QuestionSBA
QuestionChoice
Severe pneumonia can present within 48hrs and can be precipitated by poor inspiratory effort from abdominal pain, resulting in mucous plugging, atelectasis, and poor clearing of secretions. Often to develop into fulminant chest sepsis, the patient either has an acute precipitant e.g. aspiration, is immunosuppressed, or has poor residual lung function. This patient does not have evidence of these from the information above and so pneumonia would be a less likely cause of rapid respiratory deterioration in a patient with pancreatitis. The patient's chest x-ray shows interstitial fluid from pulmonary oedema and small bilateral pleural effusions, providing further evidence of acute respiratory distress syndrome over pneumonia
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Severe bilateral lobar pneumonia
QuestionChoice
The patient has signs and symptoms of acute pulmonary oedema. Differentiating between cardiogenic and non-cardiogenic pulmonary oedema can be challenging, although the patient's history, cardiac history, fluid balance, and echocardiography signs can provide useful information. This patient has no cardiac history and has only been resuscitated with 2L intravenous fluid per day for two days with only mild pedal oedema on examination. It is unlikely that the pulmonary oedema is cardiogenic based on this information, and given the history of acute pancreatitis, acute respiratory distress syndrome is more likely
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d
Fat embolism syndrome
QuestionChoice
The patient has signs and symptoms of acute pulmonary oedema. Differentiating between cardiogenic and non-cardiogenic pulmonary oedema can be challenging, although the patient's history, cardiac history, fluid balance, and echocardiography signs can provide useful information. This patient has no cardiac history and has only been resuscitated with 2L intravenous fluid per day for two days with only mild pedal oedema on examination. It is unlikely that the pulmonary oedema is cardiogenic based on this information, and given the history of acute pancreatitis, acute respiratory distress syndrome is more likely
33204
b
Acute cardiogenic pulmonary oedema
QuestionChoice
Acute interstitial pneumonitis (AIP) presents as acute respiratory distress and is the only acute form of idiopathic interstitial pneumonitis. It has a similar presentation and chest x-ray appearance as ARDS due to extensive diffuse alveolar damage. It usually occurs following a prodromal viral upper respiratory tract infection and then 1-2 weeks later rapidly progresses into respiratory failure. It is a very rare disease, not associated with pancreatitis, and is therefore a less likely cause of this patient's deterioration than ARDS
33207
e
Acute interstitial pneumonitis (Hamman-Rich syndrome)
QuestionChoice
This patient has presented with an acute respiratory deterioration on a background of acute pancreatitis. Examination findings and chest x-ray point to pulmonary oedema as the likely cause. The patient has no cardiac history and has been resuscitated with 2L intravenous fluid per day. It is unlikely that the pulmonary oedema is cardiogenic based on this (although is common as patients with pancreatitis are often given aggressive fluid resuscitation). The most likely cause of this patients rapid deterioration and new florid pulmonary oedema is acute respiratory distress syndrome (ARDS) secondary to acute pancreatitis. The patient will likely be in the initial exudative phase of ARDS, characterised by diffuse alveolar damage, microvascular injury, type I pneumocyte necrosis, and influx of inflammatory cells. The mechanism of this is likely a consequence of systemic inflammatory response with increased endothelial and epithelial barrier permeability, resulting in leakage of protein-rich substances into the alveolar space and interstitial tissues. Increased cytokines and chemokines result in increased pulmonary infiltration of neutrophils into the interstitial tissue where they cause breakdown of pulmonary parenchyma
33203
a
Acute respiratory distress syndrome
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why does ards cause leg oedema
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# Summary

Acute respiratory distress syndrome (ARDS) is a syndrome of non-cardiogenic pulmonary oedema and diffuse lung inflammation, which may be secondary to a lung injury or systemic illness. Key signs and symptoms include acute onset respiratory failure, severe dyspnoea, tachypnoea, confusion, and presyncope (crucially, not explained by heart failure or volume overload). Key investigations include chest X-ray and CT showing bilateral alveolar infiltrates, and ABG to assess oxygenation. Management involves treating the underlying cause, and supportive management usually in an intensive care setting. This may involve intubation and ventilation, maintaining cardiac output with haemodynamic support, DVT prophylaxis, nutritional support and regular repositioning to prevent pressure ulcers.

# Definition

Acute respiratory distress syndrome (ARDS) is defined as acute lung damage leading to non-cardiogenic pulmonary oedema, with a wide variety of potential causes. The pathophysiology involves diffuse alveolar damage with hyaline membrane formation. Mortality is around 50%, with many survivors developing fibrotic lung disease.

**Criteria:**

The Berlin criteria are used to determine if a patient has ARDS - they need to have all of the following:

* Acute onset (< 1 week)
* Chest X-ray shows bilateral opacities
* Decreased ratio of arterial to inspired oxygen concentrations (PaO₂/FiO₂) ≤300


# Pathophysiology

ARDS is an acute form of respiratory failure occurring within one week of a trigger. It involves diffuse bilateral alveolar injury, with endothelial disruption and leakage of fluid into the alveoli from pulmonary capillaries. There is also a decrease in surfactant production, although it is important to differentiate ARDS from neonatal respiratory distress syndrome which is caused by insufficient lung surfactant production due to prematurity.

# Aetiology

Common causes of ARDS include:

- Sepsis
- Pneumonia
- Aspiration
- Pancreatitis
- Major trauma

Other causes include:

- Fat embolism
- Drowning
- Burns
- Transfusion reactions (transfusion-related acute lung injury)
- Drug overdose
- Disseminated Intravascular Coagulation (DIC)

# Signs and Symptoms

Patients with ARDS present with acute onset respiratory failure which progressively worsens, often with an identifiable trigger such as trauma or critical illness.

Symptoms include:

- Severe dyspnoea
- Tachypnoea
- Confusion and presyncope (secondary to hypoxia)

Patients are critically unwell, often with multiorgan failure, and appear in respiratory distress. Commonly there will be diffuse crepitations on auscultation of the chest.


# Differential Diagnosis

The differential diagnosis of ARDS includes other causes of acute respiratory failure in an unwell patient:

- **Cardiogenic pulmonary oedema** (i.e. acute heart failure): suspect this in patients with a history of cardiac disease or acute myocardial infarction, chest X-ray may show cardiomegaly, BNP levels will be raised and an echocardiogram can help to differentiate this from ARDS.
- **COVID-19**: many patients with severe pneumonia secondary to COVID-19 may meet the criteria for ARDS and they present similarly with no difference in imaging findings.
- **Bilateral pneumonia**: patients may have the same signs and symptoms as in ARDS with severe pneumonia but may not meet the criterion for severe hypoxaemia (low oxygen levels in the blood).
- **Diffuse alveolar haemorrhage**: patients can bleed into the airways for a range of reasons, including vasculitis, mitral stenosis, lupus and medications. This can be differentiated from ARDS as bronchoalveolar lavage will be bloody.


# Investigations

- Respiratory viral swab: looking for COVID-19, Influenza and other possible viral triggers.
- Sputum, blood and urine cultures: septic screen for any triggering infection.
- Arterial blood gases: important to determine severity of hypoxaemia.
- Serum amylase: screening for pancreatitis (common cause of ARDS)
- Chest X-ray: bilateral alveolar infiltrates without other features of heart failure (such as cardiomegaly and Kerley B lines).

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- CT chest: can further characterise changes found on X-rays and may show evidence of an underlying pulmonary disease causing the ARDS (e.g. pneumonia).

# Management

Identification and treatment of the underlying cause is key, for example antibiotics if sepsis is suspected. Patients are usually treated in an intensive care setting, as most require intubation and ventilation.

**Key points to consider in management are:**

- Ventilatory support using a “protective strategy” - for example, using low tidal volumes to limit trauma to damaged lungs, consider proning to improve oxygenation.
- Haemodynamic support - aim for a mean arterial pressure (MAP) > 60mmHg, transfuse if haemoglobin < 70 to maintain oxygen delivery.
- Nutritional support - the enteral route is preferred e.g. via an NG tube.
- Regular repositioning to help prevent pressure ulcers.
- DVT prophylaxis whilst immobile.
- PPI cover to prevent gastric ulceration (common in critically unwell patients).


# References
[Patient UK - ARDS](https://patient.info/doctor/acute-adult-respiratory-distress-syndrome)

[Radiopaedia - ARDS](https://radiopaedia.org/articles/acute-respiratory-distress-syndrome-1?lang=gb)
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The appearance of ARDS on a chest x-ray.
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Acute respiratory distress syndrome
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Respiratory Physiology
Acute respiratory distress syndrome
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Respiratory Physiology
A 54-year-old woman with severe gallstone pancreatitis is reviewed after 2 days of worsening condition, now requiring oxygen. She received 4L IV fluids over 48 hours for nausea and vomiting, with examination findings showing intravascular depletion of fluid.


She has no known cardiac history


On examination her respiratory rate is 35, peripheral oxygen saturations 94% on 10L (40%) Venturi mask, heart rate 115, blood pressure 105/58, temperature 35.6°C.

Respiratory exam reveals diffuse bilateral coarse crepitations and reduced bibasal air entry. Mild pedal oedema extends to the knees. Abdominal exam shows epigastric guarding with mild distension; her abdomen is otherwise soft and non-tender.

Portable chest x-ray is shown below

Which of the following is the most likely diagnosis?
a