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Acute Respiratory Distress Syndrome Dr. Vanya Chugh University College of Medical Sciences & GTB Hospital, Delhi.

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Presentation on theme: "Acute Respiratory Distress Syndrome Dr. Vanya Chugh University College of Medical Sciences & GTB Hospital, Delhi."— Presentation transcript:

1 Acute Respiratory Distress Syndrome Dr. Vanya Chugh University College of Medical Sciences & GTB Hospital, Delhi

2 Timeline In 1967 – Ashbaugh, Bigelow, Petty, Levine - described Acute Respiratory Distress Syndrome in adults In 1971, Petty and Ashbaugh modified its name from ‘acute’ to ‘adult’ Respiratory Distress Syndrome; to differentiate it from its newborn counterpart In 1974, Webb and Tierney confirmed the existence of ventilator associated lung injury In 1990, Hickling et al introduced the concept of permissive hypercapnia

3 Timeline In 1992, American European Consensus Conference (AECC) gave standardized definition for ARDS In 1997, Tremblay et al introduced the concept of biotrauma In 1998, Amato et al, conducted RCT - decrease in mortality using low tidal volume ventilation and high PEEP (open lung strategy) In 2000, ARDS network trial demonstrated the benefits of low tidal volume and PEEP ventilation

4 Definitions of ARDS Ashbaugh and colleagues, 1967 Severe dyspnea Tachypnea Cyanosis refractory to oxygen therapy Decreased pulmonary compliance Diffuse alveolar infiltrates on chest radiograph.  Loosely defined criteria  Definition of hypoxemia inconsistent

5 Chest Radiology findings Score No alveolar consolidation 0 One quadrant1 Two quadrant2 Three quadrant3 Four quadrant4 Oxygenation status (Hypoxemia Score) PaO2 / FiO2 > 300 mmHg mmHg mmHg mmHg3 < 100 mmHg4 Murray & Mathay Lung Injury Score(1988)

6 Pulmonary compliance Score Compliance (ml/cmH2O) > < 194 PEEP settings (when ventilated) PEEP (cmH2O) < > 154 Acute lung injuries assessed by dividing sum by 4 0 points = No pulmonary injury points =Mild to moderate > 2.5 points=Severe (ARDS)

7 Murray & Mathay Lung Injury Score Advantages : Ventilatory settings included Disadvantage : Complex Lacks prospective validity

8 Bernard and colleagues, 1992 (American European Consensus conference definition) A three-criteria system including chest radiograph, oxygenation score, and exclusion of cardiogenic causes: Acute onset, bilateral infiltrates on chest radiography, Acute lung injury ~ PaO 2 /FIO 2 ≤ 300 ARDS subset~ PaO 2 /FIO 2 ≤ 200 Pulmonary-artery wedge pressure of <18 mm Hg or the absence of clinical evidence of left atrial hypertension

9 Bernard and colleagues, 1992 (American European Consensus conference definition) Problems Acute onset : arbitrary; <1 week Bilateral infiltrates: inter observer variation, b/l pneumonia, atelectasis, cardiogenic pulmonary edema PAOP of <18 mm Hg /absence of clinical evidence of left atrial hypertension : PAOP: poor estimate of PVH, falsely raised with high airway pressures Acute lung injury present if PaO 2 /FIO 2 is 300 : new and arbitrary value

10 Delphi definition (2005) of ARDS Diagnosis : 1- 4 present with 5a and/or 5b 1. PaO 2 /FiO 2 ratio ≤ 200 on PEEP ≥ Bilateral airspace disease : ≥ 2 quadrants, frontal chest X-ray 3. Onset within 72 hours. 4. No clinical evidence/subjective finding of CHF (including use of PA catheter and/or echo if clinically indicated) 5a. Static respiratory compliance < 50ml/cm H2O (patient sedated, TV 8ml/kg, PEEP ≥ 10. 5b. Presence of direct or indirect risk factor associated with lung injury.

11 Delphi definition of ARDS contd. Airspace disease – presence of one or more of the following- 1.Air brochogram 2.Acinar shadows 3.Coalescence of acinar shadows 4.Silhoutte sign Specificity : delphi = LIS > AECC Sensitivity : delphi = LIS = AECC Delphi criteria provisional, need further testing

12 Synonyms of ARDS Shock lung Pump lung Traumatic wet lung Post traumatic atelectasis Adult hyaline membrane disease Progressive respiratory distress Acute respiratory insufficiency syndrome Haemorrhagic atelectasis Hypoxic hyperventilation Postperfusion lung Oxygen toxicity lung Wet lung White lung Transplant lung Da Nang lung Diffuse alveolar injury Acute diffuse lung injury Noncardiogenic pulmonary edema. Progressive pulmonary consolidation

13 Epidemiology of ARDS Difficult to estimate Lack of standardization of the definition Difference in methodology KCLIP study ( ) done on ARDS patients as per AECC criteria estimated - - incidence of ALI – 78.9/lakh person years - mortality rate – %

14 Precipitating Factors Direct Lung Injury Pneumonia Aspiration of gastric contents Pulmonary contusion Near-drowning Toxic inhalation injury Indirect Lung Injury Sepsis Severe trauma Multiple bone fractures Flail chest Head trauma Burns Multiple transfusions Drug overdose Pancreatitis Post-cardiopulmonary bypass

15 Differential risk factors Chronic alcohol abuse Absence of DM Age Gender Severity of illness – APACHE score Excessive blood transfusion Cigarette smoking

16 Pathophysiology in ARDS Based on the histological appearance - Exudative phase (0-4 days) Alveolar and interstitial edema Capillary congestion Destruction of type I alveolar cells Early hyaline membrane formation Proliferative Phase (3-10 days) Increased type II alveolar cells Cellular infiltration of alveolar septum Organisation of hyaline membranes Fibrotic Phase (>10 days) Fibrosis of hyaline membranes and alveolar septum Alveolar duct fibrosis

17 Pathology in ARDS Mechanisms in early phase - Release of inflammatory cytokines – TNF alpha, IL- 1,6,8 Failure of alveolar edema clearance, epithelial and endothelial damage Increased permeability of alveolo – capillary membrane Neutrophil migration and oxidative stress Procoagulant shift – fibrin deposition Surfactant dysfunction Mechanism in late (repair) phase – Fibroproliferation -TGF beta, MMPs, thombospondin, plasmin, ROS Remodelling - matrix and cell surface proteoglycans, MMP, imbalance of coagulation and fibrinolysis.

18 Pathophysiology of ARDS

19 D/D : Hydrostatic pulmonary edema  PCWP ≥ 18 mmHg  Causes : Cardiogenic – LVF (eg. MI, myocarditis) cardiac valvular disease (aortic, mitral) Vascular – systemic HTN, pulmonary embolism Volume overload - excessive iv fluids, renal failure

20 Cardiogenic vs Non-cardiogenic edema 1. Prior h/o cardiac disease 2.Third heart sound 3. Cardiomegaly 4. Infiltrates : Central distribution 5. Widening of vascular pedicle No widening of vascular pedicle ( ↑ width of mediastinum) 6. PA wedge pressure 7. Positive fluid balance Cardiogenic Absence of heart disease No third heart sound Normal sized heart Peripheral distribution Peripheral distribution N or  PA wedge pressure Negative fluid balance Non-cardiogenic

21 Management Treatment of the precipitating cause Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation - 1.Fluid restriction 2.Permissive hypercapnia 3.Prone positioning 4.Recruitment maneuvers

22 Management contd. Non conventional/ Salvage interventions a.High frequency ventilation b.Airway pressure release ventilation c.Tracheal gas insufflation d.Inverse ratio ventilation e.Inhaled nitric oxide f.Inhaled prostacyclin g.Corticosteroids h.Surfactant administration i.Liquid ventilation j.Extracorporeal membrane oxygenation Supportive therapy – nutrition, prevention of infection

23 Concept of VALI  Mechanical ventilation - Basic care in critically ill ICU patients  May cause or worsen lung injury – ventilator induced/associated lung injury  Components – Barotrauma Volutrauma Atelectrauma Biotrauma

24 VALI and MODS

25 Concept of ‘baby lung’ Put forward by Gattinoni and colleagues first in 1987 Lung injury in ARDS - non homogenous, basal Edema and consolidation > dependent lung regions - ↑ density of dorsal regions Aerated ventral regions – ‘baby lung’ ( gms) – high compliance Ventilation of baby lung with normal tidal volumes and pressures – alveolar over distension – injury to functional lung tissue

26 Management Lung protective ventilation ARDS network protocol Goals  Oxygenation : PaO mmHg, or SpO 2 88 – 94% (excluding pregnancy, intracranial hypertension or stroke where SaO 2 goal>94%)  Ventilation : Tidal volume : 4-6 ml/kg ideal body weight Plateau pressure : <30cmH 2 O Ph: I:E ratio of 1:1 – 1:3

27 Management contd. Oxygenation Initially high Fio 2 given (1.0) to correct hypoxia Fio 2 and PEEP adjusted to the lowest level compatible with the oxygenation goals Fio 2 and PEEP adjusted in the following fixed combinations {fio 2 /PEEP(mmHg)} FIO 2 PEEP

28 Management contd Initial ventilator set up and adjustments STEP 1- Calculation of ideal body weight(IBW):  For males, IBW(kg) = {height(inch)– 60} Or IBW(kg)= {height(cm)–152.4}  For females, IBW(kg) = {height(inch)– 60} Or IBW(kg)= {height(cm)–152.4}

29 Management contd STEP 2 - Volume assist control selected as ventilator mode  Initial tidal volume (TV) set at 8ml/kg IBW  TV reduced by 1ml/kg IBW 2 hourly until TV = 6ml/kg IBW  Initial ventilator rate set to maintain baseline minute ventilation( not >35/min)  TV and respiratory rate adjusted to achieve the pH and plateau pressure goals  Inspiratory flow rate set above patients demand (usually >80L/min)

30 Open Lung Approach Introduced by Amato et al in 1998 – use of low tidal volume + high PEEP+ recruitment (Open lung strategy) – reduce mortality in ARDS Maintaining inflation & deflation between 2 inflection points during entire respiratory cycle Ventilatory settings - PEEP >P flex & TV reduced so that P plat < UIP Advantages- avoids repetitive opening and closing of alveoli (VALI) - minimizes shear injury

31 Open Lung Approach Pressure-Volume Curve

32 Management Treatment of the precipitating cause Mechanical ventilation –  Core ventilator management – protective lung ventilation strategy role of ‘open lung approach’  Adjuncts to core ventilation – 1.Fluid restriction 2.Permissive hypercapnia 3.Prone positioning 4.Recruitment maneuvers

33 Fluid restriction in ARDS Rationale – alveolar flooding depends on : 1.Capillary hydrostatic pressure 2.Oncotic pressure 3.Alveolar–capillary permeability Capillary permeability increased in ARDS ↓ hydrostatic pressure and ↑ oncotic pressure may help.

34 Fluid therapy in ARDS Recommended : Central venous pressure guided therapy – mmHg ( ARDS Network Trial 2003) Restricted fluid intake Increased urine output – Diuretics or RRT Not recommended : Vasodilators Albumin

35 Management Treatment of the precipitating cause Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation – 1.Fluid restriction 2.Permissive hypercapnia 3.Prone positioning 4.Recruitment maneuvers

36 Permissive Hypercapnia Hickling and colleagues 1990 “Degree of hypercapnia permitted in patients subjected to lower tidal volumes” Upper limit – not defined; >100 mmHg avoided  Advantages Increased surfactant secretion (animal models) – improved V/Q match, oxygenation (improved compliance) Increased cardiac output and oxygen delivery (sympathoadrenal effects predominate over cardiodepressant effects) Increased cerebral blood flow and tissue oxygenation

37 Permissive Hypercapnia  Concerns Increase in pulmonary vascular resistance Impaired diaphragmatic function (impairs afferent transmission) Decrease in cardiac contractility Raised intracranial tension  Individualize and treat

38 Management Treatment of the precipitating cause Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation – 1.Fluid restriction 2.Permissive hypercapnia 3.Prone positioning 4.Recruitment maneuvers

39 Prone Position Ventilation First suggested by Piehl and Brown in 1976 Offers improved oxygenation by: Increased FRC Change in regional diaphragm motion Distribution of perfusion Better clearance of secretions

40 Prone Position Ventilation Sud and colleagues conducted – meta-analysis of 13 RCTs (1559 patients) on supine and prone position ventilation in ARDS/ALI patients Median MV of 12 hours ( 4-24hrs) for 4 days( 1-10 days) Conclusion -cannot be recommended for routine Mx -no evidence of improved survival Gattinoni et al suggested no overall reduction in mortality except in very sick patients ( SAPS II Score >50) No decrease in ventilator associated pneumonia

41 Problems of prone position Facial edema Airway obstruction Difficulties with enteral feeding Transitory decrease in oxygen saturation Hypotension & Arrhythmias Vascular and nerve compression Loss of venous accesses and probes Loss of chest drain and catheters Accidental extubation Apical atelectasis d/t incorrect positioning of the tracheal tube Increased need for sedation

42 Management Treatment of the precipitating cause Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation – 1.Fluid restriction 2.Permissive hypercapnia 3.Prone positioning 4.Recruitment maneuvers

43 Recruitment maneuvers High pressure inflation maneuver aimed at temporarily raising the transpulmonary pressure above levels typically obtained with mechanical ventilation Types – Elevated sustained pressures : 40 cm H2O for 40 seconds Sigh breaths : ↑ tidal volume / PEEP for one or several breaths Extended sigh breath : VCV with PEEP well above LIP for a longer time More effective in early ALI and those with more homogenous disease; atelectasis > consolidation.

44 Recruitment maneuvers Adverse effects Hypotension Barotrauma Raised ICP Haemodynamic instability

45 Management contd. Non conventional/ Salvage interventions a.High frequency ventilation b.Airway pressure release ventilation c.Tracheal gas insufflation d.Inverse ratio ventilation e.Inhaled nitric oxide f.Inhaled prostacyclin g.Corticosteroids h.Surfactant administration i.Liquid ventilation j.Extracorporeal membrane oxygenation Supportive therapy – nutrition, prevention of infection

46 High Frequency Ventilation Mechanical ventilatory support using higher than normal breathing frequencies Smaller tidal pressure swings (within inflection points) along with apt mpaw Smaller tidal volumes and higher mean pressure utilized for lung protection Special ventilators required Types - High Frequency Jet Ventilation (HFJV) High Frequency Oscillatory Ventilation (HFOV)

47 HFV HFJV A nozzle/injector creates high velocity ‘jet’ of gas directed into the lung Injectors – 1-3mm diameter Expiration is passive Frequencies available – upto 600 breaths/min Available for neonatal and paediatric use only HFOV Characterized by rapid oscillations of a diaphragm (at 3 to 10 hertz i.e 180 to 160 breaths/min) driven by a piston pump Frequencies available – breaths/min Expiration is also active – risk of air trapping minimal

48 HFV contd Advantages Better oxygenation and ventilation Aids lung recruitment (high mpaw) Reduces oxygen toxicity (high mpaw) Minimizes VILI Disadvantages Delivered tidal volumes difficult to monitor Deep sedation and/or paralysis required Inadequate humidification Direct physical airway damage

49 Airway Pressure Release Ventilation Alternative mode of ventilation that applies a form of CPAP that is released periodically, augmenting CO 2 release. Pressure limited, time cycled mode Permits spontaneous ventilation throughout the respiratory cycle Based on the ‘open lung’ concept – maximize and maintain recruitment throughout the respiratory cycle

50 APRV contd Uses 2 airway pressures – P high and P low ; 2 set time periods – T high and T low, usually T high >T low P high is set above the closing pressure of recruitable alveoli (lower inflection point) Set T high maintains the P high for several seconds T low helps remove CO 2

51 APRV contd Potential benefits : ↑ V/Q match ↓ diaphragmatic atrophy during critical illness ↑ cardiac output and oxygen delivery ↑ splanchnic perfusion ↑ renal and hepatic function Fewer days on mechanical ventilation Fewer days in ICU

52 Tracheal Gas Insufflation Normal ventilatory cycle - bronchi and trachea filled with alveolar gas at end expiration In the next inspiration, CO2 laden gas forced back into alveoli. TGI - stream of fresh gas (at 4-8L/min) insufflated through a small catheter/channels in the wall of endotracheal tube into the lower trachea CO2 laden gas flushed out of the trachea before next inspiration

53 Tracheal Gas Insufflation contd. Disadvantages Dessication of secretions Inadequate humidification Airway mucosal injury Accumulation of secretions in the TGI catheter Creation of auto PEEP from expiratory flow and resistance of the ventilator-exhalation tubes and valve

54 Inverse Ratio Ventilation Alternative mode of ventilation Entails use of prolonged inspiratory times (I:E>1) using volume or pressure cycled mode of mechanical ventilation Proposed mechanism of action – alveolar recruitment at lower airway pressures, optimal distribution of ventilation Concerns – generation of auto PEEP reduced cardiac output ( ↑ MAP)

55 Inhaled Nitric Oxide NO – endogenous vasodilator, from endothelium Vasodilatation of alveolar circulation reduces shunt and pulmonary hypertension Problems: toxic nitrogen compounds methemoglobinemia pulmonary edema, acute RHF (interrupted flow) rebound pulmonary hypertension expensive Routine use not recommended

56 Inhaled Prostacyclin Cause vasodilation, inhibit platelet aggregation, reduction of neutrophil adhesion and activation, ↓ pulmonary hypertension, improved oxygenation Minimal systemic effects, harmless metabolites, no requirements for monitoring Both positive and negative results obtained in various trials Presently not recommended

57 Corticosteroids Established ARDS – characterized by alveolar fibrosis Anti-inflammatory and antifibrotic properties of steroids – probable role in ARDS No role in preventing but may help in treating ARDS

58 Surfactant Therapy Reduces alveolar surface tension Prevents alveolar collapse Anti inflammatory properties Anti microbial properties Exogenous surfactant – successful in neonatal respiratory distress syndrome (reduced surfactant production) ARDS in adults – increased surfactant removal, altered composition, reduced efficacy, reduced production Surfactant therapy not recommended in adults

59 Liquid Ventilation Involves filling the lung with liquid Removes the air liquid interface and supports alveoli, prevents collapse Perfluorocarbons – have low surface tension, dissolve oxygen and carbon dioxide readily, non toxic, minimally absorbed, eliminated by evaporation though lungs Lowered surface tension may improve alveolar recruitment, arterial oxygenation, increased lung compliance Can recruit dependent alveoli (advantage over PEEP)

60 Liquid Ventilation contd. Types : Total – filling the entire lung with liquid, ventilated with a special ventilator - Expensive Partial - filling the lung to FRC with liquid, ventilated with conventional ventilator - Appropriate dose of PFC still to be determined - ↑ chances of pneumothoraces, hypoxic episodes, hypotensive episodes PFC radiodense – impossible to detect infection or follow the progress of healing in a chest radiograph Liquid ventilation is not FDA approved

61 Extracorporeal Membrane Oxygenation Invasive, complex form of cardiopulmonary bypass Provides temporary gas exchange and blood circulation outside the body Severe but potentially reversible respiratory failure Such periods of “lung rest” allow the lungs to recover Used when conventional strategies fail No good evidence available over conventional management

62 ECMO contd. Types Veno - arterial – a catheter placed in both vein and artery. Provides support both for heart and lungs Veno - venous – single double lumen catheter placed in the vein. Provides support only for lungs ECMO allows ventilator pressures and volumes to be decreased to prevent further VILI Reduction in intra - thoracic pressure allows fluid removal from lungs with less risk of cardiovascular instability

63 ECMO contd Complications : Haemorrhage Renal failure Haemolysis Hypotension/ hypertension Pneumothorax Infections

64 Management contd. Salvage interventions a.High frequency oscillatory ventilation b.Airway pressure release ventilation c.Tracheal gas insufflation d.Inverse ratio ventilation e.Inhaled nitric oxide f.Inhaled prostacyclin g.Corticosteroids h.Surfactant administration i.Liquid ventilation j.Extracorporeal membrane oxygenation Supportive therapy – nutrition, prevention of infection

65 Nutrition Enteral over parenteral High fat – low carbohydrate diet advocated - ↓ CO 2 Immuno modulatory nutrients -amino acids - arginine and glutamine -ribonucleotides -omega-3 fatty acids Diet rich in fish oil, γ-linolenic acid, and antioxidants Standard nutritional formulations recommended

66 Antibiotics Infection - present initially : nonpulmonary sepsis Develop later - nosocomial infections : pneumonia and catheter- related sepsis. Aim : identify, treat, and prevent infections. Most pneumonia > 7 days Prompt initiation of appropriate empiric therapy. Hand washing by medical personnel New areas : - continuous suctioning of subglottic secretions to prevent their aspiration -development of new endotracheal tubes - resist formation of bacterial biofilm that can be embolized distally with suctioning.

67 Management Treatment of the precipitating cause Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation - 1.Fluid restriction 2.Permissive hypercapnia 3.Prone positioning 4.Recruitment maneuvers

68 Management contd. Non conventional/ Salvage interventions a.High frequency ventilation b.Airway pressure release ventilation c.Tracheal gas insufflation d.Inverse ratio ventilation e.Inhaled nitric oxide f.Inhaled prostacyclin g.Corticosteroids h.Surfactant administration i.Liquid ventilation j.Extracorporeal membrane oxygenation Supportive therapy – nutrition, prevention of infection

69 Complications associated with ARDS Pulmonary: barotrauma,volutrauma, pulmonary embolism, pulmonary fibrosis, ventilator-associated pneumonia (VAP), Oxygen toxicity Gastrointestinal: haemorrhage (ulcer), dysmotility, pneumoperitoneum, bacterial translocation Cardiac: Arrhythmias, myocardial dysfunction Renal: acute renal failure (ARF), fluid retention Mechanical: vascular injury, tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube) Nutritional: malnutrition, anaemia, electrolyte deficiency

70 Long term sequelae of ARDS Pulmonary function – mild impairment, improves over 1 year Neurocognitive dysfunction Post traumatic stress disorder Physical debilitation

71 Infantile Respiratory Distress Syndrome Hyaline membrane disease Deficiency of surfactant : insufficient production in immature lungs, immature babies Genetic mutation in one of the surfactant proteins, SP-B – rare, full term babies Prevention : avoidance of premature birth, corticosteroids Treatment : surfactant replacement

72 References Harrison’s Principle of Internal Medicine, 16 th ed. Christie JD, Lanken PN. Acute lung injury and the acute respiratory distress syndrome. Critical Care – Hall Foner BJ, Norwood SH, Taylor RW. Acute respiratory distress syndrome. Critical Care, 3 rd ed. Civetta Wiener-Kronish JP, et al. The adult respiratory distress syndrome : definition and prognosis, pathogenesis and treatment. BJA 1990; 65: Clinical Anaesthesia. Barash, 6 th ed. Egans Respiratory Care, 7 th e

73 References Acute respiratory distress syndrome network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;242: Brower RG, Morris A, MacIntyre N, et al. Effects of recruitment maneuvers in patients with acute lung injury and acute respiratiry distress syndrome ventilated with high positive end expiratory pressure. Crit Care Med.2003;31: Hickling KG, Henderson SJ, Jackson R. Low mortality associated with low volume pressure limited ventilationwith permissive hypercapnia in severe adult respiratory distress syndrome. Intensive care med. 1990;16: Hickling KG, Walsh J,Henderson S, Jackson R. Low mortality rate in acute respiratiry distress syndrome using low volume pressure limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med.1994;22:


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