ALOK SINHADepartment of Medicine

Manipal College of Medical SciencesPokhara, Nepal

• Serious disease characterised by damage to alveolar epithelium & capillary endothelium resulting in alveolar oedema with high protein fluid

• It results from increased alveolar capillary permeability

• NOT CARDIOGENIC IN ORIGIN

alveolar epitheliumCapillary endothelium

severe end of a spectrum of acute lunginjury due to many different insults.Essentially it is diffuse alveolar injury

Acute, persistent, lung inflammation

Increased vascular permeability

Bilateral and extensive infiltrates (seen in the CXR)

Very poor oxygenation despite PEEP

Not due to clinical left ventricular failure – associated with a wedge pressure of over 18 mmHg (non-cardiogenic)

Most commonly seen on the ICU where about 10% of such patients will have ARDS

PCWP Normal: 8-12mmHg

International criteria1. Acute onset of symptoms

2. PaO2 : FIO2 (fraction of inspired oxygen) – 200 mm Hg or lessFor Example normal PaO2 = 100, FiO2 = 20% or 1/5 so the above ratio = 100/1/5 = 500 mm Hg

3. Bilateral infiltrates on CXRs

4. Pulmonary arterial wedge pressure of 18 mm Hg or less (or no clinical signs of left atrial hypertension)

Increased alveolar-arterial (A-a) gradient

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What is this situation ?

1. Acute onset of symptoms

2. PaO2 : FIO2: between 300 to 200 mm Hg

3. Bilateral infiltrates on CXRs

4. Pulmonary arterial wedge pressure of 18 mm Hg or less or no clinical signs of left atrial hypertension

•Acute lung injury (ALI)

ALI ARDSMild

Pathogenesis of ARDS

Inflammatory damage to the alveoli– by locally produced pro-inflammatory mediators– remotely produced and arriving via

pulmonary arteryThrough inhalation (eg gastric contents)

Increased pulmonary capillary permeability - fluid and protein leakage into the alveolar spaces with pulmonary infiltrates

Alveolar surfactant is diluted with loss of its stabilizing effect, resulting in diffuse alveolar collapse and stiff lungs. This leads to:

1. Gross impairment of V/Q matching with shunting causing arterial hypoxia – usually enough remaining functioning alveoli to

maintain CO2 clearance- Normal CO2– Pulmonary hypertension will develop secondary to

the hypoxia (helpful – counters V/Q matching)

2.Reduced compliance (stiff lungs), due to loss of functioning alveoli alveolar collapse, filled with fluid and protein hyperinflation of remaining alveoli to their limits of

distension

Decrease transfer of gases in alveoli3.

Causes of mediator release leading to ARDSSepsis/pneumonia

Gastric aspiration

Major trauma

Smoke/ gas inhalation

Acute pancreatitis

Drug toxicity - tricyclic antidepressants, opiates, cocaine, aspirin

Fat emboli

Direct effects of large amounts of necrotic tissue

(secondary risk factors) alcoholism

cigarette smoking

Less common causes

Near drowning

Following upper airway obstruction: mechanism unclear

Acute form of Interstitial Pneumonia: Also known as acute Hamman-Rich syndrome

Post-bone marrow transplant as bone marrow recovers

Amniotic embolism

Massive haemorrhage

Multiple transfusions

DIC

Massive burns

Head injury– Raised ICP– Intracranial bleed

Cardio-pulmonary bypass

Acute liver failure

Course of ARDS

Phase 1 - early period of alveolar damage and hypoxaemia with pulmonary infiltration

Phase 2 -develops after a week as pulmonary infiltrates resolve– associated with an increase in

type II pneumocytes (surfactant producers)

Myofibroblasts

collagen formation

Phase 3 -if the patient survives, is the fibrotic stage that leaves the lung with –Cysts–deranged micro-architecture – fibrosis on histology

leading to Cor Pulmonale

ARDS should be considered in any patient with a predisposing risk factor develops severe hypoxaemia stiff lungswidespread diffuse pulmonary infiltrate

Approximately 1 to 2 days following the clinical presentation of the precipitating cause

Rapidly worsening dyspnoea Dry cough HypoxaemiaCoarse crackles in the chest

DIFFERENTIALS

Aspiration Pneumonia

Congestive Heart Failure

Pneumonia Atypical Bacterial Pneumonia

Pneumocystis Carinii

Pneumonia Viral

To exclude other more specifically treatable conditions

Left ventricular failure excluded – on clinical grounds– by echocardiography– wedge pressure measurement <18 mmHg.

Diffuse alveolar haemorrhage can occur in Goodpasture's, Leptospirosis

Oher clinical features of these disorders will be present

Some pulmonary infections – Mycobacteria– Legionella– PCP– viral pneumonia

may mimic ARDS & lavage fluid may reveal these

Occasionally cancer and lymphangitis carcinomatosa can also mimic ARDS – will show on a lung biopsy

CXRABG (consider arterial line as regular samples may be required)CBC,LFTs, coagulation profile, and CRPSeptic screen (culture blood, urine, sputum)ECGConsider drug screenAmylase if history suggestive

Pulmonary artery catheter to measure – PCWP– cardiac output– mixed venous oxygen saturation – calculation of haemodynamic parameters

Other investigations if appropriate–CT chest–Broncho alveolar lavage for microbiology &

cell count (?eosinophils)

Treat the precipitating cause

Provide best supportive care with adequate oxygenation

I.V. fluids – – to be used judiciously– Can increase pulmonary oedema

Inotrope and/or vasopressor support is commonly required and the choice of agent is – dobutamine – dopamine– epinephrine, norepinepherine

Patients invariably require higher oxygen concentrations (non-rebreather masks with reservoir FiO2 ~60- 80%) or CPAP

Consider transfer to HDU/ICU

Different oxygen delivery systems

Nasal canulaNon re breather masks

Indications for mechanical ventilation– Inadequate oxygenation (PaO2 <60mm

(8kPa) on FiO2 >0.6 or 60%)–Rising or elevated PaCO2 (> 45 mm or 6kPa)–Clinical signs of incipient

respiratory/cardiovascular failure

Mechanical ventilation with PEEP -almost always required to maintain oxygenation, with high inflation pressures

Is this the meaning of PEEP ?

PEEP: required to counter atelectasis

High inflation pressures may worsen ARDS directly (micro-barotrauma)– try to maintain plateau pressures <30 mmHg

Special ventilation techniques have been tried to reduce the high inflation pressures resulting from the stiff lungs (low compliance)

Using low tidal volumes to reduce inflation pressures (6 ml/kg ideal body weight compared to 12 ml/kg) reduces mortality by 10%

This results in Reduced minute ventilation

Rise in PaCO2 – permissive hypercapnia

• Inverse ratio ventilation • may improve oxygenation, but pCO2 may

rise further

• Prone positioning• improves oxygenation in ~70% of patients

with ARDS

• Inhaled pulmonary vasodilators (nitric oxide, nebulized prostacyclin): • may improve oxygenation

Extracorporeal oxygenation/CO2 removal will buy time and allow the lung to recover, but these techniques are very expensive and it is difficult to demonstrate any long-term benefit

High-dose steroids ––some evidence of overall improved survival – later use possibly beneficial if nosocomial

infection rates are not increased

Cardiovascular supportMost patients haemodynamically compromised

due to – underlying condition – ventilatory management

Benefit from fluid resuscitation. This may risk worsening capillary leak in the lung and compromise oxygenation/ventilation. Aim for a low-normal intravascular volume whilst maintaining cardiac index and mean arterial pressure

Management of other associated conditions• Renal failure • Enteral feeding • Coagulopathy -severe/DIC may be present expert

advice should be sought• Sepsis

empiric antibiotics guided by possible pathogens, and following an appropriate sensitivity tests Antibiotics should be modified or discontinued in light of microbiological results

Complications

High ventilation pressures lead to barotrauma: –pneumothorax –surgical emphysema –pneumomediastinum – Nosocomial infections

Non-specific problems of – venous thromboembolism– GI haemorrhage– inadequate nutrition

Prognosis

has improved over the last 20 years due to improvements in supportive care of –Early deaths due to the precipitating condition – later deaths to complications

Over half the patients will survive with varying residual lung damage, pulmonary function tests often show only minor restrictive abnormalities

Future developments

The optimal level of PEEP is difficult to predict. – Inadequate PEEP allows more atelectasis – too high PEEP contributes to overdistension of

remaining alveoli and further barotrauma

Ways to estimate the best PEEP are under investigation

Liquid ventilation with perfluorocarbons has been tried

Nitric oxide (NO) has been tried with clear improvements in oxygenation but very little effect on survival

Inhaled prostacyclin: is unconvincing

bilateral patchy opacities in mostly the middle and lower lung zones

Normal size heart No pleural effusion

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It appears he is ticking ‘n’ alive