Categories
  Encyclosphere.org ENCYCLOREADER
  supported by EncyclosphereKSF

Acute respiratory distress syndrome pathophysiology

From Wikidoc - Reading time: 4 min

Acute respiratory distress syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Acute respiratory distress syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnostic study of choice

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

Echocardiography

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Mechanical Ventilation Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Acute respiratory distress syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Acute respiratory distress syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Acute respiratory distress syndrome pathophysiology

CDC on Acute respiratory distress syndrome pathophysiology

Acute respiratory distress syndrome pathophysiology in the news

Blogs on Acute respiratory distress syndrome pathophysiology

Directions to Hospitals Treating Acute respiratory distress syndrome

Risk calculators and risk factors for Acute respiratory distress syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Brian Shaller, M.D. [2]

Overview[edit | edit source]

ARDS is a syndrome of inflammation and increased permeability with the lung parenchyma that leads to loss of type I pneumocytes, impaired gas exchange, inappropriate cell proliferation within alveoli, and, in survivors, fibrosis.

Pathophysiology[edit | edit source]

ARDS typically develops within 24 to 48 hours of the provoking illness or injury and is classically divided into three phases:[1][2][3]

  • Exudative phase (within 5 to 7 days): Systemic inflammation results in increased permeability of the alveolar-capillary barrier and leads to the formation of hyaline membranes along alveolar walls, accumulation of proteinaceous exudate within the alveolar air spaces (non-cardiogenic pulmonary edema), and extravasation of inflammatory cells (predominantly neutrophils) into the lung parenchyma, leading to extensive alveolar damage and, occasionally, diffuse alveolar hemorrhage
  • Proliferative phase (within 7 to 21 days): Fibroblast proliferation, collagen deposition, and early fibrotic changes are observed within the pulmonary interstitium as alveolar exudate and hyaline membranes begin to be absorbed
  • Fibrotic phase (within several weeks): Many patients with ARDS will develop some degree of pulmonary fibrosis, of which at least one-quarter will go on to develop clinically apparent fibrotic lung disease with a restrictive ventilatory defect on pulmonary function tests;[4] the development and extent of pulmonary fibrosis in ARDS correlates with an increased mortality risk[5]

Genetics[edit | edit source]

The role of genetics in the development of ARDS is an ongoing area of research. While studies have demonstrated associations between certain genetic factors (including single nucleotide polymorphisms and allelic variants of angiotensin-converting enzyme) and increased susceptibility to the development of ARDS, the nature and implications of these relationships remain uncertain.[6][7][8]

Pathology[edit | edit source]

On gross pathology, the following are characteristic findings of ARDS:

  • Firm, boggy, and dusky lungs
  • Generally increased weight compared to healthy lungs due to edema

On microscopic histopathological analysis, the following are characteristic findings of ARDS:

Hyaline membranes - very high magnification












References[edit | edit source]

  1. Katzenstein, A. L., C. M. Bloor, and A. A. Leibow. “Diffuse Alveolar Damage--the Role of Oxygen, Shock, and Related Factors. A Review.” The American Journal of Pathology 85, no. 1 (October 1976): 209–28.
  2. Tomashefski, J. F. “Pulmonary Pathology of Acute Respiratory Distress Syndrome.” Clinics in Chest Medicine 21, no. 3 (September 2000): 435–66.
  3. Thille, Arnaud W., Andrés Esteban, Pilar Fernández-Segoviano, José-María Rodriguez, José-Antonio Aramburu, Patricio Vargas-Errázuriz, Ana Martín-Pellicer, José A. Lorente, and Fernando Frutos-Vivar. “Chronology of Histological Lesions in Acute Respiratory Distress Syndrome with Diffuse Alveolar Damage: A Prospective Cohort Study of Clinical Autopsies.” The Lancet. Respiratory Medicine 1, no. 5 (July 2013): 395–401. doi:10.1016/S2213-2600(13)70053-5.
  4. Burnham EL, Janssen WJ, Riches DW, Moss M, Downey GP (2014). "The fibroproliferative response in acute respiratory distress syndrome: mechanisms and clinical significance". Eur Respir J. 43 (1): 276–85. doi:10.1183/09031936.00196412. PMC 4015132. PMID 23520315.
  5. Martin C, Papazian L, Payan MJ, Saux P, Gouin F (1995). "Pulmonary fibrosis correlates with outcome in adult respiratory distress syndrome. A study in mechanically ventilated patients". Chest. 107 (1): 196–200. PMID 7813276.
  6. Jerng JS, Yu CJ, Wang HC, Chen KY, Cheng SL, Yang PC (2006). "Polymorphism of the angiotensin-converting enzyme gene affects the outcome of acute respiratory distress syndrome". Crit Care Med. 34 (4): 1001–6. doi:10.1097/01.CCM.0000206107.92476.39. PMID 16484896.
  7. Cardinal-Fernández P, Ferruelo A, El-Assar M, Santiago C, Gómez-Gallego F, Martín-Pellicer A; et al. (2013). "Genetic predisposition to acute respiratory distress syndrome in patients with severe sepsis". Shock. 39 (3): 255–60. doi:10.1097/SHK.0b013e3182866ff9. PMID 23364437.
  8. Tejera P, Meyer NJ, Chen F, Feng R, Zhao Y, O'Mahony DS; et al. (2012). "Distinct and replicable genetic risk factors for acute respiratory distress syndrome of pulmonary or extrapulmonary origin". J Med Genet. 49 (11): 671–80. doi:10.1136/jmedgenet-2012-100972. PMC 3654537. PMID 23048207.

Licensed under CC BY-SA 3.0 | Source: https://www.wikidoc.org/index.php/Acute_respiratory_distress_syndrome_pathophysiology
1 | Status: cached on July 17 2024 00:21:27
↧ Download this article as ZWI file
Encyclosphere.org EncycloReader is supported by the EncyclosphereKSF