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Edema pulmonar no cardiogénico

Autor: Dr. Michael M. Givertz
Redactor de sección: Dr. Stephen S. Gottlieb
Redactor adjunto: Dra. Geraldine Finlay

Todos los temas se actualizan a medida que se dispone de nueva evidencia y se completa nuestro proceso de
revisión por pares .

Revisión de la literatura actual hasta:  octubre de 2022. | Última actualización de este tema:  14 de junio de
2022.

INTRODUCCIÓN

El edema pulmonar se debe al movimiento de exceso de líquido hacia los alvéolos como
resultado de una alteración en una o más de las fuerzas de Starling. En el edema pulmonar
cardiogénico, una presión capilar pulmonar alta (estimada clínicamente a partir de la presión
de enclavamiento de la arteria pulmonar) es responsable del movimiento anormal del líquido [
1,2 ]. (Consulte "Fisiopatología del edema pulmonar cardiogénico" y "Abordaje del diagnóstico y
evaluación de la insuficiencia cardíaca aguda descompensada en adultos" .)

Por el contrario, el edema pulmonar no cardiogénico es causado por varios trastornos en los
que otros factores además de la presión capilar pulmonar elevada son responsables de la
acumulación de proteínas y líquidos en los alvéolos [ 3 ]. La distinción entre causas
cardiogénicas y no cardiogénicas no siempre es posible, ya que el síndrome clínico puede
representar una combinación de varios trastornos diferentes. Sin embargo, el diagnóstico es
importante porque el tratamiento varía considerablemente según los mecanismos
fisiopatológicos subyacentes.

LA RELACIÓN STARLING

El equilibrio de líquidos entre el intersticio y el lecho vascular en el pulmón, como en otras

microcirculaciones, está determinado por la relación de Starling, que predice el flujo neto de
líquido a través de una membrana. Esto se puede expresar en la siguiente ecuación:

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Filtración neta = (Lp x S) x (presión hidráulica delta - presión oncótica delta)

= (Lp x S) x [(Pcap - Pif) - s(πcap - πif)]

dónde:

● Lp es la unidad de permeabilidad (o porosidad) de la pared capilar.

● S es el área superficial disponible para el movimiento de fluidos.
● Pcap y Pif son las presiones hidráulicas del fluido capilar e intersticial.
● πcap y πif son las presiones oncóticas del líquido capilar e intersticial; la presión oncótica
intersticial se deriva principalmente de las proteínas plasmáticas filtradas y, en menor
grado, de los proteoglucanos del intersticio.
● s representa el coeficiente de reflexión de las proteínas a través de la pared capilar (con
valores que van desde 0 si es completamente permeable hasta 1 si es completamente
impermeable).

En los microvasos normales, hay una filtración continua de una pequeña cantidad de líquido
bajo en proteínas. En el edema pulmonar no cardiogénico, el mecanismo más frecuente de
aumento de la filtración transcapilar es un aumento de la permeabilidad capilar. Ante un
aumento dado de la permeabilidad capilar, la tasa de acumulación de líquido pulmonar está
relacionada en parte con la capacidad funcional de los vasos linfáticos para eliminar el exceso
de líquido.

DEFINICIÓN DE EDEMA PULMONAR NO CARDIOGÉNICO

El edema pulmonar no cardiogénico se identifica clínicamente por la presencia de evidencia

radiográfica de acumulación de líquido alveolar sin evidencia hemodinámica que sugiera una
etiología cardiogénica (es decir, presión de enclavamiento de la arteria pulmonar ≤18 mmHg).
La acumulación de líquido y proteínas en el espacio alveolar conduce a una disminución de la
capacidad de difusión, hipoxemia y dificultad para respirar.

Las principales causas de edema pulmonar no cardiogénico son el síndrome de dificultad

respiratoria aguda (SDRA) [ 2 ] y, con menos frecuencia, el edema pulmonar neurogénico y de
gran altura. Otras causas menos comunes incluyen edema pulmonar debido a una sobredosis
de opioides, embolia pulmonar, eclampsia, lesión pulmonar aguda relacionada con
transfusiones y lesión renal aguda (a veces denominada “pulmón urémico”) [ 4 ]. La
hipoalbuminemia por sí sola no es causa de edema pulmonar. (Consulte 'Ausencia de edema
pulmonar con hipoalbuminemia' a continuación).

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PERMEABILIDAD EDEMA PULMONAR POR SDRA

La membrana alvéolo-capilar se daña y presenta fugas en casos de edema pulmonar por

permeabilidad, lo que permite un mayor movimiento de agua y proteínas desde el espacio
intravascular hacia el espacio intersticial. En la mayoría de los pacientes, la concentración de
proteína en el intersticio supera el 60 % del valor plasmático, en comparación con menos del 45
% en el edema pulmonar cardiogénico [ 5 ].

El edema pulmonar por permeabilidad es la característica más destacada del síndrome de

dificultad respiratoria aguda (SDRA) [ 6 ]. En el pasado, muchos autores equipararon el
trastorno clínico del SDRA con la entidad patológica del edema pulmonar por permeabilidad.
Sin embargo, estos dos términos no deben usarse indistintamente. Aunque un cierto grado de
edema de permeabilidad está invariablemente presente al inicio del ARDS, otras anormalidades
estructurales importantes del pulmón típicamente emergen a medida que evoluciona el ARDS.
Además, muchos episodios de edema pulmonar por permeabilidad nunca resultan en el
deterioro fisiológico severo que se requiere para la designación ARDS. (Consulte "Síndrome de
dificultad respiratoria aguda: características clínicas, diagnóstico y complicaciones en adultos" .)

El SDRA se puede observar en varios trastornos, que incluyen sepsis, infección pulmonar
aguda, traumatismo no torácico, toxinas inhaladas, coagulación intravascular diseminada,
shock pulmonar, tabaquismo de cocaína base libre, injerto de derivación arterial poscoronario
(especialmente en pacientes con amiodarona ), inhalación de altas concentraciones de oxígeno
y neumonitis aguda por radiación. Independientemente de la etiología, el escenario clínico es
similar en la mayoría de los pacientes una vez que se ha producido el daño de la membrana. La
liberación de citocinas inducida por sepsis o isquemia, como la interleucina-1, la interleucina-8 y
el factor de necrosis tumoral, puede desempeñar un papel importante en el aumento de la
permeabilidad de los capilares pulmonares, al menos en parte a través del reclutamiento de
neutrófilos [ 7 ]. . (Ver "Síndrome de dificultad respiratoria aguda: epidemiología, fisiopatología,
patología y etiología en adultos" .

Presentación y diagnóstico  :  los pacientes con ARDS se presentan con dificultad respiratoria
grave (disnea) asociada con la aparición aguda de infiltrados radiográficos de tórax difusos e
hipoxemia. El inicio del ARDS a menudo ocurre dentro de las primeras dos horas después de un
evento desencadenante, aunque esto puede demorarse entre uno y tres días. Las radiografías
de tórax generalmente progresan a un patrón de llenado alveolar bilateral. El diagnóstico de
edema pulmonar por permeabilidad requiere distinguirlo del edema pulmonar cardiogénico y
de otras causas de enfermedad o lesión pulmonar.

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Los pacientes con edema pulmonar no cardiogénico (o cardiogénico) rara vez tienen edema
unilateral [ 8-10 ]. El edema pulmonar no cardiogénico unilateral puede ser causado por
condiciones ipsolaterales al edema, como aspiración, contusión, reexpansión y oclusión de la
vena pulmonar (p. ej., enfermedad venooclusiva o compresión extrínseca) y por condiciones
contralaterales al edema, como embolia pulmonar y lobectomía [ 8 ]. Estas lesiones deben
distinguirse del edema pulmonar cardiogénico unilateral, que es causado principalmente por
insuficiencia mitral excéntrica [ 11 ] o después de una cirugía cardíaca mínimamente invasiva [
12 ].

Distinción de la insuficiencia cardíaca  :  clínica y radiográficamente, el ARDS se parece

mucho al edema pulmonar cardiogénico grave. La distinción entre estos trastornos suele ser
evidente a partir de las circunstancias clínicas al inicio de la dificultad respiratoria. Como
ejemplos, el edema pulmonar que ocurre en el contexto de un síndrome coronario agudo casi
siempre es cardiogénico, mientras que el que ocurre en el contexto de una sepsis sugiere
fuertemente una etiología no cardíaca. El edema pulmonar que ocurre en el contexto de
transfusiones múltiples podría deberse a una combinación de edema pulmonar cardiogénico
(p. ej., debido al volumen) y lesión pulmonar aguda. (Ver "Manifestaciones clínicas y diagnóstico
del shock cardiogénico en el infarto agudo de miocardio" y “Aproximación al diagnóstico y
evaluación de la insuficiencia cardiaca aguda descompensada en adultos” .

● Catéter de arteria pulmonar: se debe colocar un catéter de arteria pulmonar (o Swan-

Ganz) si no se puede discernir con confianza el mecanismo de formación del edema. Una
presión de enclavamiento de la arteria pulmonar inferior a 18 mmHg favorece la lesión
pulmonar aguda sobre el edema pulmonar cardiogénico. (Consulte "Cateterización de la
arteria pulmonar: indicaciones, contraindicaciones y complicaciones en adultos" .)

Es importante tener en cuenta que el cateterismo de la arteria pulmonar puede ser engañoso
en ciertos entornos. Lo que es más importante, la isquemia miocárdica puede causar una
disfunción ventricular izquierda grave pero transitoria, lo que lleva a un edema pulmonar
"flash". Si la presión de enclavamiento se mide por primera vez después de que se haya
resuelto la isquemia (y haya mejorado la función del ventrículo izquierdo), se puede obtener un
valor relativamente normal, lo que lleva a la conclusión errónea de que la dificultad respiratoria
fue causada por una lesión pulmonar aguda. (Consulte "Abordaje del diagnóstico y evaluación
de la insuficiencia cardíaca aguda descompensada en adultos" .)

Por otro lado, una presión de enclavamiento de la arteria pulmonar elevada no excluye la
posibilidad de una lesión pulmonar aguda. Se estima que hasta el 20 por ciento de los
pacientes con ARDS tienen disfunción ventricular izquierda concomitante [ 7 ], y los porcentajes
son mucho más altos en pacientes con ARDS secundario a sepsis [ 13 ]. La dilatación del
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ventrículo derecho también suele estar presente en el SDRA, mientras que la disfunción del
ventrículo derecho puede estar presente en los casos más graves y predecir peores resultados [
14 ].]. El diagnóstico de lesión pulmonar aguda no se puede hacer fácilmente cuando la presión
de enclavamiento es elevada; por lo tanto, se debe observar el curso clínico a medida que la
presión de enclavamiento responde al tratamiento. Si los infiltrados pulmonares y la hipoxemia
no mejoran apreciablemente dentro de las 24 a 48 horas posteriores a la restricción de líquidos
(con o sin diuresis) y la normalización de la presión de enclavamiento, es probable que la lesión
pulmonar aguda coexista con edema cardiogénico.

● BNP plasmático: la medición del péptido natriurético tipo B (BNP) en plasma, o pro-BNP N-
terminal, se ha utilizado para distinguir la insuficiencia cardíaca (BNP alto) de la
enfermedad pulmonar (BNP normal o levemente elevado) como causa de disnea con un
alto grado de precisión incluso en pacientes con enfermedades pulmonares y cardíacas [
15 ]. Sin embargo, los valores intermedios a menudo no son útiles. El papel de estos
biomarcadores en el diagnóstico de edema pulmonar ha sido menos estudiado. Los datos
en el entorno de la UCI sugirieron una capacidad limitada para discriminar el SDRA del
edema pulmonar cardiogénico [ 16 ], ya que los niveles pueden aumentar con el
desarrollo [ 17 ] y la gravedad [ 18 ] del SDRA. (Ver "Abordaje del diagnóstico y evaluación
de la insuficiencia cardiaca aguda descompensada en adultos".)

Se han desarrollado herramientas de predicción clínica para distinguir la lesión pulmonar

aguda del edema pulmonar cardiogénico [ 19 ]. Estos pueden proporcionar una guía para
acelerar la terapia inicial, pero requieren una evaluación prospectiva adicional. También se han
propuesto una serie de nuevos biomarcadores para ayudar en esta distinción [ 20 ].

Otras enfermedades pulmonares  :  dos trastornos pulmonares a veces se confunden con el
SDRA: hemorragia alveolar difusa y cáncer.

● La hemorragia alveolar difusa, a menudo debida a una capilaritis pulmonar o daño

alveolar difuso, debe considerarse siempre que se desarrolle dificultad respiratoria en
asociación con una caída importante, de otra manera inexplicable, en la concentración de
hemoglobina en sangre. La hemoptisis puede ser mínima o estar ausente antes de la
intubación; sin embargo, la broncoscopia después de la intubación invariablemente revela
secreciones sanguinolentas en las vías respiratorias durante una hemorragia activa.

La hemorragia alveolar blanda, que se caracteriza por hemorragia en los espacios alveolares sin
inflamación o destrucción de las estructuras alveolares, puede ser causada por presión
diastólica final del LV elevada, coagulopatía y, en raras ocasiones, terapia anticoagulante o
antiplaquetaria. (Ver "Los síndromes de hemorragia alveolar difusa" .)

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● El cáncer a veces se disemina por los pulmones con tanta rapidez que la insuficiencia
respiratoria subsiguiente puede confundirse con ARDS. Esto se debe con mayor frecuencia
a linfoma o leucemia aguda [ 21 ], pero la diseminación linfangítica de tumores sólidos, la
toxicidad aguda de la quimioterapia (p. ej., mitomicina [también conocida como
mitomicina-C], metotrexato ) y la CID asociada al cáncer ocasionalmente se comportan de
manera similar. manera similar [ 22 ]. Los tratamientos contra el cáncer más nuevos,
incluidos los inhibidores de puntos de control inmunitarios, también se han asociado con
neumonitis [ 23 ]. (Consulte "Toxicidades asociadas con la inmunoterapia con inhibidores
de puntos de control" .)

Tratamiento  :  actualmente no se conocen medidas para corregir la anomalía de la

permeabilidad en el ARDS. El manejo clínico implica el tratamiento de la enfermedad
subyacente (p. ej., antibióticos para la infección) y medidas de apoyo para mantener la función
celular y metabólica, mientras se espera que se resuelva la lesión pulmonar aguda. Estas
medidas de apoyo incluyen ventilación mecánica, mantenimiento de una nutrición adecuada y
monitoreo hemodinámico cuando sea necesario para guiar el manejo de líquidos y el soporte
cardiovascular [ 24 ]. Los pacientes con SDRA grave pueden necesitar oxigenación por
membrana extracorpórea además de terapias médicas de apoyo [ 25 ]. (Consulte "Estrategias
de manejo del ventilador para adultos con síndrome de dificultad respiratoria aguda" y "Acute
respiratory distress syndrome: Supportive care and oxygenation in adults" and "Evaluation and
management of suspected sepsis and septic shock in adults".)

Lowering the pulmonary artery wedge pressure with diuretics and fluid restriction can improve
pulmonary function and perhaps outcome [26,27]. One study, for example, analyzed survival
and length of stay in the intensive care unit for 40 patients with ARDS [26]. The patients were
divided into two groups: those with a reduction in pulmonary capillary wedge pressure (PCWP)
of at least 25 percent; and those with less or no reduction in PCWP. Survival was greater in the
patients with a large fall in PCWP (75 versus 29 percent). This difference remained statistically
significant after stratifying patients by age and by the APACHE II severity of illness index. In a
later study in which 1000 patients with acute lung injury were randomized to a conservative
versus liberal fluid management strategy, the conservative strategy improved oxygenation and
shortened duration of mechanical ventilation and ICU stay, but did not reduce the incidence of
shock, use of dialysis or mortality during the first 60 days [28]. (See "Predictive scoring systems
in the intensive care unit".)

A number of pharmacologic therapies for ARDS have been evaluated [29]. These include
inhaled vasodilators (nitric oxide, prostacyclin), anti-inflammatory therapies (glucocorticoids,
statins [30], prostaglandin E1), antioxidants (dietary oil supplementation), and exogenous

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surfactant. Novel mechanical ventilation strategies, including high-frequency ventilation, liquid

ventilation, and prone positioning [31], as well as preventive strategies (eg, aspirin) [32] have
also been investigated. At present, NONE has shown consistent and unequivocal clinical benefit
[33]. Preclinical and early clinical data suggest that human mesenchymal stem cells may
attenuate lung injury and promote tissue repair in ARDS. (See "Acute respiratory distress
syndrome: Investigational or ineffective therapies in adults".)

Prognosis — The outcome of patients with ARDS has improved over time; hospital mortality
was approximately 60 percent in the years 1967 to 1981 and declined to 30 to 40 percent in the
1990s. As an example of this trend, one study evaluated 918 patients with ARDS at a single
institution between 1983 and 1993 [34]. The mortality from sepsis-related ARDS declined from
67 percent in 1990 to 40 percent in 1993; the improvement was largely confined to patients
under age 60. In a systematic analysis of ARDS studies published between 1994 and 2006, a
decline in overall mortality rates of 1.1 percent per year was demonstrated [35]. The enhanced
survival is probably related to a variety of improvements in supportive care. Despite these
encouraging data, ARDS remains a world-wide problem with high mortality that is both under
recognized and undertreated [36].

Most deaths are due to the severity of the underlying disease, particularly multiorgan failure,
rather than the respiratory disease. While early deaths are typically due to the underlying cause
of the ARDS, later deaths often result from nosocomial pneumonia and sepsis. Long-term
survivors of ARDS typically show only mild abnormalities in pulmonary function and are usually
asymptomatic, although long-term physical, cognitive, and psychological sequelae have been
described [37,38]. (See "Acute respiratory distress syndrome: Prognosis and outcomes in
adults".)

OTHER NONCARDIOGENIC FORMS OF PULMONARY EDEMA

Other more unusual types of noncardiogenic pulmonary edema, often with unclear
pathophysiology, have been described.

High altitude pulmonary edema — High-altitude pulmonary edema (HAPE), which generally

occurs among individuals who rapidly ascend to altitudes above 12,000 to 13,000 feet (3600 to
3900 m), accounts for a majority of deaths due to high altitude disease [39,40]. An abnormally
pronounced degree of hypoxic pulmonary vasoconstriction at a given altitude appears to
underlie the pathogenesis of this disorder [14]. (See "High-altitude illness: Physiology, risk
factors, and general prevention" and "High-altitude pulmonary edema".)

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Neurogenic pulmonary edema — Neurogenic pulmonary edema occurs after a variety of

neurologic disorders and procedures, including head injury, intracranial surgery, grand mal
seizures, subarachnoid or intracerebral hemorrhage, and electroconvulsive therapy [41].
Sympathetic overreactivity, with massive catecholamine surges, shifts blood from the systemic
to the pulmonary circulation with secondary elevations of left atrial and pulmonary capillary
pressures [42]. Pulmonary capillary leak caused by pressure-induced mechanical injury and/or
direct nervous system control over capillary permeability may play a contributory role. The
clinical presentation is characterized by acute hypoxemia, tachypnea, tachycardia, diffuse rales,
and frothy sputum or hemoptysis. Symptom onset tends to be rapid and most cases resolve
within 48 to 72 hours. The outcome is determined by the course of the primary neurologic
insult. It is important to distinguish neurogenic pulmonary edema from cardiogenic pulmonary
edema in the setting of stress cardiomyopathy. (See "Neurogenic pulmonary edema" and
"Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)

Reperfusion pulmonary edema — Reperfusion pulmonary edema appears to represent a

form of high-permeability lung injury that is limited to those areas of lung from which proximal
thromboembolic obstructions have been removed. It may appear up to 72 hours after surgery
and is highly variable in severity, ranging from a mild form of edema resulting in postoperative
hypoxemia to an acute, hemorrhagic and fatal complication [43-45]. At experienced centers,
venovenous extracorporeal life support has been used as a bridge to recovery or transplant
when all other conventional strategies have failed [46,47] (see "Chronic thromboembolic
pulmonary hypertension: Pulmonary thromboendarterectomy"). A similar condition may occur
following lung transplantation due to ischemia-reperfusion injury. (See "Primary lung graft
dysfunction".)

Re-expansion pulmonary edema — Re-expansion pulmonary edema (RPE) usually occurs

unilaterally after rapid re-expansion of a collapsed lung (typically for greater than three days) in
patients with a pneumothorax [48], with rates ranging from 16 to 33 percent. Risk factors
include diabetes, size of pneumothorax, and presence of pleural effusion [49,50]. It may rarely
follow evacuation of large volumes of pleural fluid (>1 to 1.5 liters) (<1 percent) [51-54] or
removal of an obstructing endobronchial tumor.

The pathophysiologic mechanism is unknown. Proposed mechanisms include direct injury from
surfactant dysfunction in chronic atelectatic lung, increased transpleural pressures when
excessively negative pleural pressures are created during fluid or air removal in the setting of
an unexpandable lung, or indirect injury from reperfusion.

RPE appears to be related to the rapidity of lung re-expansion and to the severity and duration
of lung collapse. However, a study examining development of re-expansion pulmonary edema
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following thoracentesis found that it was independent of the volume of fluid removed and
pleural pressures, and recommended that even large pleural effusions be drained completely
as long as chest pain or end-expiratory pleural pressure less than -20 cm H2O does not develop
[53].

Patients typically present soon (minutes to hours) after the inciting event, although
presentation can be delayed for up to 24 to 48 hours in some cases. The clinical course varies
from isolated radiographic changes to complete cardiopulmonary collapse but most patients
present with acute onset dyspnea, cough and hypoxemia. Typical CT findings include ipsilateral
ground-glass opacities, septal thickening, focal consolidation, and areas of atelectasis [55].

A mortality rate as high as 20 percent has been described in one small review [56]; however
consistent with our experience, the mortality is much lower with later and larger series
reporting a mortality rate less than 5 percent [52,53,57].

Treatment is supportive, mainly consisting of supplemental oxygen and, if necessary,

mechanical ventilation. The disease is usually self-limited.

Opioid overdose — First described by Osler in 1880 [58], pulmonary edema can sometimes
complicate an overdose of heroin or methadone [59]; other related agents, including fentanyl
and naloxone, have also been implicated [60]. Risk factors include male sex and shorter
duration of heroin use. Most cases occur immediately or within hours of drug injection. The
chest radiograph usually demonstrates a nonuniform distribution of pulmonary edema.

The pathophysiology of this form of pulmonary edema is unknown; a combination of direct

toxicity of the drug, hypoxia, and acidosis secondary to hypoventilation and/or cerebral edema
has been proposed [61,62]. The observation that edema fluid contains protein concentrations
nearly identical to plasma and that pulmonary artery wedge pressures, when measured, are
normal suggests an alveolar-capillary membrane leak as the initiating cause. Resolution of this
form of pulmonary edema is rapid once hypoventilation and hypoxia are reversed by the
institution of assisted ventilation. In one case series, 9 of 27 patients (33 percent) required
mechanical ventilation; all but one were extubated within 24 hours [63]. Supportive care also
includes use of naloxone to reverse the opioid effects. The alarming increase in opioid use and
dependency suggests that clinicians will see more cases of pulmonary edema related to opioid
overdose in the emergency room and intensive care unit [64,65].

Salicylate toxicity — Aspirin is one of many drugs occasionally associated with the

development of noncardiogenic pulmonary edema. Salicylate-induced noncardiogenic
pulmonary edema and acute lung injury (ALI) generally occur in older patients with chronic
salicylate intoxication [66,67], but should be considered in all patients following aspirin
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overdose. The medical history is critical to making the diagnosis, as misdiagnosis or delayed
diagnosis can lead to a significant increase in morbidity and mortality [67]. Salicylate-induced
ALI and pulmonary edema can complicate volume resuscitation and administration of sodium
bicarbonate, two mainstays of treatment in this setting. Thus, the presence of salicylate-
induced pulmonary edema is considered an absolute indication for hemodialysis [68]. (See
"Salicylate (aspirin) poisoning in adults".)

Other exogenous agents — Several commonly-prescribed medications have been associated

with noncardiogenic pulmonary edema, including amiodarone, bortezomib, and
immunosuppressive agents (eg, sirolimus, everolimus) [69,70]. It may be difficult to distinguish
noncardiogenic pulmonary edema from heart failure in cardiac patients or infection in
immunosuppressed patients. Additional objective data, including invasive hemodynamics and
tissue biopsy, may be helpful in these cases. Acute lung injury and death have also been
reported with use of electronic cigarettes (vaping), and direct injury to lung epithelial cells with
capillary leak has been proposed as a mechanism. (See "E-cigarette or vaping product use-
associated lung injury (EVALI)" and "Vaping and e-cigarettes".)

Pulmonary embolism — Acute pulmonary edema in association with a massive pulmonary

embolus (PE) or multiple smaller emboli is uncommon but well described [71,72]. PE can cause
pulmonary edema by injuring the pulmonary and adjacent pleural systemic circulations,
elevating hydrostatic pressures in pulmonary and/or systemic veins, and perhaps by lowering
pleural pressure due to atelectasis. PE may also decrease the exit rates of pleural fluid by
increasing the systemic venous pressure (thereby hindering lymphatic drainage) or possibly by
decreasing pleural pressure (thereby hindering lymphatic filling). The effusions are typically
small and unilateral, and may become loculated if the diagnosis is delayed [73]. Older studies
showed that 20 percent of PE-related effusions are transudates, suggesting that hydrostatic
changes can also be important [74]. However, in a later case series, 26 of 93 patients with
effusions following PE underwent thoracentesis and all of the fluids met Light's criteria for
exudate (see "Diagnostic evaluation of a pleural effusion in adults: Initial testing"), suggesting a
primary role for vascular injury [75].

Viral infections — Rapidly progressive noncardiogenic pulmonary edema associated with

profound hypotension and a high case fatality rate has been described with hantavirus
infection (see "Hantavirus cardiopulmonary syndrome") [76], dengue hemorrhagic
fever/dengue shock syndrome (see "Dengue virus infection: Clinical manifestations and
diagnosis"), and most recently with COVID-19 infection (see "COVID-19: Clinical features").
Enteroviral 71 infection in young children [77] and SARS coronavirus infection in adults [78] are
other causes of viral-induced noncardiogenic pulmonary edema and hemorrhage (see "Severe

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acute respiratory syndrome (SARS)"). The strain of H1N1 influenza A that caused the 2009 to
2010 pandemic caused severe ARDS in some patients (see "Seasonal influenza in adults: Clinical
manifestations and diagnosis"). There have also been reports of vascular leakage and
respiratory failure in the setting of severe Ebola virus disease [79].

Pulmonary veno-occlusive disease — Pulmonary veno-occlusive disease is a cause of

pulmonary hypertension and noncardiogenic pulmonary edema. This condition is discussed in
detail separately. (See "Epidemiology, pathogenesis, clinical evaluation, and diagnosis of
pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis in adults".)

Transfusion-related acute lung injury — Transfusion-related acute lung injury (TRALI) is a rare

but potentially fatal complication of blood product transfusion that involves neutrophil
activation and pulmonary edema. Further details are provided separately. (See "Transfusion-
related acute lung injury (TRALI)".)

ABSENCE OF PULMONARY EDEMA WITH HYPOALBUMINEMIA

In older patients with heart failure with preserved ejection fraction, hypoalbuminemia due to
age, malnutrition, or sepsis may lower colloid osmotic pressure and facilitate the onset of
pulmonary edema [80]. In patients with acute heart failure, hypoalbuminemia has also been
associated with pleural effusions [81], and is an independent predictor of in-hospital and post-
discharge mortality [82]. In a study of more than 7000 patients with acute coronary syndrome,
serum albumin level ≤3.50 g/dL was an independent predictor of new-onset heart failure and in-
hospital mortality [83].

Although hypoalbuminemia can lead to peripheral edema by lowering the transcapillary oncotic
pressure gradient, it does not generally produce pulmonary edema. The pulmonary capillaries
appear to have a greater baseline permeability to albumin and therefore have a higher
interstitial oncotic pressure (about 18 mmHg) than do peripheral capillaries [84]. A fall in the
plasma albumin concentration is associated with a parallel decline in the pulmonary interstitial
oncotic pressure. The net effect is little or no change in the transcapillary oncotic pressure
gradient and therefore no pulmonary edema, unless there is a concurrent rise in left atrial and
pulmonary capillary pressures. (See "Pathophysiology and etiology of edema in adults", section
on 'Compensatory factors'.)

SUMMARY

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● Overview – Noncardiogenic pulmonary edema is caused by various disorders in which

factors other than elevated pulmonary capillary pressure are responsible for protein and
fluid accumulation in the alveoli. In contrast, a high pulmonary capillary pressure is
responsible for the abnormal fluid movement in cardiogenic pulmonary edema.
Noncardiogenic pulmonary edema may be difficult to distinguish from cardiogenic
pulmonary edema and a mixed picture can occur. (See 'Introduction' above.)

● Pathogenesis – Fluid balance between the interstitium and vascular bed in the lung, as in
other microcirculations, is determined by the Starling relationship, which predicts the net
flow of liquid across a membrane. In noncardiogenic pulmonary edema, the most
common mechanism for a rise in transcapillary filtration is an increase in capillary
permeability. Hypoalbuminemia alone is not a cause of pulmonary edema but can
contribute to pleural effusions and increased mortality in patients with acute heart failure
as well as in those with acute coronary syndrome. (See 'The Starling relationship' above
and 'Absence of pulmonary edema with hypoalbuminemia' above.)

● Definition – Noncardiogenic pulmonary edema is identified clinically by the presence of

radiographic evidence of alveolar fluid accumulation without hemodynamic evidence to
suggest a cardiogenic etiology (ie, pulmonary artery wedge pressure ≤18 mmHg). (See
'Definition of noncardiogenic pulmonary edema' above.)

● Etiologies

• The most common cause of noncardiogenic pulmonary edema is acute respiratory

distress syndrome. (See 'Permeability pulmonary edema due to ARDS' above.)

• Less common causes are high altitude and neurogenic pulmonary edema. (See 'High
altitude pulmonary edema' above and 'Neurogenic pulmonary edema' above.)

• Others include reperfusion and re-expansion pulmonary edema, heroin overdose or

use of vaping products, and salicylate or other drug toxicity. (See 'Reperfusion
pulmonary edema' above and 'Re-expansion pulmonary edema' above and 'Opioid
overdose' above and 'Salicylate toxicity' above and 'Other exogenous agents' above.)

• Other less common causes include pulmonary edema due to pulmonary embolism and
eclampsia, viral infections, pulmonary veno-occlusive disease, and transfusion-related
acute lung injury. (See 'Pulmonary embolism' above and 'Viral infections' above and
'Pulmonary veno-occlusive disease' above and 'Transfusion-related acute lung injury'
above.)

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Topic 3456 Version 23.0

Contributor Disclosures
Michael M Givertz, MD Sin relación(es) financiera(s) relevante(s) con compañías no elegibles para
revelar. Stephen S Gottlieb, MD Subvención/Investigación/Apoyo de ensayos clínicos: BTG International
[Disfunción renal];Cytokinetics [Insuficiencia cardíaca];Ionis [Amiloidosis, insuficiencia cardíaca];Pfizer
[Amiloidosis]. Consultor/Consejos Asesores: Citocinética [insuficiencia cardíaca]. Todas las relaciones
financieras relevantes enumeradas han sido mitigadas. Geraldine Finlay, MD No hay relación(es)
financiera(s) relevante(s) con compañías no elegibles para revelar.

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