Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 678 - файл
.pdf
32
https://t.me/medicina_free
Table 2.3 Genetic conditions associated with increased risk of thyroid malignancy
Age of
Genetics
NMFTC
FAP AD; APC gene mutation Chr 5>25yo 1/50 GIT polyposis syndrome
Cowden’s
disease
Peutz-Jegher’s
syndrome
fMTC
MEN IIa Germline mutation RET
MEN IIb Germline mutation RET
Non-MEN
familial MTC
AD; PTEN tumour
suppressor gene mutation
AD; STK-11 tumour
suppressor gene mutation
proto-oncogene Chr 10
proto-oncogene Chr 10
Germline mutation RET
proto-oncogene Chr 10
(50% of patients)
increased risk Incidence Clinical manifestation
Thyroid cancer=PTC (cribriform/
hobnail variants)
4th–5th
decades of
life
Late teens Up to
Early teens 1/30,000 C-cell hyperplasia + MTC (nearly
Early
childhood
(<10yo)
4th–5th
decades of
life
1/200,000 GIT hamartomatous syndrome
Thyroid cancer=PTC
GIT hamartomatous syndrome
1/50,000
1/30,00050,000
Thyroid cancer=PTC and FTC
all patients)
Phaeochromocytoma (50%).
Hyperparathyroidism (20–30%)
MTC (100% of patients)
Phaechromocytoma (40–50%)
Marfanoid stature, mucosal
neuromas, GIT
ganglioneuromatoses
MTC (relatively indolent clinical
course)
S. Craig
(NMFTC). Although medullary thyroid cancer is
uncommon, it is estimated that 20–25% of MTCs
are familial (fMTC). Table 2.3 demonstrates the
incidence and clinical characteristics of each
disease.
2.5 Hyperthyroid Conditions
Hyperthyroidism affects 2–3% of the population.
The most common cause in Australia and other
iodine-replete countries is Graves’ disease. Other
causes include neoplasia (multinodular goitre
and solitary toxic nodules), autoimmune
(Hashimoto’s, Riedel’s, and De Quervain’s disease), pregnancy and medications (amiodarone
and contrast). Most cases of hyperthyroidism are
managed medically, but there are some specic
scenarios detailed below, which may require surgical involvement.
2.5.1 Graves’ Disease
Graves’ disease is an autoimmune, inammatory
disorder in which TSH receptor auto-antibodies
bind to, and stimulate, the TSH receptor, resulting in hyperthyroidism. Graves’ disease affects
more women than men, with a peak incidence in
the fth decade of life.
2.5.1.1 Clinical Manifestations
In addition to the clinical features of hyperthyroidism, Graves’ disease can be manifest in several characteristic eye signs, including:
• Exophthalmos. This is a process by which
t-cell-mediated Ab release stimulates the proliferation of orbital adipocytes and broblast
production of glycosaminoglycans (hydrophilic). In turn, this increases retro-orbital
water content + fat deposition, which anteriorly displaces the globe.
• Chemosis-conjunctival oedema.
• Keratitis and conjunctivitis.
• Lid lag and lid retraction.
2.5.1.2 Treatment Options
There are three treatment options for Graves’ disease; medication, RAI and surgery. In Australia,
rst-line therapy for Graves’ disease consists of
anti-thyroid medication. However, relapse with
2 Thyroid
https://t.me/medicina_free
33
medical treatment occurs in about 50% of cases.
131
RAI
is indicated where patients are refractory
to medical management or have a contraindication to anti-thyroid medication. Graves’
ophthalmopathy may be exacerbated by RAI
and as such, it is a relative contra-indication.
Total thyroidectomy should be considered in
patients for whom medical therapy has failed,
and who are unwilling or unable to tolerate RAI
therapy. Surgery has a near complete cure rate for
Graves’ disease. However, it is the most invasive
treatment option and involves more signicant
risks than medication or RAI.
131
,
2.5.2 Neoplastic
2.5.2.1 Toxic Multinodular Goitre
(MNG)
Trophic changes due to TSH release result in
hypertrophy of parts of the gland. Recurrent episodes of parenchymal involution associated with
inammation result in patchy brosis. The trophic effect of constant stimulation of follicular
cells by TSH can result in autonomous thyroid
hormone production. Management of toxic multinodular goitre is similar to management of
Grave’s disease.
2.5.2.2 Toxic Nodule
Toxic (papillary) thyroid adenomas are benign
thyroid lesions with no malignant potential. They
are typically solitary, homogenous and wellencapsulated nodules. Surgery is considered in
cases refractory to medical management, for
patients unable to tolerate RAI, and for large
(typically >3–4cm) or symptomatic adenomas.
2.5.3 Preparation forSurgery
inHyperthyroidism
action, the clinical effect takes much longer due
to signicant protein-bound thyroid hormone
storage that can last weeks.
2.5.3.1 Methimazole
Methimazole directly inhibits TPO.It has a quick
onset of action and can clinically improve hyperthyroidism within 6 weeks. It has a lower side
effect prole (especially compared to propylthiouracil) and requires only a single daily dosing.
Methimazole has been associated with birth
defects, foetal hypothyroidism and goitre formation. Hence, it should be used cautiously in pregnancy, especially during the rst trimester.
2.5.3.2 Carbimazole
In addition to its effects on TPO, carbimazole
reduces the uptake of inorganic iodine by the thyroid. It is a pro-drug that is metabolised to its
much more active form (methimazole) to exert its
action. Carbimazole should be used cautiously in
pregnancy.
2.5.3.3 Propylthiouracil (PTU)
In addition to its effects on TPO, PTU inhibits the
peripheral conversion of T4 to T3. PTU may be
hepatotoxic. It should be considered second-line
therapy, especially for patients with liver disease.
PTU requires multiple daily dosing and takes
longer to achieve its clinical effect than either
carbimazole or methimazole. PTU has a reasonable safety prole in pregnancy and can be used
as rst-line therapy for hyperthyroidism in the
rst trimester.
2.5.3.4 Beta-Blockade
Beta-blockers exert dual effects during hyperthyroidism. They treat the hyperthyroidism-related
tachycardia and inhibit the peripheral conversion
of T4 to T3, reducing thyroid hormone stores.
Control and optimisation of hyperthyroidism for
surgery should always be done with input from
an experienced endocrinologist. Thionamides are
the primary medical treatment for hyperthyroidism. Thionamides are a group of compounds that
inhibit the activity of thyroid peroxidase (TPO).
Although they generally have a rapid onset of
2.6 Thyroidectomy: Operative
Steps
We describe here a simple, safe and stepwise
approach to thyroidectomy. We acknowledge that
there are many different approaches and techniques for thyroidectomy. However, the inherent
34
https://t.me/medicina_free
S. Craig
principles should always remain the same. The
aim of thyroidectomy is the safe removal of all
thyroid tissue and the identication and preservation of two nerves (EBSLN and RLN) and two
parathyroid glands (superior and inferior) on
each side. This is achieved by capsular dissec-
tion: that is, dissecting and ligating the tertiary
branches of blood vessels as they intersect with
the capsule of the thyroid. Such dissection should
thereby preserve the parathyroid glands and their
vascular pedicles, as well as minimally expose
the RLN and not disturb its blood supply.
2.6.1 Preparation
2.6.1.1 Vocal Cord Function
Detection of vocal cord palsy is a signicant nding that can inuence operative planning and surgical extent. The rate of idiopathic vocal cord
palsy is 1%. It is recommended that all patients
undergo a preoperative exible nasoendoscopy
or laryngoscopy to document vocal cord function, especially if they have voice symptoms.
2.6.1.2 Nerve Monitoring
Recurrent laryngeal nerve monitoring is now
common practice in Australia. A NIMS (Nerve
Integrity Monitoring System) comprising integrated surface electrodes within a specialised
endotracheal tube is placed adjacent to the true
vocal cords during intubation to monitor EMG
activity. An NIMS reects an intact circuit from
the descending vagus nerve to the recurrent
laryngeal nerve to the larynx. Loss of signal
detection during thyroidectomy can signify a
break in the circuit and nerve injury. Notably,
there is now clear evidence that nerve monitoring
systems can reduce the rate of nerve injury. NIMS
can also aid in nerve identication, detection of a
nerve injury, and be helpful in intraoperative
decision making should a nerve injury be
encountered.
2.6.1.3 Positioning
The patient is positioned with a head ring and
shoulder roll to facilitate slight neck extension,
with both arms tucked in. The operating table
can be positioned in slight reverse Trendelenberg
to reduce venous pressure in the neck. The
patient is prepped and draped from the angles of
the mandible to the mid-sternum and from shoulder to shoulder. Adherent drapes are useful
around the contours of the neck to maintain a
sterile eld.
Always begin by operating on the most patho-
logical side of the thyroid rst.
2.6.2 Stepwise Operative Approach
2.6.2.1 Step 1: Incision andSubPlatysmal Flaps
Stand on the contralateral side of the lobe being
dissected.
A 5–6cm transverse incision is made in a skin
crease at or just below the cricoid. This incision
is carried through the investing layers of cervical
fascia and platysma, avoiding the anterior jugular
veins which lie just deep into the platysma.
Superior and inferior sub-platysmal aps are
raised by developing the avascular plane immediately deep into the platysma and pushing the
anterior jugular veins down. Raise the subplatysmal aps cranially to the thyroid cartilage
and caudally to the sternal notch.
2.6.2.2 Step 2: Separation
andMobilisation oftheStrap
Muscles
Divide the midline raphe (pre-tracheal fascia)
longitudinally from the thyroid cartilage to the
sternal notch to expose the sternohyoid (supercial) and sternothyroid (deep). Dissect the
plane between the sternohyoid and sternothyroid muscles to expose the jugular vein and
ansa cervicalis nerve. Assess the sternothyroid
muscle for involvement in thyroid cancer, and
if suspected, resect this muscle en bloc with the
thyroid. The sternothyroid muscle may also be
divided to facilitate exposure in very large
goitres.
Develop the plane between the thyroid and the
strap muscles by lifting the strap muscle anteri-
2 Thyroid
https://t.me/medicina_free
35
orly with a Kocher retractor, and dissect the broareolar tissue with a combination of blunt
dissection and diathermy.
2.6.2.3 Step 3: Ligation oftheMiddle
Thyroid Vein andMobilisation
oftheThyroid Lobe
Identify the middle thyroid vein at the anterolateral edge of the thyroid lobe and ligate between
ligaclips. The lobe can then be retracted medially,
and the lateral tissue dissected bluntly down to
the carotid sheath. Open the carotid sheath along
the anterior surface of the common carotid
artery– once the middle thyroid has been divided,
there are no other vascular structures crossing the
anterior surface of the common carotid so this is
a safe landmark along which to dissect. The visceral thyroid fascia is continuous with the carotid
sheath, so clearing the anterior surface of the
common carotid allows free retraction of the thyroid lobe up into the wound. The broareolar tissue medial to carotid, and above the ITA, should
be spread gently to expose the pre-vertebral
fascia.
2.6.2.4 Step 4: Ligation oftheSuperior
Pole Vessels
Dissection of the superior pole of the thyroid
begins in the ‘space of Reeves’, an avascular window between the cricothyroid muscle and the
superior pole. Capsular dissection is especially
important to avoid inadvertent injury to the external branch of the superior laryngeal nerve where
it crosses the STA.Ligate the superior pole vessels between ligaclips with an energy device over
the surface of the superior pole. Continue to
ligate the branches of the superior pole vessels
until the upper-pole is fully mobilised.
2.6.2.5 Step 5: Identication oftheRLN
Before the inferior lobe is mobilised, identify the
RLN.This is achieved by dissecting along a line
made by bisecting the angle between the ITA and
the trachea, starting high adjacent to the thyroid.
Use a Crile forceps to gently fenestrate the fascia
and expose a small portion of the nerve. Use the
NIMS probe to conrm its location once visually
identied.
Other reliable landmarks for orientation of the
RLN include:
• Medial position to the Tubercle of
Zuckerkandl. The nerve passes in a groove
between the tubercle and the thyroid lobe.
• Deep to the main branch of the ITA.
• At the level of the trachea-oesophageal groove
(when distal to the ITA).
Beware that in large goitres, the RLN and/or
the typical anatomical landmarks can be displaced signicantly. Extra care needs to be taken
to safely identify the nerve before undertaking
extensive dissection and ligation of structures.
2.6.2.6 Step 6: Exposure oftheTrachea
intheMidline at Inferior Border
ofGland
The anterior trachea in this position is relatively
avascular. It provides a safe landmark for depth
of dissection around the inferior pole. Once the
RLN and anterior trachea are identied and
exposed, it is safe to proceed with the mobilisation of the inferior pole.
2.6.2.7 Step 7: Ligation ofInferior Pole
Vessels
Mobilise the inferior pole from medial to lateral
by capsular dissection. This is important to avoid
damage to the RLN as it crosses the secondary
branches of the ITA. Division of the ITA with
clips and an energy device should be present on
the thyroid gland (at the level of the tertiary
branches) to preserve perfusion to the superior
and inferior parathyroid glands and prevent RLN
injury.
2.6.2.8 Step 8: Dissection
oftheThyroid fromRLN,
Ligament ofBerry andSuperior
Parathyroid Gland
The dissection of the nal 1 cm of the RLN
before it enters the larynx is the most dangerous,
and it is important to slow down at this stage.
Bleeding around the nerve at this point can be
caused by small branches crossing over the
RLN. Great care must be taken when ligating
36
https://t.me/medicina_free
S. Craig
these ne vessels as bleeding here can be difcult
to control without risking nerve damage. Trace
the course of the RLN into the larynx to avoid
inadvertent damage to an early branching nerve.
Once the thyroid has been bluntly dissected away
from the RLN, use an energy device to divide
Berry’s ligament and separate the thyroid from
the trachea. Divide the thyroid isthmus with an
energy device if hemithyroidectomy is being
performed.
2.6.2.9 Step 9: Closure
Irrigate the surgical eld with water. Perform a
Valsalva manoeuvre and ensure meticulous haemostasis, although take great care with electrocautery in the vicinity of the RLN.Re-approximate
the strap muscles and platysma, and close the
skin with absorbable sutures. There is no evidence to support the use of drains in
thyroidectomy.
2.6.3 Postoperative Care
Patients should be nursed with the head up 30
degrees and with ice packs to the neck. Patients
who undergo total thyroidectomy should be commenced on a weight-based dose of thyroxine
replacement.
Post-operative blood is not required for
hemithyroidectomy. Following total thyroidectomy, we recommend performing postoperative
serum calcium (corrected or ionised) and PTH in
recovery. The half-life of PTH is only 2–3min,
so signicant reductions in PTH levels reect
some degree of loss of parathyroid gland function. Patients in whom the PTH is <10pmol/L are
at greater risk of postoperative symptomatic
hypocalcaemia [6].
If the PTH <10pmol/L
• Commence patients on 4–6g daily of calcium
and synthetic vitamin D (calcitriol 0.25 μg
BD).
est and most cost-effective approach to
post-operative calcium management. The
dose range is 2–6 g daily, titrated to symptoms. In patients who develop symptoms of
hypocalcaemia, the addition of calcitriol
seems to provide a benet [6].
A PTH and calcium level should be rechecked
again at follow-up in 3–4weeks. If normal, calcium supplementation can be discontinued. If
persistent hypocalcaemia or hypoparathyroidism
occurs, consider referral to an endocrinologist.
2.7 Thyroidectomy:
Management
ofComplications
2.7.1 Haematoma
Post-thyroidectomy haemorrhage is a potentially
life-threatening complication that occurs in 1–2%
of operations in high-volume centres [7].
Clinically, the patient may manifest with neck
swelling, dyspnoea (exacerbated by recumbency), stridor or frank hypoxia.
Bleeding in the thyroid bed, and subsequent
expanding haematoma, cause venous compression and congestion in the central compartment.
This results in laryngeal oedema and subsequent
laryngospasm, which is thought to be the main
cause of respiratory distress. In severe cases,
mechanical displacement and compression of the
trachea may occur. Releasing the haematoma by
cutting surgical sutures at the skin and fascial
level should take place on the ward as soon as
identied because signicant improvement in
respiratory function can occur within minutes of
doing so. A plan should then be made for an
immediate return to the theatre for denitive control of bleeding.
2.7.2 RLN Injury/Neuropraxia
If the PTH >10pmol/L
• Commence all patients on calcium supplementation. This has been shown to be the saf-
High-volume centres report temporary RLN neuropraxia in 3% of total thyroidectomies and permanent nerve dysfunction in 0.3% of them [8].
2 Thyroid
https://t.me/medicina_free
37
In a total thyroidectomy, the ‘pathological’
side should be operated on rst. Loss of nerve
signal may prompt the surgeon to perform a
hemithyroidectomy instead, thus preventing
potentially catastrophic bilateral nerve injury.
The majority of non-transected RLN injuries
recover, but this can take up to 12 months to
occur. Full recovery may take several weeks to
months but allows for a staged total thyroidectomy if required.
In experienced hands, if complete nerve tran-
section is identied intraoperatively, immediate
nerve reconstruction with an ansa cervicalis
anastomosis or autograft can be performed.
2.7.3 Hypocalcaemia
Hypocalcaemia may be attributed to impaired
perfusion to parathyroid glands, direct handling
of the parathyroid glands or failure to identify
glands in the resected specimen.
Temporary and permanent hypocalcaemia
occurs in up to 20% and <1%, respectively, of
total thyroidectomies. Permanent hypocalcaemia
is dened as the persistence of hypocalcaemia
that requires medication beyond 6months.
Patients demonstrating severe hypocalcaemia
(serum corrected calcium <1.9 mM) should
receive intravenous calcium replacement
(100mL of 10% calcium gluconate in 1L normal
saline infused at a rate of 100mL/h until normocalcaemia is achieved).
2.7.3.1 Clinical Manifestations
Calcium stabilises nerve–muscle function by
limiting sodium entry into nerve cells, modulating the extent of depolarisation. This inhibition is
mitigated in hypocalcaemia, resulting in nerve
excitability (paraesthesia of lips/ ngers and
toes), muscular tetany and cardiac arrhythmia.
Chvostek’s sign – tapping over the region of
the facial nerve results in twitching of the ipsilateral facial muscles.
Trousseau’s sign – ination of a blood pres-
sure cuff over the arm to 30mmHg greater than
systolic blood pressure for 30s, resulting in carpopedal spasm.
2.7.4 Surgical Site Infection (SSI)
SSIs occur in <1% of thyroidectomies. They can
range from minor cellulitis to the development of
frank abscesses. Independent risk factors include
prolonged surgical time, obesity and return to
theatre or re-exploration.
Top Five Takeaway Pearls for Thyroid
1. There are three principal questions when
assessing a thyroid nodule; Is the nodule
hyperfunctional, is the nodule malignant and
is the nodule causing symptoms?
2. TSH level directs the appropriate rst imaging modality for a thyroid nodule; If TSH is
normal or elevated– ultrasound, and if it is
suppressed – a functional radionuclide thyroid scan.
3. The extent of surgery (hemi vs. total±central
neck dissection) for differentiated thyroid
cancer is contentious; if in doubt, present the
case in an appropriate thyroid cancer MDT
pre-operatively.
4. To identify the RLN, dissect along a line made
by bisecting the angle between the ITA and
the trachea using a Crile forceps.
5. The safest and most cost-effective approach to
post-operative calcium management is to
commence ALL patients on oral calcium supplements, and re-check calcium and PTH levels at 3weeks.
References
1. Grant EG, Tessler FN, Hoang JK, Langer JE, Beland
MD, Berland LL, etal. Thyroid ultrasound reporting
lexicon: white paper of the ACR thyroid imaging,
reporting and data system (TIRADS) committee. J Am
Coll Radiol. 2015;12(12):1272–9.
2. Cibas ES, Ali SZ.The Bethesda system for reporting
thyroid cytopathology. Thyroid. 2009;19(11):1159–65.
3. Alexander EK, Heering JP, Benson CB, Frates MC,
Doubilet PM, Cibas ES, Marqusee E.Assessment of
nondiagnostic ultrasound-guided ne needle aspirations of thyroid nodules. J Clin Endocrinol Metabol.
2002;87(11):4924–7.
4. Haugen BR, Alexander EK, Bible KC, Doherty GM,
Mandel SJ, Nikiforov YE, et al. 2015 American
Thyroid Association management guidelines for adult
patients with thyroid nodules and differentiated thy-
38
https://t.me/medicina_free
S. Craig
roid cancer: the American Thyroid Association guidelines task force on thyroid nodules and differentiated
thyroid cancer. Thyroid. 2016;26(1):1–133.
5. Wells SA Jr, Asa SL, Dralle H, Elisei R, Evans DB,
Gagel RF, etal. Revised American Thyroid Association
guidelines for the management of medullary thyroid
carcinoma: the American Thyroid Association guidelines task force on medullary thyroid carcinoma.
Thyroid. 2015;25(6):567–610.
6. Carter Y, Chen H, Sippel RS.An intact parathyroid
hormone–based protocol for the prevention and treat-
ment of symptomatic hypocalcemia after thyroidectomy. J Surg Res. 2014;186(1):23–8.
7. Zhang X, Du W, Fang Q.Risk factors for postoperative
haemorrhage after total thyroidectomy: clinical results
based on 2,678 patients. Sci Rep. 2017;7(1):1–5.
8. Wong KP, Mak KL, Wong CKH, Lang
BHH.Systematic review and meta-analysis on intraoperative neuro-monitoring in high-risk thyroidectomy. Int J Surg. 2017;38:21–30.
Parathyroid
https://t.me/medicina_free
TamaraPreda, PeterCampbell,
andYeowChunTee
3
3.1 The Importance ofCalcium
toLife
Calcium (atomic number 20) is the fth most
abundant element in the earth’s crust and the
third most abundant metal. Calcium ions are
essential for a range of biochemical processes
including as second messengers in signal transduction, neurotransmitter release and muscle cell
contraction. It is a cofactor for many enzymes
and is responsible for maintaining the potential
difference across excitable cell membranes.
Calcium is essential for bone formation and
protein synthesis. Mammals need to both concentrate and store large quantities of calcium for
their endoskeletons and keep the remainder of
calcium ions within narrow bands for optimal
function.
T. Preda (*)
Department of Surgery, School of Medicine,
University of Notre Dame, Sydney, NSW, Australia
P. Campbell · Y. C. Tee
Liverpool Hospital, Sydney, NSW, Australia
3.2 A Brief History
ofParathyroid Surgery
andRelated Discoveries
In 1849, Sir Richard Owen was gifted the decaying carcass of the Indian Rhinoceros from the
London Zoo. It was this animal in which parathyroids were rst described: ‘a small compact yel-
low glandular body, attached to the thyroid at the
point where the veins emerge.’
1852 Lucien
Corvisart
1880 Ivar Sandstrom ‘Glandulae
1891 Eugene Gley Tetany in dogs after
1891 Friedrich Von
Recklinghausen
1904 Max Askanazy Observed osteitis brosis
1906 Jakob Erdheim Identication of the role of
1907 Jakob Erdheim Recognised parathyroid
Tetany post thyroidectomy
noted
parathyroidiae’ rst
described in humans
removal of parathyroids
Described osteitis brosa
cystica osteoclastic demineralisation and
peri-trabecular brosis as
the exemplar end organ
manifestation of untreated
populations with
parathyroid disease
cystica and parathyroid
hyperplasia
parathyroids in calcium
metabolism
hyperplasia/hypertrophy in
autopsy studies of patients
with osteomalacia
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
B. Ashford (ed.), Head and Neck Surgery for General Surgeons,
https://doi.org/10.1007/978-981-19-7900-2_3
39
40
https://t.me/medicina_free
T. Preda et al.
1907 Halsted and
Evans
1915 Freidrich
Schlagenhaufer
1917 MaCallum and
Voegtlin
1923–5Hanson and
Collip
1925 Felix Mandl First intentional
1926 Edward
D.Churchill
1929 Fuller Albright Published work on
1936 Churchill and
Cope
1937 Windaus and
Bock
1948 Fuller Albright Calcium metabolism
1953 Laurentius
Underdahl
1954 Paul Wermer Autosomal dominant
1959 Rasmussen and
Craig
1962 Rasmussen and
Craig
Parathyroid blood supply
described primarily from
ITA
Parathyroid adenoma
causing osteitis brosa
cystica
Calcium—the cause and
cure of tetany
Independently isolated
parathyroid hormone
parathyroidectomy for
bone disease (EU)
Parathyroidectomies
captain Martell (USA)
calcium and phosphate
metabolism relating to
hyperparathyroidism
Parathyroid clinical
presentations and surgery
codied. The issues of
single adenoma vs.
multi-gland hyperplasia
had been delineated. The
relationship of parathyroid
disease to renal stones was
understood, mediastinal
tumours had been found
and resected, and the
clinical priorities of an
asymptomatic vs.
obstructive renal calculus
and the metabolic effects
of the parathyroid disease
were understood. The size
range of normal and
pathological glands and
the various cells seen in
parathyroids as well as the
phenomenon of fat
depletion had been
established
Vitamin D3 isolated
systematised
14 cases of MEN-1
reported
nature of MEN-1
described
Parathyroid hormone
puried
Parathyroid polypeptide
structure established
1963 Rolayn Yallow Parathyroid immunoassay
enables routine
measurement
1982 Russell and
Edis
1993 Edward
M.Brown
Surgery for asymptomatic
primary
hyperparathyroidism
established
Calcium sensing receptor
(CaSR) identied
3.3 Parathyroid Embryology
During the fourth and fth weeks of foetal development, six pharyngeal arches and pouches
appear and the parathyroids arise from the endoderm of the third and fourth pharyngeal pouches
as well as the migrating neural crest.
The third pharyngeal pouch divides into dorsal and ventral wings, the dorsal giving rise to the
inferior parathyroid gland and the ventral forming the thymus. In the seventh week, the parathyroids and thymus descend caudally and medially
from the pharynx; the inferior parathyroid disconnects from the thymus, which descends into
the anterior mediastinum.
The fourth pharyngeal pouch also divides into
a dorsal wing, which develops into the superior
parathyroid gland, and a ventral wing, which
develops into the ultimobranchial body that fuses
to the posterolateral thyroid and contributes the
parafollicular C-cells.
The height of the inferior parathyroid glands
varies due to the longer route of descent.
Ectopic nests of parathyroid tissue can be
found anywhere along their pathway of descent.
These may be hyperplastic in secondary and tertiary hyperparathyroidism.
3.4 Parathyroid Anatomy
3.4.1 Macroscopic
The parathyroids are separate endocrine glands
normally on the posterior aspect of the thyroid
gland, within the pre-tracheal fascia.
3 Parathyroid
https://t.me/medicina_free
41
Typically, there are paired superior and inferior glands. They exist in their own capsules, are
‘London Tan’ in colour and typically weigh
between 25mg and 50mg. Shape is most commonly oval but can be bean or spherical. They
may be bilobar (5%) or multilobulated (1%).
3.4.1.1 Superior (‘P4’) Parathyroid
Glands
These are normally located on the postero-lateral
surface of the thyroid at its middle to superior
lobe. They typically lie posterior and lateral to
the RLN, under the investing fascia of the thyroid. The tubercle of Zuckerkandl is used as a
surgical landmark (inferior and lateral to the
superior parathyroid gland). The inferior thyroid
artery (ITA) enters the thyroid gland 1cm inferior to the superior parathyroid gland. The superior parathyroid glands may be undescended.
Other ectopic locations include the tracheoesophageal groove (45%), retropharyngeal space
(20%) and posterior mediastinum (15%).
3.4.1.2 Inferior (‘P3’) Parathyroid
Glands
The inferior parathyroid glands are usually found
just above or in the anterior mediastinum. They
are most commonly in the thyrothymic tract or
just deep into the thyroid capsule on the inferior
surface of the thyroid lobe.
They classically lie anterior and medial to the
RLN, approximately 1cm below the insertion of
the ITA into the thyroid gland and within a 2cm
space between the ITA and the RLN.
Ectopic inferior glands can be anywhere along
their course of descent from the base of the skull,
through the carotid sheath, and into the anterior
mediastinum. They can also be located within the
thyroid parenchyma (1%) or thymus (9%).
About 10–15% of the population have ectopic
parathyroid glands. Eighty-four per cent of
patients have four glands, 13% have additional
glands and <3% of the population have only
three. Eighty per cent of parathyroid glands
exhibit positional symmetry.
3.4.1.3 Blood Supply
Superior and inferior parathyroid glands are both
supplied by end artery branches of the ITA.The
superior thyroid artery may also supply the superior parathyroid. The superior, middle and inferior thyroid veins drain parathyroid outow to the
internal jugular and innominate veins. Parathyroid
lymphatic drainage is to the paratracheal and
deep cervical nodes.
3.4.2 Microscopic
The main parathyroid cell types are chief cells
and oxyphil cells. In pathological states water
clear cells may also be seen (Fig.3.1).
Chief cells—Synthesise and secrete
PTH.They stain dark purple on H&E stain with
pale pink cytoplasm and have large round nuclei.
Oxyphil cells—Are poorly understood. On
H&E stain, they are larger than chief cells with
smaller nuclei and more eosinophilic cytoplasm.
Соседние файлы в папке @xirurgi_2025