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PARATHYROID & ITS
DISORDERS
DR. DHIRENDRA TAK
DEVELOPMENT
 Endodermal proliferation of 3rd and 4th pharyngeal pouches
Diagrammatic representation of development of PTG
Diagrammatic representation of development of PTG
ANATOMY
 Usually 2 pairs of glands 80 – 97%
 But number may be range from 2-6 (some reported 12
glands)
 size - 6 mm in craniocaudal dimension, 3–4 mm in
transverse diameter.
 Light yellowish to reddish brown
 Each gland weighs 30–40 mg. If a single gland’s
weight is greater than 60 mg, it is considered
pathological.
 Combined weight of the glands in adults
120 mg in men
142 mg In women
 Percentage fat 17–50% normally ;
while in abnormal gland - Complete absence or very
marked reduction
 Supernumerary glands most commonly found in the
cervical thymus (39%) or within the mediastinal thymus
itself (6%).
 Normal superior parathyroids can occasionally be
found in the posterior neck, retropharyngeal–
oesophageal space, carotid sheath and posterior
mediastinum (1–4%).
Ectopic sites
LOCATION
 Around 85% of superior glands are within a 2 cm
diameter of a point 1 cm above the crossing of the inferior
thyroid artery and recurrent laryngeal nerve.
 The inferior glands are frequently situated below the
artery level or within 1 cm of the lower pole of the thyroid
gland.
ARTERIAL SUPPLY
 In some cases when inferior thyroid artery is absent, a branch from
the superior thyroid artery supplies the inferior parathyroid gland
 20-45% of cases, superior parathyroid glands receive significant
vascularity from posterior branch of superior thyroid artery.
MICROSCOPY
PHYSIOLOGY
 Calcium homeostasis is mediated by complex interactions of
PTH, an active metabolite of vitamin D and calcitonin.
 Average human contains 800-1000 g of calcium, of which 99
percent is skeletal and a small fraction is extracellular.
 Fifty percent of plasma calcium exists in its free (ionized) form,
which is metabolically active and under tight hormonal regulation.
 The remainder is bound to albumin, and small amounts are
bound to pyruvate, citrate and lactate
 Half life - 2 to 4 minutes
 Secretion : ionized calcium levels via calcium sensing
receptors ( CaSR)
 CaSR are GPCR present on the chief cells.
 expressed on the surface of the parathyroid cell
Physiology of calcium metabolism
Hyperparathyroidism
 Elevated serum PTH is the most common
pathological condition affecting the parathyroid
glands.
It is classified into
A. Primary
B. Secondary and
C. Tertiary hyperparathyroidism
Type Definition Cause Pathological changes
Primary Over-production of PTH
due to intrinsic
abnormality of one or
more glands
PTG adenoma 85%
PTG carcinoma 1%
PTG hyperplasia 14%
Sporadic
MEN1
MEN2
Familial isolated
hyperparathyroidism
Familial hypocaluric
hypercalcemia
Adenoma or carcinoma
changes
Chief cell hyperplasia
Reduced or absent inta-
parenchymal fat
Diffuse or nodular
changes
Secondary Compensatory
hyperplasia of PTG due
to decrease ser. Ca+
usually resulting in
normocalcemia
Chronic renal failure
Malabsorption
Vit D Deficiency
R.T.A
Hyperplasia of all
glands. May be
indistinguishable from
prim. Hyper. PTH.
Multi-nodular or diffuse
Tertiary Autonomous PTG hyper
function following
secondary
hyperparathyroidism
Any cause of
secondary
hyperparathyroidism
Very similar to
secondary hyper.PTH
May rarely be a/w
adenoma or Ca
Parathyroid adenoma
 Usually solitary (mean wt. 0.55 gm)
 Predominant cause of primary
hyperparathyroidism.
 More commonly affects inferior PT
glands.
 Macroscopically, PT gland
adenomas are well marginated, soft
and vary from yellow-red to orange-
brown in colour.
 It may occur spontaneously or within the context of
various syndromes.
 Irradiation of the neck is a potential risk factor.
 Parathyroid adenomas occurring in heterotopic sites ,
eg mediastinum, thyroid gland or oesophagus.
 most common site ectopic parathyroid- para
esophagus.
 Adenomas are ovoid soft reddish brown
tumours
 Most adenomas are composed of chief cells,
though oncocytic (oxyphil) cells and/or water-
clear cells are often present, either dispersed
or in nodular aggregates.
Attributes of normal and abnormal
PTG
Source: Scott-Brown’s Otorhinolaryngology Head and Neck Surgery 8th edition
Variants of parathyroid gland
adenoma
Lipoadenoma (parathyroid hamartoma)
 It is a very rare
 Consisting of parenchymal cells with copious mature
adipocytes
 About 50% of lipoadenoma associated with
hypercalcaemia.
Oxyphil adenoma (oncocytic adenoma)
 It composed entirely of mitochondrial rich oncocytic cells and
may or may not be functional.
 It must be differentiated from nodular oxyphilic cell changes
with advancing age and hurthle cell neoplasm of thyroid
gland.
Papillary adenoma-
 very rare, apt to be mistaken for papillary thyroid carcinoma
Clear cell adenoma-
 Wholly composed of water clear cells
 It may be confused with malig of thyroid gland.
Follicular variant-
 shows a predominant follicular (acinar) architecture often with
intraglandular secretions and may be
 misinterpreted as a follicular thyroid neoplasm.
ECTOPIC ADENOMA
Inferior gland > superior
CECT/MRI neck
Mediastinal PTH adenoma
Sternotomy
GIANT PTH ADENOMA
> 3 cm
May be
palpable in
the neck PTH
• Due to bigger size we found it easier to locate the gland, which is
sometimes a problem in smaller adenomas, however the risk of
RLN injury is more.
S. PTH
S. Calcium
RLN injury
Clinical Presentation
 Symptomatic: Aphorism “bones, stones, groans and psychic moans”
Muscle weakness
Muscle and bone aches and
pains
Depression
Constipation
Tiredness
Peptic ulceration
Pancreatitis
Renal impairement
Nephrogenic diabetic insipidus
Nephrolithiasis
Shortened QT interval
Band keratoipathy
Thirst and polyuria
 Patients may also be diagnosed while screening for osteopenia,
osteoporosis or nephrolithiasis.
 Very rarely, patients may present with significant bone disease
(osteitis fibrosa cystica).
 most clearly seen on x-rays of the middle phalanges showing
subperiosteal bone resorption.
 Skull- salt and pepper appearance
How to evaluate preoperatively?
Detailed
history Lab
investigations
Imaging
FNAC
All systems
should be
included
S. Calcium
S. PTH
S. ALP
S. Phosphorus
S. Vit D
USG neck
Tc99m
Sestamibi
scan
4D-CT neck
MRI neck
Removal of
adenoma
Lab Investigations
 Estalish elevated serum calcium ( if
borderline repeat 2-3 samples)
 Corrected calcium.
 Rule out other causes
Source: Scott-Brown’s Otorhinolaryngology Head and Neck Surgery 8th edition
 Ser. PTH
 Vit D3
 Chest X-ray to rule out mets
 Excretory urogram
 24 hour urinary calcium
 Evaluation of men syndrome
IMAGING
USG NECK
Tc99m SESTAMIBI SCAN
4D-CT neck
Single gland
adenoma
Pre-Operative Imaging & Localization
High-resolution ultrasound
 Sensitivity 65-95% for adenoma; 30-90% for enlarged gland
 Results are suboptimal in patients with multinodular thyroid
disease, with short thick neck, ectopic glands (15-20%).
CT with contrast
 Sensitivity of 46-87%
 Good for ectopic glands in the chest
USG and CT scan demonstrate high sensitivity but low
specificity and are not used as the first imaging investigation.
MRI ( T2 –weighted)
 Sensitivity of 65-80% , more sensitive than CT scan.
 Good for ectopic glands
SESTAMIBI scan :
 Functional imaging of parathyroid tissue by the use of
99mTc-labelled isonitriles.
 Parathyroid adenomas concentrate sestamibi because of
higher metabolically active mitochondria particularly in PT
adenoma.
 Both Thyroid and
parathyroid s
 Washes out of thyroid
around 1 hour
 Sensitivity in identification of
solitary adenomas as 88%
and for multigland
hyperplasia 44%.
washout imaging
 The subtraction scan better than
plain 99mTc-sestamibi
 allows the recognition of the site to
be related to the thyroid tissue
when the parathyroid is in normal
position in the neck.
subtraction imaging
 4DCT
 Axial, coronal and saggital
 4th dimension being “ contrast enhancement”
a) Plain contrast
b) Arterial phase
c) Delayed phase
 A small arterial enhancing nodule with washout in delayed
phase
Disadvantage : High radiation
Axial non contrast Axial contrast phase
Axial delayed phase
F.N.A.C
 Fibrosis due to FNAC – mimicking malignancy
 Seedling along the tract
Intraoperative localization techniques
Use of the Gamma probe :
 it depends on the identification by a gamma probe of a
radioisotope injected preoperatively and selectively
concentrated within parathyroid tissue.
 Technetium 99m sestamibi tends to be the isotope of
choice.
 The procedure depends on strict timing between radioisotope
injection and time of surgery
PTH levels
Graph of intraoperative parathyroid hormone (PTH) dynamics
 A drop in hormone level more than 50% from the highest peak (pre-
excision sample) before tumor excision meets criterion for predicting
postoperative eucalcemia.
Medical Management
 As the majority of newly diagnosed patients now a days are
asymptomatic.
 maintenance of a good state of hydration is advisable in
these patients and thiazide diuretics should be avoided as
they reduce calcium excretion
 Patients opting not to have surgery
I. serum calcium level drawn every 6 months,
II. PTH and RFT monitoring
III. should have annual bone densitometry.
Medical Management Primary HPT
1) Most frequently, BISPHOSPHONATES are
prescribed as firstline treatment.
 They function by decreasing bone turnover and they
also decrease serum and urinary calcium levels.
 Studies have shown increase in lumbar spine and
femoral neck mineral density.
2) Most recently, Calcimimetic Drugs, such as the second-
generation CINACALCET, have gained in popularity.
They rapidly bring about a decrease in serum PTH levels, but
are expensive.
3) Oestrogen replacement therapy is also used in
postmenopausal women
4) Calcium/Vitamin D
Treatment of hypercalcemia
 Normal saline infusion ( 2-4 Ls/day)
 Loop diuretics
 Bisphosphanates – usually 24 to 48 hours before
surgery
 Calcitonin
Indications for surgery
 Symptomatic patients
And in following asymptomatic patients
Parathyroidectomy in asymptomatic primary
hyperparathyroidism
• Less then 50 years old
• Unable to be effectively followed up
• Serum calcium > 1.0 mg/dl above the normal range
• Urinary calcium > 400mg/24 hours
• Thirty % decrease in renal function
• Complications of HPT: nephro-calcinosis, osteoporosis
( T-score <2.5 s.d at lumbar spine, hip or wrist)
• Severe psycho-neurologic disorder
Surgical Management
 Management of primary HPT is mainly surgical
Technique:
Conventional/ Traditional Four gland exploration
The principles
 Dissection should be as bloodless as possible.
 The superior gland is more constant and should be
identified first.
 An enlarged parathyroid is easier to identify than a
suppressed normal gland.
 Variability in development means that the relative
 positions of the parathyroids may be reversed
When to perform Bilateral
parathyroid exploration
 Suspected multigland disease
 Parathyroid cancer
 Failed pre-operative localization
 Failed MIP
Surgical Steps
Creation of subplatysmal flaps
Dividing strap muscles in the midline
Retracting of strap muscle laterally
and the thyroid medially with left
thumb
Separating strap muscles from the
thyroid anteriorly
Normal lateral view of anatomy
after taking the middle thyroid vein
Digital exploration of the
tracheoesophageal groove.
SEARCH FOR THE SUPERIOR PT
GLAND
 An enlarged superior gland often descends in the space
behind the thyroid lobe and oesophagus ,deep to the
recurrent laryngeal nerve and inferior thyroid artery.
 Inspection of this potential space will frequently expose the
adenoma.
 The inferior thyroid artery is readily identified deep to the
carotid sheath and followed bluntly to the thyroid lobe.
 The next step is further exploration of the recurrent
laryngeal nerve which is gently explored including deeply up
to the cricothyroid joint.
 Majority of superior parathyroids are within 1 cm of the
cricothyroid joint.
 nerve is a good constant landmark for identification of the
superior parathyroid position, and the plane of both superior
and inferior glands.
 Superior PT gland related to the Tubercle of Zuckerkandl and
are usually found posteriorly at the level of the upper two-thirds
of the thyroid, about 1cm above the crossing point of the RLN
and inferior thyroid artery (ITA)
SEARCH FOR THE INFERIOR GLAND
 The inferior gland normally lies on or just below inferior pole
of thyroid lobe, although it is ventral to coronal plane of
recurrent nerve.
 For this reason, excision of an inferior adenoma can often be
safely achieved without recurrent nerve identification,
 as long as dissection, often with bipolar diathermy forceps,
proceeds directly on surface of the gland.
 Superior parathyroid lie posterior and inferior parathyroid lie
anterior to recurrent laryngeal nerves.
MINIMAL ACCESS PARATHYROIDECTOMY/
VIDEO-ASSISTED/LAPAROSCOPIC
PARATHYROIDECTOMY
 The development and improvement of pre-operative
parathyroid gland imaging techniques have led to further
development of focused and minimally invasive surgical
techniques.
 With accurate localization, unilateral explorations and
single-gland targeted excisions through incisions of
1.5 cm become realistic options.
• A curvilinear line at the site of a standard collar incision
is marked.
• For a superior PTH adenoma, a small incision 1cm
superior to the neck crease line (A).
• For an inferior PTH, the incision is placed 1 cm inferior to
the neck crease line and medial to the medial margin of
the sternomastoid muscle (B)
MINIMAL ACCESS PARATHYROIDECTOMY
 The key for success of technique relies mainly on the
accuracy of the preoperative localization procedures.
 The focused excision has many advantages over the
traditional parathyroid exploration, namely;
 Less pain,
 Small skin incisions,
 Low morbidity with
 Less complications, and
 Decreased hospital admission time.
Complications of Parathyroid
Surgery
 Persistent HPT - 1-20% (experience dependent)
 Hungry bone syndrome (25-90% in radiological
evidence of bony disease )
 Nerve injury - recurrent or superior laryngeal -1-10%
 Bleeding - <5%
Surgical management in special
situations
1. If not found IOP
a) If super. Gland
b) If infer. Gland
c) Intra-op USG
d) PTH sampling
e) Explore chest in second stage
2. what to do in MEN syndrome
 Toneli F et al - Total parathyroidectomy is TOC
( multiple adenoma )
3. In PTH hyperplasia
 3.5 gland removed
 30-50 mg left behind
 Leave the smallest gland as remnant
 Half gland auto transplantation
 Nonabsorbable suture/ clip as a tag
Parathyroid carcinoma
 Uncommon endocrine malignancy
 0.5 to 2% of all cases of primary hyperparathyroidism
 It occurs most frequently in fifth and sixth decades
 Slow growing but local invasive progressive tumor
metastasize(30%) later.
 Death is usually attributable to the metabolic complications of
hypercalcaemia rather than overwhelming tumour burden.
Clinical Presentation
 Most patients are severely hypercalcaemic(>14mg/dl) with
active bone and renal disease at presentation. ( with raised
PTH 3 to 10 ten times)
 more often a palpable neck mass.
 Roughly 30 per cent develop metastasis, typically late in its
course, generally to regional lymph nodes (30 %), lungs (40
per cent), liver (10 per cent) and bone.
 The immunohistochemical proliferation marker
Ki67 (MIB-1) is slightly higher in parathyroid
carcinoma than adenoma,
 although there is overlap, with a proliferative
index greater than 5 per cent suggestive of
malignancy.
Surgical Treatment
 en bloc resection of the
tumour mass, together with
the ipsilateral thyroid lobe,
central neck dissection and all
other involved structures.
 Following surgery approximately
30% patient suffer local recurrence
usually within three years.
 Tumor is radioresistant
 Local recurrences should therefore be treated
by further surgical resection, and
bisphosphonates and calcimimetics are
useful for symptom control.
ATYPICAL PARATHYROID GLAND ADENOMA
 Atypical parathyroid gland adenoma (parathyroid neoplasm of
uncertain malignant potential or ‘equivocal’) is a diagnostic
term attributed to a parathyroid gland tumour.
The most common microscopical features include –
 Intracapsular Entrapment Of Tumor (87 %)
 Intratumoral Fibrosis (75 %), Peritumoral Fibrosis
 Haemosiderosis (58 %)
 Cyst Formation (50 %) And Mitoses.
 The Ki67 proliferative index typically lies intermediate
between adenoma and frank carcinoma.
ATYPICAL PARATHYROID GLAND ADENOMA
Familial Hyperparathyroidism
is much less common, but exists in clearly defined syndromes
 MEN I
 MEN IIA
 Familial Hypo-calciuric Hypercalcemia(FHH)
 Hyperparathyroidism-jaw tumor syndrome
 Fibro-osseous jaw tumors
 Renal cysts
 Solid renal tumors
 Familial isolated hyperparathyroidism( HPT-IF)
 Neonatal severe HPT (NSHPT)
MEN I (Wermer syndrome)
 Gene on Chromosome 11
 can present with:3P
 Parathyroid adenoma(95%)
• Most common and earliest endocrine
manifestation
 Pituitary tumor (66%)
 Pancreatic tumors
Gastrinoma (50%)
Insulinoma (20%)
Hyperparathyroidism in MEN I
 Early onset
 Multiple glands affected
 Primary HPT, hypercalcemia
 Surgical intervention needed
 Subtotal parathyroidectomy B/L neck exploration
with excision of three and one half glands
 20-50mg remnant of vascularized parathyroid tissue is
left intact to maintain normocalcemia.
MEN IIA (Sipple’s Syndrome)
 Features:
 Medullary thyroid carcinoma (95%)
 Pheochromocytoma(50%)
 Hyperparathyroidism(20%) – usually solitary
adenoma but may have multi-gland hyperplasia
 Cutaneous lichen amyloidosis
 Hirshsprungs disease
Pseudohypoparathysoidism
 A rare familial disorder with target tissue resistance to
PTH.
 There is hypocalcaemia, hyperphosphataemia, with
increased parathyroid gland function.
 Congenital defects include:
 Short stature, Mental retarded
 Short metacarpal and metatarsal bones
 Round face
 Subcutaneous calcification
Thank you

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Parathyroid gland anatomy, its disorders and manangement

  • 2. DEVELOPMENT  Endodermal proliferation of 3rd and 4th pharyngeal pouches
  • 3. Diagrammatic representation of development of PTG
  • 4. Diagrammatic representation of development of PTG
  • 5. ANATOMY  Usually 2 pairs of glands 80 – 97%  But number may be range from 2-6 (some reported 12 glands)  size - 6 mm in craniocaudal dimension, 3–4 mm in transverse diameter.  Light yellowish to reddish brown
  • 6.  Each gland weighs 30–40 mg. If a single gland’s weight is greater than 60 mg, it is considered pathological.  Combined weight of the glands in adults 120 mg in men 142 mg In women  Percentage fat 17–50% normally ; while in abnormal gland - Complete absence or very marked reduction
  • 7.  Supernumerary glands most commonly found in the cervical thymus (39%) or within the mediastinal thymus itself (6%).  Normal superior parathyroids can occasionally be found in the posterior neck, retropharyngeal– oesophageal space, carotid sheath and posterior mediastinum (1–4%).
  • 9. LOCATION  Around 85% of superior glands are within a 2 cm diameter of a point 1 cm above the crossing of the inferior thyroid artery and recurrent laryngeal nerve.  The inferior glands are frequently situated below the artery level or within 1 cm of the lower pole of the thyroid gland.
  • 11.  In some cases when inferior thyroid artery is absent, a branch from the superior thyroid artery supplies the inferior parathyroid gland  20-45% of cases, superior parathyroid glands receive significant vascularity from posterior branch of superior thyroid artery.
  • 13. PHYSIOLOGY  Calcium homeostasis is mediated by complex interactions of PTH, an active metabolite of vitamin D and calcitonin.  Average human contains 800-1000 g of calcium, of which 99 percent is skeletal and a small fraction is extracellular.  Fifty percent of plasma calcium exists in its free (ionized) form, which is metabolically active and under tight hormonal regulation.  The remainder is bound to albumin, and small amounts are bound to pyruvate, citrate and lactate
  • 14.
  • 15.  Half life - 2 to 4 minutes  Secretion : ionized calcium levels via calcium sensing receptors ( CaSR)  CaSR are GPCR present on the chief cells.  expressed on the surface of the parathyroid cell
  • 16.
  • 17.
  • 18. Physiology of calcium metabolism
  • 19. Hyperparathyroidism  Elevated serum PTH is the most common pathological condition affecting the parathyroid glands. It is classified into A. Primary B. Secondary and C. Tertiary hyperparathyroidism
  • 20. Type Definition Cause Pathological changes Primary Over-production of PTH due to intrinsic abnormality of one or more glands PTG adenoma 85% PTG carcinoma 1% PTG hyperplasia 14% Sporadic MEN1 MEN2 Familial isolated hyperparathyroidism Familial hypocaluric hypercalcemia Adenoma or carcinoma changes Chief cell hyperplasia Reduced or absent inta- parenchymal fat Diffuse or nodular changes Secondary Compensatory hyperplasia of PTG due to decrease ser. Ca+ usually resulting in normocalcemia Chronic renal failure Malabsorption Vit D Deficiency R.T.A Hyperplasia of all glands. May be indistinguishable from prim. Hyper. PTH. Multi-nodular or diffuse Tertiary Autonomous PTG hyper function following secondary hyperparathyroidism Any cause of secondary hyperparathyroidism Very similar to secondary hyper.PTH May rarely be a/w adenoma or Ca
  • 21. Parathyroid adenoma  Usually solitary (mean wt. 0.55 gm)  Predominant cause of primary hyperparathyroidism.  More commonly affects inferior PT glands.  Macroscopically, PT gland adenomas are well marginated, soft and vary from yellow-red to orange- brown in colour.
  • 22.  It may occur spontaneously or within the context of various syndromes.  Irradiation of the neck is a potential risk factor.  Parathyroid adenomas occurring in heterotopic sites , eg mediastinum, thyroid gland or oesophagus.  most common site ectopic parathyroid- para esophagus.
  • 23.  Adenomas are ovoid soft reddish brown tumours  Most adenomas are composed of chief cells, though oncocytic (oxyphil) cells and/or water- clear cells are often present, either dispersed or in nodular aggregates.
  • 24. Attributes of normal and abnormal PTG Source: Scott-Brown’s Otorhinolaryngology Head and Neck Surgery 8th edition
  • 25. Variants of parathyroid gland adenoma Lipoadenoma (parathyroid hamartoma)  It is a very rare  Consisting of parenchymal cells with copious mature adipocytes  About 50% of lipoadenoma associated with hypercalcaemia.
  • 26. Oxyphil adenoma (oncocytic adenoma)  It composed entirely of mitochondrial rich oncocytic cells and may or may not be functional.  It must be differentiated from nodular oxyphilic cell changes with advancing age and hurthle cell neoplasm of thyroid gland.
  • 27. Papillary adenoma-  very rare, apt to be mistaken for papillary thyroid carcinoma Clear cell adenoma-  Wholly composed of water clear cells  It may be confused with malig of thyroid gland. Follicular variant-  shows a predominant follicular (acinar) architecture often with intraglandular secretions and may be  misinterpreted as a follicular thyroid neoplasm.
  • 28. ECTOPIC ADENOMA Inferior gland > superior CECT/MRI neck
  • 30. GIANT PTH ADENOMA > 3 cm May be palpable in the neck PTH
  • 31. • Due to bigger size we found it easier to locate the gland, which is sometimes a problem in smaller adenomas, however the risk of RLN injury is more. S. PTH S. Calcium RLN injury
  • 32. Clinical Presentation  Symptomatic: Aphorism “bones, stones, groans and psychic moans” Muscle weakness Muscle and bone aches and pains Depression Constipation Tiredness Peptic ulceration Pancreatitis Renal impairement Nephrogenic diabetic insipidus Nephrolithiasis Shortened QT interval Band keratoipathy Thirst and polyuria
  • 33.  Patients may also be diagnosed while screening for osteopenia, osteoporosis or nephrolithiasis.  Very rarely, patients may present with significant bone disease (osteitis fibrosa cystica).  most clearly seen on x-rays of the middle phalanges showing subperiosteal bone resorption.  Skull- salt and pepper appearance
  • 34. How to evaluate preoperatively? Detailed history Lab investigations Imaging FNAC All systems should be included S. Calcium S. PTH S. ALP S. Phosphorus S. Vit D USG neck Tc99m Sestamibi scan 4D-CT neck MRI neck Removal of adenoma
  • 35. Lab Investigations  Estalish elevated serum calcium ( if borderline repeat 2-3 samples)  Corrected calcium.  Rule out other causes Source: Scott-Brown’s Otorhinolaryngology Head and Neck Surgery 8th edition
  • 36.  Ser. PTH  Vit D3  Chest X-ray to rule out mets  Excretory urogram  24 hour urinary calcium  Evaluation of men syndrome
  • 37. IMAGING USG NECK Tc99m SESTAMIBI SCAN 4D-CT neck Single gland adenoma
  • 38. Pre-Operative Imaging & Localization High-resolution ultrasound  Sensitivity 65-95% for adenoma; 30-90% for enlarged gland  Results are suboptimal in patients with multinodular thyroid disease, with short thick neck, ectopic glands (15-20%). CT with contrast  Sensitivity of 46-87%  Good for ectopic glands in the chest USG and CT scan demonstrate high sensitivity but low specificity and are not used as the first imaging investigation.
  • 39. MRI ( T2 –weighted)  Sensitivity of 65-80% , more sensitive than CT scan.  Good for ectopic glands SESTAMIBI scan :  Functional imaging of parathyroid tissue by the use of 99mTc-labelled isonitriles.  Parathyroid adenomas concentrate sestamibi because of higher metabolically active mitochondria particularly in PT adenoma.
  • 40.  Both Thyroid and parathyroid s  Washes out of thyroid around 1 hour  Sensitivity in identification of solitary adenomas as 88% and for multigland hyperplasia 44%. washout imaging
  • 41.  The subtraction scan better than plain 99mTc-sestamibi  allows the recognition of the site to be related to the thyroid tissue when the parathyroid is in normal position in the neck. subtraction imaging
  • 42.  4DCT  Axial, coronal and saggital  4th dimension being “ contrast enhancement” a) Plain contrast b) Arterial phase c) Delayed phase  A small arterial enhancing nodule with washout in delayed phase Disadvantage : High radiation
  • 43. Axial non contrast Axial contrast phase Axial delayed phase
  • 44.
  • 45. F.N.A.C  Fibrosis due to FNAC – mimicking malignancy  Seedling along the tract
  • 46. Intraoperative localization techniques Use of the Gamma probe :  it depends on the identification by a gamma probe of a radioisotope injected preoperatively and selectively concentrated within parathyroid tissue.  Technetium 99m sestamibi tends to be the isotope of choice.  The procedure depends on strict timing between radioisotope injection and time of surgery
  • 47. PTH levels Graph of intraoperative parathyroid hormone (PTH) dynamics  A drop in hormone level more than 50% from the highest peak (pre- excision sample) before tumor excision meets criterion for predicting postoperative eucalcemia.
  • 48. Medical Management  As the majority of newly diagnosed patients now a days are asymptomatic.  maintenance of a good state of hydration is advisable in these patients and thiazide diuretics should be avoided as they reduce calcium excretion  Patients opting not to have surgery I. serum calcium level drawn every 6 months, II. PTH and RFT monitoring III. should have annual bone densitometry.
  • 49. Medical Management Primary HPT 1) Most frequently, BISPHOSPHONATES are prescribed as firstline treatment.  They function by decreasing bone turnover and they also decrease serum and urinary calcium levels.  Studies have shown increase in lumbar spine and femoral neck mineral density.
  • 50. 2) Most recently, Calcimimetic Drugs, such as the second- generation CINACALCET, have gained in popularity. They rapidly bring about a decrease in serum PTH levels, but are expensive. 3) Oestrogen replacement therapy is also used in postmenopausal women 4) Calcium/Vitamin D
  • 51. Treatment of hypercalcemia  Normal saline infusion ( 2-4 Ls/day)  Loop diuretics  Bisphosphanates – usually 24 to 48 hours before surgery  Calcitonin
  • 52. Indications for surgery  Symptomatic patients And in following asymptomatic patients Parathyroidectomy in asymptomatic primary hyperparathyroidism • Less then 50 years old • Unable to be effectively followed up • Serum calcium > 1.0 mg/dl above the normal range • Urinary calcium > 400mg/24 hours • Thirty % decrease in renal function • Complications of HPT: nephro-calcinosis, osteoporosis ( T-score <2.5 s.d at lumbar spine, hip or wrist) • Severe psycho-neurologic disorder
  • 53. Surgical Management  Management of primary HPT is mainly surgical Technique: Conventional/ Traditional Four gland exploration The principles  Dissection should be as bloodless as possible.  The superior gland is more constant and should be identified first.  An enlarged parathyroid is easier to identify than a suppressed normal gland.  Variability in development means that the relative  positions of the parathyroids may be reversed
  • 54. When to perform Bilateral parathyroid exploration  Suspected multigland disease  Parathyroid cancer  Failed pre-operative localization  Failed MIP
  • 55. Surgical Steps Creation of subplatysmal flaps Dividing strap muscles in the midline
  • 56. Retracting of strap muscle laterally and the thyroid medially with left thumb Separating strap muscles from the thyroid anteriorly
  • 57. Normal lateral view of anatomy after taking the middle thyroid vein Digital exploration of the tracheoesophageal groove.
  • 58.
  • 59. SEARCH FOR THE SUPERIOR PT GLAND  An enlarged superior gland often descends in the space behind the thyroid lobe and oesophagus ,deep to the recurrent laryngeal nerve and inferior thyroid artery.  Inspection of this potential space will frequently expose the adenoma.  The inferior thyroid artery is readily identified deep to the carotid sheath and followed bluntly to the thyroid lobe.
  • 60.  The next step is further exploration of the recurrent laryngeal nerve which is gently explored including deeply up to the cricothyroid joint.  Majority of superior parathyroids are within 1 cm of the cricothyroid joint.  nerve is a good constant landmark for identification of the superior parathyroid position, and the plane of both superior and inferior glands.
  • 61.  Superior PT gland related to the Tubercle of Zuckerkandl and are usually found posteriorly at the level of the upper two-thirds of the thyroid, about 1cm above the crossing point of the RLN and inferior thyroid artery (ITA)
  • 62. SEARCH FOR THE INFERIOR GLAND  The inferior gland normally lies on or just below inferior pole of thyroid lobe, although it is ventral to coronal plane of recurrent nerve.  For this reason, excision of an inferior adenoma can often be safely achieved without recurrent nerve identification,  as long as dissection, often with bipolar diathermy forceps, proceeds directly on surface of the gland.
  • 63.  Superior parathyroid lie posterior and inferior parathyroid lie anterior to recurrent laryngeal nerves.
  • 64. MINIMAL ACCESS PARATHYROIDECTOMY/ VIDEO-ASSISTED/LAPAROSCOPIC PARATHYROIDECTOMY  The development and improvement of pre-operative parathyroid gland imaging techniques have led to further development of focused and minimally invasive surgical techniques.  With accurate localization, unilateral explorations and single-gland targeted excisions through incisions of 1.5 cm become realistic options.
  • 65. • A curvilinear line at the site of a standard collar incision is marked. • For a superior PTH adenoma, a small incision 1cm superior to the neck crease line (A). • For an inferior PTH, the incision is placed 1 cm inferior to the neck crease line and medial to the medial margin of the sternomastoid muscle (B)
  • 67.  The key for success of technique relies mainly on the accuracy of the preoperative localization procedures.  The focused excision has many advantages over the traditional parathyroid exploration, namely;  Less pain,  Small skin incisions,  Low morbidity with  Less complications, and  Decreased hospital admission time.
  • 68. Complications of Parathyroid Surgery  Persistent HPT - 1-20% (experience dependent)  Hungry bone syndrome (25-90% in radiological evidence of bony disease )  Nerve injury - recurrent or superior laryngeal -1-10%  Bleeding - <5%
  • 69. Surgical management in special situations 1. If not found IOP a) If super. Gland b) If infer. Gland c) Intra-op USG d) PTH sampling e) Explore chest in second stage
  • 70. 2. what to do in MEN syndrome  Toneli F et al - Total parathyroidectomy is TOC ( multiple adenoma ) 3. In PTH hyperplasia  3.5 gland removed  30-50 mg left behind  Leave the smallest gland as remnant  Half gland auto transplantation  Nonabsorbable suture/ clip as a tag
  • 71.
  • 72. Parathyroid carcinoma  Uncommon endocrine malignancy  0.5 to 2% of all cases of primary hyperparathyroidism  It occurs most frequently in fifth and sixth decades  Slow growing but local invasive progressive tumor metastasize(30%) later.  Death is usually attributable to the metabolic complications of hypercalcaemia rather than overwhelming tumour burden.
  • 73. Clinical Presentation  Most patients are severely hypercalcaemic(>14mg/dl) with active bone and renal disease at presentation. ( with raised PTH 3 to 10 ten times)  more often a palpable neck mass.  Roughly 30 per cent develop metastasis, typically late in its course, generally to regional lymph nodes (30 %), lungs (40 per cent), liver (10 per cent) and bone.
  • 74.  The immunohistochemical proliferation marker Ki67 (MIB-1) is slightly higher in parathyroid carcinoma than adenoma,  although there is overlap, with a proliferative index greater than 5 per cent suggestive of malignancy.
  • 75. Surgical Treatment  en bloc resection of the tumour mass, together with the ipsilateral thyroid lobe, central neck dissection and all other involved structures.  Following surgery approximately 30% patient suffer local recurrence usually within three years.
  • 76.  Tumor is radioresistant  Local recurrences should therefore be treated by further surgical resection, and bisphosphonates and calcimimetics are useful for symptom control.
  • 77. ATYPICAL PARATHYROID GLAND ADENOMA  Atypical parathyroid gland adenoma (parathyroid neoplasm of uncertain malignant potential or ‘equivocal’) is a diagnostic term attributed to a parathyroid gland tumour. The most common microscopical features include –  Intracapsular Entrapment Of Tumor (87 %)  Intratumoral Fibrosis (75 %), Peritumoral Fibrosis  Haemosiderosis (58 %)  Cyst Formation (50 %) And Mitoses.
  • 78.  The Ki67 proliferative index typically lies intermediate between adenoma and frank carcinoma. ATYPICAL PARATHYROID GLAND ADENOMA
  • 79. Familial Hyperparathyroidism is much less common, but exists in clearly defined syndromes  MEN I  MEN IIA  Familial Hypo-calciuric Hypercalcemia(FHH)  Hyperparathyroidism-jaw tumor syndrome  Fibro-osseous jaw tumors  Renal cysts  Solid renal tumors  Familial isolated hyperparathyroidism( HPT-IF)  Neonatal severe HPT (NSHPT)
  • 80. MEN I (Wermer syndrome)  Gene on Chromosome 11  can present with:3P  Parathyroid adenoma(95%) • Most common and earliest endocrine manifestation  Pituitary tumor (66%)  Pancreatic tumors Gastrinoma (50%) Insulinoma (20%)
  • 81. Hyperparathyroidism in MEN I  Early onset  Multiple glands affected  Primary HPT, hypercalcemia  Surgical intervention needed  Subtotal parathyroidectomy B/L neck exploration with excision of three and one half glands  20-50mg remnant of vascularized parathyroid tissue is left intact to maintain normocalcemia.
  • 82. MEN IIA (Sipple’s Syndrome)  Features:  Medullary thyroid carcinoma (95%)  Pheochromocytoma(50%)  Hyperparathyroidism(20%) – usually solitary adenoma but may have multi-gland hyperplasia  Cutaneous lichen amyloidosis  Hirshsprungs disease
  • 83. Pseudohypoparathysoidism  A rare familial disorder with target tissue resistance to PTH.  There is hypocalcaemia, hyperphosphataemia, with increased parathyroid gland function.  Congenital defects include:  Short stature, Mental retarded  Short metacarpal and metatarsal bones  Round face  Subcutaneous calcification