ENDOCRINE SURGERY
Surgical management of
parathyroid disease
Sheila Fraser
Abstract
Primary hyperparathyroidism is a common endocrine disorder caused
by excessive PTH production by one or more parathyroid glands. The
diagnosis is via biochemistry and surgery is the only definitive treat-
ment. All patients may be considered for surgery, particularly those
under 50 years of age, symptomatic disease or evidence of end-
organ damage. Imaging studies are often used to plan surgical strat-
egy. The majority of patients with primary hyperparathyroidism have
single gland disease. Positive imaging studies allow patients to un-
dergo targeted surgery. Patients with negative imaging should be
offered a traditional four-gland bilateral neck exploration. Secondary
hyperparathyroidism is most commonly caused by vitamin D defi-
ciency and renal failure. Medical management is the first-line treat-
ment, followed by parathyroidectomy in selected cases with renal
disease and extremely high PTH levels. Tertiary hyperparathyroidism
is seen in patients with continued autonomous function of the parathy-
roid glands after removal of the underlying stimulus. It is commonly
seen in renal transplant patients and parathyroidectomy has a role.
Keywords Hypercalcaemia; parathyroidectomy; primary hyperpara-
thyroidism; secondary hyperparathyroidism; sestamibi; SPECT-CT;
tertiary hyperparathyroidism
Embryology and development (see pages 00-00 of this
issue for more detail)
An understanding of the embryology and development of the
parathyroid glands is vital when considering parathyroid sur-
gery. The parathyroids are the first endocrine glands to develop,
usually during the 5the6th weeks of gestation. There are two
pairs of parathyroid glands, a superior and inferior pair. The
superior glands arise from the dorsal aspect of the fourth bran-
chial pouch, while the inferior develop from the dorsal aspect of
the third branchial pouch. The pairs of parathyroid glands are
usually symmetrically arranged on opposite sides of the neck.
The inferior parathyroid glands descend caudally and anteri-
orly along with the thymus. They have a longer decent than the
superior glands and therefore have a more variable location.
Over two-thirds of inferior parathyroid glands are found near the
lower pole of the thyroid; however, they may lie anywhere along
the line of the descent of the thymus, most commonly within the
thyrothymic tract, but also within the superior mediastinum and
rarely (when descent is impaired) anterior to the carotid sheath.
The superior parathyroid glands descend with the thyroid,
following the migration of the ultimobranchial bodies. Due to the
shorter migration the superior parathyroids tend to show less
Sheila Fraser MBChB MD FRCS is a Consultant Endocrine Surgeon at
St. James’s University Hospital, Leeds Teaching Hospitals NHS
Trust, Leeds, UK. Conflicts of interest: none declared.
SURGERY xxx:xxx
Please cite this article as: Fraser S, Surgical management of parathyroid disease, Surgery, https://doi.org/10.1016/j.mpsur.2020.10.004
anatomical variation and are usually found just outside the
thyroid’s fibrous capsule, more posterior and medial than the
inferior parathyroid glands. The majority are located just above
the junction of the inferior thyroid artery and recurrent laryngeal
nerve (RLN). Ectopic superior parathyroid glands are often
located in a para-oesophageal or retro-oesophageal position.
Around 20% of parathyroid glands lie in an ectopic position
and this is a common cause of failed parathyroid surgery. A small
number, up to 4% have been found completely within the thy-
roid. Supernumerary glands have been quoted as present in up to
13% of patients on random autopsies, frequently seen in the
thymus or the along the embryological descent of the inferior
parathyroid glands. Supernumerary parathyroids are thought to
be due to tissue fragmentation during migration of the glands,
rather than true extra glands. Furthermore, about 3% of patients
are thought to have an absent parathyroid gland.
Function of the parathyroid glands (see pages 00-00 of this
issue for more detail)
Over 99% calcium in the body is located within the bones, with
only 1% in other tissues and fluids. Serum calcium concentration is
kept in a very tight range. The key regulator of calcium homeo-
stasis is parathyroid hormone (PTH), produced by the chief cells of
the parathyroid glands. PTH is released in response to small drops
in serum calcium levels that activate calcium-sensing receptors
(CaSR) on the chief cells. Increased PTH levels raise serum calcium
levels by instigating additional reabsorption of calcium by the renal
tubules and stimulate osteoclasts causing bone resorption. PTH
also activates the enzyme 1-ahydroxylase in the proximal tubules
of the kidneys, causing conversion of 25-hydroxyvitamin D to its
active metabolite 1,25-dihydroxyvitamin D stimulating absorption
of calcium and phosphate in the gastrointestinal tract.
Definition of hyperparathyroidism
Hyperparathyroidism is defined as excess parathyroid hormone
production resulting in hypercalcaemia and is classified as pri-
mary, secondary and tertiary hyperparathyroidism.
Primary hyperparathyroidism (PHPT)
PHPT is the most common cause of hypercalcaemia in the outpatient
setting. One or more parathyroid glands are overactive, causing
hypercalcaemia due to inappropriately high and unregulated PTH
levels. PHPT is a biochemical diagnosis with raised calcium and
normal or high PTH levels. Normal PTH levels on the background of
hypercalcaemia are considered abnormal and in keeping with pri-
mary hyperparathyroidism, as PTH secretion should be suppressed
with high serum calcium levels. Primary hyperparathyroidism is
associated with normal or high urinary calcium excretion.
Symptoms of primary hyperparathyroidism
The clinical presentation of PHPT has changed significantly since
the introduction of PTH testing in the 1970s. Previously patients
presented with the clinical manifestations of hypercalcaemia,
classically summarized by the old adage ‘stones, bones, abdom-
inal groans and psychic moans’. The majority of patients now are
found on routine biochemical testing or have non-specific symp-
toms, in particular lethargy, muscle weakness and bony pains.
1 Ó 2020 Published by Elsevier Ltd.
 ENDOCRINE SURGERY
Stones refers to nephrolithiasis and nephrocalcinosis, pa-
tients may also report polyuria and polydipsia. All patients not
known to have renal calculi should have a renal ultrasound.
Bones represents osteopenia and osteoporosis frequently seen
in patients with PHPT due to increased continuous osteoclast
activity. Rarely, osteitis fibrosa cystica, brown tumours and
pathological fractures are seen. DEXA bone scan to measure
bone mineral density is recommended, especially at the distal
third of the radius, as PTH predominantly has an effect on
cortical bone.
Abdominal pain can present as peptic ulcer disease, due to
increased gastric acid production, pancreatitis or constipation.
Memory impairment, depression, irritability and lack of con-
centration are frequently seen.
Incidence and aetiology
Primary hyperparathyroidism is the third most common endo-
crine disorder, with a prevalence of 1e7 per 1000 people in the
general population. The frequency increases with age, and is the
highest in post-menopausal women with a 3e4:1 ratio of women
to men. Prior exposure to ionizing irradiation and lithium ther-
apy are risk factors for PHPT. Patients who received previous
irradiation to the head and neck region are at increased risk of
PHPT, frequently around 20e40 years after exposure. Long-term
lithium treatment is associated with PHPT in up to 15% people
with an increased incidence of multi-gland disease.
The majority of patients (85e90%) diagnosed with PHPT have
a single adenoma while 3% have double adenomas. Multi-gland
disease (four-gland hyperplasia) occurs in 10e15% patients and
parathyroid carcinoma is a rare cause in less than 1% of patients.
The majority of cases of PHPT are sporadic and less than 10%
are associated with familial inherited syndromes. Genetic con-
ditions include multiple endocrine neoplasia (MEN) type 1 and
2a, familial isolated primary hyperparathyroidism, and
hyperparathyroidism-jaw tumour syndrome (HPT-JT). Around
15% patients under 40 presenting with apparently sporadic
PHPT have an underlying genetic syndrome and young patients
should be referred for genetic counselling and screening.
The prevalence of PHPT varies in each syndrome. Hyper-
parathyroidism is usually the first endocrinopathy in patients
with MEN1 to be diagnosed and occurs in up to 90% of patients.
In MEN2a, 20e30% patients develop PHPT, with MTC and
phaeochromocytomas being more frequently diagnosed. Both
MEN1 and 2a are autosomal dominant conditions with MEN1
caused by inactivating mutations of the MEN1 gene and MEN2a
due to activating mutations of the RET oncogene.
Hyperparathyroidism-jaw tumour syndrome (HPT-JT) is an
autosomal dominant disorder with mutations in the CDC73 (also
called HRPT2) gene. It is characterized by parathyroid tumours
(of which 10e15% are parathyroid carcinomas), and fibro-
osseous tumours of the jawbone. HPT-JT patients are also
prone to renal abnormalities, including Wilm’s tumours,
hamartomas and polycystic disease, and women can present
with benign or malignant uterine tumours. The syndrome usu-
ally manifests at a young age, either in late adolescence or early
adulthood.
Familial isolated PHPT is an autosomal dominant condition
that may be due to different mutations in either MEN1 and
CDC73 genes; where the predisposition is only to PHPT.1
SURGERY xxx:xxx
Please cite this article as: Fraser S, Surgical management of parathyroid disease, Surgery, https://doi.org/10.1016/j.mpsur.2020.10.004
It is important to rule out familial hypocalciuric hyper-
calcaemia (FHH) during investigations for PHPT. FHH is an
autosomal dominant disorder usually due to inactivating muta-
tions in the gene for the calcium-sensing receptor (CaSR). This
should be considered in young patients with mildly elevated
calcium and PTH levels and low urinary calcium levels. Low
vitamin D levels can interfere with 24-hour urinary calcium
levels, but this can be corrected and urine calcium rechecked if
there are any concerns. Confirmation is via calcium/creatinine
urinary clearance ration (CCUCR) and if this is less than 1%,
patients should be referred to an endocrinologist or geneticist
rather being planned for surgery. Patients with FHH are largely
asymptomatic and do not need parathyroid surgery.
Indications for surgery (Table 1)
Surgery remains the only definitive treatment for PHPT. All pa-
tients with evidence of end organ damage or symptomatic patients
with a biochemical diagnosis of PHPT should be offered surgery.2
There remains debate about whether or when to intervene in
patients with mild asymptomatic PHPT with no end-organ
damage, who do not fulfil the criteria above for surgery.
Studies have demonstrated that there is a slow decline in bone
mineral density over several years and that this improves after
surgery. Increased cardiovascular morbidity has also been
recognized in patients with apparent asymptomatic hyperpara-
thyroidism; however, data on potential cardiovascular manifes-
tations is still not yet definitive. Many endocrinologists prefer
conservative management in mild, asymptomatic disease unless
patients fit one of the criteria mentioned in Table 1.3
When patients do not fulfil the criteria for surgery or are unfit
or unwilling to proceed they should be regularly monitored
(Table 2). The current protocol for follow up is that suggested by
the 2009 National Institute of Health Consensus Conference and
the NICE guidance from 2019.
Medical treatment for PHPT
Patients with mild asymptomatic PHPT should be monitored as
advised above. Medical management may be required in selected
patients.
Cinacalcet is a calcimimetic which can lower serum calcium
and PTH values. Cinacalcet is an agonist of the CaSR, changing
the structural configuration and increasing sensitivity to serum
calcium, therefore reducing PTH and calcium levels. It is
Current indications for parathyroid surgery
Symptomatic patients Asymptomatic patients
Hypercalcaemic crisis Age <50 years
Renal calculi Serum calcium level >0.25 mmol/L above
the upper limit of normal
Fragility fractures Creatinine clearance reduced to <60 ml/min
Osteoporosis T-score < 2.5 at any site or presence
of vertebral fractures
Any suspicion of Silent renal calculi or nephrocalcinosis
parathyroid cancer on imaging
Symptoms of Urine calcium excretion of
hypercalcaemia >10 mmol/day
Table 1
2 Ó 2020 Published by Elsevier Ltd.
 ENDOCRINE SURGERY
currently indicated in patients with contra-indications to surgery,
those who had unsuccessful surgery or have declined an opera-
tion. It is usually started in patients with adjusted calcium levels
over 2.85 mmol/L who are very symptomatic or in any patient
with adjusted calcium over 3.00 mmol/L. Patients may be started
on cincalcet to control levels until they can undergo surgery.
However, many patients cannot tolerate cinacalcet and it does
not affect the underlying bone density or renal disease.
Bisphosphonates will reduce PTH driven bone resorption, so
increasing bone density but no reduction in serum calcium
levels has been observed (unless high intravenous doses are
used). PTH levels may actually increase with bisphosphonate
treatment.
Imaging
PHPT is a biochemical diagnosis and imaging should not be used
to select patients for parathyroid surgery. However there has
been a move away from the traditional four-gland bilateral neck
exploration to minimally invasive surgery. Therefore most pa-
tients undergo preoperative imaging to identify those with single
gland disease, in whom focused surgery can be performed.
Although imaging can help plan operative strategy, it should not
deter an experienced surgeon from proceeding to a bilateral neck
exploration if the diagnosis is confirmed.
Routine first-line imaging studies in PHPT are ultrasound and
technetium 99m-sestamibi scintigraphy. Neck ultrasound is a
non-invasive cheap modality without any ionizing radiation. It
has the advantage of assessment of the thyroid gland at the same
time, allowing concurrent thyroid pathology to be identified. In
skilled hands, sensitivities and specificities of over 70% are re-
ported (Figures 1 and 2); however, ultrasound is very operator
dependent. In addition, it cannot visualize the mediastinum or
retro-oesophageal areas and has reduced sensitivity in patients
with multi-nodular thyroid disease.
Sestamibi scanning has a high sensitivity, reported as ranging
from 70 to 95%, with a specificity of 90%. Increased sestamibi
uptake is seen as it concentrates in the mitochondria, and para-
thyroid adenomas have a greater concentration of oxyphilic cells
with large numbers of mitochondria. False negative results can
be seen with small parathyroid adenomas, those with reduced
oxyphil content and in multi-nodular goitres.4
The sensitivity of dual concordant imaging when a para-
thyroid adenoma has been demonstrated reaches over 95%.
Increasingly, SPECT-CT (single photon emission computed
tomography/computed tomography) in combination with sesta-
mibi is being used as a first line investigation. It provides
improved anatomical localization of parathyroid adenomas and
has been reported to slightly increase the sensitivity5 (Figure 3).
Monitoring of patients who do not undergo parathyroid
surgery
Investigation Frequency
Serum calcium Annually
Serum creatinine/eGFR Annually
Bone density Every 2e3 years
Table 2
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Please cite this article as: Fraser S, Surgical management of parathyroid disease, Surgery, https://doi.org/10.1016/j.mpsur.2020.10.004
When both the ultrasound and sestamibi/SPECT-CT are
negative, there is a higher chance of multi-gland disease. In pa-
tients with PHPT who have not had previous surgery the NICE
guidelines do not advocate further imaging but recommend a
four-gland bilateral neck exploration by an experienced surgeon.
Additional imaging has a role in persistent or recurrent disease
and there are several modalities available. 4D-CT has been used
for the detection of parathyroid adenomas not seen on traditional
imaging. It delivers both functional and anatomical information
and has reported increased sensitivity rates. However, it requires
large radiation doses, especially to the adjacent thyroid, prevent-
ing routine use and should be used with care in young patients.6
MRI scanning is generally reserved for patients where re-do
surgery is being considered. It is a better investigation in this sit-
uation as surgical clips can cause artifacts on CT scanning. It also
has a role in pregnancy, because of the lack of ionizing radiation.
More recently, new imaging techniques have been studied
using positron emission tomography (PET)-CT, although the
ideal tracer is still being debated. Both 11C-choline and 18F -flu-
orocholine PET-CT have been used with high sensitivities re-
ported for detection of parathyroid adenomas. However, the cost
effectiveness, radiation exposure and availability of the tracer all
need to be considered and there are few high quality studies.7
Surgery for PHPT
The traditional surgical approach in PHPT is a four-gland bilat-
eral neck exploration via a standard cervical collar incision. Cure
rates of over 95% are seen when performed by an experienced
surgeon. Attempts are made to identify all four parathyroid
glands and one or more enlarged glands are removed.
With the use of preoperative localization studies and the
majority of patients having single gland disease, there has been a
shift towards focused or minimally invasive parathyroid (MIP)
surgery. This refers to a limited scan-directed unilateral operation
that targets the specific gland identified on imaging. Advantages
include decreased operating time, reduced complications, espe-
cially hypocalcaemia as the remaining parathyroid glands are
undisturbed and an equally high success rate of 95%. MIP is not
recommended unless preoperative imaging is definitive for a
single parathyroid enlargement.8
MIP is usually performed through a lateral incision, situated
over the medial edge of the sternocleidomastoid muscle and
lateral aspect of the strap muscles. The common carotid artery
and thyroid are important anatomical landmarks. An inferior
parathyroid adenoma is usually in a more anterior position,
closely related to the inferior pole of the thyroid and with the
RLN deep to the adenoma. If imaging studies suggest a superior
parathyroid adenoma, this is generally deeper and care should be
taken to recognize the RLN, which maybe anterior and close to
the adenoma (Figure 4).
If the parathyroid adenoma cannot be located via a MIP or if
there is a suspicion of multi-gland disease intraoperatively, the
incision should be extended and the operation converted to a BNE.
A BNE is preferred if preoperative localization studies are
negative or not concordant and if multi-gland disease is sus-
pected. It is also recommended in patients with lithium induced
PHPT, due to the increased rate of multi gland disease.
There is controversy regarding the use of intraoperative PTH
(IOPTH) monitoring in parathyroid surgery. Although it may
3 Ó 2020 Published by Elsevier Ltd.
 ENDOCRINE SURGERY
Figure 1 Ultrasound of right inferior cystic parathyroid adenoma.
convey a marginal benefit it is costly and is not recommended for
routine, first-time parathyroid surgery in the latest NICE guidelines.
The usual surgical approach in patients with MEN1 is a
subtotal parathyroidectomy with the removal of 3e3½ glands
or a total parathyroidectomy with auto-transplantation of single
gland. The aim is to correct hypercalcaemia and prevent
persistent or recurrent hypercalcaemia, while trying to avoid
long term hypoparathyroidism. MEN1 patients usually present
with multigland disease, although the glands show asymmetric
and asynchronous growth. There is also an increased incidence
of ectopic or supernumerary parathyroid tissue, particularly
within the thymus. A thymectomy should be performed in all
patients.9
Figure 2 Ultrasound of left inferior parathyroid adenoma.
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Please cite this article as: Fraser S, Surgical management of parathyroid disease, Surgery, https://doi.org/10.1016/j.mpsur.2020.10.004
Parathyroid cancer is rare and may not be recognized prior to
surgery. Extremely high calcium and PTH may raise suspicion as
can preoperative imaging. If there is a concern regarding para-
thyroid cancer, more radical surgery, with en bloc resection of all
adherent tissue and the lymph nodes of the central compartment
have been shown to improve outcomes.10
If patients are being considered for re-do surgery due to
persistent or recurrent hyperparathyroidism, re-do imaging and
identification of remaining parathyroid glands is essential. The
main reasons for failure include unrecognized multi-gland dis-
ease and the presence of supernumerary or ectopic glands. Rare
causes include parathyroid cancer recurrence and intraoperative
errors on frozen section.
Re-do surgery is associated with a reduction in success rates
and an increase in complications. It is vital to know information
about the previous operation, which glands were seen and
removed, and the histology report. Imaging should be scrutinized
carefully, repeated as necessary and re-do surgery undertaken by
an experienced surgeon.11
Surgery for ectopic parathyroids
Around 1e2% patients with PHPT have ectopic parathyroids
located in the mediastinum, defined as completely below the
clavicle and not accessible through a cervical approach.
Conventionally, a median sternotomy or thoracotomy has been
used to retrieve these glands but less invasive techniques are
now being used more frequently. These include partial sternot-
omy, manubriotomy and video assisted thorascopic surgery
(VATS) that have reduced complication rates compared to ster-
notomy. Preoperative localization is essential when planning
surgery for mediastinal lesions (Figure 5).
Secondary hyperparathyroidism (SHPT)
This is excessive PTH production by the parathyroid glands due
to an underlying chronic biochemical stimulus. The most com-
mon causes are vitamin D deficiency and renal failure, but it is
also seen in malabsorption syndromes.
In renal failure, SHPT usually develops prior to dialysis being
required and often in conjunction with vitamin D deficiency.
There is a combination of factors that contribute to the condition.
As the kidneys fail there is a reduced ability to excrete phosphate,
causing hyperphosphataemia that directly stimulates PTH pro-
duction and is the principal cause of secondary hyperparathy-
roidism. The surplus phosphate precipitates with calcium,
creating an insoluble complex, CaHPO4, decreasing serum cal-
cium levels and further instigating PTH release.
In addition, there is reduced conversion of vitamin D to its
active metabolite 1,25-dihydroxyvitamin D, due to a lack of 1-a-
hydroxylase availability in the kidneys. The prolonged hypo-
calcaemia seen as the kidneys decline is associated with a
reduction in vitamin D receptor levels on the parathyroid glands
and impaired binding of vitamin D to the receptor, causing
vitamin D resistance.
More recently, raised levels of fibroblast growth factor 23
(FGF-23) in renal failure have been recognized to play an
important role in SHPT. FGF-23 is produced by osteocytes and
osteoblasts and usually acts physiologically in the kidney to in-
crease renal phosphate excretion in chronic kidney disease.
4 Ó 2020 Published by Elsevier Ltd.
 ENDOCRINE SURGERY
Figure 3 SPECT-CT images of left inferior parathyroid adenoma.
However, elevated FGF-23 levels also down-regulate 1-a-hy-
droxylase availability, further inhibiting the synthesis of 1,25-
dihydroxyvitamin D. High PTH levels are an important stimulus
for FGF-23 expression. Increased levels of FGF-23 in dialysis
patients have been correlated with refractory SHPT and increased
mortality.12,13
Tertiary hyperparathyroidism
This is a consequence of prolonged SHPT, where there is
persistence of hyperparathyroidism after the underlying
biochemical stimulus has been removed. The continued
autonomous excessive production of PTH results in hyper-
calcaemia. Tertiary hyperparathyroidism is most commonly
found after a renal transplant and can be seen in up to 30%
patients, however it can develop after any long-standing cause
of hypocalcaemia.14
Figure 4 Solitary parathyroid adenoma removed via MIP.
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Indications for surgery in secondary and tertiary
hyperparathyroidism
The mainstay of treatment for SHPT is medical management,
whereas surgery is the principal management for tertiary HPT. In
SHPT the aim is to correct vitamin D deficiency and reduce
phosphate levels by restricting dietary phosphate and the use of
phosphate binders. Cinacalcet also helps severe renal SHPT by
reducing PTH levels and since its introduction, the number of
patients undergoing surgery has declined.
A small proportion of patients with SHPT will still require
surgery. Indications for surgery include severe hyperparathy-
roidism with levels over 800 nanogram/L (88 pmol/L) that is
refractory to medical treatment. Surgery should also be
considered in patients with renal osteodystrophy or calciphy-
laxis, a rare disorder that causes subcutaneous vascular
calcification and cutaneous necrosis with a high mortality
rate.
In tertiary hyperparathyroidism seen after renal transplant
surgery, hypercalcaemia often resolves spontaneously in the
months after transplant. Indications for surgical treatment
include persistent hypercalcaemia 12 months after transplant,
osteoporosis and presence of symptoms.14
Routine preoperative imaging has not been traditionally per-
formed in patients with secondary or tertiary hyperparathyroid-
ism, as a bilateral neck exploration is recommended for all these
patients. Imaging maybe requested to rule out ectopic glands or a
multinodular thyroid.
Surgery for secondary and tertiary
hyperparathyroidism
Surgery should be planned in conjunction with the renal team to
facilitate dialysis and allow preoperative calcium and vitamin D
loading to reduce the risk of profound postoperative
hypocalcaemia.
5 Ó 2020 Published by Elsevier Ltd.
 ENDOCRINE SURGERY
Figure 5 Preoperative imaging showing an ectopic parathyroid adenoma (Sestamibi and fused
SPECT-CT images in the same patient).
Subtotal parathyroidectomy (with excision of 3½ parathyroid
glands) or total parathyroidectomy with or without auto-
transplantation is currently accepted as standard practice in
renal hyperparathyroidism. In auto-transplantation, the tissue is
often re-implanted into the sternocleidomastoid or forearm
muscles and marked with non-absorbable sutures or clips. A
subtotal parathyroidectomy aims to reduce the risk of post-
operative hypocalcaemia and the remnant is again marked with
sutures or a clip.
In virtually all patients, asymmetric hyperplasia is seen. A
frozen section is sometimes needed to ensure the correct tissue
has been resected. In all cases a thymectomy should be per-
formed, as ectopic and supernumerary glands are more common
and frequently located within thymic tissue.
Persistent or recurrent disease may be due to insufficient
initial surgery, the presence of supernumerary glands or a missed
ectopic gland. Over time, there is a risk of developing recurrent
disease in the residual or transplanted gland. Post-operative im-
aging is vital in this situation to determine the location of the
hyperfunctioning tissue and plan further surgery. Localization
studies in this scenario include all those discussed above and
specifically, images of the forearm should be obtained in patients
who underwent previous autotransplantation in the forearm.
Risks of surgery
Fully informed consent is essential before any parathyroid sur-
gery to ensure patients are aware of potential complications.
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These include:
1. Bleeding e neck haematoma is a rare but potentially life
threatening situation. Airway obstruction occurs due to
venous and lymphatic congestion causing venous and
laryngeal oedema. The immediate priority is to evacuate the
haematoma and stop the bleeding.
2. Recurrent laryngeal nerve injury e temporary paralysis can
occur as a result of traction or bruising intraoperatively and
will usually recover within 3 months. Permanent injury is
less common and often happens in reoperative surgery and
in those with aberrant anatomy (such as non-recurrent
laryngeal nerves).
3. Hypocalcaemia e this is seen more frequently in patients
undergoing surgery for multigland disease in PHPT and
those with SHPT. Patients with longstanding PHPT or a large
adenoma may develop temporary hypocalcaemia due to
suppression of the remaining glands. ‘Hungry bone syn-
drome’ is a recognized condition characterized by low cal-
cium and high PTH and occurs in patients that have
osteoporosis. These patients have rapid bone remineraliza-
tion after parathyroid surgery.
4. Persistently elevated PTH levels e this is common and is
usually associated with low vitamin D levels, hungry bone
syndrome and peripheral PTH resistance. No further action
is required if patients remain normocalcaemic.
5. Recurrent hyperparathyroidism e elevated PTH and calcium
levels after 6 months of seemingly successful parathyroid
surgery.
6 Ó 2020 Published by Elsevier Ltd.
 ENDOCRINE SURGERY
6. Persistent hyperparathyroidism e elevated PTH and calcium
levels within 6 months of parathyroid surgery. The diagnosis
of PHPT should be checked and the histology and operation
reports from the previous surgery reviewed. If the diagnosis
of persistent PHPT is confirmed then it is important to assess
whether the patient would benefit from further surgery and
to consider further imaging before re-exploring the neck.
Conclusion
Primary hyperparathyroidism is a common endocrine disorder,
increasingly being diagnosed in asymptomatic patients. Surgery
remains the definitive treatment for primary hyperparathyroid-
ism. Imaging studies can help direct the surgical procedure but
should not affect the decision to operate. Medical management is
the first line treatment in renal/secondary hyperparathyroidism,
but surgery is still required in a subset of patients. A Endocrinol (Lausanne) 2018 Oct; 9.
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