Maisie L.
Shindo
ABSTRACT
Primary hyperparathyroidism is characterized by autono-
mous hypersecretion of one or more parathyroid glands.
The incidence of primary hyperparathyroidism in the
United States is approximately 100,000 patients per year.
causes of hyperparathyroidism can be classified as primary
hyperthyroidism, secondary hyperparathyroidism, tertiary
hyperparathyroidism, familial hypocalciuric hypercalcemia
(FHH), and parathyroid carcinoma. Appropriate manage-
ment of these patients with hyperparathyroidism requires
a thorough understanding of the pathogenesis as well as
typical and atypical presentations, knowledge of labora-
tory tests for proper workup, and interpretation of imaging
studies for localization of parathyroid adenomas. The abil-
ity to rapidly measure parathyroid hormone (PTH) level
has allowed parathyroid swgeons to assess biochemical
cure intraoperatively. Thus, swgical treatment of primary
hyperparathyroidism has evolved primarily into minimally
invasive single-gland excision. However, bilateral explora-
tion still plays an important role in treatment of secondary
and tertiary hyperparathyroidism. This chapter discusses
clinical, laboratory, and radiologic evaluation of the hyper-
parathyroid patient as well as surgical and postoperative
management
EMBRYOLOGY AND ANATOMICAL
CONSIDERATIONS
The inferior parathyroid glands are derived from the third
pharyngeal pouch and descend caudally with the thyroid
and thymus. The superior parathyroid glands are derived
from the fourth pharyngeal pouch, attach to the posterior
surface of the superior or mid portion thyroid and migrate
caudally with it. This pattern of migration explains the vari-
ability in the final arrest of the parathyroid glands, resulting
in many possible locations of ectopic or supernumerary
parathyroid glands. The limited course of the superior
glands leads to less variability in location compared to the
inferior gland. The inferior parathyroid glands can typi-
cally be found inferior, lateral or posterior to the inferior
pole of the thyroid, anterior to a plane drawn through the
recurrent laryngeal nerve. They can be quite variable in
location. The superior parathyroid glands are less variable
in location, the vast majority of them typically located near
the cricothyroid joint, just superior to where the recurrent
laryngeal nerve courses medially to enter the larynx. The
blood supply to the parathyroid glands is primarily from
the inferior thyroid artery, and in some there is contribu-
tion from the superior thyroid artery.
Humans typically have four parathyroid glands, two
superior and two inferior. Approximately 3% to 13o/o of
adults have supernumerary glands, and 5% have fewer
than four (1). Normal parathyroid glands vary consider-
ably in shape, size, and color. They are usually 2 to 3 mm
in width, 1 to 2 mm in thickness, and 4 to 6 mm in length.
Each gland weighs an average of 30 mg.
CALCIUM HOMEOSTASIS
Maintenance of extracellular calcium homeostasis involves
the interaction of calcium, PTH, calcitonin, and vitamin D
upon several target organs (kidney, bone, intestines, and
parathyroid). Parathyroid cells respond to minute changes
in the extracellular ionized calcium concentration, such
that a small change in calcium concentration results in a
change in the release rate of PTH in the opposite direction.
This calcium-sensing property of parathyroid cells allows
for the precise regulation of the extracellular ionized cal-
cium concentration within a narrow range, normally
1.2 to 1.3 mmol/L. The calcium-sensing ability of para-
thyroid cells is believed to be mediated by a G-protein-
coupled receptor on the parathyroid cell surface, known
as calcium-sensing receptor (CaSR) (2). Hypocalcemia
2131
2132 Section VII: Head and Neck Surgery
f SOH.VitD
1-25(0H)2Vil0 '
Increase osteoclast
activity Gl
ea>+ reabsorption Increase Ca 2•
absorption
Po4 ~~tlon /
' Figure 134.1 Actions of PTH.
induces PTH secretion, which raises the plasma calcium
level toward normal by effecting the release of calcium
from bone, increasing renal calcium reabso~ption, and
stimulating the production of 1,25-dihydroxyvi.tamin D.
Vitamin D in tum increases inttstinal absorption of cal-
cium. Osteoclasts and certain cells of the renal tubule also
exhibit calcium-sensing properties (Fig. 134.1 ).
PARATHYROID GLAND HISTOLOGY
The parenchyma of the parathyroid gland comprises pri-
marily chief cells that are small, round, and light in color
because of veJY weakly staining acidophilic cytoplasm.
The nucleus is centrally placed. Chief cells synthesize
PTH. Oxyphilic cells are less frequent. entirely lacking in
small children under 6 yea15, and increase in number with
age. Their cytoplasm is strongly acidophilic; the nucleus
is small and uniformly intensely basophilic. They con-
tain large amounts of mitochondria. These parenchymal
cells are arranged in anastomosing chords surrounded
by delicate connective tissue septa with abundant capil-
laries. A colllJiderable number of fat cells infiltrate the
gland beginning around puberty and may account for
about half the weight of the parathyroid glands in adults
(F'tg. 134.2).
Figure 134.2 Histology of nonnal parathyroid gland showing
chief cells and abundant fat cells.
HYPERPARATHYROIDISM
Hype~parathyroidism is classified into primary, second-
ary, and tertiary. Other rare causes of hyperparathyroidism
include parathyroid carcinoma and FIDI. It is important to
understand the different causes of elevated P1H in swgical
treatment considerations.
Primary Hyperparathyroidism
Primary hype~parathyroidism ( 1 o HPf) is characterized by
autonomous hypersecretion of one or more parathyroid
glands. The incidence of 1 • HPT in the United States is
approximately 100,000 patients peryeat and its prevalence
is estimated to be between 0.2% and 1% (3). It predomi-
nandy affects those between the ages of 55 and 70 with a
female-to-male ratio of2:1. Recent reports &om large series
indicate that the etiology is a single parathyroid adenoma
in 89% of cases, and hyperplasia or multiple adenomas
in the remainder (4). The incidence of double adenomas
ranges &om 4% to 16% (5-7).
Secondary and Tertiary Hyperparathyroidism
Secondru:y hypelparathyroidism (rHPf) is character-
ized by elevation of PIH level as a result of chronic hypo-
calcemia. most commonly &om chronic renal failure. but
it can also be caused by chronic vitamin D deficiency. In
chronic renal failure, renal tubular excretion of phosphate is
impaired. leading to hyperphosphatemia and binding with
free calcium. In addition, renal hydroxylation of vitamin D
is impaired leading to hypovitaminosis D. Vitamin D defi-
ciency leads to decreased calcium abso~ption from both
the gut and reabso~ption of calcium in the renal tubules.
1he end effect is lower extracellular calcium, which in Wl11.
stimulates the parathyroid glands to secrete PlH, resulting
in hyperplasia of the parathyroid glands and elevation of
PTH Jerel. Other possible causes of elevated PIH associated
with normal or low calcium are low calcium intake. inef-
ficient calcium abso~ption from gastrointestinal disorders,
and deficiency in intake of vitamin D; all these conditiolllJ
result in low calcium and a compen.satoty rise in P1H level.
In tertiru:y hypelparathyroidism, the chronically hyperplas-
tic glands autonomously secrete PTH, which usually ocaus
after successful renal transplantation but can also occur after
long-standing hypocalcemia of any other cause is corrected.
Parathyroid Carcinoma
Malignancy of the parathyroid gland is a vecy rare cause of
hypeiparathyroidism, representing less than 0.2% of patients
with 1 °HPT (7). It can rarely ocwrin association with hyper-
thyroid-jaw bone syndrome Patients with this syndrome
are cani.em of the HRPI2 gene (8). This condition tnJically
manifests with extremely high plasma calcium levels, usually
greater than 13 mg/dL. Rarely a mass may be palpable (9).
 Chapter 134: Hyperparathyroidism: Evaluation and Surgery
Familial Hypocalciuric Hypercalcemia
FHH is an autosomal dominant genetic disorder character-
ized by mutations in the intracellular part ofthe CaSR ( 10, 11 ).
The result is a defect in the CaSR of the parathyroid cell result-
ing in a lack of PIH suppression in the setting of hypercalce-
mia. Genetic linkage studies have shown that chromosome
3q is the major; but not the sole, locus for FHH-causing gene
(11,12). There are at least two other genetic loci, one linked
to chromosome 19p and another family desaibed in which
linkage to 3q and 19q loci has been excluded but the FHH-
causing gene has not yet been identified (13,14). While this
condition is usually diagnosed at a younger age, it may mani-
fest for the first time in older patients who have not sought
medical attention throughout life. It typically has a benign
course without the hypercalcemia-induced morbidities and
is therefore generally not a surgical disease ( 15, 16).
CLINICAL MANIFESTATIONS
The clinical presentation and complications of hyperpara-
thyroidism depends on the degree of hypercalcemia and
the rapidity in which the condition develops. The classic
symptoms and manifestations of the disease are
1. Musculoskeletal: bone and joint pai~ muscle pain,
muscle wealmess, osteopenia, osteoporosis, pseudog-
out, renal osteodystrophy
2. Genitourinary: nephrolithiasis, renal insufficiency, noc-
turia, polyuria
3. Gastrointestinal: constipation, peptic ulcers, hearth~
pancreatitis, abdominal pain, nausea
4. Neuropsychiatric: depression, anxiety, confusion,
memory loss, impaired thinking or "brain fog"
A popular mnemonic for remembering these symptoms is
"bones, stones, groans, and psychiatric overtones." Other
manifestations that can also be seen are fatigue, calciphy-
laxis (soft tissue calcification), cardiocalcinosis, and band
keratopathy.
EVALUATION
Evaluation ofthe hypercalcemic or hyperparathyroid patient
starts with a good history and determination of what man-
ifestations of the disease the patient has. Information on
use of medications that can cause hypercalcemia should be
elicited, specifically thiazide diuretics, lithium, dietary sup-
plemental calcium, and vitamin D. Family history of hyper-
calcemia or hyperparathyroidism should be attained, as the
patient may have familial hyperparathyroidism or FHH.
Laboratory Studies
The diagnosis of 1 "HPT is made based on plasma cal-
dum and PTH levels. Plasma calcium and PTH levels
should be drawn on the same day. Normal range for
2133
plasma calcium in most laboratories is 8.5 to 10.2 mgjdL
(or 2.2 to 2.5 mmolfL). Since most of the body's plasma
calcium is bound to albumin, a decrease in plasma albu-
min will lower the plasma calcium level even though the
free calcium remains the same. Therefore if the albumin
level is low, the plasma calcium should be corrected such
that 0.8 mgjdL should be added to the total calcium for
every drop in albumin of 1.0 gjdL. Alternatively, one can
measure ionized calcium, which represents free calcium.
Normal range for ionized calcium in most labs is 1.14
to 1.28 mmol/L. PTH is an 84 amino acid peptide chain
with a C-terminal and anN-terminal. Laboratories in the
past measured PTH levels by measuring theN-terminal or
C-terminal. Today, the most accurate assessment of PTH
level is measurement of the entire chain, known as intact
P'IH. Normal range for PTH in most laboratories is 15 to
72 pgjmL. The classic laboratory findings of 1 "HPT are
elevated plasma calcium level and high intact PTH level.
Some patients may present with elevated plasma calcium
levels and PTH levels only in the midrange to upper lim-
its of normal. In the absence of 1 "HPT, elevated plasma
calcium should suppress the PTH level. Therefore, unsup-
pressed PTH in the setting of elevated plasma calcium
is "inappropriate" and indicates 1 "HPT. In addition to
plasma calcium and intact PTH levels, it is also helpful to
look at 24-hour urine calcium and serum phosphate lev-
els. Typically in 1 o HPT, the serum phosphate is low, and
the 24-hour urine calcium is normal or elevated. Some
patients may present with only periodic elevations of
plasma calcium. In patients with mildly elevated or nor-
mal calcium, if the PTH levels are persistently elevated,
the serum phosphate is low and 24-hour urine calcium
is high (greater than 350 mg), the diagnosis of 1 °HPT
is likely. In a patient with normal or occasional mildly
elevated calcium levels, intermittent mild elevation of
P'IH, normal phosphate and low to normal 24-hour urine
calcium, the diagnosis of 1 o HPT is somewhat question-
able. If the diagnosis is uncertain, it would be prudent
to repeat calcium and intact PTH levels and follow the
laboratory values. Other than 1 o HPT, the differential
diagnosis of hypercalcemia includes thiazide diuretics,
immobilization, and hypercalcemia of malignancy and
granulomatous diseases. Contrary to 1 °HTP, the PTH
level is generally low in these conditions.
Elevated plasma calcium and PTH with a low 24-hour
urine calcium is suggestive of FHH. The diagnosis of FHH
should be considered if there is a family history of hyper-
calcemia, PTH is not markedly elevated, or the 24-hour
urinary calcium is low. In that setting 24-hour urine for
calcium, plasma calcium, serum creatinine and 24-hour
urine creatinine levels should be obtained to calculate
calcium-creatinine clearance ratio. These tests should all
be performed at the same time. FHH manifests with hyper-
calcemia and mildly elevated or normal PTH levels (17,18).
In FHH, the 24-hour urine calcium is below normal range.
The calcium-creatinine clearance ratio, calculated using
2134 Section VII: Head and Neck Surgery

the following formula, is helpful in differentiating FHH the diagnosis of 1 • HPT can be confirmed if the imaging
from 1 o Hl!f. study Wlequivocally detects a parathyroid adenoma. The
two most commonly used imaging studies are parathyroid
24- hour urine calcium serum creatinine ulttasound and technetium-99m-sestamibi parathyroid
serum.calcium x 24-hoururinecreatinine (MIBI) scan. The sensitivity of each test varies considerably,
depending on the equipment and more importantly how
A ratio that is greater than 0.01 is consistent with 1 °HPf, experienced is the individual performing or interpreting
though does not absolutely exclude FHH, and less than the study. In the hands of a highly experienced ultraso-
0.01 is suggestive ofFHH. nograph~ which can be radiologist, surgeon, or endocri-
Some patients may also present with plasma calcium nologist. the sensitivity is 80% to 85%. On ulttasoWld,
values in the mid to upper normal range but exhibit ele- parathyroid adenomas appear hypoechoic and hypervas-
vated ionized calcium. In recent yean, a new entity known cular (Fig. 134.3). Generally ultrasound should be able
as normocalcemic hyperparathyroidism has been recog- to detect adenomas located dorsal to the esophagus. The
nized where calcium level, including ionized calcium, limitation of ulttasound is detecting adenomas located
is normal and l!fH is elevated (19,20). It has been pro- rettoesophageally or in 1he mediastinum. The principle
posed that there is a generalized Wgeted tissue resistance of sestamibi parathyroid scanning is that ~~ MIBI tracer
to PIH in patients with this entity. A study by Maruani is taken up by both the thyroid and parathyroid adenoma
et al. (21) showed PIH-dependent functions of the kid- but washes out of the thyroid faster than 1he parathyroid.
ney to be attenuated in the normocalcemic hype:rparathy- lherefore early images at 20 minutes after injection are
roid patients despite an identical primary hyperseaetion obtained, followed by delayed images typically at 2 hours
of PIH. They concluded that: (a) PIH induces milder (Fig. 134.4A). It is quite specific; howeve~;. its sensitivity
biologic bone effects than in hypercalcemic patients; {b)
Calcium absorption in the renal tubular system is lower in
patients with normocalcemic 1 o Hl!f compared to that of
patients with hypercalcemic form of the disease. (c) The
ability of l!fH to decrease tubular phosphate reabsorption
and stimulate synthesis of 1,25-dihydroxyvitamin D is also
blunted in the patients who remain normocalcemic, com-
pared with those who are hypercalcemic. Normocalcemic
1 • Hl!f can be difficult to diagnose. and 2 • J.7fH from other
conditions such as chronic vitamin D deficiency; renal
insufficiency; and renal calcium leak need to be excluded
:first In 2 • HYf, the typical laboratory finding is elevated
J.7fH but unlike 1 •HPT, 1he plasma calcium level is low or
normal. Those with 2 •HJ!f &om chronic renal failure also
exhibit elevated blood urea nitrogen, serum creatinine. and
phosphate.
Vitamin D levels should also be measured. In 1 ° HPf, the
25-hydroxy form will typically be low; and 1,25-hydroxy
form is often elevated. Vitamin D levels are generally not
used to make a diagnosis of 1 ° HPr but may be helpful
in differentiating rHPT due to chronic vitamin D defi-
ciency from •normocalcemic• 1 •HPf. Since both condi-
tions will present with normal calcium and elevated PIH,
ifthe 25-hydroxyvitamin D level is low; one can correct the
vitamin D deficiency and follow the calcium level. If the
calcium level becomes elevated or the PrH level does not
correct back down to normal range with vitamin D replace-
ment,. the diagnosis is likely to be 1 °HPr.

Imaging Studies
While imaging studies are used primarily to localize
para1hyroid adenomas for surgical planning, they may
Figure 134.3 Ultrasound of left Inferior parathyroid adenoma.
also be helpful in confirming the diagnosis of 1 °HPf. If '1bp: adenoma (P) between the trachea and carotid artery; Bottom:
the lab values are intermittently or only mildly elevated, adenoma Is at the inferior tip of the thyroid.
 Chapter 134: Hyperparathyroidism: Evaluation and Surgery
20 min
A on Ute transverse and sagittal views.
can be low in detecting small glands. One of ita limitations
is that conau:rent thyroid disease can result in a false-
positive study. Another limitation is that the images are
two-dimensional (20) planer views and therefore do not
provide information on the depth of the adenoma. This
information is important for glands that are located infe-
rior to the thyroid. On a 20 planer anterior-posterior view,
without the information on the depth of the gland, a ret-
roesophageal or paraesophageal gland can look virtually
identical to an anteriorly located inferior gland. Oblique
views or single photon emission computerized tomogra-
phy (SPEer) obtained in conjlUlction with the 20 planer
sestamibi scans can be helpful in providing informa-
tion on the anterior-posterior location of the adenoma
(Fig. 134.48). Knowing this information obviates unneces-
saxy mensive or mi8sed exploration. If localization with
sestamibi scan and ulttasound performed in experienced
hands fail, thin-cut cr with intravenous contrast may be
helpful. It is especially useful in detecting ectopic glands
such as paraesophageal, retroesophageal, or mediastinal
glands (Fig. 134.5).
2135
io-----~--
Transverse
Figu,. 134.4 Sestamibi parathyroid scan. A: 20 planer images
showing a left. inferiorly located adenoma 1: SPECT revealing Ute
adenoma (arrow) to be located posterior to Ute plane of the thyroid
INDICATIONS FOR SURGERY
Parathyroidectomy is indicated in patienta with 1 • HPTwho
have complications of the disease, such as nephrolithiasi!,
hypen:::alcemic crisis (calcium greater than 12.5 mw'dL),
or are symptomatic with musruloskeletal pain, muscle
weakness, or severe neuropsychiatric dysfunction (irritabil-
itf, fatigue, oonfusion, or insomnia). However, since the
gamut of musa:ilar and neuropsychological symptoiJUI is
broad, it is often diffirult to determine if the symptoms
are truly due to 1 • HPT. The indications for swgecy in the
asymptomatic patient were first establi!hed in 1990 by a
NIH sponsored consensus panel and modified in 2002
(Table 134.1) (22). In2009, theguidelineswe:rere:reviewed
at the Third International Workshop on Asymptomatic
Primaxy Hyperparathyroidism, and the recommendations
basically remained the same except for three changes: (a)
hypen:::alciuria (24-hoururine calcium greater than 400 mg)
was eliminated,. (b) creatinine clearance was changed &om
less than 30% to less than 60 ml/min, and (c) bone density
T-score at any site less than -2.5 and/or previous &acwre or
2136 Section VII: Head and Neck Surgery

SF-36 survey; aself-ranked 36-item Slli'Vey that assesses gm-

eral health. as well as the Parathyroidectomy Assessment
of Symptoms sw:vey. Both have been shown to improve
quickly after surgery (24-27). Furthermore, these improve-
ments are sustained long term (24,27,28). Bone density
and hyperlipidemia have also been shown to improve with
parathyroidectomy (29,30).
Indications for parathyroidectomy in 2 °HPT have been
based mostly on presence of musculoskeletal symptoms,
such as bone and joint pain, muscle weakness, or radio-
logic evidence of renal osteodystrophy. In recent years
treatment with vitamin D and its analogs have allowed
the majority of these patients to be managed by medi-
cal treatment for many years without severe symptoms
of high bone turnover. Nevertheless, chronic high values
of phosphate, calcium, and PTH in renal failure patients
have been shown to be associated with increased mortal-
FiguN 134.5 CT with contrast demonstrating a right paraesoph- ity, mainly due to cardiovascular complications induced
ageal adenoma (arrow).
by ectopic calcifications (31,32). Therefore, tile main indi-
cation currently for parathyroidectomy in these patients
bone fragility (Thble 134.1) (23 ). Since parathyroidectomy is when serum phosphate, calcium, and PTH levels can-
traditionally has been performed under general anesthesia not be maintained within target ranges with vitamin D or
and required bilateral exploration, which has potential sig- D-analog therapy (32,33). The introduction of cinacalcet
nificant rislcB, many asymptomatic patients had gmerally a new allosteric modulator of the CaSR on parathyroid
been obseiVed rather than treated swgically. Howe:va; in cells that reduces 1!.11-l secretion, has also reduced the need
recent years, parathyroid swgery has evolved into mini- for parathyroidectomy by 90% (34). Swgecy is indicated
mally invasive focused exploration often under local anes- when cinacalcet cannot be continued due to adverse side
thesia, with significantly lower surgical risb. Therefore, effects or poor compliance, or if the condition is refractory
swgical consideration should be given to asymptomatic to cinacalcet therapy. Several studies have shown that para-
patients, even in healthy elderly patients with a reasonably thyroidectomy in dialyBis patients with advanced 2 o HPT is
long life expectancy, if they are appropriate candidates for associated with reduced incidence of major cardiovascular
minimally invasive parathyroidectomy (MIP). events and overall lower mortality (35-38).
Multiple studies in the last decade have proven the ben-
efits of parathyroidectomy for 1 o HPT. Studies on quality of
PARATHYROIDECTOMY
life postparathyroidectomy have been performed using the
Bilateral Exploration
While the majority of parathyroid surgeries today are per-
formed using a targeted approach exploring only a single
INDICA110NS FOR gland (see next section), surgeons still need to be thor-
PARATHYROIDECTOMY IN oughly familiar with the principles of 4-gland exploration,
ASYMPTOMA11C PATIENTS which is essential for treatment of hyperplasia, 2 o HPT, and
2002 2009 tertiary hyperparathyroidism. Knowledge of parathyroid
gland locations is the key to successful4-gland exploration.
Ca2+ > 1 mg/dL above upper Ca2+ > 1 mg/dL above upper Embryologically, the inferior parathyroid glands arise from
limit of normal limit of normal
Creatinine clearance reduced Creatinine clearance <60 mLimin
the dorsal wing of the third phat:yngeal pouch, and the
by30% vmttal wing of the third brachial pouch differentiates into
Reduction in bone density Reduction in bona density (hip, the thymus. lhe thymus then migrates caudally, pulling
(hip, L Spina, Radius) L Spine, Radius) T-score the parathyroids with it Descent of the inferior parathy-
T-score< -2.5 < -2.5; Previous fracture or roid glands usually stops at tile dorsal (posterior) surface
bone fragility
of the inferior thyroid outside of its fibrous capsule. At
Under 50 y of age Under 50 y of age
Medical surveillance not Medical surveillance not feasible times the inferior parathyroids may not lose its connection
feasible (e.g., coexistent (e.g., coexistent illness) or not to the thymus and thus descend into the anterior medias-
illness) or not possible (e.g., possible (e.g., poor follow-\lp) tinum with the thymus. The superior parathyroid glands
poor follow-up) arise from the dorsal wing of the fourth pharyngeal pouch
2~ urine calcium >400 mg
and descend with the thyroid. lhe superior parathyroids
 Chapter 134: Hyperparathyroidism: Evaluation and Surgery 2137

are generally located more posterior and medial than the

inferior parathyroids, and their final resting point is usu-
ally on the doiSal surface of the mid or superior pole of
the thyroid. However, they may also be ectopically located
lateral or posterior to the esophagus. Rarely can they be
located superior to the superior pole. Parathyroid glands
can also be located in the carotid sheath or inside the
fibrous capsule of the thyroid (intrathyroid).
When performing 4-gland exploration, it ia impor-
tant to search for each gland systematically moving from
one quadrant to the next in the expected locations of the
parathyroid glands. If the glands are not identified in the
expected locations, the ectopic locations of the missing
gland should then be systematically explored. For exam-
ple, if a superior gland ia missing, the paraesophageal and
rettoesophageal areas should be explored. If an inferior
parathyroid is missing, exploration should be directed
first at the most common ectopic location for the inferior
glands-the thymus and superior mediastinum. Ifthe miss-
ing parathyroid is not found in these locations the carotid
sheath should be explored. 1he last location to consider
ia intrathyroid, in which case a hemithyroidectomy on the
side of the missing gland may be necessary. An alterna-
tive to hemithyroidectom:y for identifying an intrathyroid
adenoma is to perform intraoperative thyroid ultrasound
with a small probe. If a hypoechoic nodule adjacent to the
posterior capsule is found (F"tg. 134.6), needle aspiration
of the lesion can be performed. The sample can be rinsed
with approximately 2 mL of normal saline and a rapid PfH
assay can be performed intraoperatively. The PTH level will
be high if the lesion is a parathyroid adenoma.
When performing subtotal parathyroidectomy, it is
important to not completely excise or dewscularize each
parathyroid gland as soon as it is identified. As each. one is
identified, it is best to biopsy part of the gland for confinna- Figure 134.6 Ultrasound showing lntrathyrold parathyroid.
tion and temporarily keep a portion in situ. Once all four
glands are histologically confirmed, the most viable residual
gland should be selected for preservation in situ, and then reimplant some of the excised parathyroid tissue in the
erosion of the other glands can be performed. Some of the forearm, although one could ;ugu.e that if the IOPTH at the
excised parathyroid glands should be ayopreserved for pos- end of the exploration is in midnormal range, reimplan-
sible future use. Approximately 30 to 40 g of parathyroid ti• tation may not be necessaif. Regardless, some of the ti•
sue should be prepared for reimplantation. It is preferable sue should be ayopreserved. Extent of parathyroidectomy
to reimplant into the brachioradialis muscle of the patient's is more conttoversial for 2 o HPf or tertiar:y hypeq>arathy-
nondominant hand. The parathyroid tissue ia incised into roidism. Unlike 1 °HPT, chronic renal failure with hypo-
approximately 1x 1x 3 mm pieces (Fig. 134.7A) and each calcemia is a strong stimulus for parathyroid hyperplasia.
piece is miaoswgically reimplanted into the brachiora- 1herefore, if subtotal parathyroidectomy is performed,
dialis muscle. Each reimplantation site should be marked any glandular tissue left behind can become hyperplastic
with hemoclip and/or colored permanent suture for ease again in the future in these patients. Consequently, some
of identification if the need arises to someday excise hyper- argue that total parathyroidectomy with reimplantation
plutic reimplanted tissue (Fig. 134.78). in the forearm is preferred in these patients to obviate the
The decision to perform subtotal versus total parathy- need for neck recxploration. Elevated preoperative cal-
roidectomy depends on the disease and to some extent sur- dum and post-op IOPTH levels were significant predictors
geon's preference. Those with hyperplasia due to 1 °HPI' for reaurent disease, while postoperative PTH less than
should undetgo subtotal parathyroidectomy, with the goal 10 pmol/L had a positive predictive value of 97.5% for
for the intmoperative rapid parathyroid hormone (IOPTH) cure (39). For those who are younger patients, post kid-
to return to the mid-normal range. Most would also ney transplants, or candidates for kidney transplantation,