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Diffuse alveolar damage

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Diffuse alveolar damage
Micrograph showing hyaline membranes, the key histologic feature of diffuse alveolar damage. H&E stain.
SpecialtyRespirology

Diffuse alveolar damage (DAD) is a histologic term used to describe specific changes that occur to the structure of the lungs during injury or disease. Most often DAD is described in association with the early stages of acute respiratory distress syndrome (ARDS).[1] It is important to note that DAD can be seen in situations other than ARDS (such as acute interstitial pneumonia) and that ARDS can occur without DAD[1].

Definitions

  • Diffuse alveolar damage (DAD): an acute lung condition with the presence of hyaline membranes.[2] These hyaline membranes are made up of dead cells, surfactant, and proteins[3]. The hyaline membranes deposit along the walls of the alveoli, where gas exchange typically occurs, thereby making gas exchange difficult.
  • Acute respiratory distress syndrome (ARDS): a potentially life threatening condition where the alveoli are damaged thereby letting fluid leak into the lungs which makes it difficult to exchange gases and oxygenate the blood.[4] It is the general practice of the medical community to use the Berlin criteria to diagnose ARDS. All criteria must be present to make a diagnosis of ARDS.

Berlin Criteria: as stated on UpToDate (2020)[5]

  1. Timing: onset of respiratory symptoms within one week of a injury/insult.
  2. Chest Imaging: can consist of chest x-ray or CT scan and must show bilateral opacities that cannot be fully explained by other conditions such as effusion, lung/lobar collapse, or lung nodules.
  3. Origin of Edema: respiratory failure that cannot be fully explained by cardiac failure or fluid overload, this needs objective assessment such as an echocardiogram.
  4. Impaired Oxygenation: this can be determined by looking at the ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2) that can be obtained based on an arterial blood gas test. Note: all PaO2/FiO2 ratios used in the determination of the severity of ARDS require that the patient be on a ventilator at a setting that includes 5 cm H2O or more of positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP).
Level of ARDS PaO2/FiO2 Range PEEP/CPAP
Mild ARDS 201-300 ≥5 cm H2O
Moderate ARDS 101-200
Severe ARDS <100

Histology/Progression

The epithelial lining of alveoli are composed of two different types of cells. Alveolar type I epithelial cells comprise about 80% of the alveolar surface area and are primarily responsible for gas exchange[6]. Alveolar type II epithelial cells play the critical roles of producing surfactant, moving water out of the airspace, and regenerating alveolar epithelium[6]. The alveolar type II epithelial cells are more resistant to damage, so after an insult to the alveoli, most of the damage will occur to the alveolar type I epithelial cells[6].

Left side demonstrate the structure of a normal alveolus including the difference between type I and type II alveolar epithelial cells. Right side depicts what occurs after injury to the alveolus during the acute/exudative phase.

Once the initial insult has damaged the alveoli and begun the process of DAD, the condition will typically progress in three phases: exudative, proliferative, and fibrotic[7]. Below are the description of the phases, paraphrased from Sweeney et al (2016)[7] and Manicone (2009)[6]

  • Exudative Phase (1-7 days): After the initial insult to the alveoli immune cells (neutrophils and macrophages) are recruited to the alveoli, which can cause more damage through their nonspecific defensive mechanisms. Since the epithelial lining is damaged it allows plasma and proteins to leak in to the airspace, accumulating fluid or otherwise known as edema. Additionally, since the epithelial lining is damaged there is limited ability to pump this edema out of the airspace and back in to the interstitium. The presence of this edema has the following detrimental impacts:
    • The edema contributes to the deposition of a hyaline membrane (composed of dead cells, surfactant, and proteins) along the alveolar walls. Hyaline membranes are characteristic of DAD.
    • The edema interferes with the naturally occurring surfactant, which is critical for reducing surface tension and allowing alveoli to remain open and allow in air for gas exchange.
  • Proliferative/Organizing Phase (1-3 weeks): This phase is characterized by recovery. The epithelial lining is repopulated with alveolar type II epithelial cells which will eventually differentiate into alveolar type I epithelial cells. While the type II epithelial cells are repopulating the epithelial surface they are also performing the critical task of transporting the edema out of the airspace and back into the interstitium. Meanwhile in the airspace, macrophages are clearing cellular debris.
  • Fibrotic Phase (after 3 weeks, if occurs): not all courses of DAD result in a fibrotic phase. This phase occurs if the alveolar collagen that is deposited during the acute exudative phase fails to be resorbed, resulting in limitations of alveolar expanse and subsequently gas exchange.

Prevalence

It is a common biopsy finding.[8] Through histology, diffuse alveolar damage goes through several stages:

  1. Exudative phase - similar to pulmonary edema. The alveoli become flooded with exudate
  2. Hyaline membrane production. Hyaline membranes are fibrinous structures resulting from organization of the exudate.
  3. Organising phase

References

  1. ^ a b Cardinal-Fernández, Pablo; Lorente, José A.; Ballén-Barragán, Aída; Matute-Bello, Gustavo (2017-06). "Acute Respiratory Distress Syndrome and Diffuse Alveolar Damage. New Insights on a Complex Relationship". Annals of the American Thoracic Society. 14 (6): 844–850. doi:10.1513/AnnalsATS.201609-728PS. ISSN 2329-6933. {{cite journal}}: Check date values in: |date= (help)
  2. ^ Berry, Gerald J; Rouse, Robert V (November 20 2010). "Acute Interstitial Pneumonia - Diffuse Alveolar Damage". surgpathcriteria.stanford.edu. Retrieved 2020-04-03. {{cite web}}: Check date values in: |date= (help)CS1 maint: url-status (link)
  3. ^ O'Morchoe, Patricia J; Thursh, Donald R; Levy, Allan H. "Lung, Hyaline Membrane Disease, Respiratory Distress". Urbana Atlas of Pathology. Retrieved 2020-04-03.{{cite web}}: CS1 maint: url-status (link)
  4. ^ "Acute Respiratory Distress Syndrome (ARDS) | American Lung Association | American Lung Association". www.lung.org. Retrieved 2020-04-03.
  5. ^ Siegel, Mark D (March 2020). "Acute Respiratory Distress Syndrome: Clinical Features, Diagnosis, and Complications in Adults". UpToDate. Retrieved 2020-04-03.{{cite web}}: CS1 maint: url-status (link)
  6. ^ a b c d Manicone, Anne M (2009-01-01). "Role of the pulmonary epithelium and inflammatory signals in acute lung injury". Expert review of clinical immunology. 5 (1): 63–75. doi:10.1586/177666X.5.1.63. ISSN 1744-666X. PMC 2745180. PMID 19885383.
  7. ^ a b Sweeney, Rob Mac; McAuley, Daniel F. (2016-11-12). "Acute respiratory distress syndrome". The Lancet. 388 (10058): 2416–2430. doi:10.1016/S0140-6736(16)00578-X. ISSN 0140-6736. PMID 27133972.
  8. ^ Parambil JG, Myers JL, Ryu JH (August 2006). "Diffuse alveolar damage: uncommon manifestation of pulmonary involvement in patients with connective tissue diseases". Chest. 130 (2): 553–8. doi:10.1378/chest.130.2.553. PMID 16899858.



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