Urgent considerations
See Differentials for more details
Pulmonary embolism
A potentially life-threatening condition that can cause sudden death from hypoxaemia, shock, and haemodynamic compromise.
The clinical probability of pulmonary embolism (PE) in haemodynamically stable patients is assessed using a combination of the Pulmonary Embolism Rule-Out Criteria (the PERC rule), the Wells (or Geneva) score, plus D-dimer testing if indicated.[60][61][62][63][64] [ PERC Rule for the Assessment of Possible Pulmonary Embolism Opens in new window ] [ Pulmonary Embolism Wells Score Opens in new window ] [ Revised Geneva Score for Estimation of the Clinical Probability of Pulmonary Embolism in Adults Opens in new window ]
If there is a low clinical suspicion of PE, it can effectively be ruled out in any patient who meets the PERC rule.[63] If clinical suspicion of PE is high or the patient does not meet the PERC rule, the Wells or Geneva score can be used to categorise the patient as 'PE likely' or 'PE unlikely'.[60][64]
In haemodynamically stable patients with low or intermediate clinical probability of PE, D-dimer measurement is recommended to assess the need for laboratory. In patients with very low clinical probability of PE, D-dimer testing is reserved for those who do not meet the PERC rule.[63]
Those with a high clinical probability of PE, or with a positive D-dimer, should proceed immediately to computed tomographic pulmonary angiography (CTPA; or ventilation-perfusion [V/Q] lung scan if CTPA is contraindicated). In patients with high pretest probability of PE, anticoagulation should be initiated while awaiting laboratory results.[64][65]
Haemodynamically unstable patients require urgent primary reperfusion, anticoagulation, and supportive care.[65] CTPA is indicated in patients with suspected PE who are haemodynamically unstable at presentation provided it is immediately available and the patient is well enough to have it. In practice this is often not the case and echocardiography is used instead.
Cardiogenic pulmonary oedema
Acute cardiogenic pulmonary oedema results from increased end-diastolic left ventricular pressure and presents with dyspnoea worsened by exertion, orthopnoea and paroxysmal nocturnal dyspnoea, elevated neck veins, peripheral fluid retention, an S3 gallop rhythm on cardiac auscultation, and pulmonary congestion (fine bibasal rales) on chest auscultation. The patient may have a history of heart failure.
Typical chest x-ray features include characteristic signs of pulmonary venous congestion, and there may be cardiomegaly. Echocardiography may show atrial fibrillation and enables differentiation between systolic and diastolic heart failure, and estimation of left ventricular ejection fraction. Bedside ultrasound study showing B-lines strongly suggests acute pulmonary oedema in an appropriate clinical setting.[66]
A low B-type natriuretic peptide (BNP) level (<100 ng/L [<100 picograms/mL]) or a low N-terminal pro-BNP (NT-proBNP) level (<300 ng/L [<300 picograms/mL]) is helpful in excluding congestive heart failure.[67]
Depending on the specific aetiology of congestive heart failure, a combination of diuretic, pre-load and afterload reduction with nitrates, angiotensin-converting enzyme (ACE) inhibitors, and non-invasive mechanical ventilation can be used.
Tuberculosis
If tuberculosis (TB) is suspected clinically, the patient should be isolated, chest x-ray obtained, and 3 sputum samples sent for acid-fast bacilli smear and culture. Nucleic acid amplification tests should be performed on at least one respiratory specimen when a diagnosis of TB is being considered.[68] When clinical suspicion of TB is high, empirical treatment with a standard antimicrobial regimen is generally initiated after sputum samples are collected.
Acute idiopathic eosinophilic pneumonia
This can lead to respiratory failure. Initial neutrophilic leukocytosis precedes subsequent eosinophilia. Peripheral eosinophilia is rare at the time of presentation of acute idiopathic eosinophilic pneumonia. It resolves rapidly with corticosteroids.
Diffuse alveolar haemorrhage
Diffuse alveolar haemorrhage (DAH) may accompany collagen vascular disease and can be suggestive of Goodpasture's syndrome.[69][70] It is associated with increased mortality in patients with collagen vascular disease. Lupus pneumonitis can accompany life-threatening alveolar infiltrate. DAH and acute lupus pneumonitis are life-threatening conditions that present as alveolar infiltrations in systemic lupus erythematosus. The mainstay of the treatment of acute lupus pneumonitis is systemic glucocorticoids and other immunosuppressive drugs.[71] Patients with DAH require supportive management and treatment of the underlying cause. Potentially causative medicines should be discontinued, and any anticoagulant therapy should be stopped and reversed. DAH is often treated with high-dose intravenous methylprednisolone followed by a tapered oral corticosteroid. If there is no response, other immunosuppressive drugs (e.g., cyclophosphamide) should be considered.
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