Since FLUS is used in critically ill patients in a variety of settings (e.g. prehospital, ED, ICU, OR) it may not always be possible to perform a standardised FLUS examination.
By using FLUS in a standardised and systematic approach, however, the examination still has a very high feasibility and the diagnosis and exclusion of important diagnoses such as pneumothorax, pleural effusion and interstitial syndrome can often still be made.
Normally B-mode is sufficient when performing FLUS.
Other modalities such as M-mode or colour Doppler can be used in some cases where there is doubt whether lung sliding is present or not (see lesson on pneumothorax).
Some patients with respiratory emergencies can not be placed in a supine position due to dyspnoea.
Anterior, lateral and posterior surfaces are then scanned with the patient in the sitting position.
In comparison, some critically ill patients may not be able to sit up for the assessment of the posterior zones.
The posterior surfaces can then either be scanned with the patient lying on the side or alternatively the transducer can be inserted in between the mattress and the patient making it possible to scan at least a part of the posterior surface.
Once the anterior and lateral surfaces have been scanned, the patient is asked to sit up and the squares on the posterior surface are scanned using the same principles as described for the anterior and lateral surfaces.
Again in each scanning zone it is noted whether pneumothorax, pleural effusion or multiple B-lines are present or whether only normal findings are present.
With the patient in the supine position the transducer is quickly placed in each of the scanning squares.
The transducer is placed in a longitudinal axis over an intercostal space.
In each square it is noted whether pneumothorax, pleural effusion or multiple B-lines are present or whether only normal findings are present.
As with other kinds of sonography, FLUS findings cannot stand alone and should be used as an adjunct to clinical assessment and other diagnostic modalities
Presence or absence of the interstitial syndrome is a powerful tool with both a high sensitivity and specificity for ruling in and ruling out pulmonary edema in patients with acute dyspnoea
The interstitial syndrome has many causes why it is less specific in some settings such as a intensive care unit
In ARDS the changes found with LUS are not necessarily gravity dependent
Hence, the number of B-lines are not necessarily most pronounced in the dependent part of the lungs
Furthermore, spared areas with no B-lines are often seen
As in interstitial lung disease, in ARDS the visceral pleura is also often affected, and therefore in areas can appear thickened and fragmented
Not all interstitial lung disease causes interstitial syndrome
In interstitial lung disease the pulmonary changes are not gravity dependent, hence the number of B-lines are not necessarily most pronounced in the dependent part of the lungs
Furthermore, spared areas with no B-lines are often seen
In interstitial lung disease, such as idiopathic pulmonary fibrosis, the visceral pleura is also affected
The visceral pleura therefore in some areas can appear thickened and fragmented which is often not the case in simple pulmonary edema
LUS cannot differentiate between cardiogenic and non-cardiogenic pulmonary edema
Supplementary focused assessed transthoracic echocardiography (FATE) is an ideal tool which can be used to assess whether interstitial syndrome is of cardiogenic origin or not
In both cardiogenic and non-cardiogenic pulmonary edema the grade of increased density of the lungs are most severe on the posterior surface of the lungs compared to the anterior surface (if the patient has been lying down)
The number of B-lines tend to be higher more posteriorly than anteriorly and there are no sparred areas with no B-lines in the dependent regions of the lungs
The visceral pleura are not affected by pulmonary edema and the pleural line therefore appears normal.
The video is of LUS of the right upper anterior quadrant (1R) of a patient with cardiogenic pulmonary edema
