Parathyroid & surgeon

DR. AJAY KUMAR
1ST YEAR PG
MKCG, MCH

AIM OF THE TOPIC
 INTRODUCTION AND HISTORY
 SURGICALANATOMYAND PHYSIOLOGY
 DISORDERS ASSOCIATED WITH
PARATHYROID
 INVESTIGATION
 TREATMENT OPTION
 TAKE HOME MESSAGE

INTRODUCTION AND HISTORY
 The parathyroid glands are small, yellowish-brown,
ovoid or lentiform structures.
 Lying between the posterior lobar borders of the
thyroid gland and its capsule.
 In 1852 , Owen discovered Parathyroid in Indian
Rhinoceros.
 Sandstrom, a Swedish medical student discovered
parathyroid gland in human.

 Gley, a Physiologist, documented the function of
Parathyroid in 1891.
 In 1908, Mac Callum described their role in Calcium
metabolism.
 PTH was first isolated by Hansen in 1923, followed by
Collip in 1925

DEVELOPMENT OF PARATHYROID
 Inferior Parathyroid - 3rd pharyngeal pouch.
 Superior Parathyroid - 4th pharyngeal pouch.
 Primordia of inferior parathyroid along with
primordia of thymus migrate downward &
finally comes to rest on inferior part of dorsal
surface of thyroid gland.

ANATOMY OF PARATHYROID
 Number – 2 pairs.
 Weight – 30 to 50 mg.
 Size – 3 to 5 mm.
 Location :–
Sup. – Posteromedial surface of sup. Thyroid lobe.
Inf. – Just below the inf. portion of thyroid lobe &
anterior to RLN.
Blood supply – Mainly Inferior Thyroid vessels.

PHYSIOLOGY OF PARATHYROID
Chief cells of parathyroid secrets PTH.
SYNTHESIS OF PTH :-
 PTH is a linear polypeptide with a molecular weight of
9500 that contains 84 amino acid residues .
 It is synthesized as part of a larger molecule containing
115 amino acid residues called preproPTH.

 On entry of preproPTH into the endoplasmic
reticulum, a leader sequence is removed from the
amino terminal to form the 90-amino-acid
polypeptide proPTH.
 Six additional amino acid residues are removed from
the amino terminal of proPTH in the Golgi apparatus,
and the 84-amino-acid polypeptide PTH is packaged
in secretory granules and released as the main
secretory product of the chief cell.

FUNCTION OF PTH
It acts by increasing the conc. of Calcium in the blood by :
- Bone :- Stimulates osteoclasts bone breaks
down Ca2+ released.
- Intestines :- Increases uptake of Ca2+ from intestine.
- Kidney :- Stimulates reabsorption of Ca2+ from the
kidney tubules

DISORDERS OF PARATHYROID GLAND
 Hypoparathyroidism
 Congenital Hypoparathyroidism
 Pseudo-Hypoparathyroidism
 Hyperparathyroidism
 Hypercalcemic crisis
 Calciphylaxis
 Parathyroid carcinoma

HYPOPARATHYROIDISM
 It occurs when there is inadequate PTH secretion.
 Results in Hypocalcaemia & Hypophosphataemia.
 Cause includes :-
a) Post Surgical
b) Trauma to parathyroid
 Features :-
- Circumoral tingling, numbness, paraesthesia.
- Carpopedal spasm.
- Stridor.

TROUSSEAU SIGN
• When BP cuff is inflated
20mmHg above SBP and
arterial blood flow to hand
is occluded for 3 to 5 min.
• Carpopedal spasm occurs.
• Flexion at wrist
• Flexion at MCP Joints
• Extension of IP Joints
• Adduction of thumb &
fingers.

Feet are extended
and adducted

• When Facial nerve is tapped
at the angle of jaw, facial
muscle on the same side of the
face contract due to hyper
excitability of nerve.
• Also called WEISS SIGN..
CHVOSTEK SIGN

CONGENITAL HYPOPARATHYROIDISM
 It is an extremely rare cause of hypoparathyroidism.
 Causes are :-
a) Di George syndrome – Pt. born without adequate
parathyroid tissue.
b) Pregnant mother with hyperparathyroidism.

PSEUDOHYPOPARATHYROIDISM
 Body fails to respond to PTH.
 Patients have :-
Low Calcium
High Phosphate
High PTH due to Hypocalcaemia
 3 Types :-
a) Type 1a :- Albright Hereditary Osteodystrophy.
Short 4th & 5th metacarpals.
Cause :- TSH Resistance

b) Type 1b :- Cause is Methylation defect
Lack of phenotypic appearance.
c) Type 2 :- Inherent abnormalities in Calcium
regulation

HYPERPARATHYROIDISM
 Primary hyperparathyroidism
 Secondary hyperparathyroidism
 Tertiary hyperparathyroidism
 Persistent hyperparathyroidism
 Recurrent hyperparathyroidism

PRIMARY HYPERPARATHYROIDISM
 MC cause of hypercalcaemia.
 Occurs due to intrinsic abnormalities in PT gland.
 Abnormal gland enlarges High PTH High
Ca2+.
 85% have single PT gland enlargement called PT
Adenoma.

 RISK FACTORS :-
a) Radiation to head and neck.
b) MEN 1 Syndrome : Symmetrical enlargement of
all 4 PT gland.
c) MEN 2A Syndrome : Asymmetrical PT
enlargement.
d) Parathyroid carcinoma

MECHANISM OF HYPERCALCAEMIA
 High PTH Binds to receptors in the bone
Increase osteoclast activity Hypercalcaemia.
 Increased Renal absorption of Calcium .
 Increased absorption of Calcium from GIT.

CLINICAL FEATURES :-
 SYMPTOMS :-
Bone pain, Muscle ache.
Polyuria.
Nausea, Vomiting, Constipation, Pain abdomen.
Fatigue, Poor Concentration, Insomnia, Irritability
 SIGN :-
Osteoporosis.
Pathological Fractures.
Nephrolithiasis .

SECONDARY HYPERPARATHYROIDISM
 Due to physiological secretion of PTH by PT gland in
response to Hypocalcaemia.
 CAUSE :-
- Vit D deficiencies.
- CRF
- Malabsorption syndrome : Celiac disease, Cystic
fibrosis, Short gut syndrome.
- Medication : Lithium, Diuretics.
- Metabolic : Hyperphosphataemia.

 MECHANISM :-
Vit D deficiency :-
Decrease serum 25(OH)D Decrease 1,25(OH)2D
Increase PTH to normalize 1,25(OH)2D
Increase bone Resorption Increase excretion
of Hydroxyproline in urine.
CRF :-
CRF Increase Phosphate & Decrease conversion
of 25(OH)D to 1,25(OH)2D Decrease Ca2+
absorption in GIT Hypocalcaemia Increase
PTH.

 TREATMENT :-
- Medical usually.
- Subtotal parathyroidectomy in refractory case.

TERTIARY HYPERPARATHYROIDISM
 Advanced form of sec. hyperparathyroidism.
 Life threatening & need surgical intervention.
 CAUSE :-
- Long standing CRF
- Post Renal transplant.
 EFFECT :-
- Hypercalcaemia.
- Normal PTH.
 TREATMENT:-
Subtotal Parathyroidectomy.

PERSISTENT HYPERPARATHYROIDISM
 Hypercalcaemia persists after 1st neck exploration.
 Preoperative investigation, operative finding & pathology
must be reviewed.
 Cause – missed adenoma, ectopic.
 Combination of investigations are required to diagnose.
 Treatment :- Surgical

RECURRENT HYPERPARATHYROIDISM
 Hypercalcaemia recurs more than 12 months after an
initially curative operation.
 CAUSE :-
- Missed pathology at 1st operation.
- Development of 2nd adenoma ( rare ).
- Hyperplasia in auto transplanted tissue.
- Parathyromatosis.

NON PARATHYROID HYPERCALCAEMIA
CAUSES :-
 Endocrine causes :-
- Hyperthyroidism
- Adrenal insufficiency
- Pheochromocytoma
 Granulomatous diseases :-
- Tuberculosis
- Sarcoidosis
- Histoplasmosis

Cont…
 Malignancies :-
- Solid tumours ( Lung, Breast, Bone )
- Lymphoma/ Leukemia
- Lytic bone Mets.
 Medication :-
- Lithium
- Diuretics
- Hormone therapy
- Vitamin/ Mineral intoxication

MECHANISM :-
1. Release of Cytokines by osteolytic mets
Activate osteoclast
Bone destruction
2. Tumour secretion of PTHrP ( homology)
Binds with PTH1R
3. Tumour production of Calcitriol by Malignant
lymphocyte & macrophage.

HYPERCALCAEMIC CRISIS
 Significantly elevated serum Ca level in association
with End Organ Dysfunction .
 Occurs when serum Ca2+ >14mg/dl
 Represent medical/surgical emergency.
 CAUSES :-
- Malignancy
- Long standing PHPT

CLINICAL FEATURES :-
- Fatigue
- Depression, Confusion
- Constipation, Pain abdomen
- Oliguria/ Anuria

TREATMENT:-
- Aggressive Fluid (200ml/hr)
- Diuretics ( Inhibit Ca absorption)
- Dialysis
- Glucocorticoid (200 to 400 mg/day x days)
- Calcitonin ( Inj. Calcinase 100U x TDS)
- Bisphosphonate (In malignancy associated)
Urgent parathyroidectomy once Ca level reduced.

CALCIPHYLAXIS
 Also called Calcific Uremic Arteriopathy.
 Characterized by :-
- Vascular calcification
- Thrombosis
- Skin Necrosis with severe pain
 Result in chronic non healing ulcer.
 Can be Fatal

CAUSES :-
1. ESRD
2. Non Uraemic calciphylaxis
- PHPT
- Alcoholic liver cirrhosis
- Breast cancer treated with Chemo.
- Cholangiocarcinoma
- SLE
- Rheumatoid Arthritis

DIOGNOSIS :-
 Skin Biopsy :
- Small arterial calcification
- No vasculitis
 Bone Scintigraphy :- Increase tracer accumulation in
soft tissue.
TREATMENT :-
Aggressive subtotal parathyroidectomy.

PARATHYROID CARCINOMA
 Rare malignancy
 Prevalence – 0.005%.
 Age – 4th to 5th decade
 C/F :-
- Uncontrolled hypercacaemia
- Renal Failure
- Cardiac arrhythmias
- Hoarseness of voice
T/t :- Total Parathyroidectomy.

DIAGNOSIS OF PHPT
 Increased PTH
 Increased Calcium
 24hr Urine Calcium
 Ca2+ : Creatinine Ratio in urine
- Distinguish PHPT & Familial hypocalceuric
hyppercacaemia.

Criteria for Surgical Referral for Asymptomatic
Patients with Hyperparathyroidism
 Age: - <50yrs.
 Serum Ca2+ :- >1mg/dl above upper limit of normal.
 Renal function:-
- Creatinine clearance <60ml/min.
- Radiological evidence of renal stone.

 Bone Density :-
• T-Score <2.5
• Z-Score <2.5
• Vertebral fracture on radiology

PARATHYROID GLAND LOCALISATION
NON INVASSIVE :-
1. Sestamibi Scintigraphy :-
- Accumulate in mitochondria.
- Abnormal PT gland have abundant mitochondria
2. USG Neck :-
- PT Adenoma :- Hypo echoic.
- Accuracy is operator dependent.
- Mediastinal PT Lesion can be missed.

3. 4D CT SCAN :-
- 4th dimension is time.
- Differentiate perfusion characteristic between
hyperfunctioning PT & surrounding structure.
4. MRI Neck :-
- Mainly used in pregnant lady.
5. PET SCAN

INVASSIVE :-
1. SELECTIVE VENOUS SAMPLING :-
- Catheterisation of Common Femoral Vein to obtain
baseline PTH.
- Followed by SVS from small venous branches of
neck & mediastinum.
- 2 times from baseline :- +VE.
Indication :-
- Persistent hyperparathyroidism.
- Recurrent hyperparathyroidism.
2. USG Guided Biopsy

TREATMENT
 Bilateral Neck Exploration
 Minimally Invasive Open Parathyroidectomy
 Endoscopic Parathyroidectomy
 Video Assisted Parathyroidectomy
 Other Techniques

BILATERAL NECK EXPLORATION
 Removal of enlarged PT Gland.
 Cure rate – 95%.
 Complication rate – 2%.
 Anaesthesia – GA/ Regional Cervical block.
 Principle :-
- Identify normal/abnormal gland.
- Distinguish between single/multi gland disease.
- Resect abnormal tissue.
- If subtotal resection, leave adequate viable
remnant in one location.

MINIMAL INVASIVE PARATHYROIDECTOMY
 Cure rates are improved.
 Complication is less.
 Operation time is reduced by 50%.
 Hospital stay reduced by 7 times.
 Drawback:-
- Require extensive experience.
- Require intraoperative PTH assay.

ENDOSCOPIC PARATHYROIDECTOMY
 First described in 1996.
 CO2 insufflation through a small 1.5 to 2cm cervical
incision.
 Complication :-
- Hypercarbia
- Subcutaneous emphysema
 Modification :-
- Low pressure insufflation
-Transaxillary/ Postauricular approach.

VIDEO ASSISTED PARATHYROIDECTOMY
 First described by Miccoli and colleagues.
 Incision :-
- Cervical
- Transaxillary
- Transthoracic
- Retro auricular
 1.5cm transverse cervical incision 2cm above sternal
notch.
 5mm & 10mm trocar sites beneath strap muscle for
endoscope & videoscopic instrument.
 High cosmetic satisfaction

OTHER TECHNIQUES
 Endoscopic approach through:-
- Axilla
- Chest
- Retro auricular space
- Floor of mouth
 Robotic Parathyroidectomy

Parathyroid & surgeon

In this document

More Related Content

What's hot

Similar to Parathyroid & surgeon

Recently uploaded

Parathyroid & surgeon