Acute Respiratory Distress Syndrome

Write about Acute Respiratory Distress Syndrome here.


• A form of acute respiratory failure due to permeability pulmonary oedema resulting from endothelial damage developing in response to an initiating injury or illness

• Lung damage and release of inflammatory mediators cause increased capillary permeability and non-cardiogenic pulmonary oedema often accompanied by multi-organ failure


Pressure Pulmonary Oedema (NOT ARDS)


Permeability Pulmonary Oedema - ARDS

The characteristic feature of permeability pulmonary oedema in ARDS is that the Pulmonary Capillary Wedge Pressure (PCWP) is not elevated


Clinically:


ARDS develops in response to injury or illness to the lungs -> direct (pneumonia etc) or indirect (pancreatitis)

• 12-48 hours later patient develops respiratory distress with increasing dyspnoea and tachypnoea

• ABG show deteriorating hypoxaemia, poorly responsive to O2 therapy

• CXR => Diffuse bilateral infiltrates in the absence of CARDIOGENIC pulmonary oedema

• Spectrum of ARDS - Full Blown ARDS:

• Hx of initiating injury or illness

• Hypoxaemia , refractory to O2 therapy (e.g. Po2<8 kPa or 60 mmHg on 40% O2)

• This is due to shunting of blood through areas of lung not being ventilated due to alveoli filled with exudate and undergoing atelectasis

• PO2/FiO2 <26 (FiO2:100% O2 = FiO2 of 1 = fractional inspired O2 concentration... FiO2:50% O2 = 0.5)

• Bilateral diffuse infiltrates on CXR

• No evidence of cardiogenic pulmonary oedema (e.g. PCWP < 18 mmHg)


Treatment:

• Initiating injury treatment and optimisation

Respiratory Support 

• CPAP can prevent alveolar atelectasis - V/Q mismatch reduced

• ET intubation and mechanical ventilation necessary in most - indications = PO2 <8.3 despite 60% O2, PCO2 >6

• => ITU

• Conventional ventilation & reduced lung compliance may lead to high peak airway pressure ± pneuomthorax

• PEEP increases oxygenation but reduces venous return, cardiac output and kidney and liver perfusion

• High pressure + high O2 concentration may -> microvascular damage perpetuating initial permeability problems (ventilator lung/oxgen toxicity)

• Techniques to overcome this

• Inverse ratio ventilation (inspiration longer than expiration, but may cause progressive air trapping)

• High-frequency jet ventilation (small volumes often)

Circulatory Support:

• Invasive haemodynamic monitoring allows guidance of use of diuretic and vasodilators (of pulmonary arteries)

• Balance between low pulmonary artery pressure (reduce fluid leak) and adequate system blood pressure (to maintain perfusion)

• Most drugs used to vasodilate the pulmonary arteries (nitrates, Ca antagonists) also cause systemic vasodilation, with hypotension and impaired organ perfusion

• Inotropes and vasopressor agents, such as dobutamine and noradrenaline may be needed to maintain systemic BP and CO particularly in patients with sepsis syndrome - sepsis with systemic vasodilation

• Inhaled NO can be used as a selective pulmonary vasodilator (rapidly inactivated by haemoglobin)

General Management:

• Correction of anaemia

• Nutritional support

• Steroids don't help in acute phase but may help >7 days


Prognosis:

• Overall mortality = 50 - 75%

• Varies with:

• age

• cause of ARDS (pneumonia = 86%, trauma = 38%)

• Number of organs involved (3 organs involved for > 1/52 => invariably fatal)