ARDS 7-3_2016

‫العظيم‬ ‫هللا‬ ‫صدق‬
‫أية‬ ‫طه‬ ‫ة‬‫ر‬‫سو‬(25‫و‬26)

ARDS
BY
DR AHMED FAYED
PULMONARY SPECIALIST
ERSM- ESCTM- RICUD
KAASH
2016

• ARDS 1st known after the 1st world war as adult respiratory distress syndrome
•In 1994 the term acute respiratory distress syndrome is used instead of adult respiratory
distress syndrome by the American European consensus conference ( AECC) as it occurs in
both adult and children
HISTORICAL BACK GROUND

DEFINITION
• A life threatening acute persistent diffuse lung inflammation with increase in vascular permeability Ch by
1. Acute onset of tachypnea and tachycardia
2. Refractory hypoxemia
3. Diffuse bilateral alveolar infiltrate in CXR
4. P/F ratio < 300
5. Pathologically DAD
6. Exclusion of cardiac failure or fluid overload
( ECHO )
According to Berlin definition of ARDS 2012

• Mild P/F ratio 200-300
• Moderate P/F ratio 100-200
• Sever P/F ratio < 100
CLASSIFICATIONS
According to Berlin definition of ARDS 2012

• Direct lung injury
• Indirect lung injury
AETIOLOGY
Paul L. Marino, 2014. the ICU book, 4th edition

• Pneumonia
• Aspiration of gastric contents
• Toxic inhalation
• Fat embolism
• Amniotic fluid embolism
• Lung contusion
• Near drowning
• Drugs as paraquat
• Radiation
DIRECT LUNG INJURY

• Sepsis
• Multiple trauma
• Multiple blood transfusion
• Acute pancreatitis
• DIC
• Sever burn
• Anaphylaxis
• Cardioplumonary bypass
• Toxic ingestion as aspirin
INDIRECT LUNG INJURY

• Exudative phase
• Proliferative phase
• Fibrotic phase
PATHOPHYSIOLOGY
Richard S. Irwin and James M. Rippe, 2012. Intensive care medicine 7th edition

• 1st 7 days
• Accumulation of fluid rich in ptn and inflammatory cells ( neutrophils and cytokines) in the interstitium with
dilution of alveolar surfactant and collapse
• Pulmonary vascular injury and obliteration by microthrombi and fibronodular proliferation
DAD
EXUDATIVE PHASE

• Stage of recovery
• 2nd and 3rd Wks
• Organization of alveolar exudate and Increase in pneumocyte type II with Early collagen deposition
• Shifting from neutrophilic to lymphocytic infiltration
PROLIFERATIVE PHASE
Stiff lung or shocked lung

• Progressive vascular occlusion with PHTN
• Extensive fibrosis with distortion of acinar architecture and emphysematous like changes with
lung bullae
FIBROTIC PHASE

• Surfactant abn
• Alv. Collapse
• Gas exchange defects
• Altered lung mechanics
• Incr pulm. shunt
• Incr dead space ventilation
• Decr lung compliance
• incr WOB
• Pulmonary hemodynamics defect with PHTN
• Hypoxemia
COLLECTIVELY

• Progressive dyspnea
• Non productive cough
• Tachypnea and tachycardia
• Cyanosis
• Incr WOB with using accessory Ms of Resp
• Agitation and restlessness
• Scattered insp. Crepitations
• Systemic hypertension
typically started within 12-48 hs of the evolving event but may be longer
CLINICAL PICTURE

• Imaging
• Laboratory
• Others
INVESTIGATIONS

• CXR) cannot reliably differentiate hydrostatic edema, i.e., cardiogenic edema,
from ALI and ARDS. )
IMAGING
ECHO
Chest CT
Chest US

• No specific lab for ARDS
• BAL
• BNP
• ABG (In addition to hypoxemia initially shows respiratory alkalosis from hyperventilation however in case of sepsis may shows metabolic acidosis with or without resp. compensation )
• ESR and CRP
• Cardiac enzymes (creatine phosphokinase and troponins) are useful for evaluating the
presence of myocardial infarction or cardiac ischemia ( troponins, have been reported to be elevated in patients
with sepsis or septic shock in the absence of coronary artery disease.)
• Liver and renal function tests
LAB0RATORY

• the most reliable method for confirming or excluding diagnosis of ARDS
• neutrophils in normal subject less than 5% but in ARDS up to 80%
• ptn BAL rich in ptn suggest evidence of lung inflammation and in relation to serum ptn the
following criteria can be applied:
L/S ptn less than 0.5% suggest hydrostatic edema while if more than 0.7% suggest lung
inflammation
• The main reason for performing bronchoscopy in ARDS is to rule in or rule out acute
processes that may have specific therapies for example, acute eosinophilic
pneumonia ( more than20% eosinophils ), diffuse alveolar hemorrhage (red cells and
hemosedrin laden macrophage), acute HP or BOOP ( high lymphcytosis).
BAL

• in patient with hypoxic respiratory failure and bilateral alveolar infiltrates BNP level less than
100 pg/ml favor diagnosis of ARDS rather than cardiogenic palm. Edema while BNP greater
than 500 pg/ml indicates that CHF is likely .
BNP

• No specific ttt ?
• principles
1- ttt of the underlying condition
2- management of respiratory failure ...........ttt of hypoxia
3- supportive care … fluid management.... inotropes...anti co agulant....VAP bundle ... nutritional care
4- other novel therapies surfactant .. anti oxidants(N acetyl cistein).... anti inflammatory( steroids,
statins and macrolides) inhaled BD (No and prostacycline) granulocyte monocyte +++ factor and ECMO
6_ future therapies ……..stem cell therapy.....APRV
PRINCIPLES OF MANAGMENT

• Decr O2 consumption
Common causes incr O2 consumption fever, pain, anxiety and use of resp.Ms
• Incr O2 delivery ……….MV?
TTT OF HYPOXIA

• People with acute respiratory distress syndrome (ARDS) are by definition severely hypoxemic,
and nearly all require invasive mechanical ventilation
• Yet mechanical ventilation itself can further injure damaged lungs (so-called ventilator-induced
lung injury) So low tidal volume ventilation is applied for ARDS
• Patient with mild ARDS may benefit from NIMV which may protect them from IMV
• NIV is proven to Increase oxygenation, Reduce dyspnea, Unload respiratory muscles.
• New modes for ARDS ……..APRV, ECMO, HFV and IRV
• Aim ?
Rajesh and Subhash, 2012. ICU protocols, respiratory system, basic of mechanical ventilation.
MV

• People with acute respiratory distress syndrome (ARDS) are by definition severely hypoxemic,
and nearly all require invasive mechanical ventilation
• Yet mechanical ventilation itself can further injure damaged lungs (so-called ventilator-induced
lung injury) So low tidal volume ventilation is applied for ARDS
• Patient with mild ARDS may benefit from NIMV which may protect them from IMV
• NIV is proven to Increase oxygenation, Reduce dyspnea, Unload respiratory muscles.
• New modes for ARDS ……..APRV, ECMO, HFOV and IRV
• Aim ? Open lung and keep it open
recruitment of lung and prevent de-recruitment
Airway pressure release ventilation
MV

• Low TV
• Plateau less than 30 cm H2O
• Permissive hypercapnia
• Optimal PEEP
• Use recruitment manuvers
• Patient sedation to improve synchrony with ventilator and NMB frequently needed
PRINCIPLES OF LTVMV

• It is safe to allow pH to fall to at least 7.20.
• The actual pCO2 is of little importance.
• When pH falls below 7.20, many physicians choose to administer sodium bicarbonate
• Conditions in which permissive hypercapnia for ARDS could theoretically be harmful include:
1. Acute cerebrovascular disorders, e.g., stroke or seizures
2. Increased intracranial pressure from any cause
3. active coronary artery disease; arrhythmias
4. Hypovolemia or GI bleeding
5. Severe pulmonary hypertension
6. Right ventricular failure
7. Uncorrected severe metabolic acidosis
8. Sickle cell anemia
9. Pregnancy
PERMISSIVE HYPERCAPNIA

It can cause severe hemodynamic compromise and barotrauma So contraindicated when the patient
is hemodynamically unstable, or in the presence of intracranial hypertension, bronchospasm, lung
bullae, or an untreated pneumothorax
Clude Guerin et al, 2011. efficacy and safety of recruitment maneuvers in ARDS. Annals of intensive care 2011

Contraindications
Shock
Acute bleeding
Multiple trauma
Spinal instability
Pregnancy
Raised intracranial pressure
Abdominal surgery
PRONE POSITION
Prone positioning improves ventilation
Clude Guerin et al, 2011. efficacy and safety of recruitment maneuvers in ARDS. Annals of intensive care 2011

• 1st pain control by opioids for non neuropathic pain and non opioids to decrease the amount of
opioids
• Gabapentin or carbamazepine may added to opioids for neuropathic pain
• Non benzodiazepine sedatives are preferred (propofol and dexmedetomidine)
• Light sedation is preferred than deep sedation with daily sedation vacation after 48 hours
• Short term NMB for up to 48hs is safe and potentially benefit
• Aim??? Improve patient ventilator synchrony and elimination of muscle activity with
subsequent decr in oxygen consumption
Juliana Barr et al, clinical practice guidelines for management of pain, agitation and delirium in adullt patient in ICU. Critical care medicine 41(1) 2013
SEDATION

• conservative strategy of fluid management (target a CVP <4 mmHg or PAOP <8 mmHg)is
needed in patients with ARDS, as long as hypotension and organ hypoperfusion can be
avoided.
• The conservative strategy improved:
1. oxygenation index
2. lung injury score
3. ventilator-free days
4. ICU-free days.
SEPSIS??
FLUID MANAGEMENT

PROGNOSIS
• Mortality rate from 24% in age between 15-19 y to 60% in age 85y and more
• Exercise impairment and decrease quality of life related to both physical and
neuropsychological factors with Decr Dlco and abnormal 6 min walking test

• The clinical hallmark of ARDS is persistent hypoxemia
• The pathological hallmark of ARDS is DAD
• MOF is the most common cause of death
•While no pharmacological therapy have been shown to incr survival in ARDS LTV MV is life
saving
•Mortality rates have been decr but still high with survivors show many problems
• Defined as A life threatening acute persistent diffuse lung inflammation with increase in
vascular permeability OF Acute onset, Refractory hypoxemia, Diffuse bilateral alveolar
infiltrate in CXR, P/F ratio < 300 AND Exclusion of cardiac failure or fluid overload
• Caused by direct and indirect lung injury but sepsis is the most common cause
• Pathogenesis include 3 stages with the affection of alveolocapillary membrane is most
important
• Not a disease but A syndrome so no specific diagnostic tool or specific treatment
conclusion

• A syndrome started as …………
ending as ………..
summary

• A syndrome started as SIRS
ending as ………..
summary

• A syndrome started as SIRS
ending as MOF
summary

pulmonary capillary wedge pressure (ie, pulmonary artery occlusion pressure

ARDS 7-3_2016

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