ACUTE RESPIRATORY

DISTRESS SYNDROME ( ARDS )

DR. SEHAJ ROOP KAUR

DEPARTMENT OF GENERAL MEDICINE
SMS MEDICAL COLLEGE & HOSPITAL
• A 55 year old male recently diagnosed with H1N1, presented to the
Emergency Department, accompanied by his wife with worsening
shortness of breath, fever, and productive cough. He is non- smoker,
non- alcoholic, no history of diabetes, HTN or any co-morbidity.
• Primary assessment revealed BP – 90/50mmHg, PR- 106/min, oxygen
saturation of 61% on room air.
• On ABG, pH- 7.42 , pCO2 – 40, pO2 – 45, saO2 – 65%
• NIV used but his respiratory status continues to deteriorate .
• Patient was tachypneic, hypotensive, had tachycardia.
• On examination he had diffuse bilateral crepitations in both lung fields
, Chest X-Ray revealed diffuse pulmonary infiltrates , predominantly in
lower lobes.
• Investigations –
• Hb – 15.1gm/dl
• TLC – 10.2
• Platelet count – 3.25 lakhs/mm3
• Serum Sodium – 143 mEq/l
• Serum Potassium – 3.9 mEq/l
• Serum Chloride – 97mEq/l
• Serum Urea – 35 mg/dl
• Serum Creatinine – 1.2 mg/dl
• BNP – 18 pg/ml
• Scrub typhus - Negative
4-5 days back CXR CXR AT ADMISSION
 INTRODUCTION

• First described as clinical syndrome in 1967 by Ashbaug and Petty

- Described 12 patients with
- tachypnea
- refractory hypoxemia
- diffuse opacities on CXR
- prominent hyaline membranes lining alveolar spaces
 DEFINITION OF ARDS
• ARDS defined as a clinical syndrome of severe dyspnea of rapid onset,
hypoxemia and diffuse pulmonary infiltrates leading to respiratory
failure.
• By expert consensus, defined by three categories based on degree of
hypoxemia.
• These stages associated with mortality risk and duration of
mechanical ventilation
 DIAGNOSTIC CRITERIA FOR ARDS
SEVERITY: ONSET CHEST ABSENCE OF
OXYGENATION RADIOGRAPH LEFT ATRIAL
HYPERTENSION
MILD : PaO2/FiO2- ACUTE BILATERAL PCWP<18mmHg or
201 to 300mmHg; ALVEOLAR OR no clinical evidence
27% mortality INTERSTITIAL of increased left
MODERATE: INFILTRATES atrial pressure
PaO2/FiO2-101 to
200mmHg;32%
mortality
SEVERE: <100mmHg;
45% mortality
 AECC DEFINITION BERLIN CRITERIA
TIMING Acute onset Within 1 week of known clinical
insult or new or worsening
[Link]

OXYGENATION PaO2/FiO2<200 Mild- PaO2/FiO2<300mmHg

Moderate- PaO2/FiO2<200
Severe- PaO2/FiO2< 100
PEEP REQUIREMENT None Minimum 5 cmH2O PEEP required
by IMV

CHEST IMAGING Bilateral infiltrates seen on Bilateral opacities not fully

chest radiograph explained by effusions, lobar/lung
collapse or nodules by chest
radiograph or CT

ORIGIN OF EDEMA PCWP<18mmHg when Respiratory failure not fully

measured or no evidence of explained by cardiac failure or fluid
left atrial hypertension overload
• Clinical terms synonymous with ARDS
- Acute respiratory failure
- Capillary leak syndrome
- Double pneumonia
- Shock lung
- Traumatic wet lung
- Adult hyaline membrane disease
EPIDEMIOLOGY

• INCIDENCE – Estimates range from 10 to 86 cases per 1,00,000

• Approx. 10% of all ICU admissions are of acute respiratory failure;
20% meet the criteria for ARDS
• Increases with advancing age, because of incidence of underlying
causes
 16 cases per 100000 person-years aged 15-19 years
 306 cases per 100000 person-years aged 75 and above
• MORTALITY- Until 1990s , reported to be 40-70%
- Now, in the range of 30-40%
AGE AND RISK-SPECIFIC INCIDENCE OF AND AGE-SPECIFIC MORTALITY FROM ALI
ETIOLOGY OF ARDS
DIRECT LUNG INJURY INDIRECT LUNG INJURY
Pneumonia Sepsis
Aspiration of gastric contents Severe trauma and hemorrhagic shock
Pulmonary contusion Multiple transfusions
Near- drowning Drug overdose
Toxic inhalation injury Pancreatitis
Postcardiopulmonary bypass
Major burn injury
Reperfusion edema after lung
transplantation or embolectomy
• Several other clinical variables associated with development of ARDS

 Older age
 Chronic alcohol abuse
 Metabolic acidosis
 Severity of critical illness
CONDITIONS THAT MAY MIMIC ARDS
• Congestive heart failure
• Interstitial lung disease ( AIP, NSIP, Cryptogenic organizing
pneumonitis, Acute eosinophilic pneumonia, Hypersensitivity
pneumonitis , Pulm. Alveolar proteinosis )
• Connective tissue diseases such as Polymyositis
• Diffuse alveolar hemorrhage from vasculitis or Goodpasteur’s
syndrome
• Drug induced ( bleomycin or amiodarone) including vascular leak
syndrome from immunotherapy
• Cancer (T cell or B cell lymphomas or metastatic carcinoma )
• Endobronchial tuberculosis
PATHOGENESIS
• Natural history of ARDS marked by 3 phases –
 Exudative
 Proliferative
 Fibrotic
• Each with characteristic clinical and pathological features

Edema Hyaline Interstitial inflammation Fibrosis

membranes

0 2 7 14 21
EXUDATIVE PHASE

• Exudative phase in the first 7

days, patient experiences onset
of symptoms
• Dyspnea develops with a
sensation of rapid shallow
breathing and an inability to
get enough air.
• Tachypnea- work of breathing
and respiratory fatigue,
ultimately- Respiratory failure
PROLIFERATIVE PHASE

• Usually lasts from day 7 to 21.

• The initiation of lung repair, organization of alveolar exudates and a
shift from neutrophil to lymphocyte predominant pulmonary
infiltrate.
• Most patients recover rapidly and liberated from Mechanical
ventilation.
• Some develop progressive lung injury and enter fibrotic phase.
• Type II pneumocytes synthesize new pulmonary surfactant and
differentiate into type I pneumocytes.
FIBROTIC PHASE

• Seen after 3-4 weeks of injury

• Histologically, there is extensive
alveolar duct and interstitial
fibrosis
• Require long term support on
Mechanical ventilation and/or
supplemental oxygen
• Bad prognosis
• Increased mortality
Bullae formation :

• Acinar architecture is markedly disrupted, leading to emphysema like

changes with large bullae.

Vascular occlusion :

• Intimal fibroproliferation in the pulmonary microcirculation leads to

progressive vascular occlusion and pulmonary hypertension.
 Classical sign of alveolar injury –
• Condensed plasma proteins aggregate with
cellular debris and dysfunctional pulmonary
surfactant to form hyaline membrane whorls.
• Alveolar edema predominantly involves
dependent portions of the lung, leading to
decreased aeration and atelectasis.
• Decreased lung compliance in the dependent
area.
• Consequently, intrapulmonary shunting and
hypoxemia develop and increase work of
breathing and dyspnea.
• Consequences of lung injury include :

- Impaired gas exchange

- Decreased compliance
- Increased pulmonary arterial pressure
 LACK OF SPECIFICITY : ( Diagnostic dilemma )

• The diagnosis of ARDS based on clinical

criteria can be problematic.

• Because many of the clinical features of

ARDS are shared by other causes of Acute
Respiratory Failure.
 Features shared by ARDS & other causes of acute respiratory
failure
FEATURE ARDS SEVERE PULMONARY CARDIOGENIC
PNEUMONIA EMBOLISM [Link]
ACUTE ONSET    

FEVER,    IF ACUTE MI
LEUKOCYTOSIS
BILATERAL   
INFILTRATES
PaO2/FiO2<200   
mmHg
PACP<18 mmHg   
TREATMENT OF ARDS
• GENERAL PRINCIPLES :
1. Recognition and treatment of underlying medical and surgical medical
and surgical disorders ( Sepsis, aspiration, trauma ).
2. Minimization of procedures and their complications.
3. Prophylaxis against
- Venous thromboembolism
- Gastrointestinal bleeding
- Aspiration
- Excessive sedation
- Central venous catheter infections.
4. Prompt recognition of nosocomial infections.
5. Provision of adequate nutrition.
MANAGEMENT OF HYPOXEMIA

• By definition, patients of ARDS are severely hypoxemic.

• Options for improving arterial oxygen saturation include –
- Use of high fractions of inspired oxygen ( FiO2 )
- Decrease oxygen consumption
- Improve oxygen delivery
- Manipulate mechanical ventilatory support
 Ventilatory based strategies in the management of ARDS –

 Currently, the only therapy proven to be effective at reducing

mortality in ARDS is a Protective ventilatory strategy.

Low volume ventilation and PEEP

LUNG PROTECTIVE VENTILATION

• Since the introduction of positive – pressure ventilation, large

inflation volumes have been used to decrease tendency for atelectasis
during mechanical ventilation

• In patients with ARDS, these large inflation volumes have a marked

decrease in functional volume - VOLUTRAUMA
• ARDS , a heterogenous disorder, principally involving dependent
portions of the lung with relative sparing of other regions

• Because compliance differs in affected versus “normal” areas of the

lung, attempts to fully inflate consolidated lung may lead to over-
distension of and injury to the more normal areas

Ventilator induced Lung injury

LOW TIDAL VOLUME VENTILATION
• Also referred to as lung protective ventilation

• A large scale randomized controlled trial sponsored by National

Institutes of Health and conducted by ARDS Network compared low
tidal volume ventilation (6 ml/kg of predicted body weight) to
conventional tidal volume ventilation (12 ml/kg predicted body
weight ) .

• Mortality rate significantly lower in low VT patients (31%) than

conventional VT patients ( 40% )
• LTVV caused hypercapnic respiratory acidosis, which is quite
expected.

• Permissive hypercapnia : One of the consequences of LTVV.

• Permitted because of the mortality benefit with low tidal volume

• The degree of hypercapnia can be minimized by -

1. Using the highest respiratory rate that does not induce
Auto-PEEP
2. Shortening the ventilator tubing to decrease dead space
PLATEAU PRESSURE GOAL

• In ARDS, the plateau pressure < 30cm of H2O, as part of ARDS Net
Protocol

• If Pplat is >30cm of water, ARDS protocol recommends, decrease Tidal

Volume by 1ml/kg of PBW ( predicted body weight ) to a minimum of
4 ml/kg of PBW.
Positive end-expiratory pressure ( PEEP )
• PEEP is an adjunct to the mode of ventilation, that increase the end
expiratory pressure to a value more than atmospheric pressure.

• Routine use of high PEEP is not recommended in ARDS, as it has no

proven mortality benefit .

• But, in patients refractory to standard methods of mechanical

ventilation, high PEEP strategy can be used, importantly in those with
recruitable lung ( i.e. oxygenation improves with high PEEP strategy )

• The effects of applied PEEP can be directly visualized by Lung

Ultrasound, may prove useful in future.
• BENEFIT –
Higher levels of PEEP benefit by opening collapsed alveoli, which in
turn serves to decrease alveolar overdistension because the volume
of each subsequent tidal breath shared by more open alveoli.

More alveoli remain open throughout the respiratory cycle, cyclic

atelectasis is also reduced.

• HARM –

Can cause ventilator associated lung injury by increasing plateau

airway pressure
RECRUITMENT MANEUVERS

• Proposed for improving arterial oxygenation and enhancing alveolar

recruitment.
• Brief application of high level of continuous positive airway pressure,
such as 35 to 40cm of H2O for 40 seconds, to open up collapsed
alveoli.
• Particularly beneficial after a patient been disconnected from the
ventilator (e.g. tubing changes, transport), because even a brief
moment without PEEP can result in alveolar collapse.
• That’s why repeated suctioning not advised in ARDS.
• Insufficient evidence to support routine use recruitment maneuvers in
ARDS patients.

• Meta-analyses do not report convincing benefit on mortality, length

of hospital stay, or the incidence of barotrauma, despite improving
the arterial oxygen tension (PaO2).

• May be performed in those with refractory hypoxemia despite low

tidal volume/high PEEP strategies.

• PaO2 usually rises within 2 hours of recruitment maneuver.

• For all patients, Tidal volume and Respiratory rate be managed using
Low Tidal Volume Ventilation ( LTVV ) strategy.

• INITIAL VENTILATOR SETTINGS :

 Calculate predicted body weight ( PBW )
Males – 50 + 2.3 [ height(inches) – 60 ]
Females – 45.5 + 2.3 [ height(inches) – 60 ]
 Set mode to Volume assist-control
 Set initial Tidal Volume to 6ml/kg PBW
 Set initial ventilator rate< or equal to 35 breaths/min to match
baseline minute ventilation.
• SUBSEQUENT TIDAL VOLUME ADJUSTMENT –

 Plateau pressure goal : Pplat< or equal to 30 cm H2O

 Check inspiratory plateau pressure with 0.5 second inspiratory pause
at least every 4 hours and after each change in PEEP or tidal volume
- If Pplat>30 cm H2O, decrease tidal volume in 1ml/kg PBW steps to
5 or if necessary to 4 ml/kg PBW
- If Pplat<25 cm H2O and tidal volume< 6ml/kg, increase tidal
volume by 1ml/kg PBW until Pplat>25 cm H2O or tidal volume=6
ml/kg
- If breath stacking(autoPEEP) or severe dyspnea occurs, tidal vol.
may be increased to 7 or 8ml/kg PBW, if Pplat remains<30cm H2O
• ARTERIAL OXYGENATION AND PEEP –

 Oxygenation goal : 55 to 80 mmHg or SpO2 88 to 95%

 Use these FiO2/PEEP combinations to achieve oxygenation goals –

SUPPORTIVE CARE
 Sedation –
Critically ill patients who require mechanical ventilation are often
given continuous intravenous infusions of sedative drugs to treat
anxiety , decrease excessive oxygen consumption and facilitate
nursing care.
Daily interruption of infusion of sedative drugs :
-Shortened the duration of hospital stay and length of stay in ICU.
-Early detection of neurologic dysfunction , from new insult
-Cost-effective
Neuromuscular blockade :

Administration of a short term( upto 48 hrs) neuromuscular blocking

agent early in the course of severe ARDS improves
-90 day survival rate
-Increased number of ventilator-free days and days outside ICU
-Did not significantly improve overall 90 day mortality

 MECHANISM :
-Facilitate lung protective ventilation by improving patient-ventilator
synchrony
-Decrease in lung or systemic inflammation
Hemodynamic monitoring :

Hemodynamic monitoring should be done by Central venous

catheter( CVC) .

CVC, when compared to that by Pulmonary Artery Catheter (PAC) in

patients with ARDS resulted in no difference in mortality, lung
function, ventilator-free days, organ failure free days or ICU-free days
at day 28

But, PAC group had approx.2 fold increase of catheter-related

complications.
Nutritional support :

Enteral nutrition support refers to provision of calories, protein,

electrolytes, vitamins, minerals and fluids via an enteral route
For most critically ill patients for whom enteral nutrition is prescribed,
a standard formulation of enteral nutrition(grade 2B) suggested
Routine supplementation of enteral nutrition with omega-3 fatty
acids, antioxidants, glutamine, arginine, prebiotics, probiotics, fiber or
immune modulators not recommended
For all critically ill patients receiving enteral nutrition, gastric feeding
is preferred than post-pyloric feeding and 30 to 45 degrees of backrest
elevation is advised
 Glucose control :

Hyperglycemia associated with poor clinical outcomes in critical

patients

Blood glucose target of 140 to 180 is suggested for critically ill adults

Careful monitoring of blood glucose necessary to achieve glycemic

control while avoiding potential harmful effects of hypoglycemia.
Nosocomial pneumonia:
Risk factors for HAP ( HOSPITAL AQUIRED PNEUMONIA ) –
- Most significant is Mechanical Ventilation
- Increasing age (>55 years)
- Chronic lung disease
- Depressed consciousness
- Aspiration
- Reintubation or prolonged mechanical ventilation
- Frequent ventilator circuit changes
- Total opioid exposure
- Paralysis
- Use of muscle relaxants or glucocorticoids
 Practices recommended to prevent Ventilator acquired pneumonia:
- Manage patients without sedation whenever possible
- Interrupt sedation daily
- Assess readiness to extubate daily
- Perform spontaneous breathing trials with sedatives turned
off
- Utilize endotracheal tubes with subglottic secretion drainage
ports for patients expected to require prolonged mechanical ventilation
- Elevate the head of the bed to 30 to 45 degrees
- Regular oral care with chlorhexidine
- Saline instillation before tracheal suctioning
 DVT Prophylaxis :
- All patients admitted to intensive care units require some form
of thromboprophylaxis

 GI Prophylaxis :
- Patients requiring prolonged mechanical ventilation are at
increased risk for gastrointestinal bleeding .
Role of STEROIDS in ARDS
 Systemic glucocorticoids should be started when ARDS has been
precipitated by Steroid-responsive process ( e.g. Acute eosinophilic
pneumonia ) or in patients in whom steroids have a proven role (e.g.
Community acquired pneumonia).
 However, their administration to ARDS patients is controversial.
Randomized trials and meta-analyses consistently demonstrate that
Glucocorticoids are NOT beneficial and may be harmful when
administered late in the course of ARDS ( i.e. more than 14 days )
Rationale for avoidance of glucocorticoids in early ARDS is lack of
proven mortality benefit and the potential for adverse effects as well
as lack of clarification regarding timing, duration and dosing.
FLUID MANAGEMENT
• Conservative fluid management strategy recommended in patients
with ARDS , as long as hypotension and organ hypoperfusion is
prevented.
• A trial of 1000 patients with ARDS , randomly assigned to conservative
( CVP targeted <4mmHg ) or a liberal ( CVP of 10 to 14mmHg ) fluid
management for seven days.
• A clear benefit of conservative fluid management on mortality not
yet shown.
• But the conservative strategy does improve oxygenation index, lung
injury score , increasing ventilator-free days and ICU-free days.
PRONE POSITIONING

Prone positioning in Severe ARDS for >12 hours per day is of proven
benefit .

Mechanism – Because edema becomes gravitationally dependent in

supine ARDS patients, prone positioning improves oxygenation by
increasing alveoli recruitment of those alveoli that have been
“flooded”
INVESTIGATIONAL OR INEFFECTIVE
PHARMACOTHERAPY IN ARDS

• Therapy for ARDS is supportive, aimed at improving gas exchange and

preventing complications while addressing to the precipitating cause.
• None pharmacotherapy are currently recommended as routine
therapy.
THERAPIES FOR PREVENTION

• Aspirin has no proven benefit and trial of inhaled glucocorticoid and

beta-2 agonist combinations are awaited.
THERAPIES FOR TREATMENT
• ENHANCING LUNG REPAIR –

-GM-CSF has not become a routine therapy for adults with ARDS
because the evidence is still inconclusive.

-GM-CSF plays an imp. Role in repairing injured lung and enhancing

alveolar macrophage function and its presence in BAL of patients
with ARDS is associated with better survival, as per preclinical
studies.
2. STEM CELLS –

- Preclinical studies suggest that treatment with exogenously

administered Mesenchymal stem cells (MSCs) may help to
attenuate lung injury.
- MSCs appear to secrete growth factors and cytokines capable of
modulating local inflammation and promoting tissue repair,
bacterial clearance, and potentially differentiate into mature cells
to replace damaged ones.
ROLE OF MACROLIDE ANTIBIOTICS

• An observational study conducted using data from Lisofylline and

Respiratory Management of Acute Lung Injury (LARMA) trial.

• Patients with ARDS receiving Macrolide antibiotic within the initial 24

hours were compared with patients who did not.

• Mortality was lower in the group receiving Macrolide antibiotic

( 23 versus 36% ).
OTHER ANTI-INFLAMMATORY AGENTS

• SB-681323, a potent selective inhibitor of p38alpha, an anti-

inflammatory and anti-proliferative agent.
• Carbon-monoxide – thought to have anti-inflammatory or anti-
oxidant properties in low doses.
• Tissue factor antibody- Anti-TF , ALT-836 inhibits TF-dependent
procoagulant activity and being studied in patients with Sepsis-related
ARDS.
• IFN-beta – a potent anti-inflammatory agent
• Sevoflurane – an inhaled anesthetic gas with anti-inflammatory
properties.
INEFFECTIVE OR HARMFUL THERAPIES
• Anti-oxidant preparations – N-acetylcysteine, procysteine, glutamine,
omega-3 fatty acids, Selenium , beta-carotene , zinc, Vitamin E and C ,
Lisofylline.
• Intravenous prostaglandin E1
• Neutrophil elastase inhibitors
• Ibuprofen
• Activated protein C
• Ketoconazole
• Statins
• Surfactant
• Short-acting beta-2 agonists (inhaled and systemic)
• A 41 year old woman presents with severe community- acquired
pneumococcal pneumonia. Chest radiograph reveals diffuse bilateral
infiltrates, and hypoxemic respiratory failure develops despite
appropriate antibiotic therapy. She is intubated and mechanical
ventilation is initiated with Volume- and Pressure-limited approach for
ARDS. Over the ensuing 24 hrs, her PaO2 decreases to 40mmHg,
despite ventilatory support with FiO2 of 100% and PEEP of 20cm of
water. She is placed in prone position and neuromuscular blocking
agent is administered, without improvement in her PaO2.
What will you recommend now?
EXTRACORPOREAL MEMBRANE
OXYGENATION ( ECMO )
Term used for an extracorporeal circuit that directly oxygenates and removes carbon
dioxide from the blood.

Commonly used for patients with ARDS

Often, imprecisely referred to as “ lung rest “

This strategy may improve outcomes by further mitigating ventilator-associated lung

injury.

The best outcome in ECMO for adult respiratory failure occurs when ECMO instituted
early after onset ( 1-2 days )
INDICATION
RESPIRATORY FAILURE CARDIAC FAILURE
ALI / ARDS POST CARDIAC SUPPORT
ASPIRATION PULMONARY EMBOLUS
PNEUMONIA POST CARDIAC SURGERY
ASTHMA BRIDGE TO TRANSPLANT
LUNG TRANSPLANT CARDIOGENIC SHOCK
LUNG CONTUSION
TYPES OF ECMO

1. Veno-venous ECMO :
• Used to support patients with severe respiratory failure refractory to
conventional therapies.
• Blood is drawn from a central vein, pass through an ECMO machine
and then returned back via a central vein
2. Veno-arterial ECMO :
• Used to support patients with severe cardiac failure (with or without
respiratory failure )
• Blood is drawn from a central vein, pass through an ECMO machine
and then returned back via a central artery
ECMO serves as a BRIDGING therapy and not a curative therapy.

Used as a :
- Bridge to recovery: that is buying time for patient to recover
- Bridge to decision: provide temporary support to patient and
allow clinicians to decide on the next step
- Bridge to transplant: provide support to patient while awaiting
suitable donor organ
INDICATIONS FOR ECMO IN ARDS

Severe hypoxemia ( e.g. ratio of PaO2/FiO2<80, despite high levels of

PEEP[typically 15 to 20]) for at least 6 hrs in patients with potentially
reversible respiratory failure.

Uncompensated hypercapnia with acidemia (pH 7.15) despite the

best accepted standard of care for management with ventilator.

Excessively high end-inspiratory plateau pressure (35-45 cm of water,

according to the patient’s body size) despite the best accepted
standard of care for management with ventilator.
RELATIVE CONTRAINDICATIONS
High pressure ventilation (end-inspiratory plateau pressure>30 cm of
water) for >7 days
High FiO2 requirements (>0.8) for >7 days
Limited vascular access
Any condition or organ dysfunction that would limit the likelihood of
overall benefit from ECMO, such as severe, irreversible brain injury or
untreatable metastatic cancer

ABSOLUTE CONTRAINDICATION
Any condition that precludes the use of anticoagulation therapy
ECMO

INITIATION

MAINTENANCE

DISCONTINUATION
ECMO INITIATION

• The patient is anticoagulated with intravenous heparin and cannulae

are inserted.

• Patient is connected to ECMO circuit, the pump started with the flow
of 20ml/kg/min.

• Gradually increase every 5-10 min by 10ml/kg/min to reach the

desired flow.
ECMO REASONABLE TARGET

• An arterial oxyhemoglobin saturation of >85% for Venovenous ECMO

• Adequate tissue perfusion as determined by

- Arterial blood pressure
- Oxygen saturation
- Blood lactate level
MAINTENANCE AND MONITORING

• Once the respiratory and hemodynamic goals achieved, blood flow is

maintained at that rate

• Anticoagulation via infusion of unfractionated heparin, titrated with

activated clotting time of 180-210 seconds.
WEANING TRIAL OF ECMO

INDICATIONS :

Improvement in radiographic appearance

Improvement in oxygenation

One trial should be performed prior to discontinuing ECMO

permanently
ADVERSE EVENTS ASSOCIATED WITH ECMO

Directly related to ECMO Circuit

Oxygenator failure 17.5%
Blood clots
Oxygenator 12.2%
Other circuit 17.8%
Cannula related problems 8.4%
Other mechanical complications 7.9%
Not directly related to ECMO Circuit
Bleeding
Surgical-site bleeding 19.0%
Cannulation-site bleeding 17.1%
Pulmonary hemorrhage 8.1%
Gastrointestinal hemorrhage 5.1%
Intracranial hemorrhage 3.8%
Hemolysis 6.9%
DIC 3.7%
Culture-confirmed infection at any site 21.3%
CESAR TRIAL

• Randomised controlled trial of adult ECMO vs Conventional

Ventilatory support.

• Adults were randomized either to Venovenous ECMO at Glenfeld

hospital, Leicester, England (90 patients) or continuing conventional
care at referral hospitals (90 patients) that is conventional ventilator
support.
ECMO CONVENTIONAL
VENTILATORY SUPPORT
57 out of 90 met primary end 41 out of 90 patients met primary
point end point
Survival rate at 6 months is 63% Survival rate at 6 months is 47%

Mortality – 37% Mortality – 53%

UNITED KINGDOM H1N1 ECMO vs
CONVENTIONAL CARE

• 69 ECMO patients in 4 centres

• Conclusion : ECMO survival 76%

Conventional care 49%
MORTALITY

• Recent mortality estimates range from 30 -40% with

substantial variability.

• The underlying cause is the usual cause of death

among patients who die early.

• In contrast, sepsis due to nosocomial pulmonary

infection is the most common cause of death among
those who die later in their clinical course.
FUNCTIONAL RECOVERY IN ARDS SURVIVORS

• Cognitive, psychologic, and physical morbidity is

common among survivors of ARDS, similar to that
observed in survivors of any critical illness.

• Many of these manifestations are present for at

least 5 years and they tend to resolve slowly.

• Exercise limitation, physical and psychological

sequelae, decreased quality of life and increased
costs and use of health care services are important
legacies of severe lung injury.
MCQs
• The Berlin definition of severe ARDS includes assessment of
following?
a) PaO2/FiO2< 100 mm Hg
b) Minute Ventilation > 10L/min
c) Ventilator pressure Pplat >25
d) CXR showing pulmonary edema
• Which of the following is not true regarding High frequency oscillatory
ventilation?
a) Early initiation is associated with increased survival
b) Decreasing frequency will increase minute ventilation
c) Improvement in oxygenation within 6 hrs
d) None of the above
• Prone postioning in ARDS is associated with?
a) Increased radiographic edema
b) Reduced pressure sore rates
c) Increased VAP rates
d) Reduced mortality in severe hypoxemia
• The early use of neuromuscular blockage is associated with?
a) Contraindicated in patients with DM
b) Associated with lower mortality in ARDS
c) May be facilitated by discontinuation of sedation
d) Required with rescue treatment(HFOV, ECMO)
• Which of the following is true regarding ECMO?
a) VA-ECMO is associated with decreased mortality
compared to VV-ECMO
b) Anti-coagulants required but not associated with
increased complications
c) Transfer to a specialized center with ECMO facility is
associated with decreased mortality
d) None of the above
• The target SpO2 in ARDS patients is?
a)Above 90%
b)88-95%
c)90-100%
d)80-90%