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Non Cardiogenic Pulmonary Oedema
Non Cardiogenic Pulmonary Oedema
Definition
It is a clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure. There is diffuse inflammatory injury of the lungs which is an EXPRESSION of various diseases and is not a specific disease entity in and of itself. It is oftenbut not alwaysaccompanied by inflammatory injury of other organ systems. Inflammatory cells and proteinaceous fluid accumulate in the alveolar spaces leading to a decrease in diffusing capacity and hypoxemia.
Common
Aspiration pneumonia Pneumonia
Common
Sepsis Severe trauma Shock
Less common
Inhalation injury Pulmonary contusions Fat emboli Near drowning Reperfusion injury
Less common
Acute pancreatitis Cardiopulmonary bypass Transfusion-related TRALI Disseminated intravascular coagulation Burns Head injury Drug overdose
Etiology
ARDS - PATHOGENESIS
Insult (direct or indirect)
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant
Stages contd
3. Resolution and Recovery: The lung reorganizes and recovers. Lung function may continue to improve for as long as 6-12 months and sometimes longer, depending on the precipitating condition and severity of the injury Some experts recognize a fourth phase of ARDS. This is the period longer than 6-12 months after onset, when some patients experience continued health problems caused by the acute illness. These problems may include cough, limited exercise tolerance and fatigue. Others experience anxiety, depression and flashback memories of their critical illness, which are very similar to post-traumatic stress disorder.
Differential Diagnosis
CARDIOGENIC PULMONARY EDEMA Bronchopneumonia Hypersensitivity pneumonitis Pulmonary hemorrhage Acute interstitial pneumonia (Hamman-Rich Syndrome)
Non-Cardiogenic Infiltrates are more homogeneous No pleural effusions No Kerley Bs Radiographic evidence lags behind clinical signs and symptoms (i.e. the CXR is unimpressive given the degree of hypoxemia)
Diffuse Bilateral patchy infiltrates homogenously distributed throughout the lungs. Positive tube sign. No Kerley Bs.
No septal thickening. Diffuse alveolar infiltrates. Atelectasis of dependent lobes usually seen.
Investigations
Blood: CBC, U&E, Amylase, Coagulation, CRP, Blood cultures. ABG CXR Pulmonary artery catheter to measure PCWP (Pulmonary capillary wedge pressure)
Management of ARDS
Admit to ICU Treat underlying illness
Sepsis, etc
Nutrition Supportive care (respiratory support, circulatory support) DVT prophylaxis GI prophylaxis Medications Avoid complications (such as ventilator associated lung injury)
Respiratory support
In early ARDS, CPAP with 40-60% O2 may be adequate to maintain oxygenation. However, most patients need invasive ventilation Indications for ventilation: PaO2<8.3kPa despite 60% O2 A low tidal-volume, pressure limited approach, with either low or moderate high PEEP improves the outcomes
PEEP
Setting a PEEP prevents further lung injury due to shear forces by keeping airways patent during expiration
ARDS-net 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
Circulatory support
Invasive haemodynamic monitoring Conservative fluid management approach improves outcomes Inotropes to maintain Cardiac output and O2 delivery
Fluid management
Dry lungs are happy lungs ARDSnet RCT of 1000 patients (FACTT), Conservative vs liberal fluid strategy using CVP or PAOP (Pulmonary artery occlusion pressure) monitoring to guide, primary outcome: death. Conservative fluids
Improved oxygenation More ventilator-free days More days outside ICU No increase in shock or dialysis No mortality effects
Swan-Ganz Catheter
FACTT
Result: No difference in mortality, number of days on the ventilator or in the ICU, lung or kidney function, rates of hypotension, ventilator settings or use of dialysis between two groups. The PAC group had twice as many catheter-related complications (mainly arrhythmias).
ARDS Clinical Trial Network. 2006. Pulmonary-Artery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury. N Engl J Med. 354 (21). pp 2213-24.
Drug therapy
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
Surfactant
Multicenter trial, 725 patients with sepsis-induced ARDS, surfactant had no effect on 30-day survival, ICU LOS, duration of mechanical ventilation or physiologic function
ARDS - Prognosis
Improved survival in recent years mortality was 50-60% for many years, now 25-40% Improvements in supportive care, newer ventilatory strategies Early deaths (3 days) usually from underlying cause of ARDS Later deaths from nosocomial infections, sepsis, MOSF Severity of gas exchange at admission does not correlate with mortality Respiratory failure only responsible for ~16% of fatalities Long-term survivors usually show mild abnormalities in pulmonary function (DLCO), impaired neurocognitive function
Summary
ARDS is a clinical syndrome characterized by severe, acute lung injury, inflammation and scarring Significant cause of ICU admissions, mortality and morbidity Caused by either direct or indirect lung injury Mechanical ventilation with low tidal volumes and plateau pressures improves outcomes So far, no pharmacologic therapies have demonstrated mortality benefit Ongoing large, multi-center randomized controlled trials are helping us better understand optimal management
Thank you !
Barotrauma
Rupture alveolar membranes Pneuomothorax, pneumomediastinum
Sheer stress
Opening/closing alveoli Inflammatory reaction, cytokine release
Oxygen toxicity
Free radical formation
ARDS Network
NIH-funded consortium of 10 centers, 24 hospitals, 75 intensive care units Goal to design large RCTs to determine effective treatments Key ARDSnet studies:
Ventilator volumes Steroids PEEP Volume management/PA catheter
NEJM 2000;342:1301-8.
NEJM 2000;342:1301-8.