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SURGERY FOR METASTATIC AND LOCALLY ADVANCED THYROID CANCER
Figure 86.1 Options for tracheal resection and repair: a small defect can be closed primarily, and
a larger defect can be reconstructed with a local muscle ap.
using this method, irrespective of microscopically involved margins. Adjuvant treatment
with radioiodine may reduce recurrence, but radiotherapy should seldom be given, if at all,
particularly in the young. With intraluminal tumour extension, tracheal resection is advised.
With laryngeal invasion, the same principles apply, but laryngectomy is seldom necessary
and is usually reserved for elderly patients with undierentiated disease. In the young, intraluminal disease can be controlled by other techniques, such as laser surgery, and again radiotherapy rarely should be considered, particularly in young patients. ese decisions should
be made on a personalised and shared basis in a central unit.
Options for segmental tracheal and laryngeal resection are shown in Figures 86.1–86.4.
Involvement of the Pharynx and Oesophagus
Pharyngeal and oesophageal invasion are rare, because muscle, unlike cartilage, acts as a
good biological barrier to invasive thyroid cancer. When seen pharyngeal or oesophageal
invasion is commonly associated with airway involvement. Most patients are asymptomatic,
because invading tumour is oen restricted to the muscularis layer and does not penetrate
intraluminally. For this reason, endoscopy of the pharynx and oesophagus is oen not predictive. A history of true dysphagia, however, should prompt a thorough examination of the
aerodigestive tract. MRI is both sensitive and specic in detecting invasion.
With intraluminal breach, which is exceedingly rare, segmental resection will be required,
with the assistance of an oesophageal surgeon.
Figure 86.2 Segmental tracheal resection: Left, an end-to-end primary anastomosis; Right, a
stepped closure involving partial resection of the cricoid cartilage.
438 Head and Neck Endocrine Surgery
SURGERY FOR METASTATIC AND LOCALLY ADVANCED THYROID CANCER
Figure 86.3 Total cricoid resection: Left, trachea to cricothyroid membrane anastomosis; Right,
vertical hemilaryngectomy.
Involvement of the Vascular Compartment
Clinical signs of arterial involvement are oen minimal, but major venous involvement
should be suspected in the presence of facial ushing, oedema, or unexplained headaches.
Both the internal jugular vein (IJV) and common carotid artery can be involved by direct
primary tumour spread, although IJV compression and thrombosis is more commonly
caused by extensive nodal disease.
Where vascular involvement is suspected, pre-operative evaluation is essential. Combination
imaging, including Doppler ultrasound, MRI, magnetic resonance angiography (MRA),
and/or CT ang iography, ca n evaluate intra luminal tumour and distinguish it from th rombus.
Ipsilateral IJV involvement can be resected without reconstruction of the venous system.
In bilateral IJV involvement, due to the associated morbidity, vein gra reconstruction will
usually be required.
A completely encased carotid constitutes inoperable disease and is usually associated with
undierentiated tumour biology. e literature details ad hoc cases of carotid resection; in
these cases, formal angiography is required to assess the arterial supply to the circle of Willis.
Encasement up to 270° is usually amenable to resection if there is no direct invasion, although
surgical morbidity should be given careful consideration in discussion with a vascular surgeon.
Figure 86.4 Total laryngectomy, for advanced disease extending across the midline.
Head and Neck Endocrine Surgery 439
INVESTIGATION OF HYPERCALCAEMIA
Surgery for Locoregional Recurrent Disease
Local recurrence is commonly seen in the thyroid bed, with lateral neck disease being less
common. Patients with high-risk tumour biology have recurrence associated with higher
mortality. Surgery is the primary modality of treatment. In low-volume and low-risk disease,
surveillance may be preferable and is appropriate for many patients. If there is evidence of
structural disease progression, the approach can be re-evaluated and clearance of the central
compartment can be performed.
In treating the lateral compartment, full clearance of Levels Ila, III, IV, and Vb is the treatment of choice. Where extranodal extension aects vascular or neural structures, the surgical strategy should balance surgical morbidity with patient age and tumour biology. Where
nodal disease recurs aer previous surgery, revision surgery can be considered, following
similar principles. In general, unless nodal disease is over 10 mm, a surveillance strategy is
advised. Radiotherapy should seldom if ever be considered, and adjuvant treatments, such
as radioiodine, alcohol injection, and radiofrequency ablation, can be considered for lowvolume recurrence
Surgery for Distant Disease
Distant metastatic spread to lung, bone, so tissues, and brain reduces life expectancy by
50%. Disease progress can be slow and oen is without symptoms. In addition to radioiodine, radiotherapy should be considered for bony metastases. However, bony metastases
trap radioiodine in only 30% of patients. For lung, radioiodine is recommended. Sorafenib,
a tyrosine kinase inhibitor, can be considered, and opportunities to participate in clinical
trials should be sought by the MDT.
Surgery for isolated cerebral metastasis has demonstrated improved long-term survival in
patients with good performance status. It should be considered regardless of radioiodine
uptake, and the decision should be made in consultation with a neurosurgical team.
KEY POINTS
• Risk stratication should be included in decision-making in advance of the primary
index surgery.
• Treatment should be patient-focused and personalised.
• Patient age and tumour biology have critical importance in management.
• Microscopic residual disease does not adversely affect long-term survival.
• The extent of surgery must be a balanced decision, weighing morbidity, patient age,
and tumour biology.
• Advanced disease should be treated at a cancer centre.
87. INVESTIGATION OF HYPERCALCAEMIA
Introduction
Most patients with hypercalcaemia are asymptomatic. Very high calcium (more than
3 mmol/L) is uncommon. Primary hyperparathyroidism (PHPT) and malignancy account
for 90% of cases of hypercalcaemia. Distinguishing between these two causes is integral in
evaluating hypercalcaemia.
440 Head and Neck Endocrine Surgery
INVESTIGATION OF HYPERCALCAEMIA
Interpretation of Serum Calcium
45% of serum calcium is bound to serum proteins, mostly albumin.
•
Biologically relevant hypercalcaemia is due to an elevated ionised (free) calcium con-
•
centration—is is referred to as the adjusted calcium (most labs will report this).
Fluctuations in protein binding can aect total calcium concentration without aect-
•
ing ionised calcium. Increased binding can result from hyperalbuminaemia caused by
dehydration. Alternatively, total calcium concentration can be low when albumin is
low in conditions like chronic illness, severe malnutrition, or liver disease. In each of
these cases, ionised calcium remains unchanged.
It is important to observe the trends in calcium concentration to determine whether it is
an acute or chronic problem. Chronic, stable, and asymptomatic hypercalcaemia is usually
due to PHPT or familial hypocalciuric hypercalcaemia (FHH). FHH is an autosomal dominant condition associated with mildly elevated calcium and parathyroid hormone (PTH)
with low urinary calcium. e degree of hypercalcaemia can be useful diagnostically. Mild
hypercalcaemia (adjusted calcium <2.75 mmol/L) is usually found in patients with PHPT.
Values above 3.25 mmol/L are uncommon in PHPT and are more common in patients with
malignancy-associated hypercalcaemia.
Clinical Evaluation
Mild to moderate hypercalcaemia is usually asymptomatic. Symptoms of hypercalcaemia are
nonspecic, and other conditions may account for the patients’ symptoms. Symptoms include
weakness, lethargy, intellectual weariness, and depression.
Patients with hypercalcaemia due to PHPT are frequently asymptomatic. A history of
•
kidney stones and osteoporosis, both suggesting chronicity and end-organ dysfunction, may provide reassurance that the cause of hypercalcaemia is not neoplastic.
Malignancy-associated hypercalcaemia occurs in patients with advanced disease,
•
and the underlying disease is the initial presenting complaint, with hypercalcaemia
detected during investigation. Breast, lung, colon, and prostate cancer are the commonest solid organ tumours that metastasise to bone.
A thorough me dical a nd drug h istory i s also imp ortant i n assessi ng patients w ith hyperc alcaem ia.
Clinical evaluation should include examination of the respiratory system, breast examination
in women, and prostate examination in men to exclude occult malignancies.
Laboratory Evaluation
Once hypercalcaemia is conrmed, the next step is to determine whether it is PTH-driven
(Table 87.1). PTH-driven hypercalcaemia occurs in both HPT and FHH, but all other causes
of hypercalcaemia suppress PTH (Table 87.2).
Serum Parathyroid Hormone
Elevated or Higher End of Normal Range
Hypercalcaemia with elevated PTH is likely to be PTH-driven and is most likely due to
PHPT.
Physiologically, high calcium levels should suppress PTH production. Elevated PTH or PTH
within the upper range of normal (inappropriately elevated) with hypercalcaemia should
raise the possibility of PHPT. PTH concentration also increases with age, and one should
bear this in mind when measuring PTH in the elderly population. FHH is also a possible
diagnosis in patients with elevated calcium and PTH. A 24-hr urinary calcium/creatinine
clearance ratio should routinely be calculated to dierentiate between the two.
In chronic kidney disease, the characteristic biochemical picture is elevated PTH in response
to high phosphate and low calcitriol, with or without low serum calcium. Hypercalcaemia is
Head and Neck Endocrine Surgery 441
INVESTIGATION OF HYPERCALCAEMIA
Table 87.1 Causes of hypercalcaemia
PTH-dependent PTH-independent
PHPT Neoplastic
• Adenoma • Osteolytic skeletal metastases
• Parathyroid hyperplasia • Multiple myeloma
• Parathyroid cancer • Paraneoplastic syndrome (PTHrP)
Ectopic hyperparathyroidism (HPT) Chronic granulomatous disease (sarcoidosis)
Lithium therapy Endocrine disorders
Secondary HPT due to renal failure
Tertiary HPT as a result of chronic renal
secondary HPT
FHH
Hypovitaminosis D Medications (thiazides, hypervitaminosis A&D)
Table 87.2 Differential diagnosis of hypercalcaemia with associated changes in blood values
Ionised
serum
Condition
PHPT ↑ ⇔ or ↓ ↑ or high-normal High-normal or ↑ ⇔ or ↓
FHH ↑ ⇔ or ↓ ↑ Ca/Cr excretion
Osteolytic skeletal
metastases
Multiple myeloma ↑ ⇔ or ↑ ↓ ⇔ or ↑ ⇔
Paraneoplastic
syndrome
Vitamin D excess
(oral ingestion,
granulomatous
disease, lymphoma)
calcium Phosphate PTH Urinary Ca
↑↑ or ↑ ↓↓ ↑ ⇔
↑ ⇔ or ↑ ↓ ⇔ or ↑ ⇔
↑ ↑ or ⇔ ↓ ⇔ or ↑ ⇔ or ↑
• Hyperthyroidism
• Acromegaly
Excessive calcium intake (TPN)
Immobilisation
2+
ratio < 0.01
Vitamin D
⇔
relatively rare until the later stages of chronic kidney disease. Hypercalcaemia in this situation may occur as a progression of compensatory parathyroid hyperplasia to an autonomous overactivity of parathyroid glands. is is known as tertiary HPT. Most patients who
develop tertiary HPT also have end-stage renal failure. Hypercalcaemia may be absent in
those patients if they are on haemodialysis.
Suppressed PTH
PTH-independent causes of hypercalcaemia should be considered if the PTH is low or within
the lower half of the reference range. If the hypercalcaemia is of a short duration and very
high (>3.00 mmol/L), then malignancy should be suspected. Lung, breast, colon, kidney, and
prostate cancer can metastasise to bone and cause hypercalcaemia. In the absence of overt
bony metastases, some tumors (squamous cell carcinoma of the lung and skin and renal cell
carcinoma) can secrete PTH-related protein (PTHrP). is protein does not react with PTH
assays, and PTH in these conditions is usually suppressed.
With multiple myeloma, 30% of patients are hypercalcaemic, with associated impaired renal
function and anaemia but suppressed PTH.
442 Head and Neck Endocrine Surgery
INVESTIGATION OF HYPERCALCAEMIA
Ca
excretio
ra
L
L
24-Hr Urinary Calcium and Urine Calcium/
Creatinine Excretion Ratio
In patients with suspected PHPT, 24-hr urinary calcium excretion should be routinely measured to conrm the diagnosis (>10 mmol/day) but also exclude FHH. FHH has a biochemical prole similar to that of PHPT apart from urinary calcium—excretion is very low in
patients with FHH. e calcium/creatinine (Ca/Cr) excretion ratio should be calculated and
is preferable in helping to exclude FHH:
mmol/L
Urinecalcium
/Cr
tio
=
n
Plasma calcium
L
mmol/L
×
Plasma creatinine
×
Urinecreatinine
µ
mol
L
1000
mmol
A ratio less than 0.01 is present in 80% of patients with FHH, while the ratio is greater than
0.02 in patients with HPTH. It also important to exclude other causes of low urinary calcium,
such as low vitamin D and use of thiazide diuretics, because they can aect the sensitivity of
the ratio. Patients with low vitamin D should have the vitamin replaced before their Ca/Cr
excretion ratio is calculated.
Vitamin D Metabolites
Testing for vitamin D metabolites is useful in patients with PTH-independent hypercalcaemia. Elevated 25-hydroxycholecalciferol, 25(OH)D, is indicative of excessive ingestion of
vitamin D.
PTH catalyses the conversion of 25(OH)D to 1,25-dihydroxycholecalciferol (1,25-DHCC).
With long-standing PHPT, it is common for the substrate 25(OH)D to become depleted.
Serum calcium may dri lower with coexisting vitamin D deciency, and the true extent of
the hypercalcaemia is revealed only aer the vitamin D deciency has been corrected.
PTH-independent hypercalcaemia associated with normal or low vitamin D metabolites
may result from unsuspected stimulation of bone resorption (as in multiple myeloma, thyrotoxicosis, prolonged immobility, hypervitaminosis A), or unrecognised high calcium intake,
especially in the face of milk-alkali syndrome.
Serum Phosphate
PTH is phosphaturic, and low serum phosphate levels are found in PHPT. Vitamin D
increases phosphate reabsorption from the kidney. Hypercalcaemia that occurs in association with vitamin D excess or in granulomatous diseases is associated with high phosphate
levels. Phosphate levels are variable in FHH.
Other Tests of Endocrine Function
Thyroid Function Tests
Hypercalcaemia occurs in 15–20% of patients with thyrotoxicosis. If it persists aer control
of thyrotoxicosis, then the cause of hypercalcaemia should be investigated to exclude concomitant PHPT.
Adrenal Function
Hypercalcaemia can occur in patients with adrenal insuciency. Possible explanations
include increased bone resorption, extracellular uid volume contraction, haemoconcentration, and increased reabsorption of calcium. Administration of steroids reverses the hypercalcaemia. Patients with phaeochromocytomas may also have hypercalcaemia, which is
PTHrP driven.
Head and Neck Endocrine Surgery 443
MANAGEMENT OF HYPERPARATHYROIDISM
KEY POINTS
• The two commonest causes of hypercalcaemia are primary hyperparathyroidism and
malignancy.
• If hypercalcaemia is conrmed, it is important to determine if it is PTH-driven—elevated
PTH occurs in primary hyperparathyroidism but is suppressed with other causes.
• Clinical evaluation and laboratory investigations aid in identifying the causes of
hypercalcaemia.
88. MANAGEMENT OF HYPERPARATHYROIDISM
Introduction
Hyperparathyroidism (HPT) means excess secretion of parathyroid hormone (PTH).
e classication of HPT into primary, secondary, and tertiary allows an aetiology-based
approach to management. As the terms imply, primary HPT (PHPT) involves excess PTH
secretion due to overactivity of the parathyroid gland(s), and secondary HPT involves excess
PTH secretion due to a stimulus external to the glands (Table 88.1). erefore, removal of the
secondary stimulus should return the patient to the euparathyroid state. If this does not occur,
by denition, tertiary HPT exists. e commonest example of tertiary HPT is the existence
of HPT aer renal transplantation in a renal failure patient who previously had renal HPT.
PHPT represents a biochemical syndrome of inappropriate or unregulated hypersecretion of
PTH by one or more of the four parathyroid glands in the absence of a recognised stimulus,
leading to hypercalcaemia. Most cases are sporadic and are caused by a single parathyroid
adenoma (85–95%). Other cases are caused by multigland disease, either multiple adenomas
or four-gland hyperplasia (5–10%), with parathyroid carcinoma accounting for <1%. Rarely,
the condition is genetic.
With the generalised introduction of the serum autoanalyser in the 1970s, the clinical prole
of PHPT has shied from a symptomatic disorder with hypercalcaemia-related symptoms,
kidney stones, and overt bone disease to a symptomatically milder condition.
e annual incidence of PHPT is around 20 cases per 100,000 population. Classical skeletal complications (osteitis brosa cystica) are present in less than 5% of newly presenting
patients, and the incidence of renal stones has fallen to around 15–20%. Neuromuscular
manifestations tend to be vague and include fatigue and subjective weakness, as opposed to
a denable myopathy. Reduction in neurocognitive function that sometimes ameliorates
following successful parathyroidectomy has been described. Peptic ulcer disease and pancreatitis are associations of classical PHPT. Pancreatitis is rarely seen nowadays because most
Table 88.1 Causes of secondary HPT
Renal failure
Hypovitaminosis D
Rare causes
Malabsorption (e.g. inammatory bowel disease, post small bowel resection)
Pancreatic insufciency
Chronic lithium therapy
Hypermagesaemia
Malnutrition
444 Head and Neck Endocrine Surgery
MANAGEMENT OF HYPERPARATHYROIDISM
PHPT is ‘mild’. Peptic ulcer disease may be seen in patients who have PHPT in association
with multiple endocrine neoplasia type 1 (MEN 1). Cardiovascular risk is increased in PHPT,
particularly with respect to increased vascular stiness. ere is an increased incidence of
hypertension with PHPT, although the underlying mechanisms are not fully understood.
A number of large population-based cohort studies have demonstrated that patients with
PHPT appear to be at risk of premature death, predominantly due to cardiovascular disease.
A matched cohort study, using hospital episode statistics and mortality data, demonstrated
that patients with mild PHPT had signicantly worse cardiovascular outcomes, in terms
of mortality and nonfatal events. e risk of other comorbidities was also increased. e
adverse outcomes were subsequently shown to be linked to high baseline PTH concentration
but not baseline calcium.
Primary Hyperparathyroidism
PHPT is sporadic in the majority of cases. Parathyroidectomy is the only curative treatment
for PHPT, with rst-time cure rates exceeding 95%. Parathyroidectomy should be recommended in all patients with symptomatic PHPT or evidence of end-organ damage, such as
low bone mineral density (BMD) or kidney stones.
In asymptomatic patients, controversy exists about the need for surgery, but guidelines exist for
conser vative follow-up (Table 88.2). Studies vary in outcome, although su rgery does seem to lead
to some increase in BMD and a decrease in vascular stiness that positively aects cardiac risk.
e National Institutes of Health (NIH) have developed consensus guidelines, updated in
2014, giving specic indications for when to recommend surgery in patients with asymptomatic PHPT (Table 88.3).
In patients who decline or are unsuitable for surgery there are medical options.
Bisphosphonates and hormone replacement therapy (HRT) are treatment options for individuals with PHPT for whom the primary goal is skeletal protection, while the calcimimetic
cinacalcet eectively lowers serum calcium and PTH levels in PHPT. However, there are
few data demonstrating positive end-organ outcomes. e NHS advises cinacalcet be used
Table 88.2 Monitoring guidelines for patients with asymptomatic PHPT
Check serum calcium annually.
Estimate eGFR annually and serum creatinine
If renal stones are suspected, undertake 24-hr biochemical stone prole, renal imaging by x-ray,
ultrasound, or computed tomography (CT)
Every 1–2 years (3 sites), x-ray or vertebral fracture assessment (VFA) of spine if clinically
indicated (e.g. height loss, back pain)
Source: Bilezikian 2014.
Table 88.3 National Institutes of Health consensus guidelines for surgery in asymptomatic PHPT
• Age <50
• Serum calcium >0.25 mmol/L above upper limit of normal
• Renal
A. Creatinine clearance <60 mL/min
B. 24-hr urine for calcium >400 mg/day (>10 mmol/day)
C. Presence of nephrolithiasis or nephrocalcinosis on x-ray, ultrasound, or CT
• Bone mineral density (by DXA):
A. T-score <–2.5 at lumbar spine, total hip, femoral neck, or distal third of radius
B. Vertebral fracture on x-ray, CT, magnetic resonance imaging (MRI), or VFA
• Medical follow-up undesired or impractical
Source: Bilezikian 2014.
Head and Neck Endocrine Surgery 445
MANAGEMENT OF HYPERPARATHYROIDISM
in renal failure patients with secondary HPT refractory to standard treatments in whom
surgery is contraindicated.
Inherited Disease
Inherited PHPT occurs in fami lial isolated HP T or as part of the MEN syndromes. Germline
mutations in the MEN1 tumour suppressor gene form the commonest cause of inherited
PHPT. Additionally, CDC73 mutations lead to another autosomal dominant inherited form
of PHPT, the HPT jaw-tumour syndrome, which is associated with HPT, mandibular osseous tumours, and a higher incidence of parathyroid carcinoma. Furthermore, RET protooncogene mutations are associated with MEN 2a, which carries a risk of inherited PHPT.
Inherited PHPT characteristically presents at a younger age than sporadic HPT. Again, the
treatment of choice is surgical, but controversy exists about the surgical approach. MEN 2a is
generally mild and only enlarged glands need removal during thyroidectomy for prevention or
cure of medullary thyroid cancer. In familial isolated PHPT and MEN type 1, the decision rests
between pre-operative localisation and removal of only the largest gland(s) to minimise surgical scarring and to reduce the risk of morbidity at later second surgery, or total parathyroidectomy (TP) with thymectomy and autotransplantation in an attempt to avoid further surgery.
Renal Parathyroid Disease
Renal HPT is managed medically with a low-phosphorus diet, vitamin D analogues, phosphate binders, and calcimimetics. In many patients, these modalities fail to control the condition and surgery is performed (Table 88.4). Once again, there is debate about the optimal
surgical intervention, and dierent centres will oer procedures ranging from TP, TP with
autotransplantation, to subtotal parathyroidectomy (3.5 gland removal), with each option
including or excluding transcervical thymectomy.
Tertiary Hyperparathyroidism
Tertiary HPT is most frequently encountered aer renal transplantation. Increased ltering
of calcium through the donor kidney is thought to increase the risk of donor loss. e most
frequent surgical option in this scenario is 3.5 PT.
Parathyroid Cancer
Parathyroid cancer is rare, presenting with severe PHPT in 90% of cases. A palpable neck mass
with a serum calcium of 3 mmol/L or greater should arouse suspicion of the diagnosis. e
management of parathyroid ca ncer is surgical. In 25% of cases, t he diagnosis is oen made intraoperatively or post-operatively through histopathological analysis. Even then, the diagnosis can
be dicult, and diagnosis is sometimes made years later when metastases appear. If parathyroid
cancer is suspected, an en bloc resection involving all adherent tissues should be performed.
Nodal involvement occurs in only 8% of cases, so level 6 clearance is usually all that is required.
Chemotherapy has no proven additional survival benet and the tumours are relatively
radioresistant; however, in tumours with aggressive characteristics, adjuvant radiotherapy
Table 88.4 Indications for surgical referral in renal HPT
Medical management of renal HPT for >6 months with persistant hypercalcaemia or
hyperphosphataemia
PTH > 800 pg/mL
Calciphylaxis with documented PTH elevation
Osteoporosis (T-score –2.5 or worse) or pathological bone fracture
Symptoms/signs:
Pruritus
Severe vascular calcications
Bone pain
Myopathy
446 Head and Neck Endocrine Surgery
PARATHYROID SURGERY
is advised. Surgical removal of metastases is also worth considering for management of
hypercalcaemias and symptom relief. Survival rates are 85% at 5 years and 35–75% at 10 years.
KEY POINTS
• PHPT is caused by unregulated hypersecretion of PTH by one or more of the four
parathyroid glands. Rarely, it may be genetic.
• The clinical prole of PHPT has shifted to a symptomatically milder condition.
• Skeletal complications, renal stones, neuromuscular manifestations, peptic ulcer
disease, and pancreatitis are now rarely seen in the context of PHPT.
• Parathyroidectomy is the only curative treatment for PHPT, and if no contraindications
exist, it should be performed in all patients with symptoms or end-organ disease.
• Medical treatments can improve bone mineral density and normalise serum calcium,
but they have not been shown to improve long-term outcomes.
• Asymptomatic PHPT may have clinical sequelae, and specic indications exist for when
surgery is recommended.
• Structured follow-up is required for patients with asymptomatic PHPT who do not
fulll criteria for surgery.
• Criteria exist for the timing of surgical intervention in secondary HPT.
• The primary management of parathyroid cancer is surgical, because adjuvant therapies
have limited utility
• Although the diagnosis of parathyroid cancer may be challenging, suspect it in the
patient with a palpable neck mass and serum calcium > 3 mmol/L.
89. PARATHYROID SURGERY
Introduction
Surgery provides the only c ure for patients with pri mary hyperparathy roidism (PHPT) and is
also an option for select patients with secondary/tertiary hyperparathyroidism. Historically,
patients with PHPT underwent bilateral neck exploration (BNE) and examination of all
four parathyroid glands, with removal of macroscopically abnormal glands. However, with
improvements in pre-operative localisation and intraoperative monitoring, including technetium-99m sestamibi single-photon emission computed tomography (SPECT), 4-dimensional computed tomography (4D CT), and intra-operative assays of parathyroid hormone
(ioPTH), patients can now be oered minimally invasive parathyroidectomy (MIP), reducing morbidity and facilitating same-day surgery.
Some patients still require BNE and examination of all four parathyroid glands; therefore,
parathyroid surgeons should have expertise in both techniques.
Surgical Anatomy and Embryology
A thorough knowledge of the embryology and anatomy of the parathyroid glands is essential
to aid identication and successful removal of abnormal glands.
Parathyroid glands are usually four in number.
•
Embryologically:
•
Superior parathyroids arise from the fourth pharyngeal pouch.
•
Inferior parathyroids, as well as the thymus, arise from the third pharyngeal
•
pouch. (e shared origin of the thymus and inferior parathyroids accounts for
the occasional nding of an inferior parathyroid within the thymus.)
Superior parathyroids usually lie on the posterior surface of the thyroid gland.
•
Head and Neck Endocrine Surgery 447
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