the acute respiratory distress syndrome describe the history and evolution of the diagnosis of ards...
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THE ACUTE RESPIRATORY
DISTRESS SYNDROME
Daniel Brockman, DO
Objectives
Describe the history and evolution of the diagnosis
of ARDS
Review the diagnostic criteria for ARDS
Discuss the primary interventions in ARDS
Address salvage therapies for severe hypoxia in
ARDS.
Case Presentations
A
23 year old male college student…
18 year old female…
60 year old male SNF resident…
40 year old female with an SBO
Case presentations
...is found down after ODing on Heroin.
…comes to the ICU after DCS for abdominal trauma
from an MVC.
…is sent to the ED with a fever and cough.
…vomits on the wards and collapses.
Next they
develop severe hypoxia.
And a CXR reveals
Or this
Or this
Or maybe it was a CT to r/o PE
Epidemiology
Approximately 190,000-200,000 cases annually
reported.
Incidence estimated to be 86 case per 100,000
Increased incidence in the elderly
306 case per 100,000
Estimated mortality between 30-40%.
Historical Perspective
During the Vietnam War a clinical syndrome of
severe hypoxia was identified soldiers who suffered
serious injuries.
The Adult Respiratory Distress
Syndrome
In 1967 a case series reported 12 cases of sudden
onset severe hypoxia associated with diffuse patchy
infiltrates on chest X-ray.
The condition was termed the Adult Respiratory
Distress Syndrome.
The X-ray appeared very similar to the Infant
Respiratory Distress Syndrome.
Pediatricians are for babies
As the condition was diagnosed more it became
apparent that ARDS occurred in all ages.
Pediatricians REALLY don’t like writing the word
adult and were quite vocal about it.
Therefore the name was changed to ACUTE
Respiratory Distress Syndrome
Shortly there after
Tom Petty, MD had a new ABG machine
Discovered in a patient with what was later identified
as ARDS after trauma that retarding expiratory flow
resulted in an increase in PaO2(40->130).
This maneuver was repeated in 12 additional patients
with similar clinical picture with consistent improvements
in oxygenation.
So what is ARDS?
Diffuse pulmonary edema due to fluid leaking in to
alveolar spaces and damage to lung tissues from
inflammation and loss of oncotic forces.
So all of these:
Neurogenic Pulmonary Edema
Fat Embolism
Shock Lung
TRALI
Pump Lung
Capillary Leak Syndrome
Are just ARDS
Clinical Diagnosis
AECC Definition:
Due to the disparate causes and unclear definition a
diagnostic criteria was composed in 1994 to
standardize the definition of ARDS
Main diagnostic points were
Acute Onset
Hypoxia
Bilateral Infiltrates
Absence of Heart Failure
Refining the Diagnosis
The Berlin Criteria was devised by a panel of
experts in 2011 and released in 2012.
Provided more concrete criteria for some of the
diagnostic requirements.
Added a severity scale to diagnosis.
Not very different from AECC in actuality.
AECC vs. Berlin
Acute Onset.
Diffuse patchy infiltrates on CXR.
Absence of LV dysfunction on Echo or PAWP<18.
PaO2/FiO2 <200.
Onset within 7 days.
Diffuse patchy infiltrates on CXR or CT scan.
No clinical suspicion of heart failure or absence of LV dysfunction on Echo.
PaO2/FiO2<300 on at least 5 of PEEP or EPAP.
Berlin Criteria Severity Scale
Based on PaO2/FiO2 ratio.
Mild 201-300
Moderate 101-200
Severe <101
Correlates with mortality
Mild: 27%
Moderate: 32%
Severe: 45%
So if you want to be technical
Patient’s with cardiomyopathies can’t have ARDS.
Patient’s with a pneumonectomy can’t have ARDS
Pathophysiology
Inciting event causes release of inflammatory
markers causing damage to capillaries and alveoli
resulting in fluid exiting the vascular space into the
lung parenchyma resulting in filling of or collapse
of alveoli.
Pathophysiology
Results in patches of alveoli that receive no
ventilation causing shunting of deoxygenated
venous blood through portions of the lung without
oxygenation.
Phases of ARDS
Acute(or exudative) Phase
Edema and diffuse alveolar damage.
Generally Days 1-6
Phases of ARDS
Healthy Lung
Acute ARDS
Phases of ARDS
Proliferative Phase
Edema begins to improve,
overgrowth of Type 2
Aveolar Cells, myofibroblasts
invade into interstitium and
collagen deposition occurs.
Thank you Pediatricians
Chronic Acute Respiratory Distress Syndrome
Also called Fibrotic Phase of ARDS
Fibrosis of lung parenchyma,
formation of cysts in
damaged parts of the
Lung.
Inciting Events
Pulmonary
Pneumonia
Aspiration
Pulmonary Contusion
Near Drowning
Smoke Inhalation
Extrapulmonary
Sepsis
Severe Trauma
Burns
Pancreatitis
Blood Transfusions
Drug Overdose/Reaction
Head Injury
Cardiac Bypass
Bone Marrow Transplant
Complications
Pneumothorax
Pneumomediastinum
Decreased venous return-hypotension
Worsening of pulmonary edema and worsening oxygenation
Organ dysfunctiomn
Many are actually are complications of mechanical ventilation in ARDS
Barotrauma
Injury to lung due to High Ventilatory pressures.
Pneumothorax
Pneumomediatinum
Volutrauma
Increase in inflammatory markers caused by
distension of alveola.
Leads to further lung injury from inflammation and
extrapulmonary organ injury.
Atelectrauma
Increase in both inflammatory cytokines and
alveolar injury due to shearing caused by the
repeated opening and closing of alveolar units.
Optimizing Treatment in ARDS
Low Tidal Volume Ventilation
Controlling Plateau Pressures
Permissive Hypercapnia
Providing adequate Oxygentaion
Early Neuromuscular Blockade
The ARMA Trial
Randomized control trial
861 patients meeting AECC definition of Acute Lung
Injury (PaO2/FiO2<300)
Randomized to:
6 ml/kg(PBW) and Plateau pressure <30
12 ml/kg(PBW) and Plateau pressure <50
Stopped early due to significantly higher mortality in
12 ml/kg group
Demographics
Results
12 ml/kg 6 ml/kg P-value
Mortality 39.8% 31.0% 0.007
Ventilator free days 10 12 0.007
Days without other organ failure 11 15 0.006
Barotrauma Events 11 10 0.43
PEEP strategies
Best PEEP using flow volume loops
Super PEEP
Optimum PEEP for compliance
Minimum PEEP for oxygenation
No good evidence to support one strategy over
another for determining PEEP.
Some points about PEEP
It takes time to recruit alveoli with PEEP, don’t
expect rapid changes in oxygenation.
A lung opening procedure or recruitment maneuver
can be used to more rapidly open the lung and
improve oxygenation.
Increase PEEP to 30-40 for 20-30 seconds.
Early Neuromuscular Blockade
Randomized Double Blind Placebo Controllede Trial
340 patients with AECC definition of ARDS and
PaO2/FiO2<150 on at least 5 of PEEP
Randomized to
Deep Sedation for 24 hours
Deep Sedation plus Neuromuscular Blockade with
cisatricurium for 48 hours.
Demographics
Results
Results
Adjust 90 day Hazard Ratio for Death: 0.68 (p-value: 0.04)
Neuromuscular Blockade
Subgroup analysis based on severity of ARDS
defined by PaO2/FiO2 ratio demonstrated that
mortality benefit occurred in patients with
PaO2/FiO2 ratio <120.
Fluid Management(The FACCT Trial)
Randomized Controlled Trial
Two major questions:
Do PAC’s help management of ARDS
Keep this short: NO
Liberal(give fluid) vs restrictive(diurese) management
The FACCT Trial
1000 patient meeting AECC definition of Acute
Lung Injury (PaO2/FiO2<300)
Randomized to:
Demographics
Results
Salvage/Rescue Therapies
Proning
Inhaled Vasodilators
APRV
HFOV
ECMO
Proning
Proning
Reverses dependant areas of lung leading to
decreased V/Q mismatch.
Creates increase in extrathoracic pressure.
Recent NEJM study showed improved mortality in
patients with severe ARDS (PaO2/FiO2<100 after
36 hours of treatment) kept prone for 14 hrs a day.
Inhaled Nitric Oxide
Vasodilator
Enters opened areas of lung and dilates capillaries increasing blood flow to open areas of lung.
Improves V/Q matching.
Expensive.
Improves oxygenation but no proven mortality benefit.
Increased incidence of renal failure.
Epoprostenol
Same mechanism of action as INO.
Administered as continuous NEB @ 50 ng/kg/min
Again improves oxygenation but no proven mortality
benefit
Significantly cheaper than INO.
No evidence of increased renal failure.
Iloprost
Another inhaled vasodilator
Administered Ever 2 to 4 hours
Has the least evidence supporting its effectiveness.
Cheapest option of Inhaled Vasodilators
APRV
APRV
Alternate mode of ventilation high steady airway
pressure that drops to a lower pressure for a brief
period of time.
Allows higher airway pressures.
Some small studies show decreased rates of
developing ARDS, but no other evidence of
outcomes differences in patients with ARDS.
HFOV
HFOV
Continuous high airway pressures, a piston rapidly
pushes tiny amounts of air into and out of the lungs.
Allows higher mean airway pressures without large
tidal volumes or shearing improving recruitment and
oxygenation.
In 2 large studies no benefit or worsened outcomes
if used in early ARDS.
ECMO
ECMO
By running Venous blood through a membrane
oxygenator the patient can have effective CO2
removal and oxygenation without relying on the
lungs.
Allows for minimal vent settings to rest the lungs.
Evidence is limited but shows some potential benefit
in severe ARDS.
Key Points
ARDS is a clinical diagnosis with specific criteria.
Acute Onset <7 days
PaO2/FiO2 <300
Bilateral patchy infiltrates
Not cardiac related
Key Points
Low tidal volume ventilation improves mortality.
6 mL/kg PBW(based on Height)
Diuresis decreases ventilator days and organ failure in
hemodynamically stable patients.
Early Neuromuscular Blockade of benefit in moderately
severe cases
Variety of salvage therapies
Proning, Inhaled Vasodilators, APRV, HFOV, ECMO
Only proning has shown any mortality benefit.
Key Points
Variety of salvage therapies
Proning, Inhaled Vasodilators, APRV, HFOV, ECMO
Only proning has shown any mortality benefit.
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