Download Sonography of the Parathyroid Glands

Educational Supplement
Sonography of the Parathyroid Glands
Nicola Griffiths Grad Dip Appl. Sc. (Medical Sonography)
Nicola is a sonographer at St Vincent’s Hospital, Sydney.
Introduction
Parathyroid glands are not frequently scanned in many departments. This paper explains parathyroid scanning for those
sonographers who rarely encounter requests to scan them.
Background Anatomy
There are two sets of paired parathyroid glands, the superior and inferior glands. The superior parathyroid glands arise
embryologically with the thyroid gland from the 4th branchial cleft pouch, and the inferior parathyroid glands arise along
with the thymus from the 3rd branchial cleft pouch. As they develop, their connection with the pharyngeal pouches is
lost, and they begin to migrate to their eventual positions (Spence 1987). The superior glands are usually positioned
close to the mid to upper thyroid gland in the adult, whilst the inferior glands are more variable in their final position;
usually sitting at, or just inferior to, the posterior aspect of the lower part of the thyroid gland. A significant proportion
of parathyroid glands (most often the inferior glands) lies in ectopic locations in the neck or mediastinum (Spence 1987).
The parathyroid glands are made up of tightly packed masses or cords of cells. I
The adult parathyroid glands usually measure no more than 5mm x 3mm x 1mm, and are not routinely seen on highfrequency ultrasound unless enlarged. Normal parathyroids which are seen on ultrasound without accompanying
hypercalcaemia are not considered clinically significant (Rumack 1998)
The effects of the parathyroid hormones
The major role of the parathyroid gland is to secrete parathyroid hormone, which is a major controller of calcium and
phosphate metabolism. A decreased level of ionised plasma calcium is the major stimulant for the release of parathyroid
hormone (PTH), although the precise mechanism is not well understood (McCance 1998)
With the release of PTH, plasma calcium concentration is increased, in part by stimulating the nephrons of the kidney to
decrease calcium excretion. Plasma phosphate concentration is decreased by prompting greater excretion of phosphate
in the urine (Spence 1987). PTH also acts directly on bone, with two major effects: intense acute stimulation results in the
breakdown and resorption of bone, whilst chronic stimulation causes bone remodelling by the progressive breakdown
and consequent reformation of bone (McCance 1998).
Levels of magnesium also affect the secretion of PTH. A low level of magnesium in a person with normal calcium levels
acts as a mild stimulant to secretion of PTH, whilst excess magnesium levels can serve to decrease PTH secretion, even
if the person is hypocalcaemic.
The parathyroid glands have little ability to store PTH, and it is generally only synthesised when required (Nowak 1999).
Hyperparathyroidism
Hyperparathyroidism is abnormally increased activity of the parathyroid gland(s) and may be primary or secondary. It is
characterised by excess secretion of PTH. The primary form may be due to a benign or malignant parathyroid tumour, or
to multiple parathyroid hyperplasia (Nowak 1999)
Primary hyperparathyroidism is caused by a single adenoma in 80-90% of cases, multiple gland enlargement in 10 – 20%,
and by carcinoma in less than 1%. The cause of primary hyperparathyroidism is unknown, however, some familial
incidence has been noted (McCance 1998). In the primary condition, there is failure of the normal feedback mechanisms
which inhibit PTH secretion. Secondary hyperparathyroidism develops as a compensatory mechanism when serum
calcium levels are chronically below normal (as in a patient with chronic renal failure, vitamin D deficiency or malabsorption
syndrome). Patients with secondary hyperparathyroidism usually have multiple enlarged glands (McCance 1998).
Excess of PTH results in an alteration of the cells of bone, renal tubules and the gastrointestinal mucosa. The condition
is detected by a combination of laboratory tests for hypercalcaemia and a series of symptoms involving, among other
things, bone pain, spontaneous fractures (associated with demineralisation of bones), kidney stones, muscular weakness
and gastrointestinal symptoms (McCance 1998).
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Sonographic Technique
The patient is positioned and prepared as for a thyroid ultrasound. The patient is place in a supine position with a pillow
under the shoulders to hyperextend the neck as much as is comfortable for the patient. A high-frequency (preferably a
minimum of 10Mhz) linear array transducer is used to interrogate the region of the neck in a logical fashion. A typical
study of each side of the neck would involve transverse imaging from superior to the thyroid gland, sweeping inferiorly
to several centimetres below the inferior pole of the thyroid; and longitudinally from beyond the common carotid artery,
laterally to the trachea and thyroid isthmus, medially.
Hard copy images are taken as for the thyroid gland.
Sonographic Appearances
The sonographic appearances for enlarged parathyroid glands are essentially the same in the primary and secondary
conditions, although asymmetric enlargement is more often seen in the secondary form (Figs 1-4).
The appearances are:
•
Usually ovoid.
They may acquire an oblong, dumbbell or teardrop shape with increasing enlargement as a result of
their dissection between the longitudinal layers of the neck fascia (Rumack 1998).
•
Usually have a hypoechoic echogenicity (Rumack 1998).
Echogenicity of the parathyroid adenoma is usually much less than that of thyroid tissue. This is due
to the densely packed cellular nature of the gland, resulting in few reflective interfaces (Rumack 1998).
•
Most are homogeneously solid.
2% have internal cystic components due to cystic degeneration, or to true simple cysts.
They rarely display internal calcifications (Rumack 1998).
•
May display increased vascularity on colour flow and spectral Doppler.
Fig 1: Transverse image through the right lobe of the
thyroid, showing a hypoechoic enlarged parathyroid
gland.
Fig 2: Longitudinal image of the same parathyroid
gland.
Fig 3: Transverse image of the thyroid gland at the
isthmus. Note the hypoechoic area on the left.
Fig 4: Longitudinal image through the left lobe on the
same patient. This clearly shows the mostly anechoic
enlarged parathyroid gland.
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•
Most parathyroid adenomas are between 0.8 and 1.5cm long, but may, rarely, be up to 5cm long.
Carcinomas are usually larger than adenomas, generally measuring greater than 2cm, with an often-lobulated
contour or heterogeneous architecture.
Generally speaking, unless there is evidence of local invasion, carcinomas are indistinguishable from large
benign adenomas on sonography (Rumack).
Possible pitfalls
•
Prominent blood vessels adjacent to the posterior and lateral aspects of the thyroid gland
Use multiple scanning planes to show tubular structure of vessels.
Use colour flow and spectral Doppler to show flow in vessels.
Use Valsalva technique to show engorgement of vessels (Rumack 1998).
The left lateral border of the oesophagus may protrude from behind the trachea, simulating a parathyroid
adenoma.
Turning the patient’s head to the opposite side may accentuate the protrusion.
Transverse scanning may demonstrate the characteristic concentric ring pattern of bowel.
Longitudinal scanning will show the tubular nature of the oesophagus.
Asking the patient to swallow water through a straw will demonstrate the movement of fluid in the
oesophagus (Rumack 1998; Sanders 1998).
The longus colli muscle may simulate an adenoma in the transverse plane.
Longitudinal scanning will demonstrate the length of the muscle as well as the striations of skeletal
muscle.
Asking the patient to swallow will show movement of structures relative to the muscle, as it will not
move due to its attachment to the spine (Rumack 1998).
Thyroid nodules or cervical lymph nodes may mimic adenomas. In reality, it may be possible to differentiate
these from adenomas, but the following may assist
A posteriorly protruding thyroid nodule may mimic parathyroid adenoma. Look for a thin echogenic
rim separating the parathyroid adenoma from the thyroid gland. Thyroid nodules, because they arise
from within the gland do not show this tissue rim.
Thyroid nodules are often partially cystic and heterogeneous, unlike the usually hypoechoic
homogeneous parathyroid adenomas.
Enlarged cervical lymph nodes may look like adenomas but can often be distinguished from adenomas
by the characteristic echogenic band of the hilum (fat, blood vessels and fibrous tissue).
Cervical lymph nodes do not usually lie adjacent to thyroid tissue, although as mentioned previously,
parathyroid glands may be found distant from the thyroid gland (Rumack 1998).
Perhaps one of the major pitfalls in sonography of the parathyroid glands, when looking for gland enlargement
in hypercalcaemia, is the possibility, albeit unlikely, of these glands lying in ectopic locations. As mentioned
previously, the superior glands are usually found in their expected location adjacent to the postero-superior
aspect of the gland, with most inferior glands found posterior to the inferior thyroid pole, or in soft tissues just
below the thyroid gland. The four most common ectopic locations are:
In the retrotracheal region. Sonographic visualisation may be possible with maximal rotation of the
head to view the area posterior to the trachea.
In the upper mediastinum. Hyperextension of the neck and extreme caudal angulation may demonstrate
these, however, CT may be of greater value in this situation.
Within the thyroid gland. Although uncommon, these will be well visualised due to their hypoechoic
nature. Biopsy may be required to characterise the nature of the deposit.
Rarely, they may lie superiorly in the neck near the carotid bifurcation, and may resemble enlarged
lymph nodes (Rumack 1998).
•
•
•
•
Treatment
Initial treatment of proven hyperparathyroidism involves lowering the serum calcium level, increasing urine calcium
excretion with diuretics, and long-term utilisation of drugs that decrease the resorption of calcium from bone. Definitive
treatment is by surgical excision of the hyper-functioning glands (Rumack 1998).
References
McCance K.L., Huether S.E. (1998) Pathophysiology: The
Biologic Basis for Disease in Adults and Children. 3rd edition.
St. Louis. Mosby-Year Book Inc.
Rumack C.M., Wilson S.R., Charboneau J.W., (1998).
Diagnostic Ultrasound. 2nd edition. St. Louis. Mosby-Year Book
Inc.
Nowak T. J., Handford A.G., (1999). Essentials of
Pathophysiology: Concepts and Applications for Health Care
Professionals. 2nd edition. Boston. McGraw –Hill Companies.
Sanders R.C. (1998). Clinical Sonography: A Practical Guide.
3rd edition. Philadelphia. Lippincott.
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