Acute lung injury (ALI) and adult respiratory distress syndrome (ARDS) develop in response to lung injury. A wide variety of precipitating causes are recognised (Tables 1a and 1b). Severe sepsis is the leading cause, followed by pneumonia, aspiration of gastric contents, massive blood transfusion, multiple trauma and pregnancy-related ARDS. ALI and ARDS develop very soon after the precipitating event, usually within 12-72 hours and often within 6 hours. In 1994, The American-European Consensus Conference Committee proposed definitions for ALI and ARDS (Table 2). It can be seen that ALI is a continuum of injury. When the oxygenation abnormality is more severe, the condition is termed ARDS. There are estimated to be about 3/100,000 cases of ARDS each year. Recent improvements in critical care have seen a reduction in the mortality of ARDS but it still remains at about 50% for the general population and 25% if it is pregnancy related. Fewer than 20% of deaths are due to refractory respiratory failure. This emphasises the importance of identifying and treating the precipitating cause.
Table 1a. Causes of ARDS
Septic shock
Gastric aspiration
Pre-eclampsia
Amniotic fluid embolus
Shock of any aetiology
Major trauma
Massive blood transfusion
Severe acute pancreatitis
Drug overdose
Pneumonia
Raised ICP
High inspired oxygen concentration
Pulmonary contusion
Near drowning
Cardiopulmonary bypass
Inhalation toxic fumes
Massive burns
Typical radiological appearances of ARDS
Acute phase
Pulmonary oedema
Normal vascular pedicle
No cardiomegaly or upper lobe blood diversion
Septal lines usually absent
Subacute phase
Progressive lung destruction and transition from alveolar to interstitial opacities
Chronic phase
Fibrosis
Focal emphysema
Table 3. The clinical and pathological phases of ARDS
Initial phase
Lasts 3-5 days
Severe oxygenation defect
Reduced lung compliance
Bilateral pulmonary infiltrates
Endothelial and epithelial cell injury
Leak of protein-rich oedema fluid in interstitium and air spaces.
Abnormal surfactant/inactivation of surfactant
Neutrophil sequestration and migration in lung
Sub-acute
Starts 5-7 days after onset of ARDS
Persistent oxygenation defect
Persistently reduced lung compliance
Increased alveolar dead space
Interstitial fibrosis with proliferation of type II alveolar cells
Widespread disruption of the pulmonary micro-circulation.
Chronic
Starts about 14 days after initial insult
Persistent low lung compliance
Increase in dead space ventilation
Extensive pulmonary fibrosis
Obliteration of normal alveolar architecture
Widespread emphysema and discrete bullae.
Focus on clinical manifestations and outcome from ARDS
At the bedside, the patient is clearly in respiratory distress. Although orthopneoa may be present, the other features of congestive heart failure are seldom present. Chest X-ray reveals diffuse, bilateral infiltrates that are often patchy and asymmetric (Table 4). Arterial blood gases reveal hypoxaemia that is often refractory to oxygen therapy. An initial respiratory alkalosis invariably leads to hypercapnia as dead space ventilation increases and muscle fatigue sets in. As ARDS evolves, the cardiovascular system is commonly affected and multi-organ failure invariably ensues. Over half the patients will develop associated renal failure. Immediate prognosis is related to the number of organ systems involved. In the general population, patients with only lung involvement have 15-30% mortality. If three or more organs are involved, this becomes greater than 80%. If the multi-organ failure persists beyond 4 days, mortality is 100%.
Table 1a. Causes of ARDS
Septic shock
Gastric aspiration
Pre-eclampsia
Amniotic fluid embolus
Shock of any aetiology
Major trauma
Massive blood transfusion
Severe acute pancreatitis
Drug overdose
Pneumonia
Raised ICP
High inspired oxygen concentration
Pulmonary contusion
Near drowning
Cardiopulmonary bypass
Inhalation toxic fumes
Massive burns
Typical radiological appearances of ARDS
Acute phase
Pulmonary oedema
Normal vascular pedicle
No cardiomegaly or upper lobe blood diversion
Septal lines usually absent
Subacute phase
Progressive lung destruction and transition from alveolar to interstitial opacities
Chronic phase
Fibrosis
Focal emphysema
Table 3. The clinical and pathological phases of ARDS
Initial phase
Lasts 3-5 days
Severe oxygenation defect
Reduced lung compliance
Bilateral pulmonary infiltrates
Endothelial and epithelial cell injury
Leak of protein-rich oedema fluid in interstitium and air spaces.
Abnormal surfactant/inactivation of surfactant
Neutrophil sequestration and migration in lung
Sub-acute
Starts 5-7 days after onset of ARDS
Persistent oxygenation defect
Persistently reduced lung compliance
Increased alveolar dead space
Interstitial fibrosis with proliferation of type II alveolar cells
Widespread disruption of the pulmonary micro-circulation.
Chronic
Starts about 14 days after initial insult
Persistent low lung compliance
Increase in dead space ventilation
Extensive pulmonary fibrosis
Obliteration of normal alveolar architecture
Widespread emphysema and discrete bullae.
Focus on clinical manifestations and outcome from ARDS
At the bedside, the patient is clearly in respiratory distress. Although orthopneoa may be present, the other features of congestive heart failure are seldom present. Chest X-ray reveals diffuse, bilateral infiltrates that are often patchy and asymmetric (Table 4). Arterial blood gases reveal hypoxaemia that is often refractory to oxygen therapy. An initial respiratory alkalosis invariably leads to hypercapnia as dead space ventilation increases and muscle fatigue sets in. As ARDS evolves, the cardiovascular system is commonly affected and multi-organ failure invariably ensues. Over half the patients will develop associated renal failure. Immediate prognosis is related to the number of organ systems involved. In the general population, patients with only lung involvement have 15-30% mortality. If three or more organs are involved, this becomes greater than 80%. If the multi-organ failure persists beyond 4 days, mortality is 100%.
Mon May 08, 2023 3:14 pm by yagocom
» ultrasound of lung in critical care patients
Mon Apr 24, 2023 9:50 am by yagocom
» respiratory diseases , anaesthetic management 2023
Sat Feb 18, 2023 6:42 pm by yagocom
» thoracic anaesthesia 2023
Fri Feb 10, 2023 10:43 pm by yagocom
» indication to SICU admission
Sun Nov 20, 2022 3:21 pm by yagocom
» electrolyte disturbances
Sat Jul 23, 2022 11:11 pm by yagocom
» fluid physiology
Mon Jul 11, 2022 12:09 pm by yagocom
» TAP block USG
Mon Jul 11, 2022 11:56 am by yagocom
» Assisted ventilation for surgical patients
Fri Jul 08, 2022 10:40 am by yagocom
» nutrition in critical ill patient
Sun Jun 12, 2022 11:14 pm by yagocom
» US workshop in Mosul
Fri May 27, 2022 2:56 pm by yagocom
» Basics of ultrasound
Fri May 27, 2022 2:28 pm by yagocom
» الملتقى العلمي الاول للجمعية العراقية للتخدير والعناية المركزة والحد من الالم فرع الموصل
Mon May 09, 2022 7:15 pm by yagocom
» Geriatric anaesthesia
Sun May 08, 2022 10:35 pm by yagocom
» thoracic anaesthesia 2022
Sat Jan 15, 2022 11:14 pm by yagocom
» chronic pain management
Fri Dec 03, 2021 5:53 pm by yagocom
» anaesthesia in respiratory diseases
Mon Nov 29, 2021 8:33 pm by yagocom
» anaesthesia for plastic procedures
Mon Jul 19, 2021 11:17 am by yagocom
» ECG for candidate
Mon Jul 19, 2021 11:14 am by yagocom
» postoperative care
Tue Feb 23, 2021 10:50 pm by yagocom