ARDS

Question 1

What is the mechanism of ARDS?

Answer 1

From the OHCM “ARDS may be caused by direct lung injury or secondary to sever systemic illness. Lung damage and release of inflammatory mediators cause increased capillary permeability and non-cardiogenic pulmonary oedema, often accompanied to multiorgan failure”

Question 2

Give 6 causes of ARDS

Answer 2

Pulmonary: pneumonia, gastric aspiration, inhalation, injury, vasculitis, contusion
Other: shock, septicaemia, haemorrhage, multiple transfusion, DIC, pancreatitis, acute liver failure, trauma, head injury, malaria, fat embolism, obstetric events (eclampsia, amniotic fluid embolus), burns, drugs/toxins (aspirin, heroin, paraquat)

Question 3

What are the clinical features of ARDS?

Answer 3

Cyanosis, tachypnoea, tachycardia, peripheral vasodilation, bilateral fine inspiratory crackles

Question 4

What investigations would you order?

Answer 4

FBC with U&Es, LFTs, amylase, clotting, CRP and blood cultures. ABG. CXR, which would show bilateral pulmonary infiltrates. Pulmonary artery catheter to measure pulmonary capillary wedge pressure (PCWP)

Question 5

What is the diagnostic criteria?

Answer 5

Diagnosis requires:

1. Acute onset
2. CXR: bilateral infiltrates
3. PCWP

Question 6

How do you manage ARDS?

Answer 6

Admit to ITU, give supportive therapy, find the underlying cause.

1. RESPIRATORY SUPPORT: CPAP with 40-60% O2, though may need mechanical ventilation if PaO2 6kPa. NB. That the high airway pressure of ventilation and the reduced lung compliance may lead to high airway pressures and pneumothorax, hence a low tidal volume (pressure limited approach) with a low or moderate Positive End Expiratory Pressure (PEEP) improves outcome.
2. CIRCULATORY SUPPORT: Invasive haemodynamic monitoring with an arterial line and Swan-Ganz catheter aids the diagnosis. Conservative fluid management improves outcome. Maintain cardiac output and O2 delivery with inotropes (e.g. dobutamine 2.5-10micrograms/kg/min IVI) vasodilators and blood transfusion. Consider treating pulmonary hypertension with low dose nitric oxide. Haemofiltration may be needed in renal failure to achieve negative fluid balance.
3. SEPSIS: identify organisms and treat accordingly, and if no obvious organism then treat with appropriate broad-spec antibiotics (avoid nephrotoxic agents)
4. OTHER: nutritional support – enteral is best with high fat, antioxidant formulations. Steroids protect those at high risk of fat embolism and with pneumocystosis and may improve outcome in subacute ARDS, though their role in established ARDS is controversial.

Question 7

What is the prognosis?

Answer 7

Overall mortality is 50-70%, though varies with age of patient, the cause (Pneumonia 86%, trauma 38%) and number of organs involved (3 organs involved for >1 week is ‘invariably’ fatal)