Acute Care and Trauma Flashcards
Define acute respiratory distress syndrome
a non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness.
Respiratory distress, stiff lungs and CXR findings (bilateral, diffuse, pulmonary infiltrates)
ARDS:
- acute onset (within 1 week)
- CXR bilateral shadowing
- PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on positive end-expiratory
Explain the aetiology / risk factors of acute respiratory distress syndrome
insult to the lungs or other organs causes release of inflammatory mediators, increased capillary permeability, pulmonary oedema, impaired gas exchange and decreased lung compliance.
Common causes include sepsis, aspiration, pancreatitis, trauma/burns, transfusion, transplantation and drug overdose/reaction.
Summarise the epidemiology of acute respiratory distress syndrome
5% of hospital patients
1/6000 in the UK population
Recognise the presenting symptoms of acute respiratory distress syndrome
unexplained tachypnoea and dyspnoea
Rapid deterioration of respiratory function, dyspnoea, respiratory distress, cough, symptoms of aetiology.
Recognise the signs of acute respiratory distress syndrome on physical examination
Cyanosis, tachypnoea, tachycardia, widespread inspiratory crepitations.
Hypoxia refractory to oxygen treatment.
Signs are usually bilateral but may be asymmetrical in early stages.
Identify appropriate investigations for acute respiratory distress syndrome and interpret the results
- CXR: Bilateral alveolar and interstitial shadowing.
Blood: FBC, U&E, LFT, ESR/CRP, amylase, clotting, ABG, blood culture, sputum culture. - Plasma BNP < 100 pg/mL may distinguish ARDS/ALI from heart failure, but higher levels can
neither confirm heart failure nor exclude ARDS/ALI in critically ill patients. - Echocardiography: Severe aortic or mitral valve dysfunction or # LVEF favours haemodynamic
oedema over ARDS. - Pulmonary artery catheterization: PCWP<18mmHg (however “ PCWP does not exclude ARDS as patients with ARDS may have concomitant left ventricular dysfunction).
- Bronchoscopy: If the cause cannot be determined from the history, and to exclude differentials, e.g. diffuse alveolar haemorrhage (frothy blood in all airways, haemosiderin- laden macrophage from lavage fluid), lavage fluid for microbiology (mycobacteria, Legionella pneumophila, Pneumocystis, respiratory viruses) and cytology (eosinophils, viral inclusion bodies and cancer cells).
Define acute kidney injury (AKI)
impairment of renal function resulting in increased urea and creatinine in the urine, and oligouria
Explain the aetiology / risk factors of acute kidney injury (AKI)
pre renal: shock (septic, hypovolaemic, cardiogenic),
renal: ATN (acute tubular necrosis), glomerulonephritis, acute interstitial nephritis, vessel obstruction (renal artery thrombosis)
Recognise the presenting symptoms of acute kidney injury (AKI)
malaise, anorexia, nausea, vomiting, coma (uaemia), confusion,
Recognise the signs of acute kidney injury (AKI) on physical examination
oedema and signs of causes
Identify appropriate investigations for acute kidney injury (AKI) and interpret the results
urine dipstick: haematuria, proteinuria
Generate a management plan for acute kidney injury (AKI)
d
Identify the possible complications of acute kidney injury (AKI) and its management
d
Summarise the prognosis for patients with acute kidney injury (AKI)
d