ards 7-3_2016

صدق الله العظيم(26و 25سورة طه أية )

ARDSBY

DR AHMED FAYEDPULMONARY SPECIALIST

ERSM- ESCTM- RICUDKAASH2016

• 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, 4 th 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 7 th 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 ARDSneutrophils 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 inflammationThe 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

Paul L. Marino, 2014. the ICU book, 4 th editionRichard S. Irwin and James M. Rippe, 2012. Intensive care medicine 7 th edition

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



MANAGMENT

• 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

Rajesh and Subhash, 2012. ICU protocols, respiratory system, basic of mechanical 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

Paul L. Marino, 2014. the ICU book, 4 th editionRichard S. Irwin and James M. Rippe, 2012. Intensive care medicine 7 th edition

• 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

ContraindicationsShockAcute bleedingMultiple traumaSpinal instabilityPregnancyRaised intracranial pressureAbdominal 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 score3. 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

Thank You

ards 7-3_2016

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