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Distress Syndrome
Alice Gray, MD
Duke University Medical Center
March 21, 2007
Objectives
Pneumonia (34%)
Sepsis (27%)
Aspiration (15%)
Trauma (11%)
Pulmonary contusion
Multiple fractures
NEJM 2000;342,18:1334-1349
Risk factors for ARDS
Low serum pH
Sepsis
40% of patients with sepsis develop
ARDS
Differential diagnosis
Pulmonary edema from left BOOP or COP
heart failure Hypersensitivity
Diffuse alveolar hemorrhage pneumonitis
Acute eosinophilic Leukemic infiltrate
pneumonia Drug-induced pulmonary
Lupus pneumonitis edema and pneumonitis
Acute interstitial pneumonia Acute major pulmonary
Pulmonary alveolar embolus
proteinosis Sarcoidosis
Interstitial pulmonary
fibrosis
Excluding other diagnoses
Echo
Central venous catheter
NEJM 2000;342,18:1334-1349
Pathological findings
Hyaline membranes
Alveolar
Filling
Expansion of
interstitium with
macrophages and
inflammation
Hyaline
Membran
es
Fibroproliferative Phase
Persistent hypoxemia
Fibrosing alveolitis
Pulmonary hypertension
From obliteration of capillary bed
May cause right heart failure
Fibroproliferative phase
Chest xray shows linear opacities consistent with
evolving fibrosis
Pneumothorax in 10-13% of patients
CT: diffuse interstitial opacities and bullae
Histologically, fibrosis, mesenchymal cells,
vascular proliferation, collagen and fibronectin
accumulation
Can start 5-7 days after symptom onset
Not present in every patient with ARDS, but does
portend poorer prognosis
Fibroproliferative phase
NEJM 2000;342,18:1334-1349
Fibrosing alveolitis
NEJM 2000;342,18:1334-1349.
Recovery phase
Gradual resolution of hypoxemia
Hypoxemia improves as edema resolves via active
transport Na/Cl, aquaporins
Protein removal via endocytosis
Re-epithelialization of denuded alveolar space with
type II pneumocytes that differentiate into type I cells
Improved lung compliance
Chest xray and CT findings resolve
PFTs improve, often normalize
Management of ARDS
DVT prophylaxis
GI prophylaxis
Medications
Complications in Managing
ARDS patients
Mechanical ventilation causes:
Overdistention of lungs (volutrauma)
• Further damaging epithelium
• Increased fluid leak, indistinguishable from ARDS damage
Barotrauma
• Rupture alveolar membranes
• Pneuomothorax, pneumomediastinum
Sheer stress
• Opening/closing alveoli
• Inflammatory reaction, cytokine release
Oxygen toxicity
Free radical formation
ARDS Network
NEJM 2000;342:1301-8.
Positive End-Expiratory
Pressure (PEEP)
Titrate PEEP to decrease FiO2
Goal sat 88% with FiO2 <60%
• Minimize oxygen toxicity
PEEP can improve lung recruitment and decrease
end-expiratory alveolar collapse (and therefore
right-to-left shunt)
Can also decrease venous return, cause
hemodynamic compromise, worsen pulmonary
edema
ARDSnet PEEP trial of 549 patients show no
difference in mortality or days on ventilator with
high vs low PEEP
NEJM 2004:351(4):327-336
Other Ideas in Ventilator
Management
Prone positioning
May be beneficial in certain subgroup, but
complications including pressure sores
• RCT of 304 patients showed no mortality benefit
High-frequency oscillatory ventilation
In RCT, improved oxygenation initially, but results not
sustained after 24 hours, no mortality benefit
ECMO
RCT of 40 adults showed no benefit
Agents studied:
Corticosteroids
Ketoconazole
Inhaled nitric oxide
Surfactant
No benefit demonstrated
Steroids in ARDS
Earlier studies showed no benefit to early use steroids,
but small study in 1990s showed improved
oxygenation and possible mortality benefit in late stage
ARDSnet trial (Late Steroid Rescue Study “LaSRS” –
“lazarus”) of steroids 7+ days out from onset of ARDS
180 patients enrolled, RCT methylprednisolone vs
placebo
Overall, no mortality benefit
Steroids increased mortality in those with sx >14 days
JAMA 1998;280:159-65, N Engl J Med 2006;354:1671-84
Steroids in ARDS
NEJM 2006;354:2564-75.
Keys to management
Treat underlying illness
Supportive care
Low tidal volume ventilation
Nutrition
Prevent ICU complications
• Stress ulcers
• DVT
• Nosocomial infections
• Pneumothorax
• No routine use of PA catheter
Diuresis/avoidance of volume overload
Give lungs time to recover
Survival and Long Term
Sequelae
Traditionally mortality 40-60%
May be improving, as mortality in more
recent studies in range 30-40%
Nonetheless survivors report decreased
functional status and perceived health
79% of patients remember adverse events in
ICU
29.5% with evidence of PTSD
1 year after ARDS survival
Lung Function:
FEV1 and FVC were normal; DLCO minimally reduced
Only 20% had mild abnormalities on CXR
Functionally:
Survivors’ perception of health was <70% of normals
in:
• Physical Role: Extent to which health limits physical activity
• Physical Functioning: Extent to which health limits work
• Vitality: Degree of energy patients have
6 minutes walk remained low
Only 49% had returned to work