Chest guideline of ARDS
In 1994, a European/North American consensus conference agreed on standard
definitions of ARDS and a less severe illness, acute lung injury (ALI). TABLE 1
I. Definition
A. Acute onset (most patients develop ARDS within 5 days of their acute event);
B. PaO2/FiO2≦ 200 mmHg (regardless of PEEP level);
C. Bilateral infiltration seen on frontal chest radiograph;
D. Pulmonary artery wedge pressure≦ 18 mmHg or no clinical evidence of left
atrial hypertension.
II. Etiology TABLE 2
A. Most common diagnoses associated with ARDS are sepsis, trauma, aspiration of
gastric content, pancreatitis, drug overdose, hyprtransfusion of blood products.
B. Approximately 20% of patients with ARDS have no identified risk factor.
III. Clinical Presentation
The history is generally remarkable for evidence of the precipitating event.
A. Symptoms and sings
Cough, Dyspnea, Tachypnea, Cyanosis, Crackles, Fever.
B. Lab Studies
1. No definitive laboratory tests aid in the diagnosis of ARDS.
2. Arterial blood gases (ABGs)
a. Respiratory alkalosis and hypocarbia is an early sign of respiratory distress.
b. Hypercarbia and hypoxemia develops with worsening disease, reflecting an
increasing shunt fraction and an increased dead space.
C. Radiology study
1. CXR
With disease progression, both lung fields become more diffusely and
homogeneously opaque.
2. Chest CT
a. Reveals patchy areas of dense infiltrates and areas of normal appearing lung
tissue.
b. Posterior and gravitationally dependent areas of the lung are more infiltrated
than nondependent areas.
3. MRI
No data exist concerning the role of MRI in imaging of patients with ARDS.
D. Sonography study
1. Chest ultrasonography
The only role is to define the presence of pleural effusions.
2. Echocardiography
a. Estimate left ventricular end diastolic pressure;
b. May provide evidence of pulmonary hypertension.
IV. Diagnosis
Meet ARDS definition criteria by history (etilology), CXR, ABGs and PAWP
(Swan-Ganz catheter) data.
V. Differential Diagnosis TABLE 3
A. Pneumonia;
B. Pulmonary thromboembolism;
C. Alveolar proteinosis;
D. Congestive heart failure.
VI. Management
No treatment for ARDS is definitive. The cornerstone of management is impeccable
intensive care.
A. Treat the primary cause (eg, sepsis, pneumonia) if possible.
B. Prevent sepsis, stress ulcers, multiple organs failure if possible.
C. Correct hypoalbuminemia, electrolytes imbalance, anemia, bleeding diathesis.
D. Reduce edema and lung fluid
PCWP should be decreased to the lowest level (8-12 cmH2O) without
compromising LV function, tissue perfusion or urine output.
E. Diet
1. The standard practice of introducing early enteral feeds when possible;
2. 25-30 kcal/kg, protein 1.5 g/kg;
3. Eicosapentaenoic acid, gamma-linolenic acid, and antioxidants is associated
with a reduction in pulmonary neutrophil recruitment, improved gas exchange,
decreased requirement for mechanical ventilation, reduced length of ICU stay,
and a reduction of new organ failures.
F. Ventilator strategies FIGURE 1
Ventilation is the cornerstone of management of the patient with ARDS.
1. Goal of ventilation
a. Keep SaO2≧ 90%;
b. Keep the FiO2＜60% to minimize the risk of oxygen toxicity.
2. Lower tidal volume (Vt)
a. Lower Vt (6ml/kg) has been shown to improve mortality and ventilatorfree days for ALI or ARDS.
b. Limitation of airway pressures to a maximum inflation pressure that should
not exceed 30 to 35 cmH2O.
c. If Pplat＞30 cmH2O, decrease tidal volume by 1 ml/kg steps to 5 or 4 until
Pplat＜30 cmH2O.
3. Arterial oxygenation and pH
a. Oxygenation goal
(1) keep PaO2≧ 55-88 mmHg or SpO2≧ 88-95%;
(2) use FiO2/PEEP combinations to achieve oxygenation goal;
FiO2 0.3 0.4 0.4 0/5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0
PEEP 5
5
8
8 10 10 10 12 14 14 14 16 18 20-24
b. pH goal is 7.30-7.45
(1) If pH≧7.45
(a) Decrease set rate until patient rate＞set rate;
(b) Minimal set rate＝6/min;
(2) If pH 7.15-7.30
(a) Increase set rate until pH＞7.30 or PaCO2＜25 (maximal set rate＝
35/min);
(b) If set rate＝35/min and pH＜7.30, NaHCO3 may be given (not
required).
(3) If pH＜7.15
(a) Increase set rate to 35/min;
(b) If set rate＝35/min and pH＜ 7.15 and NaHCO3 has been
considered, tidal volume may be increased in 1 ml/kg steps until pH
＞7.15 (Pplat target may be exceeded).
4. Permissive hypercapnia
a. The most direct way to implement this form of lung protective strategy is
to set the Vt at 4-8 ml/kg.
b. Complications include acidosis, hyperkalemia, increased cerebral blood
flow, seizures, coma, and arrhythmia.
c. It is not advisable to use permissive hypercapnia in patients with IICP.
5. PEEP
a. Theoretically, PEEP increases lung volume at end expiration, thereby
increasing functional residual capacity (FRC).
b. Use of PEEP in improving oxygenation should be increased b increments of
3-5 cm, and its effects should be evaluated clinically (BP, urine output, lung
compliance) or hemodynamically (maximization of oxygen delivery at an
acceptable FiO2).
6. Volume-cycled vs pressure-controlled ventilation
a. No differences in PaO2 or PaCO2 when ALI/ARDS patients received
ventilation with volume-cycled vs pressure-controlled modes at constant
tidal volume, end-expiratory alveolar pressure, and ratio of the duration of
inspiration to the duration of expiration.
b. Volume-cycled modes provide greater control over tidal volume, which
is an important determinant of ventilator-associated lung injury.
E. Positioning
1. By turning patients prone, ventilation perfusion matching is thought to be
optimized by reducing the degree of atelectasis in dependent areas of the lung.
2. Improving gas exchange, oxygenation, resulting from prone positioning.
3. No improving survival benefit.
G. Steroids
Steroids may be beneficial when used in the fibroproliferative phase.
H. Surfactant
No benefit on oxygenation, duration of mechanical ventilation and survival.
I. Nitric oxide
1. Specific pulmonary vasodilator for persistent pulmonary hypertension.
2. Reduce right-sided pulmonary pressures, improving cardiac output that
transient improving oxygenation benefits.
3. No improving on mortality rate, ventilator-free days, or time to extubation.
J. Liquid ventilation
1. Perfluorocarbons (PFCs) which may improve V/Q matching because both
oxygen and carbon dioxide dissolve easily in PFC liquid.
2. No eveidence of improving survival.
VII. Further Inpatient Care
A. Weaning and Extubation
As MMH ICU weaning protocol.
VIII. Prognosis
A. Mortality
1. Many studies have reported data demonstrating a mortality rate in patients
with ARDS of 30-40%;
2. Higher up to 90%, if multiple organ failure or severe sepsis were developed.
B. Morbidity
1. Pulmonary complications
The most common are the air leak syndromes, frequently pneumothorax but
also pneumomediastinum, pneumopericardium, pneumoperitoneum, and
subcutaneous emphysema.
2. Extrapulmonary complication
Multiple organs failure, nosocomial infection, stress ulcers, adrenal
insufficiency, glucose intolerance, seizure, myopathy.
IX. References
1. Textbook of respiratory medicine 4th, chapter 92,
page 2413-2442 Murray
2. Harrison’s principles of internal medicine 15th,
chapter 265, page 1523-1526
3. Cecil textbook of medicine 21st, chapter 88 page 467-475
4. ARDSnet (www.ardsnet.com)
5. The acute respiratory distress syndrome. N Engl J
Med 2000; 342:1334–1349
6. Treatment of ARDS. CHEST 2001; 120:1347–1367
7. Selecting the right level of PEEP in patients with
ARDS. Am J Respir Crit Care Med 2002; 165:1182–1186
Table 1: Recommended Criteria for Acute Lung Injury (ALI) and Acute Respiratory
Distress Syndrome (ARDS)
Timing Oxygenation
Chest Radiograph
ALI
Criteria
Acute
onset
Bilateral infiltrates
seen on frontal
chest radiograph
ARDS
Criteria
Acute
onset
PaO2/FIO2≦
300 mmHg
(regardless of
PEEP level)
PaO2/FIO2≦
200 mmHg
(regardless of
PEEP level)
Bilateral infiltrates
seen on frontal
chest radiograph
Pulmonary Arterial
Occlusion Pressure
≦18mmHg when
measured or no clinical
evidence of left atrial
hypertension
≦18 mmHg when
measured or no clinical
evidence of left atrial
hypertension
Table 2: Conditions That May Lead to the Acute Respiratory Distress Syndrome
Direct injury to lung
Indirect lung injury
Aspiration of gastric contents
Diffuse pulmonary infection
Near drowning
Pulmonary contusion
Toxic inhalation
Sepsis syndrome
Severe nonthoracic trauma
Hypertransfusion
Pancreatitis
Cardiopulmonary bypass
Table 3. OVERLAPPING FEATURES OF ARDS AND OTHER CAUSES OF
ACUTE RESPIRATORY FAILURE
Feature
ARDS
Left-Heart Failure
Pneumonia
Fever, leukocytosis
Yes
Possible
Yes
Pulmonary
Embolism
Yes
Bilateral infiltrates
Yes
Yes
Possible
Unlikely
Pleural effusions
Unlikely
Yes
Possible
Possible
Wedge pressure
Normal
High
Normal
Normal
High
Low
High
High
Lung lavage protein