ARDS BY DR MUHAMMAD AKRAM KHAN QAIM KHANI

12/27/2015DR. MUHAMMAD AKRAM KHAN QAIM KHANI 1
ARDS
BY
DR MUHAMMADAKRAM
MATERNITYAND CHILDREN HOSPITAL
MAUSADIA, JEDDAH
RESIDENT ICU

INTRODUCTION
 In 1967 the investigators from university of
Colorado presented the modern concept of
ARDS.
 A type of Acute Respiratory failure of
noncardiac origin.

What is ARDS?
Definition formalized in
1992 American European
Consensus Conference
1. Acute onset, bilateral
infiltrates on CXR
2. PCWP ≤ 18 mmHg or no
clinical evidence of left
atrial hypertension
3. PaO2/FiO2 (P/F) Ratio
 ≤ 300 forALI
 ≤ 200 forARDS
Bernard et al. AJRCCM 1994;149:818-824

What is ARDS? – Berlin
Definition
The ARDS Definition Task Force. JAMA 2012;307:2526-2533

CLINICAL FEATURES
 The clinical features of ARDS usually appear within 6 to 72 hours of
an inciting event and worsen rapidly
 Patients typically present with
 dyspnea
 cyanosis (ie, hypoxemia)
 diffuse crackles.
 Respiratory distress is usually evident, including
 tachypnea, tachycardia, diaphoresis, and use of accessory muscles of
respiration.
 A cough and chest pain may also exist.

CLINICAL FEATURES
 Arterial blood gases reveal hypoxemia
 High concentrations of supplemental oxygen are generally required to
maintain adequate oxygenation.
 The initial chest radiograph typically has bilateral alveolar infiltrates
 computed tomography (CT) usually reveals widespread patchy or coalescent
airspace opacities that are usually more apparent in the dependent lung
zones.

EPIDEMIOLOGY
 The incidence of ARDS in the United States .
 Within intensive care units, approximately 10 to 15
percent of admitted patients and up to 20 percent
of mechanically ventilated patients meet criteria
for ARDS .
 The incidence of ARDS may be somewhat higher
in the United States than in other countries .

OUT COME
 Mortality varies from 40 to 60%.
 Most die of non respiratory complication during the
supportive phase of ARDS rather then hypoxia

COMPLICATIONS
Barotrauma
Delirium
Nosocomial infection

PATHOPHYSIOLOGY
 • Endothelial injury
– Endothelin-1,VWF
 • Epithelial injury
 • Neutrophil-mediated injury
– Near endothelium, retained, activated
 • Cytokines
 –TNF, IL-1, IL-8
 • Oxidative injury
 •Ventilator-induced injury
 • Hypercoagulability
 • Fibrosis
Ware LB. Sem in Resp Crit Care Med 2006

Pathology
 Like interstitial nephritis and acute hepatitis,
the term ARDS encompasses many distinct
disorders that share common clinical and
pathophysiologic features.
 The pathological features of ARDS are
typically described as passing through three
overlapping phases: exudative, proliferative
and finally fibrotic phase.

PATHOLOIC FEATURES
 Depend on the time of tissue sampling
 As the clinical disorder unfolds, there is
histologic evidence of diffuse alveolar damage
 Features include
 Presence of microthrombi of platelets andWBCs
within capillary lumen, denudation of epithelial lining
cells, swelling of the capillary endothelial cells,
infiltration by polymorph nuclear leukocytes(PMNLs),
and hyaline membrane formation within alveoli

Pathogenesis
 Lung injury is primarily initiated by a specific
insult (sepsis, trauma,VILI); with the initiation
of inflammation there is rapid and increased
recruitment of leucocytes, together with
inflammatory mediators to the site of injury,
several mechanisms had been involved in the
pathogenesis of ARDS.

Pathogenesis
Lung Insult
Inflammatory Cells Inflammatory Mediators
Cell Adhesion Molecules VILI
Surfactant Depletion Fibrosing Alveolitis
ALI/ARDS

MANAGEMENT
 Guidelines for ventilatory support of the patient with
ARDS from the ACCP Consensus Conference on
MechanicalVentilation include the following:
1. Clinicians should choose a ventilatory mode that is capable of
supporting oxygenation and ventilation and one with which they
are familiar.
2. Oxygenation target is arterial oxygen saturation of >90%.
3. End-inspiratory plateau pressures of >35 cm H2O are a concern
for the development of alveolar overdistention. In this setting,
clinicians ought to consider decreasing the tidal volume to values
as low as 5 mL/kg.

MANAGEMENT
4. To meet target end-inspiratory pressure goal, the PaCO2 may be
permitted to rise as long as there is no evidence of increased
intracranial pressure or other contraindication to permissive
hypercapnia.
5. Positive end-expiratory pressure (PEEP) is beneficial in
supporting oxygenation; however, the level of PEEP support used
should be minimized and continually evaluated.
6. The goal for FIO2 is to achieve adequate oxygenation with the
least amount of supplemental oxygen.Attempts should be made
to decrease the FIO2 to levels <0.55, if possible.The use of PEEP
may assist with the reduction in oxygen support.
7. When oxygenation is inadequate, clinicians ought to consider the
use of sedation, paralysis, or position changes and strategies to
increase tissue oxygen delivery.

MANAGEMENT STEPS
 Removal of precipitating/ underlying cause
 Ventilatory support
 Oxygenation with min. ventilatory trauma
 Low tidal volumes of 05 to 07 mls./ kg.
 Limit inspiratory pressure of <35 cmH2O
 Permissive hypercapnia
 ?? Permissive hypoxia pO2 55-65 mmHg

MANAGEMENT TECHNIQUES
 Alveolar recruitment
 PEEP inc. Pa O2 with min. FiO2 (10-20 cm)
 Ventilatory facilitated recruitment techniques
 Physiotherapy
 Ventilation strategies
 Inverse ratio / newer modes
 Nitric Oxide
 PRONEVENTILATION

Adjuncts to Improve Survival
 Daily spontaneous breathing trials
 Daily discontinuation of sedation
 Avoiding neuromuscular blocakde
 DVT prophylaxis
 HOB elevation
 Stress ulcer prophylaxis
 Enteral nutrition (when possible)

OTHER MANAGEMENT OPTION
 Steroids
 Surfactant
 PDE inhibitors
 Extrapulmonary gas exchange:-
 IVOX ( IntraVenacaval gas exchange)
 ECMO ( Extra Carporeal Membrane Oxygenation)
 ECCO2- R ( Extra Carporeal CO2 Removal)
 Ketoconazole
 Prostaglandin inhibitors.

PERMISSIVE HYPERCAPNIA
 TV is reduced to allow ventilation at lower peak airway pressure and
less risk of volutrauma
 This approach may allow better oxygenation but leads to
hypercapnia
 Gradual elevation of PaCO2 about 2.5mmHg/hr is well tolerated
 Acute elevation in PaCO2 leads to
 Increased Sympathetic activity
 Raised Cardiac Output
 High pulmonary vascular resistance
 Impaired skeletal and bronchomotor tone
 Dialated cerberal vessels
 Impaired CNS function

SURFACTANT THERAPY
 It is produced by type 2 pneumocytes, decreases
surface tension at the air-fluid interface of small
airways and alveoli
 Without surfactant the alveoli may collapse and
resist opening, even high airway pressures
 Plasma protein leak into the alveolar airspaces
inactivate the existing surfactant
 Resulting increasing surface tension leads to
Atelactesis and decreased lung compliance
 Newer preparation in current clinical trial

NITRIC OXIDE
 A powerful endogenous vasodilator
 Because it is rapidly inactivated, its effects are
restricted to the blood vessels at the site of
administration
 Inhalation dilates pulmonary vessels perfusing
aerated lung units, diverting blood flow from
poorly ventilated or shunt regions
 An ideal agent to treat Pulmonary Hypertension
and ARDS

INVERSE RATIO VENTILATION
 Inspiratory phase is prolonged and leads to an
increase in inspiration-to-expiration ratio (
between 1:1 and 4:1 )
 This approach increases the mean airway
pressure maintaining acceptable peak airway
pressure
 Disadvantages of IRV include air trapping
leading to auto PEEP.Therefore, requires heavy
sedation and neuromuscular blocked

POSITIVE END-EXPIRATORY PRESSURE (
PEEP )
 It is the pressure maintained in the lungs at the end of
expiration
 Prevents collapse of alveoli, thus increases the surface
area of O2 transfer
 High level causes over distension of the alveoli, poor lung
compliance, increase in the airway pressures, and
deleterious effect on cardiac out put
 “BEST PEEP” is a balance between the advantages and
disadvantages of PEEP
 Recommendation are to start with PEEP of 5cm H2O and
increase by 03 to 05 cm H2O to achieve Oxygen
saturation >/=90%

TRACHEAL GAS INSUFFLATION
 Physiologic dead space is elevated in ARDS, and small tidal volume
ventilation causes hypercapnia and acute acidosis
 WithTGI, a stream of fresh gas ( approximately 04 to 08 L/min. ) is
insufflated through a small catheter or through small channels in the
wall of the ETT into lower trachea, flushing CO2- laden gas out prior
to next inspiration
 It can be used throughout respiratory cycle ( continuous flow
catheter ) or only during a segment of it ( Phasic catheter flow )
 Disadvantage include:-
 Auto PEEP
 Catheter may become nidus for infection
 Desiccation of secretions and airway mucosal injury

FLUOROCARBON LIQUID-ASSISTED
VENTILATION
 Surface tension can be eliminated by filling the
lungs with a liquid such as fluorocarbon.
 It can dissolve O2 17 times more O2 than water,
has low surface tension and spreads quickly over
the respiratory epithelium, and evaporates
 Requires a liquid-gas exchange device to
oxygenate liquid, deliver the tidal volume, and
remove CO2

EXTRAPULMONARY GAS EXCHANGE
 Reduces the requirement for ventilating pressure
 Methods include
 ECMO
 ECCO2-R
 IVOX
 There has been 50% mortality reported comparing to
90% in a control group by Gatinoni in 1986.
Approximately same stands for study by Brunet while
patients were treated with low-frequency positive-
pressure ventilation ( LFPPV )

ECMO

GLUCOCORTICOID THERAPY
 High dose of glucocorticoids do not prevent the
development ofARDS in patients with sepsis
 Serum complement level are not lowered in patients
with sepsis induced ARDS
 Patients with late- phase of ARDS have persistent
inflammation, with cytokines release in the airspaces in
lungs, glucocorticoids at this stage could facilitate
recovery.
 Increase the risk of nosocomial infection, which could
diminish the chances of recovery

PROSTAGLANDIN AGONISTS/
INHIBITORS
 Ketoconazole, a potent inhibitor of thromboxane
and leukotriene synthesis, prevent the
development of ARDS
 Prostaglandin E1 is a vasodilator that blocks
platelet aggregation and decreases neutrophil
activation

PRONE POSITIONING FOR ARDS
 Indications:
 Pulmonary dysfunction despite escalating
mechanical ventilatory support
 Goals ofVentilation:
 SaO2 >92%
 PaO2/FiO2 ≥200
 pH 7.25 – 7.40
 Pplat <35 cm H2O

 Criteria for Inclusion:
 CXR with diffuse bilateral infiltrates consistent with
ALI orARDS
 Mechanical ventilation
 FiO2 ≥ 0.6 for 48 hours
 PEEP ≥ 15 cm for 48 hours (includes PCIRV, auto PEEP)
 Increasing respiratory dysfunction as evidenced by:
 PaO2/FiO2 < 200

 Exclusion Criteria:
 Closed head injury with ICH
 Unstable orthopedic fracture
 Spinal cord injury
 Hemodynamic instability
 Active intraabdominal process
 Pregnancy

 Procedure:
 Order fromAttending doctor
 ETCO2 monitor and arterial line in-place.
 Low air-loss mattress.
 Discontinue gastric feeding. Stomach to be
evacuated via NGT.
 Explanation of procedure to patient and family
 Minimum of 3 RNs, Attending doctor, and RT.

 Reposition ECG leads to patient’s back.
 Anticipate the need for frequent ETT suctioning.
 Obtain ABG 20 minutes after repositioning.
 Duration of prone positioning is dependent
upon patient’s hemodynamic status

Transfusion-Related Acute Lung
Injury
Respiratory distress, pulmonary edema, hypoxia,
hypotension and fever
• Within 2 hours of transfusion (6 at most)
• Mechanism
– Plasma in transfused product
– HLA antibodies or granulocyte specific antibodies
• 1/5000?
• 5-10% mortality
• Diagnosis:
– Difficult to tease out
– Isolation of antibodies
Popovsky et al. Guidelines for the management of TRALI. AABB 2003

Transfusion-Related Acute Lung
Injury
Stop the transfusion
• Treat pulmonary and cardiac dysfunction
• Test the transfused units
• Contact a reference lab for advice
• Subsequent transfusions to that individual
not a problem

ARDS BY DR MUHAMMAD AKRAM KHAN QAIM KHANI

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