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Acute (Adult) Respiratory Distress Syndrome

Synonyms: Adult respiratory distress syndrome (ARDS); Acute lung injury (ALI).

Acute respiratory distress syndrome (ARDS) is a common and devastating condition which affects both medical and surgical patients. It occurs when noncardiogenic pulmonary oedema (secondary to acute damage to the alveoli) leads to acute respiratory failure.

Epidemiology

Incidence is uncertain, but was reported as 17.9 per 100,000 for acute lung injury and 13.5 per 100,000 for ARDS in a Scandinavian study in 1994.1

Aetiology

Risk Factors

The more risk factors apply, the greater the chance of ARDS.

Commonest Risk Factors

  • Sepsis
  • Massive trauma with shock and multiple transfusions
  • Hypovolaemic shock
  • Pneumonia
  • Gastric aspiration

Other Risk Factors

  • Acute pancreatitis
  • DIC
  • Head injury / raised ICP
  • Fat emboli
  • Transfusions of blood products
  • Heart/lung bypass
  • Tumour lysis syndrome
  • Pulmonary contusion
Pathophysiology

Increased permeability of pulmonary microvasculature causes leakage of proteinaceous fluid across the alveolar-capillary membrane.2 This may be one manifestation of a more generalized disruption of endothelium, resulting in hypoxia and multiple organ failure.

Clinical features
  • Symptoms: History of relevant injury and increasing dyspnoea which may occur some time after the precipitating event.
  • Signs: Cyanosis (reflecting hypoxia refractory to oxygen therapy), tachypnoea, tachycardia, peripheral vasodilatation; bilateral fine inspiratory crackles.
Investigations
  • FBC, U and E, LFTs, amylase, clotting, CRP, blood cultures, ABG.
  • CXR shows bilateral alveolar shadowing, often with air bronchograms.
  • Pulmonary artery catheter to measure pulmonary capillary wedge pressure (PCWP).
Diagnostic criteria

One consensus requires these 4 to exist:3

  1. Acute onset
  2. CXR: bilateral infiltrates
  3. Pulmonary-artery wedge pressure18mmHg or a lack of clinical evidence of left atrial hypertension (i.e. CCF)
  4. Refractory hypoxaemia: acute lung injury is present when ratio PaO2:FiO2<300; ARDS is present when PaO2: FiO2<200.

20-50% of acute lung injury patients will develop ARDS within 7 days.4

Management

Admit to ITU, give supportive therapy and treat the underlying cause.

Respiratory support

In early ARDS continuous positive airway pressure (CPAP) with 40-60% oxygen may be adequate to maintain oxygenation. But most patients need mechanical ventilation.

Indications for ventilation:

  • PaO2: <8.3kPa despite 60% O2;
  • PaCO2: >6kPa.

The large tidal volumes (10-15mL/kg) produced by conventional ventilation plus reduced lung compliance in ARDS may lead to high peak airway pressures ± pneumothorax. Positive end-expiratory pressure (PEEP) increases oxygenation but at the expense of venous return, cardiac output, and perfusion of the kidneys and liver. Newer approaches include inverse ratio ventilation (inspiration > expiration), permissive hypercapnia, prone position and high-frequency jet ventilation, and other low-tidal-volume techniques.5,6 Low tidal volume ventilation i.e. ≤6mL/kg predicted body weight is the only form of ventilation associated with improved survival.7,6

Circulatory support

Circulatory support Invasive haemodynamic monitoring with an arterial line and Swan-Ganz catheter aids the diagnosis and may be helpful in monitoring PCWP and cardiac output.

Maintain cardiac output and oxygen delivery with inotropes (eg dobutamine 2.5-10μg/kg/min), vasodilators and blood transfusion. Consider treating pulmonary hypertension with low-dose (20-120ppm) nitric oxide, a selective pulmonary vasodilator.8 However, a recent systematic review and meta-analysis found that nitric oxide only provides a short improvement and does not affect survival. Furthermore, nitric oxide was associated with renal dysfunction.9 Haemofiltration may be needed in renal failure and to achieve a negative fluid balance.

Experimental therapies

More novel therapies currently in the experimental stages include activated protein C, granulocyte-macrophage colony-stimulating factor and the use of beta agonists to enhance alveolar fluid clearance.8

Sepsis

Identify organism(s) and treat accordingly. If clinically septic, but no organisms cultured, use empirical broad spectrum antibiotics. Avoid nephrotoxic antibiotics.

Nutritional support

Enteral is better than parenteral feeding. Steroids do not improve mortality in the acute phase but may be of benefit later on (>7 days), particularly if eosinophilia in blood or bronchial-alveolar-lavage (BAL).

Prognosis

Overall mortality is 50-75%. Prognosis varies with age of patient, cause of ARDS (pneumonia 86%, trauma 38%), and number of organs involved (3 organs involved for >1 week is invariably fatal). In most cases, survivors' lung function returns almost to normal within 6-12 months. There may be reduced vital capacity and some obstructive lung disease but these are usually asymptomatic.4 Interestingly, patients with acute lung injury have reduced exercise capacity up to two years after the episode and there is evidence to suggest long-term neurocognitive impairment.4


Document References
  1. Luhr OR, Antonsen K, Karlsson M, et al; Incidence and mortality after acute respiratory failure and acute respiratory distress syndrome in Sweden, Denmark, and Iceland. The ARF Study Group. Am J Respir Crit Care Med. 1999 Jun;159(6):1849-61. [abstract]
  2. Ware LB, Matthay MA; The acute respiratory distress syndrome. N Engl J Med. 2000 May 4;342(18):1334-49.
  3. Bernard GR, Artigas A, Brigham KL, et al; Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Consensus Committee. J Crit Care. 1994 Mar;9(1):72-81. [abstract]
  4. Rubenfeld GD, Herridge MS; Epidemiology and outcomes of acute lung injury. Chest. 2007 Feb;131(2):554-62. [abstract]
  5. No authors listed; Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000 May 4;342(18):1301-8.; This trial was stopped after the enrollment of 861 patients because mortality was lower in the group treated with lower tidal volumes than in the group treated with traditional tidal volumes [abstract]
  6. Wheeler AP, Bernard GR; Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007 May 5;369(9572):1553-64. [abstract]
  7. Girard TD, Bernard GR; Mechanical ventilation in ARDS: a state-of-the-art review. Chest. 2007 Mar;131(3):921-9. [abstract]
  8. Calfee CS, Matthay MA; Nonventilatory treatments for acute lung injury and ARDS. Chest. 2007 Mar;131(3):913-20. [abstract]
  9. Adhikari NK, Burns KE, Friedrich JO, et al; Effect of nitric oxide on oxygenation and mortality in acute lung injury: systematic review and meta-analysis. BMJ. 2007 Apr 14;334(7597):779. Epub 2007 Mar 23. [abstract]

Internet and Further Reading
  • Wheeler AP, Bernard GR; Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007 May 5;369(9572):1553-64. [abstract]
Acknowledgements EMIS is grateful to Dr Gurvinder Rull for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2007.
DocID: 1773
Document Version: 21
DocRef: bgp628
Last Updated: 22 May 2007
Review Date: 21 May 2009




















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