Acute Respiratory Distress Syndrome

A. Presentation

At early stage, pt may be asymptomatic, or only mildy tachypnic

 

Crackles at the bases on auscultation.

No signs of volume overload (S3, JVP)

 

B. Investigation

ABG

Respiratory alkalosis may be present at early stage.

Hypercarbia and respiratory acidosis at later stage.

FBC, U&E

Baseline tests and for sepsis

Blood culture

For sepsis

Coagulation

For liver/coagulation problems

CXR

Bilateral diffuse infiltrate

Absence of vascular redistribution

May be normal at early stage, but may rapidly progress to complete white-out of both lung fields.

C. Treatment

Initially

Cardiac monitor

Pulse-oximeter

Time-cycled BP cuff

IV access

   [Fluid if hypotensive.]

   [Volume overload may significantly worsen pulmonary oedema]

100% Oxygen

   [Keep SpO2>90%]

 

Later on

If SpO2<90% on O2, or fatigue or hypercarbia

---> Endotracheal intubation

If mechanical ventilation cannot keep SpO2>90%

---> Increase PEEP slowly

   [Higher airway pressure may decrease venous return and lead to hypotension]

PEEP (positive end-expiratory pressure) is very important as it helps minimising alveolar

 

Others

Routine or prophylatic use of antibiotics or corticosteriods ---> no proven benefit.

CXR changes, hypoxia, respiratory alkalosis ---> ICU admission.

D. Other notes

Mortality - 40 to 60%

 

Causes

Sepsis

Severe tramatic injury

•    Multiple fractures (esp long bone) [via fat embolism]
•    Head injury: via sympathetic overdrive, causing acute pulmonary hypertension
•    Pulmonary contusion

Multiple transfusion

   [Risk increases with the number of units used, and presence of liver disease or coagulation abnormality]

Near-drowning

   [More common after salt water aspiration than fresh water.]

   [Develops in 12-24 hours.]

   [Better prognosis if develops after 6 hours]

Smoke inhalation

   [via direct thermal damage, and chemical irritation]

Drugs

• Narcotics (classically heroin OD)
• Salycilates
• Tricyclic antidepressants
• Some sedatives
• Tocolytic agents
• Hydrochlorothiazide
• Protamine
• IL-2

 

Mechanisms

ARDS - pulmonary oedema in the absence of volume overload or depressed left ventricular function.

 

Injury results in loss of the integrity of the alveolar-capillary membrane and increased permeability to plasma

---> Fluid enters alveolar space, disrupting the function of pulmonary surfactant

---> Microatelectasis

---> V/Q mismatch and shunting of blood

 

Differential

Congestive Heart Failure and Pulmonary Oedema

Pneumonia

• Aspiration
• Bacterial
• Immunocompromised
• Mycoplasma

Irritant gas inhalation

 

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Things to revise/add later:

Bibliography: "eMedicine On The Go"

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