Pleural effusion pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Healthy individuals have less than 15 ml of fluid in each pleural space. Normally, fluid enters the pleural space from the capillaries in the parietal pleura, from interstitial spaces of the lung via the visceral pleura, or from the peritoneal cavity through small holes in the diaphragm. This fluid is normally removed by lymphatics in the visceral pleura, which have the capacity to absorb 20 times more fluid than is normally formed. When this capacity is overwhelmed, either through excess formation or decreased lymphatic absorption, a pleural effusion develops.

  • Increase entry of fluid versus decreased exit of fluid.
  • Lymphatics have a large reserve capacity to deal with excess fluid.

Increased Fluid Entry

  1. Increased permeability
    • Increase in fluid conductance or protein permeability.
  2. Increased microvascular pressure
    • Usually increased venous outflow pressure. Arterial pressures usually not transmitted due to capillary resistance. Thought to be lung interstitial fluid when hydrostatic pressure.
  3. Decreased pleural pressure
    • i.e. Significant atalectasis, reduces pressures around nearby vessels.
  4. Decreased plasma oncotic pressure
    • Hypoalbuminemia alone not usually enough but can lower threshold for other factors.

Decreased Fluid Exit

  • Reflects a reduction in lymphatic function.
  • Much of how is speculative.
  • There are intrinsic and extrinsic factors.
  1. Intrinsic
    • Prevent ability of lymphatic vessels to transport fluid- products of inflammation, endocrine problems (hypothyroidism), direct injury (chemotherapy, radiotherapy), infiltration with cancer.
  2. Extrinsic
    • Limitation of respiratory motion (diaphragm paralysis, lung collapse), compression of lymphatics (pleural fibrosis, pleural granulomas), blockage (pleural malignancy), increased systemic venous pressure (only acutely because chronically lymphatics can adapt), decreased liquid availability (ie after pneumothorax liquid contacts fewer lymphatic openings)
  • Common postoperative in patients undergoing cardiac surgical procedures
  • Predominantly left-sided: suggests underlying pericarditis is a causative factor.
  • Majority are small and not serious.
  • Pathogenesis may relate to immunologic cause
  • Respond to steroids and prolonged latent period from injury to onset

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