Acute care and trauma Flashcards
Define acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) is a non-cardiogenic pulmonary oedema( caused by Increased vascular permeability) and diffuse lung inflammation syndrome that often complicates critical illness. The diagnosis of ARDS is based on fulfilling three criteria:
- Acute onset (within 1 week)
- Bilateral opacities/ infiltrates on chest x-ray
- PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O. 1
- Extra criteria :pcwp <19mmHg or a lack of clinical congestive heart failure.
If no risk factors for ARDS are present, then acute pulmonary oedema as a result of heart failure should be ruled out.[Dont understand]
Explain the aetiology / risk factors of acute respiratory distress syndrome
All the risk factors below lead to injury and/ or inflammation , which can lead to ARDS
-Sepsis
-Aspiration
-Pneumonia
blood transfusions
Multiple transfusions of blood products are associated with ARDS.
lung transplantation
acute pancreatitis
history of alcohol misuse
burns and smoke inhalation(inhalation injury)
drowning
- pulmonary contusion
- cardiopulmonary bypass
- fat embolism
- disseminated intravascular coagulation
WEAK:
drug overdose
cigarette smoking
[three phases are recognised during the evolution of ARDS: 1) an exudative early phase which results from diffuse alveolar damage and endothelial injury; 2) a proliferative phase which ensues about 7–14 days after the injury, incorporating repair of the damaged alveolar structure and re-establishment of the barrier function, together with proliferation of fibroblasts; 3) a fibrotic phase with chronic inflammation and fibrosis of the alveoli, which follows in some patients.]
Summarise the epidemiology of acute respiratory distress syndrome
Overall, 10% to 15% of patients admitted to the intensive care unit meet the criteria for ARDS, [2] [3] with an increased incidence among mechanically ventilated patients meeting the criteria for ARDS
Give the details of the pathophysiology of ARDS(Extra)
The pathophysiology of ARDS is complex and incompletely understood. [13] Early in the development of ARDS, the primary pathological finding is diffuse alveolar damage, although this is not seen uniformly in all patients. The diffuse alveolar damage leads to injury to the alveolar-capillary membrane, made up of type I and type II alveolar pneumocytes and capillary endothelial cells. The alveolar air spaces are subsequently flooded with proteinaceous oedema fluid, inflammatory cells (neutrophils and activated alveolar macrophages), and inflammatory mediators, including pro-inflammatory cytokines, lipid mediators, and oxidants. Epithelial injury may be severe, with necrosis and sloughing of the type I cells exposing the basement membrane. Fibrin deposition occurs along the denuded basement membrane, resulting in the hyaline membranes that are characteristic of diffuse alveolar damage. Injury to type II cells and alveolar flooding contribute to surfactant dysfunction. Mechanical ventilation with high pressures and high volumes may further injure the lung, contributing to the pro-inflammatory cytokine cascade. The early phase of ARDS manifests clinically as acute hypoxaemic respiratory failure with an increased alveolar-arterial oxygen gradient and poorly compliant lungs. Concomitant multiple organ failure may occur, particularly if the underlying cause of ARDS is sepsis. Right ventricular dysfunction is also common and is associated with worse outcomes.
After the acute onset of alveolar flooding and inflammation, some patients have rapid resolution and return to normal lung histology and function. Pulmonary oedema fluid is cleared by active transport of sodium and chloride across the alveolar epithelium. In other patients, this early exudative inflammatory phase progresses to a fibroproliferative phase. During this later phase, the lung develops organised fibrous tissue and collagen deposition, which leads to irreversible and sometimes catastrophic lung fibrosis. [12] This phase is characterised by continued respiratory failure, high minute ventilation, and poorly compliant lungs.
Recognise the presenting symptoms of acute respiratory distress syndrome
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Recognise the signs of acute respiratory distress syndrome on physical examination
presence of risk factors
low oxygen saturation
Low despite supplemental oxygen.
acute respiratory failure
Progressively worsening respiratory failure in the setting of critical illness.
Other diagnostic factors
COMMON HIDE ALL
critically ill patient
Patients developing ARDS are critically ill, often with multi-system organ failure.
dyspnoea
Dyspnoea is the most common presenting symptom.
increased respiratory rate
Respiratory rate >20 breaths per minute.
pulmonary crepitations
Pulmonary crepitations on auscultation are common and typically diffuse. [24]
low lung compliance
Measured by tidal volume/(plateau pressure minus PEEP).
fever, cough, pleuritic chest pain
These symptoms are often present, particularly if the underlying cause of ARDS is pneumonia.
UNCOMMON HIDE ALL
frothy sputum
Presence of cough productive of frothy sputum, or frank pulmonary oedema that may be blood-tinged.{Develop on this]
Identify appropriate investigations for acute respiratory distress syndrome and interpret the results
VIEW ALL
chest x-ray
TEST:
New onset of bilateral opacities that is not fully explained by effusions, lobar/lung collapse, or nodules is part of the clinical diagnostic criteria for ARDS. [1] Therefore, chest x-ray is 100% sensitive.
Specificity is poor because other conditions may cause bilateral pulmonary infiltrates, including cardiogenic pulmonary oedema and diffuse alveolar haemorrhage.
RESULT:
Bilateral infiltrates
TEST
A PaO₂/FiO₂ (inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O is part of the diagnostic criteria for ARDS. [1]
It is 100% sensitive, but specificity is poor because many other conditions can cause hypoxaemia.
RESULT:
low partial oxygen pressure
sputum culture
TEST:
Sputum cultures are recommended to test for any possible underlying infection (as sepsis is the most common cause of ARDS).
RESULT:
positive if underlying infection
blood culture
TEST:
Blood cultures are recommended to test for any possible underlying infection (as sepsis is the most common cause of ARDS).
RESULT:
positive if underlying infection
urine culture
TEST:
A urine culture is recommended to test for any possible underlying infection (as sepsis is the most common cause of ARDS).
RESULT:
positive if underlying infection
amylase and lipase
TEST:
Serum amylase and lipase, in conjunction with clinical assessment, can be used to help establish whether the patient has acute pancreatitis, a common cause of ARDS. [42] Both tests have similar sensitivity and specificity but lipase levels remain elevated for longer (up to 14 days after symptom onset vs. 5 days for amylase). [43] Its prolonged elevation creates a wider diagnostic window than amylase.
RESULT:
amylase and/or lipase 3 times the upper limit of the normal range in cases of acute pancreatitis
Investigations to consider VIEW ALL brain natriuretic peptide (BNP) TEST:
BNP levels <100 nanograms/L (<100 picograms/mL) make heart failure unlikely and thus ARDS more likely.
BNP levels >500 nanograms/L (>500 picograms/mL) make heart failure likely and thus ARDS less likely.
BNP levels between 100 and 500 nanograms/L (100 and 500 picograms/mL) are indeterminate.
BNP levels may be difficult to interpret in patients with acute or chronic kidney failure. However, BNP levels should be <200 nanograms/L (<200 picograms/mL) in patients without heart failure with estimated glomerular filtration rate <60 mL/minute.
RESULT:
BNP levels <100 nanograms/L (<100 picograms/mL)
echocardiography
TEST:
Abnormal left ventricular systolic or diastolic function suggests cardiogenic pulmonary oedema rather than ARDS.
Some patients may have both ARDS and cardiac dysfunction.
RESULT:
usually normal
pulmonary artery catheterisation
TEST:
PAOP ≤18 mmHg suggests ARDS.
Pulmonary artery catheterisation should not be used routinely to manage patients with ARDS.
Can be used to determine whether pulmonary oedema is cardiogenic if the diagnosis is still in doubt after measuring BNP levels and carrying out echocardiography.
Some patients can have an increased left ventricular end-diastolic pressure superimposed on ARDS. For this reason, PAOP measurements are no longer included in the definition of ARDS. [1]
In the ARDS Network FACTT trial, approximately 20% of patients had an initial PAOP >18 mmHg, although elevations >24 mmHg were unusual. [37]
RESULT:
pulmonary artery occlusion pressure (PAOP) ≤18 mmHg
bronchoalveolar lavage or endotracheal aspirate
TEST:
Recommended in patients with suspected pneumonia and patients without a defined predisposing condition, to exclude a non-infectious parenchymal lung disease.
RESULT:
identification of infectious pathogens; characteristic findings of alternative diagnoses
CT scan of the thorax
TEST:
CT scanning of the thorax is not routinely required to diagnose or manage ARDS. A CT scan provides more information than a plain chest x-ray and may be helpful in some cases for diagnosing pneumonia or another underlying lung disease.
RESULT:
may be helpful in identifying pulmonary causes of ARDS such as pneumonia
