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5 Sonography ofLymph Nodes intheNeck
Fig. 5.1 Reactive, juvenile
CLN with huge diameters
57
Fig. 5.2 Characteristic
examples of a reactive CLN
with a hilum and a
longitudinal diameter less
than 18mm and a minimal
diameter less than 8mm
In various studies, the longitudinal, cross-sectional, and
minimal transverse diameters have been recommended for
the assessment of CLNs [7–11]. In a larger cohort study of
290 patients, interpretation of the ROC curve suggested that a
long-axis measurement of 18mm is a good cutoff value to
distinguish reactive from malignant CLNs (Fig. 5.2) [1].
Because the data in the literature vary signicantly, the longi-
tudinal axis is of rather poor diagnostic value, however, and
the shortest axis or the ratio of long to short axis diameters
(Steinkamp/Solbiati index) should be considered [12]. Hajek
and colleagues have suggested that reactive CLNs have a
maximal shortest axis of no more than 5mm, with a cutoff
value for the minimal diameter of 8 mm, which was conrmed by several other groups (Fig.5.2) [1, 13–15].
58
J. E. Meyer
Another interesting issue is the calculation of ratios of
diameters. On one hand, this reduces false-positive and falsenegative results, and on the other hand, it is possible to estimate two-dimensional and three-dimensional forms of a
lymph node. A ratio of long to short axis diameter above 2 is
thought to be oval and reactive. The study group led by
Vassallo presented a sensitivity of 85% and a specicity of
86% for this criterion [16]. Other published data in this eld
has concluded that the Steinkamp/Solbiati ratio (L/S, longer
to shorter diameters) is the most conclusive parameter
(Fig.5.3) [12].
There is common agreement that round lymph nodes tend
to be malignant and oval nodes tend to be benign [15, 17–
20]. However, a round-shaped CLN (L/S ratio <2) can be
found in up to 36% of healthy patients [21–25]. Furthermore,
every malignant lymph node at an early stage of conversion
can still be oval-shaped [18].
A lymph node hilum corresponds to the site where the
afferent and efferent vessels pass the capsule of the lymph
node. It can easily be visualized sonographically by both
B-mode and color duplex sonography (Fig. 5.4). A hilum
occurs in 28.6–87% of normal CLNs [21–24]. Nevertheless,
the hilar vascularization is seen in only about two thirds of
normal CLNs by B-mode grayscale sonography, so color
duplex sonography is the method of choice to clarify whether
a lymph node has hilar vascularization. The absence of a
hilum or hilar vascularization may be without signicance,
but the presence of a normal hilum virtually eliminates suspicion of malignancy in the majority of cases. Although
peripheral vascularization stands for malignant transforma-
tion of a CLN, it can also be seen in up to 18% of benign
CLNs [21–24].
Doppler ultrasonographic assessment of intranodal vascular
resistance Furthermore, Doppler sonography elicits an intrano-
dal vascular pattern of CLNs, which has been reported to have a
reproducibility of 85% [26]. Normal and reactive lymph nodes
with maximal transverse diameter greater than 5mm show a hilar
vascular pattern in about 90% of all CLNs in a normal neck,
whereas small CLNs with a maximal transverse diameter less
than 5mm usually appear avascular (Figs.5.5 and 5.6; Video 5.1)
[18, 27–31]. Evaluation of the vascular pattern of CLNs may not
distinguish between different benign nodal diseases, however, as
their vascular patterns vary with the duration of illness [32, 33].
Additionally, spectral Doppler US allows calculation of
the vascular resistance of the intranodal vessels. Because of
inconsistent results in previous studies and poor reproducibility, to date the value of spectral Doppler US evaluation of
intranodal vascular resistance is limited in routine clinical
practice, however [31, 32, 34–39].
Qualitative elastographic assessment
It is well known
that benign lymph nodes tend to be soft, whereas malignant
lymph nodes are usually rm. The rmness is classied in
qualitative real-time elastograms into four or ve grades
[40–43]. For qualitative US elastography as a single parameter to distinguish between benign and malignant conditions,
the sensitivity, specicity, and overall accuracy have been
reported to be 62.2–88.4%, 35.3–100%, and 66.3–89%,
Fig. 5.3 Large, reactive CLN
with a hilum and a ratio of
long to short axis diameter
above 2 (Solbiati/Steinkamp’s
ratio)
ab
cd
5 Sonography ofLymph Nodes intheNeck
59
Fig. 5.4 (a–d) Presentation of a classical CLN’s hilum corresponding to the site where the afferent and efferent vessels pass the capsule. (a)
Normal B-mode scan. (b) Enlarged B-mode scan. (c) Color duplex sonography. (d) Power Doppler sonography
Fig. 5.5 A small CLN with a
maximal transverse diameter
less than 5mm which usually
appears apparently avascular
without a hilum
60
a
b
J. E. Meyer
a
Fig. 5.6 A chain of small CLNs which is characteristically of reactive lymphadenopathy. (a) in a longitudinal view. (b) in a transverse view
b
respectively, whereas the combination of qualitative elastography and grayscale ultrasonography achieved an improved
sensitivity (92%), specicity (94%), and overall accuracy
(93%) [40–43].
Currently the major problems with qualitative US elastography are inconsistent scoring systems and approaches in
the assessment of CLNs, which lead to contradictory results
in the literature. Therefore, the value of real-time elastography in routine clinical practice remains unclear and limited.
Quantitative elastographic assessment
On conventional
strain elastography, benign lymph nodes tend to have a lower
strain index, whereas malignant nodes usually have a higher
strain index. Shear wave elastography (SWE) has been
reported to have variable reliability in assessing the stiffness
of neck lesions [44]. A recent study using SWE found that
malignant nodes were stiffer than benign nodes [45]. Strain
index and SWE allow quantication of lymph node stiffness,
which provides additional information for the assessment of
cervical lymphadenopathy. However, the results remain
inconsistent and highly dependent on the cutoff values chosen, so its use in routine clinical practice is limited.
In conclusion, there is currently not one single sonographic parameter that gives a precise hint as to the status of
a CLN, so the decision relies on the combination of multiple
parameters; the most signicant information currently are
the absence of peripheral vascularization, short axis diameter, and Steinkamp’s ratio [1].
5.1.2 Tuberculous Lymphadenopathy
Characteristics Can mimic all other lymphadenopathies.
Inhomogeneous, lost echostructure, induration, lymph node
packages, high vascularization, malignant appearance,
Table 5.4 Stages and sonographic appearance of tuberculous cervical
lymph nodes
Stage Clinical changes of CLNs US ndings
I Nonspecic, reactive changes as
in other lymphadenitis
II Fixation to surrounding tissues
because of periadenitis changes
III Cold abscesses Hypoechoic mass with
IV Formation of collar stud
abscesses
V Sinus tract formation Extranodal spread into
Simple nodal enlargement
or rounding
Irregular borders
inhomogeneous texture
Nodal matting
adjacent structures
hypoechoic, round, without echogenic hilum, displaced hilar
vessels, liquid areas, intranodal cystic necrosis, “collar stud”
abscess, hyperechoic spots with evident posterior acoustic
shadowing, single or multiple coarse high-echo spots created
by scattered calcications or hyalinosis, nodal matting, adjacent soft tissue edema, echogenic thin layer.
Plain grayscale ultrasonography
Suppurative, tubercu-
lous lymphadenitis can mimic any other type of CLN diseases, because different US patterns can be apparent
simultaneously in one patient who has multiple tuberculous
cervical lymph nodes (TCLN) of different stages [46, 47].
The different stages of tuberculous lymphadenitis are
depicted in Table5.4 [48].
Therefore, evaluation of clinical symptoms (such as unilateral, enlarged CLN without pain or tenderness) and of other
underlying diseases (most frequently, HIV) is very important
[48]. In most cases in developed countries, TCLNs is a differ-
ential diagnosis of malignant CLN or neck abscess formation
that usually involves the lymph nodes of the jugular chain,
posterior triangle, and supraclavicular fossa [46, 49].
According to Ying etal. [50], stage I TCLNs commonly
appear as round lesions (Fig.5.7). In their study, 79% of 315
5 Sonography ofLymph Nodes intheNeck
Fig. 5.7 Stage I of a
tuberculous-infected CLN
commonly appearing as a
hypoechoic, round lesion with
displaced hilar vessels
61
TCLNs showed a more round shape (S/L ratio more than
1/2), but the percentage was less than that of metastatic
nodes (95%) [50].
Because the shape or size of TCLNs is rather unspecic,
changes in the echogenic texture and echogenicity provide
more clues to the diagnosis of TCLNs. The presence of a
hilum within CLNs is usually a sign of benignity, whereas its
absence points toward malignancy, but an absent hilum is
also reported in 76–86% of TCLNs [50]. TCLNs are predominantly hypoechoic because of the high incidence of
intranodal cystic necrosis with posterior acoustic enhancement (Fig.5.8) [51].
By contrast, in a study reviewing CLNs in 192 patients,
84% of tuberculous nodes and 11% of metastatic nodes
showed considerable internal echoes in B-mode sonography,
whereas none of the reactive nodes had internal echoes [52].
The hyperechoic appearance is created by scattered calcications or hyalinosis in caseous necrosis, which is thought to
be highly specic for TCLNs (Fig. 5.8). Under US, they
appear as single or multiple coarse, high-echo spots located
focally in either the central or peripheral area within the
nodes [48]. In cases of stage IV (Fig.5.9) or V (Fig.5.10)
tuberculous infection, the evolving pathological process
leads to clustered calcications in several foci, which appear
as hyperechoic spots with evident posterior acoustic shadowing under US. This nding was reported in about 25% of
TCLNs [47, 53]. It is difcult, however, to differentiate
between sprinkled calcications of papillary thyroid carcinoma metastases and caseous necrosis of tuberculous nodes,
so it is important to keep this possibility in mind during the
investigation and take a routine look at the thyroid gland!
The so-called echogenic thin layer is another key US feature of TCLNs; it is usually located deep to the peripheral
margin and measures 2–3mm in thickness (Fig.5.11). It is
seen in 86.7% of pathologically conrmed cases and corresponds to the specic granulomatous tissue layer surrounding the caseous necrosis, reecting the wall of body defense
[46, 51]. Interestingly, Asai etal. showed that the concomitant presence of hyperechoic echoes and an echogenic thin
layer has a sensitivity of 100% and a specicity of 100% for
tuberculosis [51].
Further progression of the tuberculous infection leads to
periadenitis (stage II disease) and subsequently to a loss of
acoustic impedance difference between the TCLN and its
surrounding soft tissues (Fig. 5.12). This usually results
sonographically in unsharp borders of the TCLN [17]. More
advanced inammation (stage III) can leave the lymph nodes
and spread into the adjacent subcutaneous tissue, eliciting
soft tissue edema (Fig.5.13). Nodal matting or clumping is
considered to be a result of this periadenitis and adjacent soft
tissue edema [17]. This phenomenon may also be seen in
patients whose neck has been irradiated [54], but in patients
without previous radiotherapy, the presence of soft tissue
edema and nodal matting is highly suggestive of
tuberculosis.
The “collar stud” abscess or a stula tract can be seen in
stage IV/V of CLN tuberculosis (Figs.5.9 and 5.10) [47].
Doppler ultrasonographic assessment of intranodal
vascular resistance On Doppler US, the vascular pattern
of TCLNs varies depending on the degree of intranodal
necrosis and the stage of the disease. In 81% of TCLNs, an
62
Fig. 5.8 Classical TCLN
with an absent hilum,
predominantly hypoechoic
because of the high incidence
of intranodal cystic necrosis
with posterior acoustic
enhancement and hyperechoic
appearance created by
scattered calcications or
hyalinosis
J. E. Meyer
Fig. 5.9 CLN with a stage
IV tuberculous infection with
clustered calcications in
several foci appearing as
hyperechoic spots with
evident posterior acoustic
shadowing under US
intranodal cystic necrosis pushes the hilum away and causes
displaced vasculature (Fig. 5.7) [17]. As cystic necrosis
aggravates, it eventually destroys the blood vessels in
6–41% of TCLNs and results in apparent avasculature
(Fig.5.14) [29, 31]. Avasculature may also reect the healing process at later stages of the disease, when brosis and
hyalinization cause compression and obliteration of intranodal vessels [55].
Qualitative/quantitative elastographic assessment The
role of elastography is not yet fully understood, although differences between malignant, benign, and tuberculous CLNs
have been identied in case reports [56].
Ultrasound-guided ne-needle aspiration (USFNA) and
utrasound-guided core biopsy (USCB) cytology Although
typical US features exist, none are pathognomonic, and
5 Sonography ofLymph Nodes intheNeck
Fig. 5.10 TCLN in stage V
with sinus tract formation and
extranodal spread into
adjacent structures
63
Fig. 5.11 TCLN depicting
another key US feature the
“echogenic thin layer” that
shows in combination with
hyperechoic echoes a
sensitivity of 100% and a
specicity of 100% for
tuberculosis
TCLN cannot be diagnosed merely with US alone [48]. A
conrmative diagnosis depends on ancillary tests such as
USFNA, USCB, mycobacterial culture, or polymerase chain
reaction (PCR) test for the M. tuberculosis gene [57]. The
sensitivity of cultures performed on FNA specimens was
reported to reach 86%, whereas the sensitivity of microscopy was 18% and of cytology from FNA specimens was
38% [58]. Surgical biopsy has long been considered the
gold standard to obtain specimens for histology of TCLNs,
but this is often followed by stula formation and poor
wound healing [59]. Instead, USCB provides a favorable
alternative, which leaves a smaller scar and has lower
chances of complications while offering similar diagnostic
accuracy (Video 5.2) [60].
64
Fig. 5.12 TCLN with a stage II disease typically presented with peri-
adenitis and subsequently a loss of acoustic impedance difference in
comparison to its surrounding soft tissues, which is sonographically
shown by unsharp borders
Fig. 5.13 More advanced
tuberculous inammation
(stage III) spreads into the
adjacent subcutaneous tissue
eliciting soft tissue edema,
nodal matting, or clumping
J. E. Meyer
Fig. 5.14 TCLN with stage V disease. As cystic necrosis aggravates, it
destroys the blood vessels and results in apparent avasculature
5.1.3 Non-tuberculous Mycobacteria (NTM) Lymphadenopathy
Characteristics Can mimic all other lymphadenopathies,
primarily in children under the age of 6 years. Unilateral,
most commonly (in order of incidence) in submandibular,
preauricular, and parotid CLN levels; satellite-like nodules;
“malignant” appearance; heterogeneous; lost echostructure;
intranodal liquefaction with cystic necrosis (echolucent
areas); overlying skin with livid discoloration and with a
“parchment-like” shiny appearance; echogenic thin layer;
sinus-like lymphocutaneous stulas; echogenic intrinsic
reexes with and without acoustic shadowing; multiple
intranodal calcications; nodal matting; adjacent soft tissue
edema.
The term non-tuberculous mycobacteria (NTM) refers to
mycobacterial species other than the Mycobacterium tubercu-
losis complex (i.e., M. bovis, M. africanum, M. microti, M.
canetti, M. caprae, M. pinnipedii, M suricattae, and M. mungi)
and those organisms causing leprosy (M. leprae and M. lepromatosis). NTM are ubiquitous environmental organisms
mostly found in soil and water; they cause lung-, sinus-, lymph
5 Sonography ofLymph Nodes intheNeck
65
node-, joint-, CNS-, and catheter-related and disseminated
infections in susceptible individuals [61, 62].
For any given level of host susceptibility, there seem to be
a real increase in NTM infection rates, which has been associated with activities potentially increasing exposure to NTM
in water (swimming), soils (gardening), and aerosols (showering, hot tubs) [63]. Furthermore, a number of immunodeciencies have been associated with NTM infection [64, 65],
including inherited disorders of cytokine signaling [66, 67]
and immune cell function [68, 69], as well as acquired immunodeciencies, including HIV/AIDS [70]. A number of
immunosuppressive drugs, such as oral or inhaled corticosteroids [71–73] and the combined immunosuppressive therapy
used in solid organ transplantation and in anticancer chemotherapy [70], have been associated with the acquisition of
NTM infections, whereas direct person-to-person spread is
unlikely [74].
Besides the most frequent pulmonary infections, NTM
cause locally limited infections of the skin, connective tissue, eye, and bones [61, 75], as well as lymph nodes of the
neck, most often in children less than 5years of age, with a
female predilection; immunocompetent teenagers and adults
are usually not affected [76]. Predominantly isolated mycobacteria belong in 65–80% of cases to the Mycobacterium
avium/intracellulare species; only about 10% are
Mycobacteria tuberculosis, but the opposite applies to teen-
agers and adults [77]. Furthermore, the authors showed that
the increasing incidence of NTM lymphadenopathies was
linked to a change and diversication in NTM species from
M. avium/intracellulare and M. scrofulaceum to M. celatum,
M. genavense, M. haemophilum, M. interjectum, M. kansasii, M. lentiavum, M. malmoense, and the fast-growing M.
abscessus/fortuitum. The primary therapy includes the com-
plete resection of the affected lymph nodes and surrounding
tissue. Preoperative ultrasound is often the only imaging
technique that is required.
Plain grayscale ultrasonography
NTM lymphadenopathy
of the head and neck can be divided into four distinctly segmented clinical phases by ultrasound imaging (Table 5.5).
These are universal features but not entirely specic, and all
the stages are similar to TCLNs [78]. Characteristically the
submandibular nodes are most frequently involved, followed
by the preauricular and rarely by the parotid gland lymph
node levels. Most levels are unilaterally affected [79].
Stage I is characterized by a painless, hypervascular
mass (Fig.5.15). The diameter of the involved lymph nodes
ranges from 1.9cm to 4.4cm (rather large in comparison)
[79]. On sonography, marked decreases of echogenicity
were characteristic in the early stages, with development of
satellite-like nodules at the edge of the affected lymph node
[79, 80].
Table 5.5 Stages and sonographic appearance of non-tuberculous cer-
vical lymph nodes
Stages Clinical changes of CLNs US ndings
I Mostly over weeks persistent,
painless, enlarged lymph
nodes without symptoms as in
other lymphadenitis
II Fluctuation as a result of
intranodal liquefaction with
cystic necrosis
Fixation to surrounding tissues
as a result of periadenitis
changes
III Livid discoloration and
thinning with a shiny
appearance (“parchment-like”)
of overlying skin
IV Lymphocutaneous stulas/
draining wound
Unilateral, nonspecic,
reactive nodal hypervascular
enlargement or rounding
Rather large diameters
(1.9–4.4cm)
Marked decreases of
echogenicity
Development of satellitelike nodules at the edge of
the lymph node
Characteristically
submandibular and
preauricular; parotid lymph
node levels rarely involved
Hypoechoic mass with
inhomogeneous texture with
irregular borders and
posterior shadowing
Nodal matting and adjacent
soft tissue edema
Decreased distance of skin
to lesion
Echogenic intrinsic reexes,
with and without acoustic
shadows
Multiple intranodal
calcications
In stage II, lymph nodes with heterogeneous echogenicity,
incorporating intranodal echolucent areas, may indicate liquefaction with cystic necrosis, causing the mass to appear
uctuant. Additionally, nodal matting and adjacent soft tissue edema may be present in the neck (Fig.5.16) [79, 81].
In stage III, the overlying skin of the affected CLN may
develop livid discoloration and become notably thinner with
a shiny appearance (“parchment-like”) (Fig.5.17). During
stage IV, the lesion stulizes to the skin surface, causing a
sinus-like, draining wound; echogenic intrinsic reexes with
and without acoustic shadows can be seen (Fig.5.18; Video
5.3) [80, 81]. Multiple intranodal calcications are rather
characteristic of end-stage NTM infection [79, 82].
Calcication in juvenile CLNs is rather uncommon
(Fig.5.19), but calcication may also be found in metastatic
nodes from papillary carcinoma of the thyroid in children
[83, 84].
Most NTM patients present in stage III with lymph node
uctuation and violaceous skin discoloration following a
history (over weeks) of unilateral, painless, enlarged lymph
nodes without symptoms [80]. Then overnight the lymph
nodes rapidly enlarge, fuse, and develop a lymphocutaneous
stula with secretions. Sometimes both sides are affected.
Clinically the focally livid color of the skin covering the
enlarged lymph node is characteristic.
66
Fig. 5.15 Unilateral stage I
NTM lymphadenopathy of
the head and neck
characterized by a painless,
hypervascular mass
J. E. Meyer
Fig. 5.16 Stage II non-
tuberculous CLN with
heterogeneous echogenicity,
incorporating intranodal
echolucent areas indicating
liquefaction with cystic
necrosis, nodal matting, and
adjacent soft tissue edema
The differential diagnosis is challenging, including tuberculosis, cat scratch disease, EBV-driven mononucleosis, toxoplasmosis, or suppurative lymphadenitis. A clear differentiation from
tuberculosis is not possible by imaging alone. Actinomycosis
also leads to livid skin discoloration and stula development, but
it typically does not spread via the lymphatic system [85].
Doppler ultrasonographic assessment of intranodal
vascular resistance
The use of newer power Doppler
equipment has increased the sensitivity of the detection of
intranodal vascularity [86]. Still, to date no specic data
have been published on the use of Doppler US in NTM
infection. Benign processes may manifest with variable