ISSN 2398-2969      

Lung: pulmonary edema

icanis
Contributor(s):

Lesley G King


Introduction

  • Cause: left-sided congestive heart failure, altered pulmonary capillary permeability.
  • Signs: respiratory distress, cyanosis.
  • Diagnosis: auscultation, radiography.
  • Treatment: diuretics Furosemide , venodilator glyceryl trinitrate (UK only) Glyceril trinitrate , nitroprusside infusion Nitroprusside. Treat underlying cause.
  • Prognosis: edema may be managed but underlying disease is often severe.

Pathogenesis

Etiology

Increased pulmonary capillary pressures

  • Left-sided cardiac disease, congestive heart failure.

Altered pulmonary capillary permeability

Pathophysiology

  • Increased pulmonary capillary pressures:
    • Left-sided cardiac disease such as mitral valve endocardiosis Heart: mitral valve degenerative disease , dilated cardiomyopathy Heart: dilated cardiomyopathy (DCM).
    • Decreased cardiac output leads to activation of the renin-angiotensin-aldosterone system which causes renal retention of sodium and water, and gradual hypervolemia.
    • Increased cardiac preload and mitral insufficiency leads to left atrial dilation and progressive congestion of pulmonary veins.
    • Pulmonary venous congestion leads to increased pulmonary capillary hydrostatic pressure, which allows increased water diffusion out of the vasculature into the pulmonary interstitium.
    • Edema (interstitial and then alveolar) occurs when the pulmonary lymphatic system is overwhelmed and can no longer deal with the increased water movement out of the capillaries.
  • Altered pulmonary capillary permeability:
  • Direct pulmonary epithelial cell injury:
    • Due to irritants such as smoke inhalation, aspiration of gastric contents, severe pneumonia, drowning, re-expansion pulmonary edema.
    • If inflammation is severe and diffuse, alveolar inflammation extends from the alveolar epithelium through to the pulmonary capillary endothelium, leading to capillary endothelial injury and increased permeability.
  • Non-cardiogenic pulmonary edema:
    • Due to electrocution, neurogenic edema (prolonged seizures, head trauma), upper airway obstruction.
    • All of these triggers can activate reflexes that originate from brainstem neurogenic pulmonary edema centers.
    • Activation of these specific areas in the medulla and hypothalamus leads to sudden massive sympathetic discharge.
    • Stimulation of alpha receptors results in severe, acute but transient systemic vasoconstriction.
    • Acute systemic vasoconstriction leads to shunting of blood into the pulmonary vasculature, which is not affected because it lacks alpha receptors.
    • Sudden but transient overload of the pulmonary circulation leads to capillary wall stress failure and acute damage to pulmonary capillary endothelial cell tight junctions.
    • Capillary permeability edema ensues.
    • In animals with upper airway obstruction eg leash strangulation, brachycephalic Brachycephalic airway obstruction syndrome , laryngeal paralysis Larynx: paralysis etc, profound negative airway pressures further exacerbate edema formation.
  • Indirect pulmonary injury due to systemic inflammation:
    • Systemic Inflammatory Response Syndrome due to sepsis; pancreatitis; uremia; organ torsion eg GDV, lung lobe, spleen; burn, bullet or bite wounds.
    • Systemic release of inflammatory mediators into the circulation, inflammatory cytokines and cells injure the pulmonary capillary endothelial cells (mild inflammation also called Acute Lung Injury [ALI]).
    • If the pulmonary damage is extensive, inflammation extends from capillary endothelial cells to involve also the alveolar epithelial cells (severe inflammation, also called Acute Respiratory Distress Syndrome [ARDS]).

Clinical signs

  • Accumulation of fluid initially in the interstitium and then in the alveoli results in varying degrees of respiratory distress.
  • The animal may be tachypneic, dyspneic or orthopneic, have exercise intolerance or coughing, and may be cyanotic.
  • With profound alveolar flooding, blood-tinged frothy edema fluid can appear from the nostrils or from the mouth.
  • Additional clinical signs depend on underlying disease, for example:
    • Cardiac arrhythmias in primary heart disease.
    • Smoke and burn injury to skin and corneas.
    • Electricution injury burns on lips.
    • Seizures.
    • Abdominal pain, distension or vomiting.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bachmann M, Waldrop J E (2012) Noncardiogenic pulmonary edema. Compend Cont Educ Vet 34,(11), E1 PubMed.
  • Diana A, Guglielmini C, Pivetta M et al (2009) Radiographic features of cardiogenic pulmonary edema in dogs with mitral regurgitation: 61 cases (1998-2007). JAVMA 235 (9), 1058-1063 PubMed.
  • Parent C, King L G, Walker L M & Van Minkle T J (1996) Clinical and clinicopathological findings in dogs with adult respiratory distress syndrome: 19 cases (1985-1993). JAVMA 208 (9), 1419-1427 Europe PMC.
  • Drobatz K J, Sunders H M, Pugh C R, Hendricks J C (1995) Noncardiogenic pulmonary oedema in dogs and cats - 26 cases (1987-1993). JAVMA 206 (11), 1732-1736 PubMed.

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