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Acute respiratory distress syndrome (ARDS) (Diagnosis (Investigations…
Acute respiratory distress syndrome
(ARDS)
Clinical presentation
Cyanosis
Laboured breathing
Shortness of breath
Diagnosis
Examination
Resp: laboured breathing, tachycardia, tachypnoea, cyanosis, peripheral vasodilatation,
bilateral fine crackles or poor a/e
Investigations
Bedside
Obs: high RR, high HR, low sats
ECG: tachycardia
Bloods
ABG:
may show T1RF
FBC (infection), CRP (infection), U+E, LFT, bone, lactate
D-dimer
(PE),
amylase
(pancreatitis)
Blood cultures
(if suspected infection)
Swabs/samples
Sputum culture
Viral swabs e.g. COVID
Imaging
CXR: diffuse bilateral shadowing,
may progress to whiteout
(Radiopedia.org)
History
PC/HPC: sudden SOB, labroured breathing,
recent infection, trauma, or surgery/bypass
PMH: any HF, other lung pathology, previous ARDS
DH: current meds, inhalers, allergies
FH: lung disease, ARDS
SH: living arrangements, work, smoking
Diagnostic criteria
Acute onset
Bilateral infiltrates on CXR
Pulmonary capillary wedge pressure <19mmHg
or absence of cardiogenic pulmonary oedema
Refractoy hypoxaemia
Management
Conservative
Identify and treat underlying cause
ITU referral and admission
Medical
Haemofiltration
Indication: overload refractory to fluid restriction and diuretics
MOA: removal of excess fluid from vascular system
Diuretics
MOA: reduces overload by increasing diuresis
Fluid restriction
MOA: reduces overload
Prognosis
High mortality (30-40% die from sepsis and MOF)
Definition
Respiratory distress (acute lung failure/injury)
due to non-cardiogenic pulmonary oedema resulting in refractory hypoxemia
Pathophysiology
Vascular permeability
Inflammatory mediators increase vascular permeability
Intra-alveolar haemorrhagic exudate (platelets, fibrin, clotting factors)
Progressive lung changes
Exudate inactivates surfactant and causes inflammation
Results in pulmonary fibrosis and scarring
Vascular compresssion
Local oedema increases pressure in the the lung vasculature, causing pulmonary HTN
Increaed sympathetic drives causes vasoconstriction, further increasing pulmonary HTN
Aetiology
Lung
Vacular: embolism (fat, fluid etc)
Infection: pneumonia, COVID-19
Trauma: aspiration, lung contusion
Autoimmune: vasculitis
Systemic
Infection: sepsis, malaria
Trauma: burns, major haemorrhage, head injury
Iatrogenic: cardiopulmonary bypass
Metabolic: pancreatitis, acute liver failure
Drugs: aspirin, heroin, paraquat
Haematological: DIC, MOF
