Mx of ARDS 5.10

RECENT TRENDS IN MANAGEMENT OF ARDS : 

RECENT TRENDS IN MANAGEMENT OF ARDS Presenter: Lokesh M B Moderator: Dr. M. N. Awati

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General principles Mechanical ventilation Fluid management Pharmacologic principles Drugs under trial

GENERAL PRINCIPLES : 

GENERAL PRINCIPLES SUPPORTIVE CARE Recognition and treatment of underlying medical and surgical disorders Minimizing procedures and their complications Prophylaxis against venous thrombo-embolism, GI bleeding, CVC infections Prompt recognition and treatment of nosocomial infections Provision of adequate nutrition

MECHANICAL VENTILATION : 

MECHANICAL VENTILATION

VENTILATOR INDUCED LUNG INJURY : 

VENTILATOR INDUCED LUNG INJURY ARDS- heterogeneous- dependent > apex Attempts to fully inflate consolidated lung – over distension of normal lung – injury VILI by repeated over distension and recurrent alveolar collapse

VENTILATOR STRATEGY : 

VENTILATOR STRATEGY Goal: optimize oxygen delivery and hemodynamic function. Permissive hypercapnia Hickling et al intensive care med 1990 Open lung protective strategy: low tidal volumes recruitment maneuver optimal PEEP Amato et al 1998

Optimal Ventilator Strategy in ARDS: What is Still Unclear : 

Optimal Ventilator Strategy in ARDS: What is Still Unclear Mode of Ventilation Method of Setting PEEP PEEP Level Need for Lung Recruitment High Frequency Ventilation Prone Positioning Liquid Ventilation Bob Kacmarek MIH

PERMISSIVE HYPERCAPNIA : 

PERMISSIVE HYPERCAPNIA Reduction of minute volume: ↑ PaCO2, ↓ pH (6.8), resp rate 35 to achieve low tidal volume and airway pressure (plateau <30cmH2O) Safety profile not established Acceptable when necessary to limit tidal volume Limited use in preexisting metabolic acidosis and ↑ ICP Hickling et al, Crit Care Med 1994.

LOW TIDAL VOLUME : 

LOW TIDAL VOLUME In ALI can prevent progression to ARDS 6ml/kg ideal body weight Ideal body weight: NIH-ARDS 2000 Men [ 50 + 0.91 (Ht in cm) – 152.4] Women [ 45.5 + 0.91 (Ht in cm) - 152.4 ] Target: maintain plateau pressure Only intervention till date to reduce mortality from 40% (conventional) to 31% Mechanism: reduced activation of inflammatory cascade lower levels of soluble TNFRI, ↓ in IL-6, IL-8.

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A.No PEEP B.With PEEP C.With PEEP + low tidal volume D.With PEEP and normal tidal volume AAFP 2002 RECRUITMENT

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Sustained deep inflations with the intention of reopening collapsed regions of the lung. Benefit often transient if not followed by high levels of PEEP Extra pulmonary : more greater degree of edema and alveolar collapse. More amenable to recruitment Benefits negligible or short lived Oczenski Anesthesiology, 2004.

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Strategies: Richards et al Johannesburg 1999 Incremental increases in PEEP High-Frequency Oscillatory Ventilation Prone Position Spontaneous Breathing Pressure controlled ventilation with elevated cumulative product of pressure and inflation time Sustained inflations with peak inflation pressure limited to bet 30-40cm H2O Sigh

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CXR before and after recruitment maneuver Richards et al Johannesburg 1999

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Advantages: Minimize atelectasis Prevent over distension of normal alveoli Disadvantages: Worsen oxygenation by shunting blood flow to poorly aerated areas, barotrauma. Impair cardiac output – limit venous return and cardiac preload Hemodynamic compromise – hypotension Excessive over distension or repeated opening of atelectatic alveoli – injury Fujino et al, Bond et al CCM 2003

Positive end expiratory pressure PEEP : 

Positive end expiratory pressure PEEP High or low PEEP? Can’t recruit collapsed alveoli Modulate effect of RM Optimal PEEP? Doesn’t reduce edema or force fluid back to interstitium Cause redistribution of fluid within alveoli Considered when P/F ratio <150 or shunt fraction (on pulm artery catheter) >20%

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Contraindications: Absolute – presence of undrained pneumothorax Relative – ↑ ICP Hypovolemia Marginal CVS function Emphysema Cavitatory pneumonias Unilateral lung disease u/l lung ds – PEEP causes compliant lung to ↑ more than stiff lung. Selective bronchial intubation with double lumen tube and differential PEEP.

STEPS TO INSTITUTE PEEP TRIAL : 

STEPS TO INSTITUTE PEEP TRIAL Establish baseline values ↑ PEEP by 2.5 – 5 increments. Observe for immediate effects Allow 15 min for stabilization. Repeat measurements Analyze If PaO2 ↑ – reduce FiO2 (up to < 0.5) If PaO2 ↓ – reduce PEEP to original level SpO2 ↓(10%), CO ↓ (20%) – reduce PEEP PEEP can be increased till SpO2 >88% with FiO2 <0.5, or shunt fraction <20% or complications develop. ASCCA

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Guidelines for PEEP reduction: ASSCA Patient no longer have sepsis Patient on stable clinical course for at least 12 hours (PaO2 of 80mmHg or more on FiO2 of 0.4 or less) Close monitoring after trial

HIGH FREQUENCY VENTILATION : 

HIGH FREQUENCY VENTILATION Very small tidal volumes (less than or equal to dead space) delivered at a very high rate. No survival benefit Mechanisms: Exact mech not known Pendular effect of mixing gases bet lung regions of different impedance Coaxial flow with net center flow and net peripheral flow Augmented dispersion producing mixing of fresh and residual air along leading edge Molecular diffusion thru relatively still air

NON INVASIVE AND PARTIAL SUPPORT : 

NON INVASIVE AND PARTIAL SUPPORT Patient participation in triggering breaths - spontaneous breathing Improve aeration and V/Q mismatch within dependent regions d/t ↑ trans pulmonary pressure by actively moving diaphragm Advantages: Patient ventilator synchrony Lower sedation requirements Improved hemodynamics V/Q matching Non-invasive face mask- reduction of infectious complications, can safely be used Atonelli et al NEJM 1998

PARTIAL LIQUID VENTILATION : 

PARTIAL LIQUID VENTILATION Filling the lung close to FRC with PFC Perfluorocarbons: ↑ O2 carrying capacity ↓ surface tension Improved alveolar recruitment Intrinsic anti-inflammatory properties Direct attenuation of lung injury and VILI

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Success in animal models and neonatal RDS leech et al NEJM 1996 High density – settle in dependent regions – overdistension. So PFC vapour or aerosol – more homogenous distribution. Kandler et al AJCC 2001 Not proved

PRONE POSITION VENTILATION : 

PRONE POSITION VENTILATION

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Improve oxygenation and ventilation Douglas et al 1997 Mechanisms Improved ventilation of dorsal regions. Reduction of dependent lung compression by weight of heart or mediastinum Regional changes in chest wall mechanics Disadvantages: safety concern ET tube obstruction Accidental extubation ↑ pressure sores

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NEJM 2006

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No survival benefit Guerin et al JAMA 2004 Length of time prone 7 + 4.8 hours/day Ventilator strategy VT 10.3 + 2.8 ml/kg PEEP 9.6 + 30 cmH2O Rate 17.2 + 5.1/min Gattinoni NEJM 2001:345;568

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Critical care medicine 2004; 32;1

FLUID MANAGEMENT : 

FLUID MANAGEMENT Topic of controversy Prevent pulmonary edema vs adequate perfusion Conservative fluid management reduces duration of mech ventilation or ICU stay FACTT study NEMJ 2006 Maintain adequate fluid balance BP maintained by vasopressors than IV fluids Duiretics can be used to reduce fluid load Colloid vs crystalloid? Controversy Am society of Cr care an Use of pulmonary artery catheter is not indicated in routine management FACTT study

DRUGS : 

DRUGS Pulmonary vasodliators: iNO Useful in neonatal RDS In ARDS benefit transient, no survival benefit Some benefit seen in patient receiving 5ppm iNO Dillinger et al CCJM 1998 Corticosteroids: Potential to reduce inflammation No benefit in acute Bernard NEJM 87, Luce 88 or late ARDS NIH2006 Significant reduction in mortality in early ARDS tang et al 2007 meta analysis

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Surfactant replacement Large proteins: lamellar structure, tubular myelin – surfactant property Small proteins: limited surface activity ↑ small proteins in ARDS Useful in neonatal RDS No survival benefit Reasons: ? inactivated by plasma proteins Insufficient quantity delivered Distributed preferentially only to well ventilated lung

PROSPECTIVE FUTURE THERAPY : 

PROSPECTIVE FUTURE THERAPY Beta agonists: Improve alveolar fluid clearance McCauley et al CCJM 2004 Reduced no of ICU days but no reduction in mortality Anticoagulation/fibrinolysis: Fibrin in alveoli binds with and inhibit surfactant Beneficial effect of activated protein C Bernard et al NEJM 2004 Micro vascular occlusion and thrombosis – wasted ventilation

PROGNOSIS : 

PROGNOSIS Mortality rate 35-50% Milberg et al JAMA 1995 Risk factors for ↑ mortality ALI secondary to sepsis Male sex African-American race Advanced age Alcoholism Malignancy Liver disease Chronic steroid use HIV infection Diabetics have reduced risk

OUTCOME : 

OUTCOME Survivors suffer from prolonged disturbance in lung function Impairment in neorucognitive skills Protracted perception of poor quality of life Majority recover in lung function by 1 year. Few also suffer from depression, anxiety, decreased quality of life, Post traumatic stress disorder.

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Results of RCT of Treatments and Ventilation Strategies for ALI and ARDS

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