The European and American consensuses9^,10 recommend measuring IMT in specific groups (Table 1). In these groups of individuals, IMT is considered increased when above the 75 percentile for their age, gender, and ethnicity, according to one of the normative tables, assisting in the discussion of clinical treatment and change in lifestyle. If a CP is found, regardless of the obstruction degree, IMT measurement does not need to be reported, except for exams explicitly requested for this purpose. In these cases, if the CP is located in the IMT measurement, it should be included in the value.

The recommended protocol is similar to the one described by the ELSA-Brasil study13 (Table 2).

After collecting numerical IMT data, the average values will be compared with existing reference numbers, according to normative tables of the studies ELSA Brasil,13 CAPS,14 or MESA.15 The decision about which table to use will depend on the gender, age, and ethnicity of the individual.

Although the manual point-to-point measurement is less reproducible - considering the differences in ultrasound equipment used in our country -, the consensus was that it could be used if the equipment does not automatically measure IMT, strictly respecting the technical recommendations. The examiner should pay special attention when placing the cursor in the intima-lumen and media-adventitia interfaces and be very cautious not to overestimate the values. In this case, measure each side at least five times to obtain the mean value (mean IMT).16

Mean IMT [mean of measurements in the right or left common carotid artery (RCCA and LCCA, respectively)]: most types of equipment provide this measurement automatically or semi-automatically (in the latter case, the examiner can make small adjustments based on the automatic one). After calculating the mean IMT values from each side, compare them to the table to find the equivalent percentile. The individual under study is classified in the highest percentile.

To determine the percentile of IMT measurement, consult tables 3 to 5, according to the age group of the individual under study.

Describe the mean IMT on each side, in mm, in the body of the report. Also, include in conclusion if the value is above or below the 75 percentile and the table used, with its bibliographic reference.

Inform the presence of carotid plaques, with their specific characteristics and quantification, according to the criteria recommended by the recent Brazilian consensus.1

The assessment of carotid stenosis with VUS is based on measurements of flow velocity and their relationships using spectral Doppler, associated with the evaluation of two-dimensional and color Doppler imaging. With the patient in the supine position, use transverse and longitudinal ultrasound planes that allow the visualization of the right and left carotid system.

Figure 3 shows the recommendation from DCI-BSC for the sequence of evaluation of carotid stenosis.

Figure 3

2.4.1.1. Quantification of Carotid Stenosis with Hemodynamic Parameters

Arterial flow velocity measured by Doppler is presented as flow velocity waveforms (spectrum) for each site examined. Wave characteristics depend on the type of local flow, as well as changes in blood velocity resulting from conditions proximal and distal to the measurement site. In the internal carotid artery (ICA), the resistance of flow velocity waveforms is usually of low. In the external carotid artery (ECA), the resistance of velocity waveform is high, while in the common carotid artery (CCA), it is intermediate between ICA and ECA13(Figure 4).

Figure 4

Measure the velocities in the proximal and distal segments of CCA. To evaluate the velocity ratio in the quantification of ICA stenosis, assess CCA at approximately 2 cm from the bifurcation, preferably in a rectilinear segment, without plaques.4 Analyze ICA in the proximal and middle segments, since atherosclerotic lesions usually affect the proximal 2 cm. The cursor must be parallel to the vessel wall, with a volume sample smaller than the lumen, and positioned in its center and toward the flow, so the insonation angle is ≤ 60º (Figure 5).1^,26

Figure 5

After identifying the stenosis with B-scan and/or color Doppler, document the spectral tracing in this point, and pre-stenotic and post-stenotic regions. The velocity evaluation given by the spectral tracing must include the peak systolic velocity (PSV) and end-diastolic velocity (EDV) in CCA and ICA. Systolic and diastolic velocities provide the following relationships (ratios): PSV ICA/PSV CCA, PSV ICA/EDV CCA, and EDV ICA/EDV CCA.

Subocclusions are diagnosed based on the narrowing of the vessel lumen using color/power Doppler, with thin flow (string sign or trickle flow); however, it might be associated with high, low, or undetectable velocities, which occasionally hinders the diagnosis.1

In turn, carotid occlusions can be diagnosed with ultrasound as the absence of patent lumen in grayscale and undetected flow with color/power Doppler and/or spectral Doppler, in addition to the presence of high-resistance flow in CCA and staccato flow - flow with minimal velocity and very high-resistance at the occlusion or pre-occlusion site.1

The study group from DCI-BSC suggests the use of table 6 to quantify ICA stenosis.1

2.4.1.2. Quantification of Carotid Stenosis with Anatomic Parameters

The anatomical criterion (Figure 6) is based on the assessment of lumen reduction and should be used to characterize, in particular, stenosis below 50% (without hemodynamic repercussion); however, it is also a great contributor in stenosis greater than 50%, in which the hemodynamic criterion can fail to quantify stenosis accurately (e.g., severe aortic stenosis, significant contralateral carotid stenosis, among others). Lumen reduction is preferentially measured by diameter, and the result of the carotid stenosis range should be reported in intervals of 10%. It is recommended not to measure plaques smaller than 20% to avoid possible differences in the measurement of diameter reduction when the thickened intima is included or stopped being included.1

Figure 6

Velocity evaluation can be compromised in some situations that affect measurements of spectral analysis. They can be located in the carotid bifurcation - distal or proximal - or even, in the contralateral carotid. Among the conditions proximal to the bifurcation, we underline aortic valve diseases (stenosis or insufficiency), atherosclerotic stenosis, or arteritis with involvement of the aortic arch, branches, and common carotid1 (Table 7).

Anatomic evaluation can be affected in circumstances such as arterial calcification with acoustic shadowing, improper adjustment of equipment, among others.

Relevant information for the report:

Specify the type of transducer used.

Inform the technical quality of the examination (report situations that can lower its quality - e.g., presence of catheters).

Describe the presence of atherosclerotic plaques, their location, extension, morphological characteristics, and degree of stenosis - quantified in deciles according to the DCI-BSC recommendation.1

Report other findings of or related to carotid arteries (e.g., tortuosities, dissections, tumors, arteritis).

The patient’s position is the same as that adopted for the carotid study.

To evaluate the extracranial part of vertebral arteries, start the examination by the V2 segment. At this point, with the aid of color Doppler and small angulation movements, try to identify the artery (as well as its vein) and record the spectral curves, adapting the scale and insonation angle of the vessel. Past this point, the artery is displayed toward its origin. The V3 segment of the vertebral artery lies below the mastoid process of the temporal bone (anatomic mark for the study). This region presents the vessel end of the transverse foramen and its course around the mastoid process (also called “atlas loop” due to its anatomical relationship with this vertebral body).3 The typical parameters expected are:

Diameter: ranges from 2 to 4 mm. Caliber asymmetry among vertebral arteries is common (73% of cases), and the left one has a more dilated caliber in 50% of cases.28^,29 The normal standard with pulsed wave Doppler is waveforms with laminar antegrade flow of low-resistance, PSV between 20 and 60 cm/s in the V2 segment, and that can range from 30 to 100 cm/s in the origin of the vertebral artery. Due to the frequent diameter asymmetry, there is a considerable difference in PSV and resistance index (RI) among the normal vertebral arteries of an individual.27

Vertebral artery hypoplasia is defined as a vessel diameter equal to or lower than 2.0 mm (or caliber asymmetry among vertebral arteries with ratio > 1:1.7).28

Proximal stenosis (V0-V1) diagnosis results from the increase in flow velocities at the lesion site. The DCI-BSC standardization3 suggests the values presented in table 8, adapted from the study by Hua et al.30 Evaluate stenosis in the remaining segments with VUS based on multi-parameter analysis, such as turbulent flow with color Doppler, local increase in flow velocities, increase in velocity rates, and distal flow damping, since there are no tables of quantification of stenosis for these segments.

Aneurysms are defined as a local dilation equal to or greater than 50% of the proximal or normal arterial diameter, necessarily involving all vessel layers. Even though the diameter of the abdominal aorta changes with age, gender, and biotype, the mean diameter of the infrarenal aorta is approximately 2.0 cm, with upper normal limit < 3.0 cm. Thus, abdominal aortic aneurysm (AAA) is defined as an aorta that measures > 3.0 cm. AAAs are located between the diaphragm and the aortic bifurcation and can be classified as suprarenal, juxtarenal, and infrarenal. Approximately 85% of AAAs are infrarenal, and 5% involve the suprarenal aorta.31 About 25% of patients with AAA have associated iliac artery aneurysm.2

Aneurysms can be fusiform, saccular, or with eccentric shapes. The type of asymmetry can significantly influence the risk of rupture and, as aneurysms grow, they can form laminated thrombi that preserve the arterial lumen.2

VUS is the most used examination to screen and diagnose asymptomatic patients in emergency units without a prior diagnosis and symptomatic ones. Computed tomography angiography (CTA) is the examination of choice for pre- and postoperative assessment; however, VUS does not lose its value for being more accessible, costing less, and not using nephrotoxic contrast. The current availability of microbubble contrast makes VUS quite attractive, particularly in postoperative assessments.32

Screening (Table 9).

Follow-up: monitor the growth and determine the appropriate time for surgery.33

Evaluation of pulsating abdominal mass, signs of rupture, or growth.

Preoperative AAA examination: report data on the access route, abnormalities in iliac arteries, fixation site of the endoprosthesis, aspect and measurements of the aneurysmal sac, and presence of parietal thrombi.

Postoperative AAA examination.

The examination must be conducted from the subxiphoid region to the aortic bifurcation, followed by the study of right and left common iliac arteries and their external and internal branches.

The evaluation uses B-scan, with transverse, coronal, and longitudinal planes to detect atheroma plaques and measure the diameters, especially if dilations are found. Take the anteroposterior (AP) measurement of the aneurysm during the peak systolic expansion, reporting if it was made from outer wall to outer wall (OTO) or inner wall to inner wall (ITI).

• Screening: use the B-scan during the subxiphoid part of the echocardiogram or in routine abdominal ultrasound.

• Diagnosis and follow-up: screen the aorta from the subxiphoid region to its bifurcation, followed by the study of iliac arteries and branches.

• Preoperative assessment: descriptions, necessary measurements, and relevant data are described in figure 8.

Figure 8

• Postoperative assessment: inform the surgical techniques used. They are described in detail in the DCI recommendations.2

Essential information to include in the medical report (Figure 8):

• Diagnostic examination:

- Report technical difficulties.

- Measure the largest diameter of the aorta.

- Inform the presence of tortuosities or enlargement of the aorta.

- Define the location of the aneurysm: supra-, juxta-, or infrarenal.

- Describe the anatomical shape of the aneurysm: saccular, fusiform, or other.

- Inform the presence or absence of wall thrombi, the intraluminal diameter, and signs of rupture.

• Additional information for the preoperative examination:

- Diameters:

○ Neck in the lowest renal artery plane.

○ Neck 15 mm below the origin of the lowest renal artery.

○ Maximum AAA - AP transverse plane (ITI or OTO).

○ Bifurcation plane (when present).

○ Both common iliac arteries.

○ Iliac artery bifurcation.

- Longitudinal extension of the proximal neck.

- Neck angle with aneurysm axis.

- Longitudinal extension of AAA.

Symptoms of acute ischemia (distal embolism) and intermittent claudication with decreased or absent femoral pulse, gluteal claudication, erectile dysfunction, and pain at rest.

Clinical signs such as abdominal bruit and reduced ankle-brachial index.

Prior VUS showing abnormalities in the velocity curve pattern of femoral arteries.

Follow-up of grafts and endoprostheses for the treatment of aortoiliac obstruction.

Suspected diagnosis of aortic dissection.

Suspected diagnosis of arteritis.

3.2.2.1. Diagnostic Criteria

• Stenosis: measure PSV at the lesion site (V2) and 1 to 2 cm proximal to the lesion (V1) and calculate the velocity ratio (V2/V1). Determine the spectral curve with an angle ≤ 60º parallel to the turbulent flow axis (Figure 9). The degree of stenosis should be classified according to table 11.

Figure 9

• Occlusion: lack of flow in any aortoiliac segment, even with scan parameters that detect low-velocity flows. Presence of typical preocclusive waveform (high peripheral resistance, low peak systolic velocity, and lack of diastolic flow). Collateral vessels can be found in occluded pre- and post-segment (re-entry point). The post-occlusive spectrum is characterized by monophasic waveform, with reduced PSV and prolonged acceleration time - parvus/tardus (Figure 9). Hypoechoic image with a concave interface in colored flow and spectrum in preocclusive staccato pattern suggests thromboembolic occlusion.

• Essential information to include in the medical report:

- Diagnostic examination:

○ Report if there were technical difficulties during the examination.

○ In case of dilations, inform the largest diameter of the aorta and/or iliac arteries.

- Additional information for the preoperative examination:

• Inform the presence, aspect, and location of atherosclerotic plaques, as well as the degree of stenosis of lesions. Table 12 lists the general limitations of VUS examination.

Mesenteric vessels are represented by the celiac trunk (CT) and superior and inferior mesenteric arteries (SMA and IMA, respectively). Anatomically, CT starts just below the aortic hiatus of the diaphragm and originates the splenic and hepatic arteries.

SMA and IMA begin approximately 0.5 to 2 cm below CT and 4 to 5 cm above the aortic bifurcation, respectively (Figure 10).35

Figure 10

Mesenteric artery obstructive disease progresses chronically and asymptomatically. The clinical manifestation represented by postprandial abdominal pain (mesenteric angina) and/or progressive weight loss occurs when two or more mesenteric vessels are involved. Older men are more frequently affected. Atherosclerosis is responsible for more than 90% of diseases that strike mesenteric arteries and is usually dissemination of the atheromatous process that involves the entire aorta.36

Arteriography is the standard diagnostic method; however, VUS is the first examination indicated for the study of symptomatic chronic intestinal ischemia for being non-invasive and risk-free.37

The objective of VUS is to determine the presence, location, extension, and severity of the stenotic lesion. The study must include the SMA, CT, and IMA, with the evaluation of SMA and CT being more important.38

Recurrent postprandial abdominal pain (mesenteric angina).

Weight loss without a known cause.

Abdominal bruit.

The DCI recommendations describe in detail the protocols of follow-up after surgical or endovascular treatment and assessment of compression syndromes.2

• Specific examination protocol:39^,40

- Place the transducer in the epigastric region; using the transverse plane, identify the SMA anteriorly, the aorta posteriorly, and the right renal vein between these two vessels (Figure 11A). In this same location, using the longitudinal plane of the aorta, find the CT and SMA (Figure 11B).

Figure 11

- B-scan: evaluates the presence of atherosclerotic or aneurysmal disease.

- Color flow imaging: assesses vessel patency and indicates flow turbulence, suggesting the probable stenosis site.

- Spectral analysis: used to analyze PSV and EDV. Measure these velocities in the origin of the vessel and/or in places with suspicion of stenosis. Position the insonation angle toward the blood flow.

- Velocities of mesenteric vessels are influenced by respiration; therefore, patients should hold their breath during the measurement.

• Table 13 presents the ultrasonographic criteria to assess flow in CT and SMA.2^,41^-43

Report if there were technical difficulties during the examination.

Presence or absence of atherosclerotic disease.

Lesion site.

Measurement of stenosis.

Measurement of PSV and EDV.

Table 12 lists the examination limitations.

Prevalence of renal artery stenosis (RAS) changes according to the population studied. RAS is the most common cause of secondary hypertension among the general population of hypertensive patients, representing approximately 1 to 6% of cases.44^,45

The most frequent cause of RAS is atherosclerosis (85% to 90% of cases), which often strikes the origin of and/or the segment proximal to the renal artery and can be unilateral or bilateral. Its prevalence increases with age, diabetes, and atherosclerosis in other arterial sites. It is considered an independent predictor of adverse events such as acute myocardial infarction, CVA, and death due to cardiovascular causes.45^,46

Fibromuscular dysplasia - a non-inflammatory disease - is responsible for 10% of RAS cases. Its frequency among the general population is unknown, but it is more usually reported in young women. Renal artery involvement occurs in its mid-distal segment and is often bilateral.47

With the quality improvement of imaging methods, RAS diagnosis became feasible and of great interest, aiming to identify patients who would benefit not only from drug therapy but also from renal revascularization procedures. Among the imaging examinations, VUS is the initial method of choice to investigate RAS due to its advantages, such as being non-invasive, low-cost, having no risk of radiation, and, mainly, the lack of contraindications related to the use of nephrotoxic contrast. Ultrasound evaluation of renal arteries has high specificity in competent laboratories, demonstrating that, when the vessels are correctly assessed, its results rarely differ from those obtained by arteriography.45^,48^-50

Table 14 shows the main indications to investigate RAS, according to the principal American guidelines.51^,52

The principal objectives of the study of renal arteries are:

Identify the main renal arteries and, if possible, the accessory ones.

Locate and grade stenotic lesions resulting from atherosclerotic disease or not.

Monitor the progression of RAS.

Follow-up after renal artery revascularization.

Patient’s position: Supine, using transverse and longitudinal ultrasound planes to analyze the abdominal aorta and origin of renal arteries.

Lateral, using the coronal plane to assess all middle and distal segments of renal arteries. Use this plane to measure the longitudinal diameter of the kidney and analyze the intrarenal flow in segmental or interlobular arteries.2

B-scan: used to identify atheroma plaques in the renal artery and evaluate the echogenicity and size of the kidney.

Color flow imaging and/or power Doppler: evaluate artery patency. Power Doppler indicates possible stenosis sites through flow turbulence or reduction in the vessel lumen.

Spectral analysis: Essential to measure systolic and diastolic velocities (PSV and EDV). Use the transverse or coronal plane, keeping the cursor directed at the flow jet, with an insonation angle < 60° in the renal artery and 0° in intraparenchymatous arteries.53

Measure PSV and EDV at the origin of the renal artery or in any segment with suspicion of stenosis.

Use the longitudinal plane of the aorta, near the origin of the SMA, to measure its PSV and calculate the renal aortic ratio (RAR).

Diagnostic criteria for RAS are classified as direct and indirect. The first consists of evaluating the renal artery from its origin in the aorta and, if possible, in all its extension. The second analyzes the hemodynamic repercussion of the proximal lesion of the renal artery on intraparenchymatous arteries.

The direct criterion comprises renal artery PSV and EDV and aortic PSV to calculate RAR (renal artery PSV/aortic PSV). The low-resistance waveform is considered normal for the renal artery. PSV is the most accurate parameter to grade RAS, with values that range between 180 and 250 m/s from study to study. EDV and RAR are used to aid the RAS evaluation. According to several studies, RAR ranges from 3.2 to 3.7 to estimate hemodynamically significant stenosis. Situations such as aortic coarctation, severe left ventricular dysfunction, aortic dissection or aneurysm, and systolic aortic velocities > 100 cm/s or < 40 cm/s can change the velocities in renal arteries and their relationships.2

Indirect criteria, represented by the measurement of the kidney size and analysis of intraparenchymatous artery flow, should be combined with direct criteria to optimize the results. A difference of 1.5 cm in kidney size can result from hemodynamically significant stenosis or even renal artery occlusion. Regarding the analysis of intraparenchymatous artery flow, initially, there is a reduction in the first systolic peak (FSP), prolonged acceleration time (AT) with decreased acceleration rate (AR), and flattening of the systolic wave until the parvus/tardus pattern is found. AT > 70 ms is associated with 60% RAS, while the parvus/tardus flow is present in more severe stenosis (80%).2

Table 15 summarizes the criteria recommended by DCI-BSC for hemodynamically significant RAS (> 60%). All references to these criteria are detailed in the guideline.2

Renal artery occlusion might be suggested if the vessel flow is not seen during color flow imaging and/or power Doppler, and not detected with pulsed wave Doppler, associated with a longitudinal diameter of the ipsilateral kidney < 8.5 cm.

Follow-up after renal revascularization is not part of the scope of this publication and can be found in the DCI guidelines.2

Listed on table 12.

Report if there were technical difficulties during the examination.

Inform the presence or absence of atherosclerotic disease or signs of fibromuscular dysplasia.

Lesion site.

Measurement of stenosis.

Measurement of renal artery PSV and EDV.

Measurement of aortic PSV.

Measurement of pulsatility index (PI) and RI in intraparenchymatous arteries (preferably the segmental artery).

Measurement of kidney size.

• Choose the non-dominant member, if possible.

• Follow the order: 1^st option - wrist; 2^nd option - elbow; 3^rd option - prosthesis.

• Measure the arterial and venous diameter (a tourniquet can be used in the member to evaluate venous distensibility).80^,81

- Ideal venous or arterial diameter: elbow - 4 mm; wrist - 3 mm.

- Minimum functional diameter: elbow - 2 mm; wrist - 1.8 mm.72

• Measure the depth between vessels and skin surface; the ideal for puncture is < 5 mm. 79

• Measure the distance between artery and vein to be used (Figure 14).

Figure 14

• Measurements of artery, vein, and anastomosis;

- Ideal venous or arterial diameter: elbow - 4 mm; wrist - 3 mm

- Minimum functional diameter: 2 mm

• Flow volume: to obtain the effective flow volume through an AVFH, measure the diameter of the drainage vein by its inner edges (in cm), preferably with a transverse plane, to calculate its radius (R) and, consequently, its area (in cm²). Take this measurement farther from the anastomosis site of the fistula, where the color flow imaging shows no flow turbulence, usually 2 to 5 cm from the anastomosis. Find the flow in the same place of the vein where the diameter was assessed with pulsed wave Doppler. Locate the sample volume in the center of the vessel and correct the Doppler flow angle to up to 60°. Determine the mean flow velocity (V_MEAN) in cm/s with pulsed wave Doppler. Calculate the mean of 3 to 5 cardiac cycles. Apply the following formula:

The values below are used for normal flow volume of homologous and heterologous AVFH:

Brescia-Cimino fistula (radiocephalic) = 614 ± 242 ml/min.

PTFE = 464 ± 199 ml/min.

Mean normal value = 514 ml/min.

Fistulas with flow volume < 450 ml/min have a high risk of thrombosis in 2 to 6 weeks.

The minimum functional flow volume for AVFH in the elbow is ≥ 200 ml/min, and in the wrist is ≥ 150 ml/min.

Hyperflow is considered when the flow volume is > 3,000 ml/min.

Maturation protocol:73^,74^,77 AVFH maturation consists of an increase in caliber and flow of the vessels used.

Assess vessel diameter and structure (≥ 6 mm), flow volume (≥ 600 ml/min), and the distance between the vein and skin surface ≤ 6 mm.

Wait at least 14 days; the ideal scenario is individualization with follow-up for each patient and interval superior to 30 days. If possible, wait 60 or even 90 days before the first canalization.

Table 19 summarizes the main objectives of VUS findings.

Arterial: diabetes mellitus and significant atheromatosis.

Venous: fibrosis.

Anastomosis site: turbulence and intimal hyperplasia.

Significant escape through tributary veins.

Steal phenomenon, in which retrograde flow is found in the radial artery distal to AVFH (Figure 15).

Figure 15

Pronounced tortuosities.

Intimal hyperplasia (valves).

Thrombosis (dissection by puncture).

Idiopathic: puncture and surgical technique.

Significant stenosis with V2/V1 ≥ 4 (if ≥ 2 indicates stenosis > 50%; angioplasty is recommended in case of clinical and/or hemodynamic abnormalities associated).

Occlusion.

Aneurysm, dilation due to prosthesis degeneration and pseudoaneurysm.

Infection.

Hematoma, seroma, and lymphocele.

Inexistent, with rare exceptions in highly significant edemas, fibrotic scars, and presence of orthopedic devices.

1. Examination before the procedure (Table 20):

Report deep and superficial venous thrombosis; abnormalities in the arterial system; and anomalous anatomic changes, such as the number of vessels, paths, and forearm vessels that continue in the arm

Inform the measurements of calibers and proper flows.

2. Examination after the procedure (Table 21):

Describe the type of AVFH and its location; inform if it is functional, dysfunctional, or non-functional, mentioning the cause, location, and extension of the involvement

Report the afferent and efferent volumes (ml/min).

As the accuracy of the clinical diagnosis of DVT is low (< 50%), few patients with suspicion of DVT effectively have the disease (12% to 31%). Therefore, the recommendation is to perform an accurate and objective examination that can confirm or rule out DVT.87^,92^,96 The current gold standard examination to diagnose DVT is compression VUS.92^,97

Three categories of examinations are used to determine the probability of DVT:92^,98

1. Clinical probability based on anamnesis and clinical examination

2. D-dimer levels

3. Imaging studies - the most commonly used is venous VUS, and the less used are venography, CTA, and venous magnetic resonance angiography. This guideline will cover only VUS.

VUS is considered the current gold standard examination to diagnose acute DVT.99 The PIOPED II study showed 95.5% agreement between CTA and ultrasound in diagnosing or ruling out DVT. In addition, we must remember that VUS is useful not only in diagnosing DVT in symptomatic or asymptomatic (with a high risk of DVT) patients but also in identifying other conditions that cause signs and symptoms indistinguishable from DVT.

Knowledge about vascular anatomy and its variations is crucial since the frequency of variability in the number of veins is high, with the possibility of only one of them being involved, in addition to the different levels of confluences and paths.

To diagnose thrombosis, we adopt several criteria, listed below.

1. Venous compression: the normal vein has thin, smooth, and regular walls, and is completely collapsible with transducer compression (Figure 17).

Figure 17

Incompressibility is the main criterion for DVT diagnosis (Figure 16).

A few conditions might hinder this compressibility, and sometimes special maneuvers are necessary. They are:

Presence of a strong muscle group in the path to be compressed; for instance, the adductor canal requires compression in the external side of the thigh.

Neurogenic bladder needs draining through urinary catheterization.

Proximity to bone structures; for example, compression is limited in infrapatellar veins due to the size of the transducer.

2. Vein caliber: usually the vein has twice the caliber of the adjacent artery. Acute venous thrombosis presents great distension of the vessel wall, with an increase in vein caliber and loss of this relationship. Over time, with the process of recanalization, the vein caliber decreases disorderly in some segments, losing the uniformity usually observed along the vessels. In the most chronic stage, a complete vein retraction might occur, with calibers becoming smaller than those of arteries, at times, hindering their recognition during the examination.

3. Characteristics of the venous wall: parietal irregularities or diffuse parietal thickening, intraluminal trabeculations or synechia, structural valve abnormalities, loss of anatomical relationship with adjacent structures, even if tenuous, which can mean a previous DVT already recanalized.

Intraluminal echoes indicate presence of thrombus and its echogenicity can characterize or not its age.

4. Color imaging: color flow imaging is an important tool for venous thrombosis.

While color flow filling all lumen in longitudinal and transverse planes indicates normality, the lack of color or flaws in filling the vessel can point to partial or complete thrombosis, particularly in recent partial thrombi with low echogenicity.

Flow around the vessel strongly suggests acute DVT. Flow permeating the thrombus indicates recanalization and chronicity of the process.

Take precautions regarding the scale and gain of the equipment, and the proper performance of maneuvers that increase venous flow, generating a color signal.

5. Spectral analysis: the normal venous flow with spectral Doppler is spontaneous and phasic with respiration, increases with distal compression maneuvers, and ceases with Valsalva maneuvers (proximal veins) or proximal compression.85 The spontaneity of the flow might not be observed in distal veins of patients in the supine position, and distal compression maneuvers and/or mobilization of the limb to displace the blood column become necessary. Loss of phasicity, with continuous flow pattern, is an indirect sign of occlusion or proximal compression. Damped response to distal compression indicates obstruction between the compression site and the location of the sample flow.

Retrograde flow occurs when there is valve damage. Thus, valve regurgitation is a pathological sign, which can warn to the presence of previous thrombosis, and valve agenesia or venous reflux secondary to hyperflow should be ruled out.

Table 22 describes VUS characteristics that assist in the identification of stages of venous thrombosis.

Valsalva and inspiration and expiration maneuvers help and add information (Table 23).

In general, high-frequency (5 to 12 MHz) linear transducers are used for normal-weight and thin patients. In overweight/obese patients, the study of the adductor canal and even of leg veins in individuals with moderate/severe edema can use transducers of greater depth range, such as convex abdominal ones, whose frequency varies from 3 to 5 MHz.108

Presence or lack of signs of deep and/or superficial venous thrombosis.

Information about the characteristics of the thrombus.

Extension of thrombosis: essential and, if possible, with approximate measurements of anatomical reference points, such as the anterior-superior iliac spine, inguinal fold, knee, malleolar or plantar region, axillary fold, elbow fold, and wrist fold.

In case of chronic thrombosis:

- Measurements of residual thrombotic masses can be included in the report and/or images, with their locations so that they can be compared later.

- Presence of orthostatic reflux.

The basic structure of any additional examination must have:

• Patient’s identification (full name and age).

• Clinical indication (the purpose of the examination will determine the type of TCD needed).

• Technical quality of the examination (reporting possible issues that interfere in obtaining the necessary images for the study).

• Record of all ultrasound windows used, and vessels examined (justifying the cases that were impossible to study).

• Description of specific characteristics found in each technical resource used:

- Color flow imaging - lumen patency or occlusion, laminar or turbulent (“mosaic”) pattern, direction (antegrade or retrograde).

- Pulsed wave Doppler - laminar or turbulent pattern, direction (antegrade or retrograde), velocities of spectral flow curves (peak systolic, end-diastolic, and mean), and PI and resistance according to the clinical indication of the examination (e.g., sickle cell disease requires mean velocity).

- Contrast solution with “macrobubbles” - record and count of HITS in the study of patent foramen ovale and paradoxical embolism.

- Use of contrast agent with “microbubbles” (SonoVue®).

- In the intraoperative monitoring, report the occurrence and count of HITS/hour and variations in flow velocities with potential risk for ischemic CVA in the postoperative period.

Conclusion: avoid etiological diagnosis (TCD is a study of cerebral hemodynamics and findings should be correlated to the clinical indication of examination: for instance, the presence or lack of criteria for vasospasm, with grade classification and time reference to the onset of symptoms of subarachnoid hemorrhage).

Note: in cases of sickle cell disease, it is mandatory to specify, after the conclusion, the recommended date to repeat the reassessment examination (following the Brazilian Guidelines for Transcranial Doppler in Children and Adolescents with Sickle Cell Disease, 2010).123 In other pathologies, this suggestion is prohibited due to professional ethics.

A unique characteristic of contrast agents for US (non-existent in those used for MRI and computed tomography) is that they are modified by the waves used to detect them. When exposed to US, microbubble behavior changes according to the US power emitted, that is, the amplitude of the acoustic wave [called mechanical index (MI) in the equipment]. In non-contrast studies, MI ranges from 1.6 to 1.9; under this acoustic power, the microbubble always oscillates vigorously and bursts, causing two unwanted effects: a sudden increase in signal intensity with an excessive blurring of the image, and a significant reduction in contrast concentration, consequently shortening the examination time. This image mode, called “image by acoustic stimulation,” does not require equipment with contrast technology (but, on the other hand, it does not use the full potential of the contrast agent, limiting it to its echo-enhancer function).

After reducing MI to ≤ 0.1, we can not only keep the integrity of microbubbles but also make them oscillate non-linearly (initial compression followed by expansion) and resonate, emitting different frequencies (known as “harmonic frequencies”) from the fundamental one emitted by the transducer. Equipment with this technology can filter signals emitted specifically by microbubbles, leading to a more lasting study that highlights microbubble over tissue signal (virtually nulled in the image, appearing as a dark background).

This type of study, also called “contrast study with low MI”, allows the examiner to evaluate the contrast wash-in continuously in the local studied, the enhancement period, and the concentration of microbubbles in the target structure [essential for situations such as the study of vessels of vessels (vasa vasorum), carotid plaques, renal capillary (perfusion) distribution, and masses].124

An undesired effect of the contrast study with low MI is the depth limitation of the pulse wave, which undergoes greater attenuation as it moves through tissues. Some ways to minimize this effect are: adopting alternative acoustic windows that allow closer proximity with the structure of interest, using broadband transducers with lower frequencies, and, as a last resort, increasing the MI and consequently destroying more bubbles in the proximal field.128

A noteworthy equipment control in the contrast study is the image gain, which amplifies the signal received during the post-processing in the equipment. High gain produces a bright image and widespread increase in background noise, obscuring the contrast signal (once the saturation level of the equipment has been reached, there will be no margin to amplify the signal caused by contrast). Therefore, during the contrast study, the equipment gain should be reduced until the image is virtually black, except for highly echogenic structures. Some manufacturers have gain adjustment controls for contrast studies that can easily be turned on and off during the examination.

When performing a manual adjustment, make sure to have the least amount of acoustic signals before contrast injection and understand if this signal results from an increase in MI (when specific structures are seen in the image) or gain (which causes a widespread rise in noise across the image).6

A last technical aspect worth mentioning is the dose of contrast injected. High doses initially blur (saturation) the signal and attenuate (acoustic shadowing) structures in the distal field until contrast concentrations drop to a proper level. In addition, distinguishing small enhancing differences between structures is not possible, given that the upper limit of dynamic range (grayscale) of the equipment has been exceeded.128 One way of highlighting different enhancing levels caused by contrast in a structure is to adjust the dose of contrast to allow adequate opacification, without blurring or attenuation, and increase the dynamic range of the equipment. In turn, low doses will not reach the opacification level desired.