It'a a clinical non cardiogenic syndrome characterized by
severe rapid-onset dyspnoea, hypoxaemia and
widespread pulmonary infiltrates and pulmonary edema that induce respiratory failure, . Acute lung
injury (ALI) is a less severe condition but with the risk of evolving to acute
respiratory distress syndrome (acute respiratory distress syndrome, ARDS)
Incidence
• ARDS: estimated at 60 out of 100,000 people annually
• ALI: estimated at 80 out of 100,000 people annually J Prevalence
• Orca 10% of patients admitted to intensive care units have acute respiratory
failure
• 20% of these patients have the criteria of ALI or ARDS
- Old age
- Chronic alcohol abuse
- Metabolic acidosis
- Critical illness
- Patients with trauma
- A score of the Acute Physiology and Chronic Health Evaluation (APACHE)> 16
carries an increased risk of ARDS of 2.5 times
- An APACHE II score> 20 carries an increased risk of ARDS> 3 times compared to
a score <9
The T-1001G allelic variant of the pre-B cellular colonizing factor (pre-B-cell
colony-enhancing factor, PBEF) and related haplotypes are associated with an
increased likelihood of developing ARDS among high-risk patients.
The allergy variant PBEF C-1543T and related haplotypes are associated with an
increased likelihood of ARDS among patients with septic shock
Caused by alteration of the pulmonary microcirculation with lung damage widespread by several underlying medical causes and surgical complications
The activation of the inflammatory cascade is
determined by neutrophil sequestration, degranulation of the neutrophils
themselves and release of toxic substances for the alveolus-capillary endotheles.
Cytokines take part and complement is activated with formation of fibrin
microtrombi and endothelial lesions, with diffuse alveolar damage.
• > 80 % of cases is caused by:
• Sepsi
• Bacterial pneumonia
• Trauma
• Multiple transfusions
• Gastric acid material aspiration of
• Drug abuse
• Direct pulmonary damage: Pneumonia, Aspiration.-gastric contents, Pulmonary
contusion, Drowning, Inhalation of toxic gases
• Indirect Pulmonary Damage: Sepsis, Severe Trauma, Multiple Transfusions, Drug
Abuse, Multiple Bone Fractures, Thoracic Trauma, Head Trauma, Burns,
Pancreatitis, Period Following Cardiopulmonary Bypass
Although they usually present within 12-36 hours of the initial insult, symptoms
may occur after 5-7 days
• Dyspnea
• Tachypnea
• Respiratory failure
• The additional symptoms and signs are related to the underlying etiologic
disease
Chest X-ray: ARDS, interstitial infiltrates
Most common signs
• Cardiogenic pulmonary edema
• Diffuse pneumonia
• Alveolar hemorrhage
Less frequent signs
• Acute interstitial lung disease (eg, acute interstitial pneumonia)
• Acute immunological damage (eg, hypersensitivity pneumonitis)
• Toxin damage (eg, radiation pneumonia)
• Neurogenic pulmonary edema
ARDS: Oxygenation: relationship between the arterial partial pressure of oxygen
(Pa02) and the inspiratory fraction of oxygen (FI02) <200 mmHg; beginning:
acute; Chest X-ray: bilateral alveolar or interstitial infiltrates; Left atrial
hypertension: pulmonary capillary wedge pressure <18 mmHg or no clinical
evidence of increased left atrial pressure
ALI is a similar syndrome, with a ratio of Pa0 / FI02 <200-300 mmHg; The early
characteristics are not specific, so that alternative diagnoses should be
considered
Laboratory exams
Arterial blood gas analysis
• Initially shows hypoxemia
• Brain natriuretic factor (BNP): in patients with hypoxic respiratory failure,
very low BNP levels suggest a diagnosis of ARDS / ALI; conversely, very high BNP
levels suggest cardiogenic pulmonary edema. The BNP seems useful for:
a) Exclude cardiogenic pulmonary edema
b) Identify patients with high probability of ARDS
• Larger studies are needed to validate these observations. Additional
examinations are decided based on clinical presentation
• Chest radiography: in the exudative phase it shows interstitial infiltrates
and diffuse alveolar membranes; it can be difficult to distinguish from left
ventricular failure
• CT of the thorax: in the exudative phase, the dependent alveolar edema and
atelectasis predominate
Capillary pulmonary wedge pressure <18 mmHg if Swan-Ganz catheter is used
General lines of management
General principles (see Figure)
General treatment of intensive care
New ventilation strategies to decrease the current volume (Vt) maintaining
adequate oxygenation. General treatment requires: Therapy of the underlying
cause of lung injury; Reduce the procedures and their complications; Avoid
preventable complications, such as venous thromboembolism and hemorrhage of the
Gl segment, with appropriate prophylactic regimens; Recognize and treat
nosocomial infections; Proper nutritional support
• Initiate limited volume / pressure ventilation, oxygenate, reduce acidosis and
maintain diuresis.
• Monitoring of the patient
Monitor patient oxygenation, water balance and acid-base status
Emphysema alterations with large bubbles; progressive vascular occlusion and
pulmonary hypertension; pneumothorax; pulmonary fibrosis; depression and
post-traumatic stress disorder; complications of long-term intensive care; renal
failure, especially in patients with sepsis; Nosocomial infections
Natural history
• Exudative phase: typically duration of ~ 7 days; characterized by dyspnoea,
tachypnea and severe hypoxia
• Proliferative phase: duration 7-21 days; most patients recover quickly and are
weaned from mechanical ventilation during this phase
• Fibrotic phase: starting from day 21; although the majority of patients
recover within 3-4 weeks of the initial insult, some show progressive fibrosis
with the need for prolonged ventilatory support predisposing to long-term
intensive care complications. This phase may be a reaction to today's abandoned
ventilatone strategies that employed wide Vt and high pulmonary distension
pressures
• Mortality estimates: 40-65%: most deaths are due to non-pulmonary causes:
sepsis and non-pulmonary organ failure account for 80% of deaths
• Mortality decreased with the improvement of general care and the use of low Vt
ventilation
• Patients> 75 years have a significant increase in mortality (-60%) compared to
those <45 years (-20%)
• Patients> 60 years with ARDS and sepsis have a mortality rate three times
greater than those <60 years
• Pre-existing organ dysfunction from chronic liver disease, cirrhosis, chronic
alcohol abuse, chronic immunosuppression, sepsis, chronic kidney disease, any
non-pulmonary organ failure and increased APACHE II scores have also been
associated with increased mortality from ARDS
• Patients with ARDS from direct lung injury (including pneumonia, pulmonary
contusion and aspiration) have almost doubled mortality rates compared to those
with indirect causes of lung injury
* Surgical and traumatic patients with ARDS, especially those without direct
lung injury, have a better survival rate than other patients with ARDS
• Mortality can not be predicted by: Severity of hypoxemia; PEEP levels used in
mechanical ventilation; respiratory compliance; the extension of alveolar
infiltrates to chest radiographs; pulmonary damage score; the early (within 24
hours of presentation) increased dead space can predict increased mortality from
ARDS
The majority of patients who survive restores an almost normal respiratory
function despite prolonged respiratory failure and dependence on mechanical
ventilation for survival. Maximum respiratory function is generally achieved
within 6 months. One year after endotracheal extubation, more than a third of
survivors have normal spirometry and diffusion values; most of the remaining
patients have only modest changes in respiratory function. Respiratory function
restoration is inversely correlated with the extent of pol¬monary damage in
early ARDS.
Factors associated with lower recovery of lung function
• Low static respiratory compliance
• High levels of PEEP required
• Increased duration of mechanical ventilation
• High lung damage scores