Noncritical Ultrasound, Within the ICU and Other Hot Settings

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Hôpital Ambroise Paré Service de Réanimation Médicale, Boulogne (Paris-West University), France

Electronic supplementary material

The online version of this chapter (doi:10.1007/978-3-319-15371-1_36) contains supplementary material, which is available to authorized users.

This textbook deals mostly with critical ultrasound. The real ultrasonic revolution will regard the whole population in countless settings, in several decades or hopingly sooner, used by all up to the family doctor. Noninvasive ultrasound should be liberally performed each time there is a question regarding a macroscopic item.

Here is a (non-limitative) list of situations. We apologize for those who would find this chapter quite heterogeneous, but things came as they came. Not the aim of this textbook, this chapter is just a kind of appetizer on how far this method can go.

Noncritical Ultrasound Inside the ICU

Weaning Issues: Only the Diaphragm on Focus?

Weaning is a hot topic currently. Physicians devote a high energy for assessing the diaphragmatic work, the left heart, especially the diastolic function [1, 2]. We try to simplify what can be simplified. A failure of weaning can be explained by other factors.

Diffuse interstitial changes. This is probably not a good condition for weaning, either from edema (fluid overload or inflammatory) or fibrosis.
Substantial pleural effusion. It should be withdrawn. The technique is the same as the one described in Chaps. 25 and 28.
Lung consolidations.
Pneumothorax.
Venous thrombosis, either from legs or recent catheters, may give small but iterative pulmonary embolism.
Peritoneal disorders (substantial effusion) may create a hyperpressure, hampering diaphragmatic course.
Maxillary sinusitis can generate pneumonia and keep it going.
Vocal cord edema, laryngeal edema are sources of post-extubation dramas (stridor). Stridor can complicate from 2 to 15 % of extubations [3]. The cuff-leak test has good negative predictive value but poor positive predictive value. The ultrasound air-column width measurement should identify high-risk patients.

All these disorders can be radioccult.

As to the diaphragmatic dysfunction, please read Anecdotal Note 1 of Chap. 21 on the excluded patients of the BLUE-protocol. We put here some notions in order not to frustrate those who find interest to this field. Just one technical word: getting interest to vascular (linear) probes only for this application would mean expenses for little benefit (especially since our microconvex probe makes the work). Here is the minimal we consider useful for assessing the diaphragm.

The Diaphragm: Why and How to Analyze It

Why

In critical ultrasound, we never paid a lot of attention to this muscle, although a vital one. Our feeling is that, once an operator is aware of the potentials of lung ultrasound, the diaphragm appears slightly less interesting (Anecdotal Note 1). Said differently, we would advise this teaching only after priority targets are under perfect control. We remind the principle of critical ultrasound: Since we are unable to repair a paralyzed diaphragm in the night, we just give oxygen with noninvasive ventilation, or more (intubation, etc.), to these patients. Following this concept, for keeping the book thin, we devote a modest place to its analysis. The diaphragm is a real image. This is reassuring for those who are scared by lung artifacts. Therefore, the diaphragm is familiar to many intensivists today. They want to know, mainly, if a given patient can be weaned.

We do not search for looking at the diaphragm itself. Which interesting features should emerge from its vision? Tumors? Of course not. Inspiratory thickening (in spontaneous ventilation)? If it moves, it should thicken (see if necessary the subtle Fig. 16.11 of our 2010 edition). Assessing its function does not require direct visualization, and little energy is devoted in this. Indirect signs work as well as direct ones, see below.

How

How to locate it is schematically given by the BLUE-points, allowing minimal energy. The lower finger of the lower hand locates it. Observing lung items at the left of the image and abdominal items at the right ensures correct phrenic location. A location of this boundary image above the defined landmarks (phrenic line) is pathological. This being said, for those who really want to see the very diaphragm, ultrasound is probably the best tool at the bedside (and maybe the only, fluoroscopy remaining an exceptional referral). It just requires some skill, i.e., more energy. The diaphragm is a part of circle of roughly 22 cm of diameter in standard adults, for helping novice users to figure it out (see Figs. 16.4, 16.5, 16.7, and 17.5). One can apply the probe laterally (phrenic point) or two intercostal spaces below the PLAPS-point, or even posteriorly when the patient is turned laterally. The amplitude is the same.

How to assess its dynamic?

The detection of a lung sliding allows immediate recognition of a correct diaphragmatic function. Note that lung sliding is an item of the BLUE-protocol. The lung slides because the diaphragm contracts (read again how lung sliding is explained in Chap. 10).

Lung rockets, if present, enhance this dynamic since our image is sectorial.

One can also look for hepatic or splenic podal inspiratory excursion, and giving the same dynamic information maybe easier to measure.

Therefore, we don’t require the presence of pleural effusions or atelectasis which are, according to some, necessary for a correct vision of the diaphragm. Care must be taken to be longitudinal. In spontaneous ventilation in a normal subject, or in conventional mechanical ventilation in a patient without respiratory disorder, the phrenic amplitude is roughly between 15 and 20 mm. A pleural effusion, even substantial, does not affect this amplitude even in mechanical ventilation.

A pathological diaphragmatic amplitude (using direct or indirect signs) is under 10 mm, for instance 5 mm, or null, or negative (paradoxical dynamic). Pleural symphysis, atelectasis, low tidal volume, neurological diseases, or abdominal hyperpressure explain a diminished or abolished phrenic amplitude. Phrenic palsy is a complication of cardiac or thoracic surgery and nerve blockade. It yields abolished lung sliding, elevated cupola, motionless cupola or paradoxical movement, absence of inspiratory thickening, for those who can assess this. For more information, read some excellent works [4, 5].

Outside the ICU

The Issue of Pulmonary Embolism in Standard Medicine

In many areas of medicine (internal medicine, emergency room, geriatrics, etc.), the spectrum of pulmonary embolism is an issue, quite an obsession. We have the feeling that the image of pulmonary embolism, which appears as a “monobloc disease,” can be split into several subtle boxes thanks to ultrasound. Four different situations can be indeed described:

Severe dyspnea or shock plus visible venous thrombosis: extreme risk for sudden death

Severe state without visible venous thrombosis: major risk for sudden death

Good tolerance with venous thrombosis: risk for sudden death

Good tolerance without visible venous thrombosis

This last situation is interesting. Let us consider, e.g., the case of a young woman with isolated basithoracic pain, seen in the ER. The fear of the doctor to see such patients suddenly die is familiar. Yet the (laudable) energy invested in this diagnosis would imply night aggressive helical CT (without premedication), blind night heparin therapy, or blind thrombolysis, plus the remote consequences of irradiation. For decades before the advent of CT, we had the risk of the highly invasive pulmonary angiography, done day or night. At these times, ultrasound was fully operational. There is a price to pay for this behavior [6–11].

The Grotowski law speculates that, a few seconds before sudden death occurs from a massive pulmonary embolism, there is always a voluminous, floating, iliocaval, highly unstable deep venous thrombosis – easy to detect using simple ultrasound, in a patient with no or little thoracic complaint. De la Palice was said to be still alive 5 min before his death (in the year 1525). Usually, 5 min before death, people are in extremely critical shock. For drama such as massive embolism, de la Palice was possibly right: following his philosophy, we consider that massive pulmonary embolism should be anticipated – i.e., what the CLOT-protocol (described in Chap. 28) makes.

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