Acute Respiratory
Distress
Syndrome
Megan DiGuiseppe, Amos
Wu, Johnson Fong,
Julianne Gant, and Kieran
Palumbo
Clinical Presentation
Quick onset
Decrease in oxygenation
Trouble breathing
Prevalence
75 incidents per 100,000 people
Age increases risk factor
Outcomes
High mortality
Most deaths caused by “cascade”
Low recovery rate after 1 week
Pulmonary Edema
Gaps appear between capillary cells
Fluids escape
Pulmonary Edema
Impaired gas exchange
Cannot drain fluids
Inflammatory
Cascade
Inflammation at the alveoli
causes diffuse alveolar
damage
Inflammatory Cascade
Sepsis
Inflammation via the
capillaries
Decrease in Lung Compliance
Compliance: the ability for lungs and
thorax to expand
Decrease in surfactant makes it harder to
breathe and results in alveolar collapse.
Pulmonary hypertension
Destruction of alveoli obstructs
blood flow
Blood pressure increases
Scar tissue builds up
pulmonary fibrosis due to hypertension
Pulmonary Fibrosis
Thickening of the alveolar membrane
Decrease in compliance
Results in chronic hypoxia
Hypoxemia
Deprivation of oxygen in the
bloodstream
Ventilation (inspired O2) >>
Perfusion (blood in the alveoli) =
dead space
discoloration of extremities due to
hypoxemia
Dead Space: air trapped in the body
Treatments: Ventilation
Cornerstone for successful treatment is proper mechanical ventilation
- 
support breathing and allow for healing
Ventilation Technique
Prone vs. Supine ventilation
- 
improves oxygenation by
redistributing air flow
Preventing Injury
Pharmacologic paralytic agents
- 
neuromuscular blocking agents
- 
decrease injuries to lungs during
ventilation
Lung volume protection strategy
Treatment Options for Hypoxemia
Extracorporeal membrane oxygenation (ECMO)
-  intractable hypoxemia
Inhaled vasodilators therapy
-  Nitric oxide helps oxygenation
-  Immunomodulatory effect
Other Treatments: Non invasive
Ventilation
●  No invasive artificial airway
●  No risk of ventilator
associated pneumonia
●  Added comfort for the patient
A patient using a mask style NIV
New Treatments: Preemptive Ventilation
●  May be able to block the progression
of lung injury
●  Currently there is no other
preventative technique
●  The future of ARDS treatment
New Treatments: LASSBio596 with
surfactant
●  Exogenous Surfactant as a
treatment for ARDS
●  Used with LASSBio596
○  anti-inflammatory properties
○  anti-fibrogenic properties
●  Dream team?
Complications
ARDS has many complications
- 
pulmonary, cardiac,
gastrointestinal
Currently no great treatment option
- 
~45% mortality in some studies
But, much progress has
been made!
Sources used
Charalampos, Pierrakos Et Al. "Acute Respiratory Distress Syndrome: Pathophysiology and Therapeutic Options." Journal of Clinical
Research Medicine (2012): 7-16. NCBI. Web. 1 Mar. 2016.
"Hypoxemia (low Blood Oxygen)." Mayo Clinic. 25 Dec. 2015. Web. 1 Mar. 2016. <http://www.mayoclinic.org/symptoms/hypoxemia/
basics/definition/sym-20050930>.
"What Is Pulmonary Hypertension?" National Heart, Lung, and Blood Institute. US Department of Health & Human Services, 2 Aug.
2011. Web. 1 Mar. 2016. <http://www.nhlbi.nih.gov/health/health-topics/topics/pah/>.
"Noncardiogenic Pulmonary Edema Imaging." Medscape. 7 Oct. 2015. Web. 1 Mar. 2016. <
http://emedicine.medscape.com/article/360932-overview>.
Suman, Yadam, Et Al. "Acute Respiratory Distress Syndrome." Critical Care 39.2 (2016): 190-95. Wolters Kluwer Health, Inc. Web. 1
Mar. 2016.
"Noninvasive Ventilation." : Medspace. 4 April 2014. Web. 02 Mar. 2016. <
http://emedicine.medscape.com/article/304235-overview#a4>
Sadowitz, Benjamin. "Preemptive Mechanical Ventilation Can Block Progressive Acute Lung Injury." World Jounal of Critical Medical
Care, 4 Jan. 2016. Web. 1 Mar. 2016.
Silva J, D, Et Al. “Respiratory and Systemic Effects of LASSBio596 Plus Surfactant in Experimental Acute Respiratory Distress
Syndrome.” Cell Physiol Biochem 2016;38:821-835. Karger Medical and Scientific Publishers. Web. 1 Mar. 2016.