Anda di halaman 1dari 10

Acute Respiratory Distress Syndrome

Definition
A clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure. Acute lung injury (ALI) is a less severe disorder but has the potential to evolve into acute respiratory distress syndrome (ARDS).

Epidemiology
Incidence o ARDS: estimated to be 60 per 100,000 persons annually o ALI: estimated to be 80 per 100,000 annually Prevalence

Approximately 10% of patients admitted to the intensive care unit have acute respiratory failure. ~20% of these patients meet criteria for ALI or ARDS.
o

Risk Factors
Advanced age Chronic alcohol abuse Metabolic acidosis Critical illness Trauma patients o Acute Physiology and Chronic Health Evaluation (APACHE) II score 16 carries 2.5-fold increased risk of ARDS. o APACHE II score > 20 carries > 3-fold increased risk of ARDS compared with score 9. Pre-B-cell colony-enhancing factor (PBEF) T-1001G variant allele and related haplotype are associated with increased odds of developing ARDS among at-risk patients.[1] PBEF C-1543T variant allele and related haplotype are associated with decreased odds of ARDS among patients with septic shock. [1]

Etiology
Caused by diffuse lung injury from many underlying medical and surgical disorders o >80% of cases are caused by: Sepsis Bacterial pneumonia Trauma Multiple transfusions

Gastric acid aspiration Drug overdose Mechanism of action o Direct lung injury Pneumonia Aspiration of gastric contents Pulmonary contusion Near-drowning Toxic inhalation injury o Indirect lung injury Sepsis Severe trauma Multiple transfusions Drug overdose Multiple bone fractures Flail chest Head trauma Burns Pancreatitis After cardiopulmonary bypass

Symptoms & Signs


Although usually present within 1236 hours after the initial insult, symptoms can be delayed by 57 days. o Dyspnea o Tachypnea o Respiratory failure Additional symptoms and signs are related to the underlying etiology of ARDS.

Differential Diagnosis

Most common
o

Cardiogenic pulmonary edema o Diffuse pneumonia o Alveolar hemorrhage Less frequent Acute interstitial lung diseases (e.g., acute interstitial pneumonitis) o Acute immunologic injury (e.g., hypersensitivity pneumonitis) o Toxin injury (e.g., radiation pneumonitis) o Neurogenic pulmonary edema
o

Diagnostic Approach

Diagnostic criteria o ARDS

Oxygenation: ratio of arterial partial pressure of oxygen (PaO2) to inspiratory oxygen fraction (FiO2) < 200 mmHg Onset: acute Chest radiography: bilateral alveolar or interstitial infiltrates Left atrial hypertension: pulmonary capillary wedge pressure 18 mmHg or no clinical evidence of increased left atrial pressure o ALI is a similar syndrome, with PaO2/FiO2 ratio < 200300 mmHg. Early features are nonspecific, so alternative diagnoses must be considered.

Laboratory Tests

Arterial blood gas analysis


o

Imaging

Initially shows hypoxemia Brain natriuretic factor (BNP) [2] o In patients with hypoxic respiratory failure Very low BNP levels suggest a diagnosis of ARDS/ALI. Very high BNP levels suggest cardiogenic pulmonary edema. o BNP appears useful in: Excluding cardiogenic pulmonary edema Identifying patients with a high probability of ARDS o Larger studies are necessary to validate these findings. Additional testing is dictated by clinical presentation. Chest radiography (see Figure 1)
o

During the exudative phase, shows diffuse interstitial and alveolar infiltrates Can be difficult to distinguish from left ventricular failure Chest CT (see Figure 2) During the exudative phase, dependent alveolar edema and atelectasis predominate.
o

Diagnostic Procedures
Pulmonary capillary wedge pressure 18 mmHg if SwanGanz catheter in use

Treatment Approach

General principles

Specific Treatments

General critical care management New ventilator strategies to decrease tidal volume (Vt) while maintaining adequate oxygenation General care requires: o Treatment of underlying cause of lung injury o Minimizing procedures and their complications o Avoidance of preventable complications, such as venous thromboembolism and GI hemorrhage, with appropriate prophylactic regimens o Recognition and treatment of nosocomial infections o Adequate nutritional support Initial management o Initiate volume/pressure limited ventilation o Oxygenate o Minimize acidosis o Diuresis
o o

Mechanical ventilatory support Overdistention of normal lung with positive pressure can produce or exacerbate lung injury, causing or worsening ARDS. o New ventilator strategies aim to limit alveolar distention while still ensuring adequate tissue oxygenation. o Current practice is to use low Vt combined with positive end-expiratory pressure (PEEP) at levels to achieve adequate oxygenation with the lowest FiO2. o Other techniques that may improve oxygenation while limiting alveolar distention Extending the time of inspiration on the ventilator Placing patient in the prone position Stepwise approach to mechanical ventilation in ARDS (see Figure 3 )
o

o o

Calculate predicted body weight in kg. Men: 50 + 5.42[height (cm) 60] Women: 45.5 + 5.42[height (cm) 60] Ventilator mode Volume cycle, assist control Vt Initial Vt: 8 mL/kg of predicted body weight Reduce to 6 mL/kg over 24 hours if ventilation is adequate.

Goal inspiratory plateau pressures are < 30 cmH2O; reduce Vt to as low as 4 mL/kg as needed (and permitted by ventilation) to achieve this goal. Oxygenation PaO2 goal of 5580 mmHg, or pulse oximetry oxygen saturation 8895% Use the minimal amount of PEEP to keep FiO2 0.6 mmHg and meet PaO2 goal. Respiratory rate and acidosis management Goal arterial pH: 7.307.40 pH < 7.30: Increase respiratory rate to 35 breaths/min. pH < 7.30 and respiratory rate of 35 breaths/min: Consider starting intravenous bicarbonate (or equivalent buffer).

Ancillary therapies If stepwise mechanical ventilation approach fails and the patient has persistent hypoxemic respiratory failure, consider [3]: o Neuromuscular blocking agents o Recruitment maneuvers o High PEEP o Prone positioning Patients with ARDS should receive intravenous fluids only sufficient to achieve an adequate cardiac output, tissue oxygen delivery, and organ function, as assessed by urine output, acidbase status, and arterial pressure. o Goal: MAP 65mmHg, avoid hypoperfusion Glucocorticoids o Routine use of glucocorticoids or other pharmacologic therapies in ARDS, except as needed to treat the underlying cause, is not recommended. o Recent randomized, double-blind, placebocontrolled trial[4] withmethylprednisolone infusion demonstrated reductions in: Duration of mechanical ventilation Duration of intensive care unit (ICU) stay ICU mortality o The ARDS Network is currently conducting a largescale study of glucocorticoids in the late phase of ARDS. Use of nitric oxide is not currently recommended. o Meta-analysis[5]showed nitric oxide is associated with:

Limited improvement in oxygenation in patients with ALI or ARDS No mortality benefit Possible harm (renal dysfunction) Lung replacement therapy with extracorporeal membrane oxygenation provides clear survival benefit in neonatal respiratory distress syndrome.
o

No proven survival benefit in adults with ARDS

Evidence-based recommendations for ARDS therapies A: recommended therapy based on strong clinical evidence from randomized clinical trials B: recommended therapy based on supportive but limited clinical data C: indeterminate evidence; recommended only as alternative therapy D: not recommended based on clinical evidence against efficacy of therapy Mechanical ventilation o Low Vt: A o High PEEP or "open-lung:" C o Prone position: C o High-frequency ventilation: D o Extracorporeal membrane oxygenation: D Minimization of left atrial filling pressure: B Glucocorticoids: C Surfactant replacement, inhaled nitric oxide, and other anti-inflammatory therapy (e.g., ketoconazole, prostaglandin E1, NSAIDs): D

Monitoring
Regular monitoring of oxygenation, fluid balance, and acidbase status

Complications
Emphysema-like changes, with large bullae 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

Prognosis

Natural history

Exudative phase Duration typically ~7 days Marked by dyspnea, tachypnea, and severe hypoxemia o Proliferative phase Days 721 Most patients recover rapidly and are liberated from mechanical ventilation during this phase. o Fibrotic phase Day 21 onward Although the majority of patients recover within 34 weeks of the initial insult, some experience progressive fibrosis. o Necessitating prolonged ventilatory support predisposing to complications of longterm intensive care This phase may be a reaction to nowabandoned ventilator strategies that employed large Vt and high lung inflation pressures. Mortality o Mortality estimates: 4065% Most deaths are due to nonpulmonary causes. o Sepsis and nonpulmonary organ failure account for > 80% of deaths. o Mortality has decreased with improvements in general care and use of low-Vt ventilation. o Patients > 75 years have a substantially increased mortality rate (~60%) compared to those < 45 years (~20%). o Patients > 60 years with ARDS and sepsis have a 3-fold higher mortality rate compared with those < 60 years. o Preexisting organ dysfunction from chronic liver disease, cirrhosis, chronic alcohol abuse, chronic immunosuppression, sepsis, chronic renal disease, any nonpulmonary organ failure, and increased APACHE II scores have also been linked to increased mortality rates from ARDS. o Patients with ARDS from direct lung injury (including pneumonia, pulmonary contusion, and aspiration) have nearly twice the mortality rate of those with indirect causes of lung injury. Surgical and trauma patients with ARDS, especially those without direct lung injury, have a
o

better survival rate than do other patients with ARDS. o Mortality cannot be predicted from: Extent of hypoxemia Level of PEEP used in mechanical ventilation Respiratory compliance Extent of alveolar infiltrates on chest radiography Lung injury score o Early (within 24 hours of presentation) elevation in dead space may predict increased mortality from ARDS. Recovery o Of patients who survive, most recover nearly normal lung function. Despite prolonged respiratory failure and dependence on mechanical ventilation for survival o Maximum lung function is usually recovered within 6 months. o One year after endotracheal extubation: More than one-third of survivors have normal spirometry values and diffusion capacity o Most remaining patients have only mild abnormalities in pulmonary function. o Recovery of lung function is inversely related to the extent of lung injury in early ARDS. o Factors associated with worse recovery of pulmonary function Low static respiratory compliance High levels of required PEEP Longer durations of mechanical ventilation High lung injury scores

Prevention

In patients at high risk for ARDS o Careful fluid management o Aspiration precautions (e.g., elevate head of bed)

ICD-9-CM
518.5 Pulmonary insufficiency following trauma and surgery (includes adult respiratory distress syndrome) 518.82 Other pulmonary insufficiency, not elsewhere classified (includes adult respiratory distress syndrome, not elsewhere classified) 769 Respiratory Distress Syndrome (in the perinatal period)

See Also

Approach to Nosocomial Infections

Internet Sites
Professionals o Acute Respiratory Distress Syndrome ClinicalTrials.gov o Homepage American College of Chest Physicians Patients o ARDS (acute respiratory distress syndrome) MedlinePlus o Acute respiratory distress syndrome MayoClinic.com

References
1. Bajwa EK et al: Pre-B-cell colony-enhancing factor gene polymorphisms and risk of acute respiratory distress syndrome. Crit Care Med35:1290, 2007 [PMID:17414088] 2. Karmpaliotis D et al: Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema. Chest131:964, 2007 [PMID:17426196] 3. Girard TD, Bernard GR: Mechanical ventilation in ARDS: a state-of-the-art review. Chest 131:921, 2007 [PMID:17356115] 4. Meduri GU et al: Methylprednisolone infusion in early severe ARDS: results of a randomized controlled trial. Chest 131:954, 2007 [PMID:17426195] 5. Adhikari NK et al: Effect of nitric oxide on oxygenation and mortality in acute lung injury: systematic review and meta-analysis. BMJ 334:, 2007 [PMID:17383982]

General Bibliography
Bersten AD et al: Incidence and mortality of acute lung injury and the acute respiratory distress syndrome in three Australian States. Am J Respir Crit Care Med 165:443, 2002 [PMID:11850334] Chan KP, Stewart TE: Clinical use of high-frequency oscillatory ventilation in adult patients with acute respiratory distress syndrome. Crit Care Med33:S170, 2005 [PMID:15753724] Fan E, Needham DM, Stewart TE: Ventilatory management of acute lung injury and acute respiratory distress syndrome. JAMA 294:2889, 2005 [PMID:16352797]

Herridge MS et al: One-year outcomes in survivors of the acute respiratory distress syndrome. N Engl J Med 348:683, 2003 [PMID:12594312] Piantadosi CA, Schwartz DA: The acute respiratory distress syndrome. Ann Intern Med 141:460, 2004 [PMID:15381520] 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 Med342:1301, 2000 [PMID:10793162] Ware LB, Matthay MA: The acute respiratory distress syndrome. N Engl J Med 342:1334, 2000 [PMID:10793167] This topic is based on Harrisons Principles of Internal Medicine, 17th edition,chapter 262 Acute Respiratory Distress Syndrome by BD Levy and SD Shapiro.

Anda mungkin juga menyukai