Acute respiratory distress syndrome (ARDS) is a Sudden failure of the respiratory system. It Can occur in anyone over the age of one who is critically ill. It is a Life- threatening because normal gas exchange does not take place due to severe fluid buildup in both lungs. Prevention can be achieved by Limiting Blood Loss so decreasing transfusion requirements, Early Stabilization Of unstable Fractures and Early prophylactic mechanical Ventilation. Established cases with ARDS is treated in the Intensive Care Unit By Mechanical ventilation and Oxygen therapy through a ventilator, Fluids through an IV line to improve blood flow and provide nutrition and medicine to prevent and treat infections and to relieve pain.

1. Dr. Fathi Neana, MD
Chief of Orthopaedics
Dr. Fakhry & Dr. A. Al-Garzaie Hospital
January, 11 - 2019
Polytrauma
Part 2
(ARDS)
Acute Respiratory Distress
Syndrome

3. Trauma Mortality
Causes
3 Peaks
First peak (24 hours)
Second peak (2-7 days)
Third peak – delayed ( <7 days)

4. Trauma Mortality (3 Peaks)
FIRST PEAK (24 hours)
Early phase - immediate death
severe brain injury, disruption of great vessels, cardiac
disruption
Second phase – within 24 hours
subdural, epidural hematomas, hemopneumothorax, severe
abdominal injuries, multiple extremity injuries (bleeding)
SECOND PEAK (2-7 Days)
Acute Respiratory Distress Syndrome (ARDS)
40 - 50% Mortality
THIRD PEAK – DELAYED ( <7 Days)
Multisystem organ failure, Sepsis (Septic Death)
28% Mortality

5. • Define
ARDS, FES, Thromboembolic Disease, Septic Shock
(Septic Death), DIC, etc…
• Understand
Etiology & Pathophysiology of each Condition
• Understand
Prevention, Diagnosis, Treatment, Outcomes
Trauma Mortality
Objectives

6. 3 Rights
Right Patient, Right Hospital, Right Time
Delayed arrival increase Infection rate (3rd
peak of death)
Delayed or Inappropriate Surgery increase ARDS rate
(2nd
peak of Death)
Trauma centre vs. usual G. hospital
Treating Team (senior orthopedic trauma)
Trauma Mortality
Factors Affecting Mortality

7. Ventilation and Gas exchange
under the control of the autonomic nervous
system from parts of the brain stem, the
medulla oblongata and the pons
Immune functions
Metabolic and endocrine functions of the lungs
Vocalization
Temperature control
Coughing and sneezing
Air & Oxygen are free to all
The Respiratory system

8. 18
If you try to reckon up Allah's blessings, you
cannot count them. Indeed, He is Forgiving and
Compassionate, (16:18) Alnahl
Air and Oxygen are free to all

9. The right lung is slightly larger than the left.
Hairs in the nose help to clean the air we breathe as
well as warming it.
The highest recorded "sneeze speed" is 165 km per
hour.
The surface area of the lungs is roughly the same size
as a tennis court.
The capillaries in the lungs would extend 1,600
kilometers if placed end to end.
We lose half a liter of water a day through breathing.
This is the water vapour we see when we breathe
onto glass.
A person at rest usually breathes between 12 and 15
times a minute.
The breathing rate is faster in children and women
than in men.
Amazing Facts about the
Respiratory System

10. Lung Compliance
• Measurement of how easy or hard it is to inflate the lungs.
• COMPLIANCE IS RECIPROCAL OF ELASTANCE.
• Compliance = ∆ Volume
∆ Pressure
• Normal Values
– Lung 0.2 L/cm H20
– Thorax 0.2 L/cm H20
– Total 0.1 L/cm H20

11. Increased Lung Compliance
• Easier to inflate the lung
• Lower inflation pressures
• Decreased Elastance
• Causes
– Emphysema
Lung Compliance
Decreased Lung Compliance
• Higher inflation pressures
– Higher airway pressures on
the ventilator
– Increased complications
(barotrauma, decreased CO)
• Harder to inflate the lung
• “Stiff lung”
• Increased Elastance
• Causes
– Atelectasis
– Fibrosis
– Pneumothorax
– ARDS

12. (ARDS)
Acute Respiratory Distress
Syndrome

13. Acute Respiratory Distress
Syndrome (ARDS)
Acute Respiratory Distress or
Failure
40 - 50% Mortality rate
Big Cats Tigers and Lions know
how to suffocate their prey?

14. • Acute respiratory distress syndrome (ARDS) is a life-threatening
lung condition that prevents enough oxygen from getting into the
blood.
• Acute respiratory distress syndrome was first described in 1967 by
Ashbaugh and colleagues.
• ARDS is also referred with variety of terms like
• Stiff Lung
• Shock lung
• Wet lung
• Post traumatic lung
• Adult respiratory distress syndrome
• Adult hyaline membrane disease
• Capillary leak syndrome &
• Congestive atelectasis.
Mr. sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli
Acute Respiratory Distress Syndrome (ARDS)
Introduction

15. Acute Respiratory Distress Syndrome (ARDS)
Definition
Acute Respiratory Distress Syndrome (ARDS)
is a clinical syndrome:
- Severe dyspnea of rapid onset
- Hypoxemia
-Alveolar capillary membrane damage
-Diffuse pulmonary infiltrates
Inflammatory cells and proteinaceous fluid
accumulate in the alveolar spaces leading to a
decrease in diffusing capacity and hypoxemia
- Respiratory failure

16. Lung Injury
• Acute Lung Injury (ALI)
– Normal barriers to
fluid movement
within the lungs is
disrupted.
– If it is severe enough
to cause acute
hypoxemic
respiratory failure it is
termed:
• Acute respiratory
distress syndrome
(ARDS)
– Most severe gas
exchange
abnormalities
– Multiple Organ
Dysfunction
Syndrome (MODS)

17. Criteria Differentiating
ALI and ARDS
• PaO2/FiO2 ratio
• Example
– 100 mm Hg/.21 = 476
– As the number decreases, oxygenation is
getting worse
• ALI is when the ratio is LESS THAN 300
• ARDS the ratio LESS THAN 200

18. Acute lung injury (ALI) and acute respiratory
distress syndrome (ARDS)
 ALI is the term used for
patients with significant
hypoxemia (PaO2/FiO2 ratio
of ≤ 300)
 ARDS is the term used for
a subset of ALI patients
with severe hypoxemia
(PaO2/FiO2 ratio of ≤ 200)
Normal → ALI → ARD
Clinical Spectrum

19. Tissue injury
Infection
Inflammatory
Mediators
(Decompensated SIRS)
Organ
Injury
ARDS is related to Multi organ dysfunction (MOD)
Persistent release of (inflammatory mediators) results in Systemic inflammatory
response syndrome (SIRS). Inefficient compensatory anti inflammatory response
syndrome (CARS) leads to Multi organ dysfunction (MOD) including Lungs (ARDS)
Acute Respiratory Distress Syndrome (ARDS)
Pathophysiology

20. Multi organ Failure in ARDS
(ARDS) is related to Multi organ
dysfunction (MOD)

21. Systemic Inflammatory Mediators
Damage to Endothelial Lining
Increased Capillary Permeability
Fluid Extravasation
Alveolar Collapse
Decreased Pulmonary Compliance
Ventilation Perfusion Abnormalities
Arteriolar Hypoxemia
Acute Respiratory Distress Syndrome (ARDS)
Pathophysiology

22. • Injury of the lung
• Destruction of the alveolar-capillary
membrane (the barrier)
• Engorged capillaries
• Interstitial and alveolar edema
• Hemorrhage
• Decreased surfactant with atelectasis
• Hyaline Membrane formation
•
• Fibrosis
Acute Respiratory Distress Syndrome (ARDS)
Pathophysiology

23. acute respiratory
distress syndrome
(ARDS)
A normal alveolus
(left)
and a damaged
injured alveolus in
the acute phase of
acute respiratory
distress syndrome
(right).

25. The Inflammatory Response
Inflammation is an Adaptive response to noxious conditions (Infection and
Tissue injury) an attempt to restore homeostasis
1- Induced by immune recognition of infection or tissue damage (usually
good). But if the immune recognition is hypersensitive to environmental or
auto inflammatory components (autoimmune disease)
2- Inflammation depends upon the Immune Recognition of infection or tissue
damage. a very Balanced process, Normally end with Recovery but Errors, in
recognition - Hypo or Hyper sensitivity end by Death from the Disease or
Inflammation
3- Opsonisation, Antibody opsonization is the process by which the
pathogen is marked for ingestion and eliminated by the phagocytes.
4- Phagocytosis—Process in which phagocytes engulf and digest the
(Opsonised) microorganisms and cellular debris.
5- Recruitment, The Complement (Opsonin) and the Phagocytes
(Exist mainly in blood). A mechanism to recruit these elements to the
invaded tissue led to inflammatory response (inflammation)

26. Vasodilatation .. increase blood flow ..
Capillary permeability ..
Passage large immune cells + proteins
Increase in body heat .. swing the balance
of chemical reactions in favour of the host
The tissues become red. warm, swollen,
painful , Organ dysfunction
Inflammatory process once started it
continues until infection is eradicated
Phagocytes continue to consume and
destroy bacteria
The acquired immune system binds &
disposes harmful toxins
Pus is produced
The Effects of the Inflammatory Response
The Effects of the Inflammatory
Response
Cornelius Celsus in De Medicina, 1st
century A.D.
rubor et tumor cum calore et
dolore”
(Redness and Swelling with Heat
and Pain)
later “functio laesa” (Disturbance of
Function) was added

27. When the infection has been eradicated, and there is no more foreign
antigen
The helper T cells stop emitting the stay-alive signal, thus allowing the
cells involved in the inflammatory response to die off (apoptosis)
If foreign antigen is not eradicated, or if the immune cells receive the
stay-alive signal from another source, then chronic inflammation may
develop
How does the inflammatory response end ?

28. The inflammatory response
Conclusion
Acute inflammation: influx of white blood cells and fluid from blood to fight
infection and aid tissue repair
Chronic inflammation: inducer of inflammation is not removed Leads to
tissue damage and loss of tissue function (joint destruction, lung fibrosis,
etc.)
Current view: aggressively fight inflammation in certain chronic diseases to
decrease / delay progressive loss of function
Current research suggests that inflammation may play an important role in
common chronic diseases including atherosclerosis, type 2 diabetes,
neurodegeneration, and cancer

30. Sudden failure of the respiratory
system
Can occur in anyone over the age of
one who is critically ill
Life- threatening because Normal gas
exchange does not take place
Due to severe fluid buildup in both
lungs
What is Acute respiratory distress syndrome
(ARDS)?
Characterized by:
Rapid breathing
Difficulty getting enough air into the
lungs
Low blood oxygen levels
Cough and fever (if caused by
pneumonia)
Low blood pressure
Confusion & Extreme tiredness

31. Acute respiratory distress syndrome (ARDS)
Clinical Definition
– Acute onset of symptoms
– Ratio of PaO2 to FIO2 of 200 mm Hg or less
(PaO2
) =Arterial partial pressure of oxygen = 95 mm Hg
FIO2 = fraction of inspired oxygen".
– Bilateral infiltrates on CXRs
– Pulmonary arterial wedge pressure of 18 mm Hg or less or no
clinical signs of left atrial hypertension
– American-European Consensus Conference (AECC) on ARDS,
94

32. Acute respiratory distress syndrome (ARDS)
in the post traumatic period
• Incidence 5% – 8% after
polytrauma
• Much lower in isolated fracture
• Mortality up to 40 -50%
• Uncommon in Children and the
Elderly
Characterized by:
• Decreased PaO2
And
• Diffuse and often massive
extravasations of fluid from the
pulmonary vasculature to the
interstitial space of the lungs

33. Acute respiratory distress syndrome (ARDS)
Common Causes & risk factors
(Multifactorial)
• Trauma
• Shock
• Massive Transfusion
• Embolism
• Sepsis (bacterial infection of
the blood)
• Pneumonia or other lung
infection
• Aspiration , vomit , salt water
• Breathing in harmful smoke
or fumes
• Prolonged LOC
• Cardiopulmonary Bypass
• Pancreatitis
• Major Burns
• Abdominal Distension
• Narcotics
• Sedatives
• Overdoses of tricyclic
antidepressants

34. Medical history, Physical exam and Medical
tests
Abnormal Breathing or Heart sounds
Edema means heart or kidneys dysfunction
Arterial blood gas test
Chest x-ray
Chest CT scan
Blood tests for infection
Heart tests look for heart failure
ARDS usually diagnosed in a Hospitalized
patient with a Critical illness such as Shock,
Sepsis or Trauma
Acute respiratory distress syndrome (ARDS)
Diagnosis
Chest Radiograph
Autopsy Specimen
Chest CT Scan

35. • Radiopaque – white
• The more severe the ARDS, the whiter
the lungs appear
• Often described as “White Out” or
diffuse “fluffy” infiltrates
– Non-homogenous
– “Baby Lungs”
• Heart size is normal
• Air Bronchograms
• Honeycombing or Ground Glass
Acute respiratory distress syndrome (ARDS)
Chest X-ray

36. • Common complications are;
– Nosocomial Infections pneumonia
– Barotrauma
– Renal failure
• Other complications are :
– O2 toxicity,
– Stress ulcers, GI hemorrhage/gastric distension
– Tracheal ulceration,
– Blood clots, deep vein thrombosis & pulmonary embolism.
– Sepsis, micro emboli
– Disseminated Intravascular Coagulation (DIC),
– Anemia
– Pulmonary fibrosis – permanent disability
– Cardiovascular Problems
Acute respiratory distress syndrome (ARDS)
Complications

37. Image shows subtle manifestations of barotrauma, pulmonary interstitial
emphysema, and subcutaneous emphysema. This patient was being treated with
noninvasive ventilation. Importantly, recognize that barotrauma can be
associated with noninvasive ventilation.

38. • Limiting Blood Loss
Decreasing Transfusion
Requirements
• Early Stabilization Of Unstable
Fractures
• Early Prophylactic Mechanical
Ventilation
Temporary Ex-Fix For Stabilization
Acute respiratory distress syndrome (ARDS)
Prevention

39. There is no specific treatment for ARDS
ARDS is treated in the Intensive Care Unit
By Mechanical ventilation & Oxygen therapy
Treatments may include:
Oxygen through a ventilator
Fluids through an IV line to improve blood flow
and provide nutrition
Medicine to prevent and treat infections and to
relieve pain
Acute respiratory distress syndrome (ARDS)
Management

40. • Ventilator Support
– Acceptable ABG’s
Normal Value, Range. pH, 7.4, 7.35 to 7.45.
Pa02, 90mmHg, 80 to 100 mmHg.
– Avoid further alveolar damage
• Toxic FIO2
• Barotrauma
• General Organ Support
• Research
– Optimal ventilator settings
– Pharmacological agents
Acute respiratory distress syndrome (ARDS)
Management

42. • Reversal of underlying
associated disorder
• Oxygen & Diuretics (keep on
dry side)
• Steroids (after 7 days if no
infection)
• Antibiotics
• Mechanical Ventilation
• Proning or lateral rotation
therapy
• Nutritional support
Acute respiratory distress syndrome (ARDS)
Management
• Minimize O2 demand by reducing
metabolic rate
– Control fevers
– Control anxiety and pain
• Altered Style of Ventilation
– Bi-Level Ventilation (APRV)
– High frequency ventilation
– Recruitment Maneuvers
– Proning
• Experimental Treatments:
– Nitric Oxide
– Extracorporeal membrane
oxygenation (ECMO)
– Exogenous Surfactant
Administration

43. Proning
Prone positioning was first proposed in the 1970s
as a method to improve gas exchange
• Should see improvement in 1 hour
– Response should be significant
– PaO2 improves from 60 – 100
mm Hg
• Works better in indirect ARDS
– Pancreatitis
• May improve oxygenation but
does not improve mortality
• Facial Edema can be severe

45. Indications for Mechanical Ventilation
• Acute Hypercapnic
Respiratory Failure
– Respiratory Acidosis
• Acute Hypoxemic
Respiratory Failure
– PaO2 less than normal
– FiO2 greater than 60%
oxygen
• Positive End Expiratory
Pressure (PEEP)
• Set PEEP at lower infection point
to recruit alveoli and keep them
open
• Shunting will improve with
improved PaO2
• PEEP may decrease blood
pressure and cardiac output so
monitor both closely
– Do not allow oxygen delivery
to decrease

46. Ventilation Strategies
• Use higher PEEP levels (10 – 15
cm H20)
• Set low tidal volumes at 5-7
mL/kg
• KEEP ALVEOLAR (PLATEAU)
PRESSURE LESS THAN 30 – 35 cm
H20
• This may result in permissive
hypercapnia.

47. 1. Ineffective breathing pattern related to
decreased lung compliance, decreased
energy as characterized by dyspnea,
abnormal ABGs, cyanoisis & use of
accessory muscles.
2. Impaired gas exchange related to
diffusion defect as characterized by
hypoxia (restlessness, irritability & fear of
suffocation), hypercapnia, tachycardia &
cyanosis.
3. Risk for decreased Cardiac output
related to positive pressure ventilation
4. Ineffective protection related to positive
pressure ventilation, decreased pulmonary
compliance & increased secretions as
characterized by crepitus, altered chest
excursion, abnormal ABGs & restlessness.
5. Impaired physical mobility related to
monitoring devices, mechanical
ventilation & medications as
characterized by imposed restrictions of
movement, decreased muscle strength &
limited range of motion.
6. Risk for impaired skin integrity related
to prolonged bed rest, prolonged
intubation & immobility.
7. Knowledge deficit related to health
condition, new equipment &
hospitalization as characterized
by increased frequency of questions
posed by patient and significant others.
Nursing care and diagnosis

48. Nursing care and
diagnosis

49. Acute respiratory distress syndrome (ARDS)
Outcome
Mortality :
• Significant Cause of Mortality
• Polytrauma second peak 0f death (2-7
Days) 40 - 50% Mortality rate
• Major Cause of Death in Patients with the
Lowest ISS scores
– Mortality Rate Slowly Decreasing with
Changing & Improving Therapy
– Mortality rates have declined over the
past two decades to 30 – 40%

50. Recovery:
• Extent of recovery depends on:
– Severity of the initial lung injury
– Influence of secondary forms of injury
• Oxygen toxicity
• Nosocomial infections
• DIC
• Barotrauma with mechanical ventilation
• Normal lung function after 1 year
• Residual effects may result in decreased flow rates and
DLCO (Diffusing capacity of the lungs for carbon monoxide (DLCO)
Acute respiratory distress syndrome (ARDS)
Outcome

51. Acute respiratory distress syndrome (ARDS)
Outcome
Survivors:
• Good function in many
• Diffuse pulmonary fibrosis and pulmonary
hypertension in severe cases
• Prognostic markers:
– Extreme pO2 decrease
– fibrosis