ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)GUIDE - DR.SHIV.S.SHARMA

- DR.Y. JAMRACANDIDATE-DR.SARATH MENON.R

Intensive care unit,Dept.Internal Medicine

MGM MEDICAL COLLEGE & M Y HOSPITAL,INDORE

OUTLINE

Definition Clinical history Pathophysiology Diagnosis Management

CASE

35 yr old male met with an RTA was admitted in surgery icu developed severe tachpnoea,dyspnoea

within 24hrs admission o/e- pulse- 110/mt,bp- 80/50mmHg pallor+ cyanosis + no jvp S1/S2- NL Chest b/l rales present in mid/lower area p/a- soft ,no HSM Abg analysis- O2 sat 50%,pao2-40%,pco2-45% ph – 7.3

CXR – WHAT’S DIAGNOSIS ?

ARDS -DEFINITION

ARDS is a clinical syndrome of dyspnea of rapid onset,hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure.

Inflammatory cells and proteinaceous fluid accumulate in the alveolar spaces leading to a decrease in diffusing capacity and hypoxemia.

ALI V/S ARDS

ALI is the term used for patients with significant hypoxemia (PaO2/FiO2 ratio of ≤ 300)

ARDS is the term used for a subset of ALI patients with severe hypoxemia (PaO2/FiO2 ratio of ≤ 200)

Acute PaO2/FiO2 < 200 B/l interstitial

/alveolar infiltrates PCWP <18mmHg

Acute < 300mmHg Same

Same

ARDS ALI

ARDS DIAGNOSTIC CRITERIA

Acute Onset

Predisposing Condition

Bilateral Infiltrates

PaO2/FiO2 ≤ 200 mm Hg

Pulmonary capillary Wedge Pressure ≤ 18 mm Hg or no clinical evidence increase in LA pressure.

ARDS CAUSES Direct Lung Injury: a) Pneumonia b) pulmonary contusion c) near drowning d) inhalation injury f) aspiration of gastric contents

ARDS CAUSES Indirect lung injury

a) sepsis b) severe trauma w/ shock, hypoperfusion c) acute pancreatitis d) transfusion of multp blood

products

PATHOPHYSIOLOGY

Diffuse alveolar damage Lung capillaries damage Inflammatory cells Alveolar edema Severe hypoxemia Decreased lung compliance & atelectasis Pulmonary hypertension

NATURAL HISTORY OF ARDS

3 phases - exudative (0-7 d) - proliferative ( 7-21 d)

- fibrotic ( > 21 days)

HISTOLOGIC FINDINGS

Typical histological findings in ARDS alveolar inflammation,

thickened septal from protein leak (pink), congestion and decreased alveolar volume

www.burnsurgery.com/.../pulmonary/part3/sec4.htm

←Normal Lung Histology—large alveolar volumes, septal spaces very thin, no cellular congestion.

Hyaline Protein in air spaces

Cellular Congestion

CLINICAL HISTORY

Acute Critically ill Rapid –tachypnoea,dyspnoea,hypoxia Within in 12-48 hr of precipitating event Initial respiratory alkalosis Respiratory failure

LAB INVESTIGATIONS

Routine blood counts RFT CXR ABG CT chest BNP 2D Echo BAL PCWP

HOW TO DETERMINE ARDS BY CXR Can be difficult to do. Should always try to

make the diagnosis in light of the clinical picture.

Need to determine Cardiogenic vs. Non-cardiogenic edema.

Cardiogenic Non-Cardiogenic

Bilateral infiltrates predominately in lung bases. Kerley B’s. Cardiomegaly.

Diffuse Bilateral patchy infiltrates homogenously distributed throughout the lungs. No Kerley B’s.

CARDIOGENIC V/S NON CARDIOGENIC EDEMA

Patchy infiltrates in bases

Effusions + Kerley B lines + Cardiomegaly + Pulmonary vascular

redistribuition Excess fluid in alveoli

Homogenous pluffy shadows

Effusions – Kerley B lines – Cardiomegaly – No pulm.vascular

redistribuition Protein,inflammatory

cells,fluid

cardiogenic Non-cardiogenic

ARDS

early late

Cardiogenic Non-Cardiogenic

No septal thickening. Diffuse alveolar infiltrates. Atelectasis of dependent lobes usually seen .

Septal thickening. More severe in lung bases.

THERAPY- GOALS

Treatment of underlying cause Cardio-pulmonary support Specific therapy targeted at lung injury Supportive therapy.

SPONTANEOUSLY BREATHING PATIENT

In the early stages of ARDS the hypoxia may be corrected by 40 to 60% inspired oxygen .

If the patient is well oxygenated on <= 60 % inspired oxygen and apparently stable without CO2 retention then ward monitoring may be feasible but close observation( 15 to 30 Min), continuous oximetry, and regular blood gases are required

INDICATION FOR MECHANICAL VENTILATION

Inadequate oxygenation ( PaO2- < 60 with FiO2 >=0.6)

Rising or elevated PaCO2 ( > 50mmHg)

Clinical signs of incipient respiratory failure

MECHANICAL VENTILATION

The Aims are to increase PaO2 while

minimizing the risk of further lung injury

(ventilator induced lung injury)

ARDSNETVENTILATOR PROTOCOL

ARDS NET PROTOCOL -WEANING

Spontaneous breathing trial daily PaO2/FiO2-<8/<.4 or <5/ <.5 PaO2/FiO2 less than previous day Systolic BP > 90 without vasopressors No neuromuscular blockade 2 hr trial- with T piece with 1-5cm water

CPAP. ABG,RR,SPO2 monitoring If tolerated for 30 mt,consider extubation

EVIDENCE BASED RECOMMENDATIONS FOR ARDS THERAPY

TREATMENT

MECHANICAL VENTILATION

Low tidal volumeMinimize LAFPHigh PEEPProne positionRecruitment maneuversHigh frequency

ventilation Glucocorticoids Sufactant

replacement,inhaled NO,others

RECOMMENDATIONS

A B CCC D DD

MANAGEMENT: REDUCING VENTILATOR-INDUCED LUNG INJURY Low tidal volume mechanical

ventilation In ARDS there is a large amount of poorly

compliant (i.e. non-ventilating) lung and a small amount of healthy, compliant lung tissue. Large tidal volume ventilation can lead to over-inflation of the healthy lung tissue resulting in ventilator-induced lung injury of that healthy tissue.

PEEPSetting a PEEP prevents further lung injury due to

shear forces by keeping airways patent during expiration

ARDS NETWORK CLINICAL TRIALS

High TV vs low TV (12ml/kg vs 6ml/kg) - 861 pts - mortality rate 39.2 % vs 31% High PEEP vs low PEEP 13cm H20 vs 8 cm H20 –NO difference

Amato etal- optimal PEEP- 15cm H20

Inverse ratio ventilation - reduce peak airway pressure - I: E – 1:1 & 4:1 - severe hypoxemic resp.failure Permissive hypercapnea - controlled hypoventilation - PaCO2 upto 55mmhg - pH upto 7.25 Proning

OTHER METHODS

High flow ventilation ECMO Partial fluid ventilation (PLV)

EXTRA CORPOREAL MEMBRANE OXYGENATION (ECMO)

MANAGEMENT

Fluids – - conservative management - normal or low LAFP - reduce icu stay,duration of

ventilation

Steroids - Meduri et al study - methyprednisolone-2mg/kg & taper to .5-1mg/kg in 1-2wk

TREATMENT OF SEPSIS

Empirical antibiotics Culture sensitivity & change antibiotics Avoid nephrotoxic drug Enteral feeding

OTHER TREATMENT MODALITIES

NO Ketoconazole Albuterol Pentoxyphylline NSAIDS N-acetyl cysteine

PROGNOSIS

Mortality ranges-26 %-44% Risk factors- - advanced age - CKD,CLD - Chronic immunosuppression - chronic alcohol abuse ARDS from direct lung injury has double

mortality

REFERENCES

Harrison’s text book of medicine-18th edition ARDS Network clinical trials - www.ardsnet.org ARDS Foundation - www.ardsusa.org

THANK U….