ARDS

1. “Fulminant noncardiogenic pulmonary oedema following CPB is an infrequent but life threatening event, occurring in less than 1% of cases but associated with a mortality of 30—50%”

2. “. . . hypoxic, septic or traumatic injury to the lungs causes massive pulmonary oedema, atelectasis, and hyaline membrane deposits. Alveolar membranes are also injured, causing further loss of fluid into the alveoli and resulting in alveolar hypoventilation; the later development of pneumonitis and interstitial fibrosis causing a decrease in diffusion capabilities. Lung compliance and FRC are markedly reduced. Marked alveolar hypoventilation produces ventilation/perfusion mismatch and severe hypoxaemia. Hypocapnia may be present while compensatory hyperventilation occurs. Development of hypercapnia indicates severe patient deterioration. With progressive hypoxia, acidosis in unavoidable.”

CLINICAL PRESENTATION

· The syndrome usually develops insidiously 12 - 48 hours following the precipitating event but has been seen within 6 hours of uneventful CPB

· Progressive deterioration, often accompanied by sepsis & multiorgan failure leads to death within 3—4 weeks.

· Usual features are :

§ increase in intraalveolar fluid

§ increased pulmonary vascular resistance

§ intrapulmonary shunt

§ dyspnoea

§ tachypnoea

§ cyanosis

§ fine crepitations

§ hypoxaemia

§ increased A—aDO2

· As disease progresses:

o decreased lung compliance

o increased dead space:tidal volume ratio

o increased minute volume required to maintain adequate PaO2

· Pulmonary dysfunction following CPB is a common event. The (A-a) 02 gradient increases following CPB increases to a maximum 18-24 hours postoperatively. Thought to be due to increase in pulmonary interstitial fluid. In its most extreme form is a type of ARDS [called post perfusion lung syndrome.

· Etiologies include:

o loss of surfactant

o hypoxic lung damage

o pulmonary vasculitis caused by haemolysed blood

o protein denaturation

o multiple pulmonary emboli

o lung accumulation of activated neutrophils (containing lysosomal enzymes resulting in pulmonary capillary damage and subsequent leakage of plasma)

· Noncardiogenic pulmonary oedema occurs when the permeability characteristics of the alveolar capillary membrane are dramatically altered, creating a capillary leak syndrome with net migration of water and proteins into the alveolar spaces

· Lungs are diffusely congested with:

1. Intraalveolar oedema
2. Interstitial oedema
3. Haemorrhagic atelectasis

· Pulmonary vessel lumens are packed with neutrophils

· There is diffuse swelling of capillary endothelium and alveoli pneumocytes

· Pulmonary capillary endothelial injury, capillary leak, and surfactant abnormalities results in interstitial and pulmonary oedema

· Attenuated alveolar type I cells are replaced by cuboidal type II cells resulting in thickened alveoli walls

· The interstitium becomes infiltrated with inflammatory and other cells

· Alveoli are filled with proteinaceous and haemorrhagic fluid

· Pulmonary fibrosis appears and progressively obliterates pulmonary architecture including vasculature

TREATMENT

· Mechanical ventilatory support

— usually with high airway pressures

· Fluid management

—colloids may be given to increase osmotic pressure in blood to return lung interstitial fluid back to blood

—note that large volumes of fluid may be lost into the lungs resulting in a reduced MSFP (mean systemic filling pressure) and reduced cardiac output —> require aggressive fluid replacement but careful fluid management is needed to reduce fluid overload & pulmonary oedema

· Cardiac support

—to increase cardiac output and reduce filling pressures (with subsequent pulmonary oedema)

—especially in environment of high PEEP

· Corticosteroids

—may reduce lung injury by inhibiting complement-induced leukocyte aggregation and reduce capillary permeability if used early

PREVENTION

1. Minimise contact activation of complement and consequently leukocytes

· minimise suctioning

· use membrane oxygenators instead of bubble oxygenators

· adequate heparinisation to reduce whole body inflammatory response

· use of antifibrinolytic agents to reduce complement activation and fibrin split products

· minimise duration of CPB

· reduce haemolysis

· use more biocompatible surfaces

· minimise blood transfusions [anti-leukocyte antibodies activate white cells]

2. Minimise microemboli

· use of arterial filters etc