous malformation

Hantavirus pulmonary syndrome

High altitude pulmonary edema (HAPE)[33][34]

Envenomation, such as with the venom of Atrax robustus[35]

Signs and symptoms

Fluid within the alveoli (air spaces)

of the lungs

The most common symptom of pulmonary edema is dyspnea and may include other symptoms
relating to inadequate oxygen (hypoxia) such as fast breathing (tachypnea), tachycardia and
cyanosis. Other common symptoms include coughing up blood (classically seen as pink or red,
frothy sputum), excessive sweating, anxiety, and pale skin. Other signs include end-inspiratory
crackles (crackling sounds heard at the end of a deep breath) on auscultation and the presence
of a third heart sound.[3]

Shortness of breath can manifest as orthopnea (inability to breathe sufficiently when lying down
flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden
breathlessness at night). These are common presenting symptoms of chronic and cardiogenic
pulmonary edema due to left ventricular failure.

The development of pulmonary edema may be associated with symptoms and signs of "fluid
overload" in the lungs; this is a non-specific term to describe the manifestations of right
ventricular failure on the rest of the body. These symptoms may include peripheral edema
(swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to
normal when pressed upon due to fluid), raised jugular venous pressure and hepatomegaly,
where the liver is excessively enlarged and may be tender or even pulsatile.

Additional symptoms such as fever, low blood pressure, injuries or burns may be present and can
help characterize the cause and subsequent treatment strategies.
Diagnosis

Chest X-ray of Pulmonary Edema with lines and

overlay showing congestion

There is no single test for confirming that breathlessness is caused by pulmonary edema – there
are many causes of shortness of breath; but there are methods to suggest a high probability of
an edema.

Lab tests

Low oxygen saturation in blood and disturbed arterial blood gas readings support the proposed
diagnosis by suggesting a pulmonary shunt. Blood tests are performed for electrolytes (sodium,
potassium) and markers of renal function (creatinine, urea). Elevated creatine levels may
suggest a cardiogenic cause of pulmonary edema.[12] Liver enzymes, inflammatory markers
(usually C-reactive protein) and a complete blood count as well as coagulation studies (PT,
aPTT) are also typically requested as further diagnosis. Elevated white blood cell count (WBC)
may suggest a non-cardiogenic cause such as sepsis or infection.[12] B-type natriuretic peptide
(BNP) is available in many hospitals, sometimes even as a point-of-care test. Low levels of BNP
(<100 pg/ml) suggest a cardiac cause is unlikely, and suggest noncardiogenic pulmonary
edema.[3]
Imaging tests

Pulmonary edema on CT-scan

(coronal MPR)

Chest X-ray has been used for many years to diagnose pulmonary edema due to its wide
availability and relatively cheap cost.[4] A chest X-ray will show fluid in the alveolar walls, Kerley B
lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe
diversion (biased blood flow to the superior parts instead of inferior parts of the lung), and
possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated
with noncardiogenic edema.[3]

Lung ultrasounds, employed by a healthcare provider at the point of care, is also a useful tool to
diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water,
track changes over time, and differentiate between cardiogenic and non-cardiogenic edema.[36]
Lung ultrasound is recommended as the first-line method due to its wide availability, ability to be
performed bedside, and wide diagnostic utility for other similar diseases.[4]

Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may

strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous
pressures and high pulmonary artery pressures leading to pulmonary edema.

Prevention

In those with underlying heart or lung disease, effective control of congestive and respiratory
symptoms can help prevent pulmonary edema.[37]

Dexamethasone is in widespread use for the prevention of high altitude pulmonary edema.
Sildenafil is used as a preventive treatment for altitude-induced pulmonary edema and
pulmonary hypertension.[38][39] Sildenafil's mechanism of action is via phosphodiesterase
inhibition which raises cGMP, resulting in pulmonary arterial vasodilation and inhibition of
smooth muscle cell proliferation and indirectly fluid formation in the lungs.[40] While this effect
has only recently been discovered, sildenafil is already becoming an accepted treatment for this
condition, in particular in situations where the standard treatment of rapid descent
(acclimatization) has been delayed for some reason.[41]

Management

The initial management of pulmonary edema, irrespective of the type or cause, is supporting vital
functions while edema lasts. Hypoxia may require supplementary oxygen to balance blood
oxygen levels, but if this is insufficient then again mechanical ventilation may be required to
prevent complications caused by hypoxia.[42] Therefore, if the level of consciousness is
decreased it may be required to proceed to tracheal intubation and mechanical ventilation to
prevent airway compromise. Treatment of the underlying cause is the next priority; pulmonary
edema secondary to infection, for instance, would require the administration of appropriate
antibiotics or antivirals.[2][3]

Cardiogenic pulmonary edema

Acute cardiogenic pulmonary edema often responds rapidly to medical treatment.[43] Positioning
upright may relieve symptoms. A loop diuretic such as furosemide is administered, often
together with morphine to reduce respiratory distress.[43] Both diuretic and morphine may have
vasodilator effects, but specific vasodilators may be used (particularly intravenous glyceryl
trinitrate or ISDN) provided the blood pressure is adequate.[43]

Continuous positive airway pressure and bilevel positive airway pressure (CPAP/BiPAP) has been
demonstrated to reduce mortality and the need of mechanical ventilation in people with severe
cardiogenic pulmonary edema.[44]

It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in
which the cardiac output is insufficient to sustain an adequate blood pressure to the lungs. This
can be treated with inotropic agents or by intra-aortic balloon pump, but this is regarded as
temporary treatment while the underlying cause is addressed and the lungs recover.[43]

Prognosis

As pulmonary edema has a wide variety of causes and presentations, the outcome or prognosis
is often disease-dependent and more accurately described in relation to the associated
syndrome. It is a major health problem, with one large review stating an incidence of 7.6% with
an associated in hospital mortality rate of 11.9%.[2] Generally, pulmonary edema is associated
with a poor prognosis with a 50% survival rate at one year, and 85% mortality at six years.[45]
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