HYPER PARATHYROIDISM

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HYPERPARATHYROIDISM:

HYPERPARATHYROIDISM By Dr Avinash Prakash , 2 nd yr DNB surgery resident, KIMS

HISTORY of PARATHYROID:

HISTORY of PARATHYROID 1852 - 1 st identified in an Indian Rhinoceros by Sir Richard Owen in London Zoo . Sir Richard is best remembered for coining the word ' Dinosauria ' (terrible reptile) He described it as ‘a small compact yellow glandular body attached to the thyroid at the point where the vein emerged ’—now identified as the parathyroid gland

HISTORY: DISCOVERY IN HUMAN:

HISTORY: DISCOVERY IN HUMAN 1875 - 1 st identified in humans - Ivar Viktor Sandstrom ( swedish medical student ) After the discovery of the glands in dogs, cats, and rabbits he undertook a careful neck dissection in 50 autopsy cases and found that the glands were present in humans as well. He called the newly discovered glands glandulae parathyroideae Sandström was not aware of Owen’s description, which had been published in a journal with a limited circulation. Sandström's report was not well received and his work remained barely noticed for several years

HISTORY: OFC:

HISTORY: OFC 1890 : von Recklinghausen reported on a patient who had experienced recurrent fractures of several bones with negligible trauma and had subsequently shown ‘bending’ of the long bones with extensive fibrosis, cysts and brown tumours . This group of findings was subsequently termed ‘ osteitis fibrosa cystica ‘ , but he did not associate it with hyper parathyroidism OFC is also called “ Von Recklinghausen's Disease of Bone ” , not to be confused with Von Recklinghausen's disease (neurofibromatosis type I) 1903: askanzy did an autopsy in a pt who had osteomalacia and non fusing # .he noticed a large tumor adjacent to thyroid

HISTORY: BONE & PARATHYROID:

HISTORY: BONE & PARATHYROID 1906 : Erdheim ( viennese pathologist ) : He postulated that gland hyperplasia was compensatory and bone disease was primary, Eugene gley ( french physiologist ): he noticed that tetany and death caused by experimental thyroidectomy in dogs occurred only if the excised material included the glands described by Sandström 1915 : Friedrich shchlangenhaufer professor of pathology in Vienna, suggested that an enlarged parathyroid might be the cause of bone disease and not the result of it & it should be excised

HISTORY: AUTO TRANSPLANTATION:

HISTORY: AUTO TRANSPLANTATION von eiselberg ( pupil of B illroth ) did the 1 st auto Tx of parathryoid He did total thyroidectomy in cats and then auto grafted thyroid glands &parathyroid in abdo wall . Postop no tetany . HPER: neovas Halstead : exp with hypo calcemia in total thyroidectomy Even very small amount of autograft parathyroid if surviving can be of life s aving . He emphasized that interruption of vascular supply to parathyroid was a more important cause of post op hypo Ca ++ .

HISTORY: 1 st SURGERY:

HISTORY: 1 st SURGERY 1925- 1 st successful parathyroidectomy by Felix Mandll Pt with # femur ,bone pain,fatigue . Believing its compensatory p arathyroid hyperplasia he administered fresh parathyroid extaract But no relief Then he transplanted fresh parathyroid No relief Recalled schlagenhaufers suggestion Removed parathyroid tumor Immediate relief !!!

HISTORY: CHARLES MARTELL:

HISTORY: CHARLES MARTELL Charles martell , sea captain , had high Ca ++ & demineralisation . He had 6 neck exploration without success 7 th time he had by then learnt about his disease and urged for a mediastinal exploration. Oliver cope and churchill identified 3 cm tumor from mediastinum . Postop tetany was managed with supplementation Several weeks later he had renal colic and d ied of laryngospasm Finally the development of an immunoassay for the measurement of parathyroid hormone by Berson and Yalow in 1963 earned them the Nobel Prize

ANATOMY:

ANATOMY NORMAL : 5-6 mm diameter; 15-35 mg ; orange tan color ; leaf like branching pattern of vascular pedicle ABNORMAL : darker brown & reddish – brown ; do not compress easily ;firm ; knobby ; prominent vascular pedicle Lighter gray : secondary/tertiary Mottled gray –white : carcinoma usually symmetrically located

Vascular supply:

Vascular supply Superior : 20 % : sup thyroid Art Rest inf thyroid art Inferior : 10 % sup thyroid art Rest inf thyroid artery Superior thyroid artery supplies parathyroid mostly when inf thyroid art is absent Primary mediastinal parathyroid: thymic branch from IMA

Gilmores autopsy study :

Gilmores autopsy study 2 glands : 0.2 % 3 glands : 6.1 % 4 glands 87 % 5 glands : 6 % 6 glands : 0.5 %

EMBROYOLOGY : :

EMBROYOLOGY : upper parathyroid develop from dorsal endo of 4 th branchial arch 80% lie 1 cm above and behind the level at which RLN crosses the Inf Thyroid Art Lower parathyroid develop from dorsal endo 3 rd branchial arch along with thymus Within 2 cm from the lower pole of thyroid Ventral endo of 3 rd branchial arch forms thymus Ectopic locations : within thymus , along carotids , jugular, vagus , retro- esophageally

:

Excessive fragmentation thymic rests Failure to fragment intra thyroid parathyroid ( 20% ) Parathyroid is covered by extension of pre tracheal fascia that envelops the thyroid and connect it to hypo pharynx and esophagus and carotid sheath“ pseudo capsule “ Moves freely with the capsule ( unlike a thyroid nodule )

PHYSIOLOGY:

PHYSIOLOGY Chr 11 ( 11p 15 ) PTH gene Pre pro PTH Pro PTH PTH PTH 84 a.a . ( MW 9000) N-term : biological activity T ½ 2-5 min Chr 3 PTH receptor (G – protein coupled receptor) Kid, bone, brain ,heart , lung , liver , testis ↑ Ca ++ ↓PTH ↓ Ca ++ ↑ PTH ↓ Mg ++ ↓ PTH ↑ Ca ++

PowerPoint Presentation:

↑ PO4 ↓ i Ca ++ ↑ PTH Vit D ↓ PTH transcription , ↓ parathyroid proliferation Al +++ ↓ PTH Li ++, thiazide diuretic ↑ PTH Dominant regulator of PTH : Ca ++ Max PTH if Ca < 7 OR iCa < 3.5 Min PTH if Ca > 11 OR iCa > 5.5 PTH secretion is pulsatile ( > at night )

PTH rp:

PTH rp Originally in cancers SCC + hyper Ca ++ Normal skin keratocytes Lactating mammary epithelium Placenta Fetal parathyroid

PowerPoint Presentation:

Hyperparathyroidism

PowerPoint Presentation:

What is Hyperparathyroidism ?

PowerPoint Presentation:

Hyperparathyroidism is a metabolic derangement characterized by increased synthesis and secretion of PTH. Serum Calcium levels may be increased, decreased or normal depending upon renal function and a variety of other factors Primary Secondary Tertiary

PowerPoint Presentation:

What is Primary Hyperparathyroidism ?

Primary Hyperparathyroidism:

Primary Hyperparathyroidism Inappropriate elevation of PTH in the presence of hypercalcemia Rule : without hypocalciuria Familial hypocalciuric hypercalcemia - FHH

HYPERPARATHYROIDISM:

HYPERPARATHYROIDISM 80 % : SOLITORY ADENOMA 15-20 % HYPERPLASIA < 0.5 % : CARCINOMA Prevalence incr with age F : M = 3 :1 ETIO : unknown ; previous radiation to HFN > 60 yrs incr incidence Abnormalities of gene : cyclin D1 ( PRAD 1 ) , Rb , MEN 1 , MEN 2 Most common cause of hyper Ca ++ in non hospitalised pts 2 nd most common cause of hyper Ca ++ in hospitalised pts ( 1 st being ,malign )

Differential Diagnosis:

Differential Diagnosis Hypercalcemia of malignancy Familial hypocalciuric hypercalcemia Sarcoidosis Vitamin D intoxication Milk alkali syndrome Thyrotoxicosis Immobilisation hypercalcemia

HISTOPATHOLOGY: ADENOMA :

HISTOPATHOLOGY: ADENOMA Thin collagenous tissue capsule Chief cells : majority ; cyto granules Oxyphil cells : more mito , ADENOMA : inferior > superior predominant follicular architecture with colloid-like material in many of the follicles OCOCYTIC ADENOMA : rare subtype ; exclusively oxyphil cells ; F>M; abundant granular eosinophilic cytoplasm

PowerPoint Presentation:

LIPOADENOMA : adipose tissue & myxoid stroma ; tumor cells form branching cord that are surrounded by fat cells with areas of fibrosis and chronic inflammatory cells WATER CLEAR CELL ADENOMA : glycogen free cyto filled with vesicles; The tumor cells have small nuclei with dense chromatin and abundant vacuolated cytoplasm. ATYPICAL ADENOMA : atypical cytological features

PARATHYROID HYPERPLASIA :

PARATHYROID HYPERPLASIA PRIMARY SECONDARY CHIEF CELL HYPERPLASIA : 15% Stimulus is unknown Possible circulating factor 30 % have familial ( MEN ) Enlargement of all 4 WATER CLEAR CELL HYPERPLASIA : Rare ; Sup > Inf resemblance to RCC Consequence of renal failure Cannot be distinguished from primary More uniform earlier Degree of enlargement reflects severity of renal isorder Largest if disease began in childhood

PARATHYROID CARCINOMA :

PARATHYROID CARCINOMA Its uncertain whether it begins with pre existing benign parathyroid lesions Postulated to arise from primary parathyroid hyperplasia Rarely h/o radiation Metastasis is the only certain sign of malignancy Generally large tumors 30-50 % palpable Firm to hard Gray to white Adherent Rarely LN Widespread local infiltration Mets : lung , bones ,nodes Microscopic diagnosis is difficult Mitosis maybe seen Only reliable factors : mets & local infiltr

PARATHYROID CARCINOMA :

PARATHYROID CARCINOMA 70% Ca ++ > 14 80% symptomatic Definitive preop diagnosis is almost impossible Rx : en bloc resection with thyroid lobe and tracheo eso phageal soft tissues and lymphatics RLN , strap muscles may require sacrifice Central compartment dissection is important to stage Prophylactic MRND is not recommended Only if mets detected radiologically or clinically Performance of appropriate initial surgery is imp and most imp prognostic indicator Integrity of parathyroid capsule should be maintained Lung mets : resection

FAMILIAL HYPER PARATHYROIDISM :

FAMILIAL HYPER PARATHYROIDISM <5% MEN I , MEN II A , MEN II B , FAMILIAL NEONATAL HPT BFHH

MEN 1 :

MEN 1 95 % parathyroid tumors 90 % hyper Ca ++ is first manifestation 40 % pancreatic islet cell tumors Gastrinoma > insulinomas Zollinger E llison $ ( imp cause of mobidity and mortality ) PPomas : asympto Glucagonomas and VIPomas are rare 30 % : Ant pituitary tumors Prolactinomas 60% > somatotrophinomas20 % Adrenal cortical tumors 5 % Carcinoids 4 % lipomas 1 %

MEN 1 (WERNER):

MEN 1 (WERNER) Hyper parathyroidism may occur 10-15 years before the onset of other endocrine disorders Should be considered in any primary hyper parathyroidism at early age or with multi glandular disease F/H endocrinopathies Sr prolactin level , glucose , Sr Gastrin , Pancreatic Polypeptide Inability to recognize super numerary gland : persistent disease Rx : routine B/L exploration ; subtotal / total Subtotal : risk of recurrence Total + auto transplantation : graft related hyper parathyroidism

MEN II A (SIPPLE):

MEN II A (SIPPLE) 70 % pheo 20 % hyper parathyroidism : detected by screening or incidentally during surgery for MTC Mild hyper Ca ++ Lower incidence of persistent disease Presence of Pheo must be excluded : hypertensive crisis may occur Sr catecholamines , Metanephrine If present Rx is conservative Else : B/L neck exploration subtotal

NON MEN FAMILIAL HPT:

NON MEN FAMILIAL HPT At least one 1 st degree relative with surgically proven hyper parathyroidism And no f/h/o MEN r/o BFHH Young More aggressive Profound hyper Ca ++ Hyper Ca ++ crisis Persistent or recurrent disease Rx : subtotal / total with B/L cervical thymectomy with auto transplantation

FAMILIAL NEONATAL HPT:

FAMILIAL NEONATAL HPT Rare Severe hypotonia , constipation ,failure to thrive , resp distress f/h of BFHH Rx : urgent parathyroid exploration and resection of all 4 glands total with B/L cervical thymectomy with cryopreservation

HYPERPARATHYROIDISM IN PREGNANCY:

HYPERPARATHYROIDISM IN PREGNANCY Rare Degree of protection as Ca ++ is transported across the placenta Fetal hypo parathyroidism Most common presenting symptom : neonatal tetany Spontaneous abortion , prematurity , IUGR, Symptomatic : surgery 2 nd trimester 3 rd trimester : postpone after deliver

HYPER CALCEMIA IN MALIGNANCY:

HYPER CALCEMIA IN MALIGNANCY PTH – rp Ectopic pth Ectopic VIT D Lytic bone mets

DOUBLE ADENOMA:

DOUBLE ADENOMA 50 % image accurately B/L exploration is necessary At least one normal parathyroid should be identified Though biopsy is unnecessary

NON PTH , NON MALIGNANT HYPER Ca ++:

NON PTH , NON MALIGNANT HYPER Ca ++ Ovarian dermoid Thyrotoxicosis Pheo Addisons Granulomatous disorders : Sarcoidosis,TB ,Candidiasis Drugs: Vit D,A excess , thiazide , Li ++, Estrogen BFHH PAGETS LIVER FAILURE TPN Milk alkali syndrome SLE Hep B

SECONDARY HYPER -PARATHYROIDISM:

SECONDARY HYPER -PARATHYROIDISM “ physiological response to a defect in Ca ++ homeostasis “ Nearly all pts with CRF ( hydroxylation) ↓ Vit D , ↓ Ca ++, ↑ Phosph CLINICAL : Renal osteodystrophy , Osteitis fibrosa cystica , brown tumor osteomalacia Extra-osseous calcification : vascular , calciphylaxis ( excess Ca ++ dep in microvas leading to ischemia and ulcer ) Rx : Ca ++ & Vit D , Calcimimetics ( Cinacalcet ) Indications : PTH > 800 , Ca X PO4 > 55, gland > 1cm diameter Surgical option : Subtotal 3 ½ / Total PT + thymectomy + Auto Tx Surg is not a cure . Only cure is Renal Tx

TERTIARY HYPER PARATHYROIDISM:

TERTIARY HYPER PARATHYROIDISM Prolonged stimulation leads to autonomous production of PTH even after removal of stimulus leading to “ TERTIARY HYPER-PARATHYROIDISM ” . Due to loss of Ca ++ sensing & Vit D receptors . Most of them asymptomatic Those who present mimic primary hyper parathy Surgery : persist hyper Ca ++ , Phospate Wasting , Pruritis , Nephrolithiasis , Osteopenia , Gland wt > 500mg

CLINICAL FEATURES: HYPERPARATHYROIDISM:

CLINICAL FEATURES: HYPERPARATHYROIDISM ASYMPTOMATIC 50% :Kidney stones (long standing ) Osteopenia Osteoporosis Bone # ↑urination ↑thirst Abdominal aches ( consti , pancr,PU ) Neuro - cognitive changes Depression Poor mentation Insomnia Fatigue Pancreatitis Osteitis fibrosa cystica Brown tumor ( Epulis of jaw ) Bones , stones, abdominal groans & psychic moans

ACUTE HYPER Ca ++ CRISIS:

ACUTE HYPER Ca ++ CRISIS MED AND SURG EMERGENCY Ca > 15 Severe mental status changes or coma Untreated : renal failrure , dysrhythmia , sudden death Metastatic complication at corneal scleral junction ( band keratopathy ) Shortened QT Anorexia , nausea vomitng ,thirst ,poly dipsia ,polyuria

IF HYPER PARATHYROIDISM UNTREATED:

IF HYPER PARATHYROIDISM UNTREATED Some studies show benign course of untreated mild hyper parathyroidism Manifestations relate to level of Ca ++ Younger men are prone to have renal stones with mild Ca ++ Bone density decreased pronounced in post menopausal Renal failure : creatinine clearance reduce by 1/3 rd , occur silently Rarely : initially mild rapidly advancing dis may have parathyroid carcinoma Impossible to predict when progressive disease will occur Extended f/u is crucial if surgery is deferred

DIAGNOSIS:

DIAGNOSIS Elevated Sr. Ca ++ & iCa ++ Elevated PTH ( Nomal – 60 pg /ml ) Normal or high 24 hr urine Ca ++ ( if low 50 mg /dl then BFHH benign familial hypercalcemic hypocalciuria ) 10 % atypical presentation Normal Ca ++ & High PTH ( physiologic secondary hyperparathyroidism due to low Ca ++ or Vit D intake or mal- absorbtion ) Normal PTH & high Ca ++ ( r/o mets , sarcoidosis , pulm tumors, MM, PTHrp producing tumors) Current assays prevent any cross reactivity between PTH & PTH- rp

iCa ++:

iCa ++ Sr Ca ++ : 47 % bound to proteins ; of which 70 % bound to albumin Albumin has 12 Ca ++ binding regions per molecule Normally only 20 % is occupied Sr alb < 4 g /dl : decr Ca ++ by 0.8 mg / dl for every 1 gm / dl decr in Sr alb Incr in Sr alb > 4 g/dl : incr Sr Ca ++ > 0.8 mg /dl for each 1 gm / dl incr in Sr alb Acidosis : incr ionised Ca ++

LOCALISATION STUDIES : NON INVASIVE:

LOCALISATION STUDIES : NON INVASIVE Tc 99 THALLOUS CHLORIDE IMAGING USG Tc 99 SESTAMIBI SCAN 4D- CT MRI Imaging studies are not intended for diagnosing but for localizing

Tc 99 SESTAMIBI SCAN:

Tc 99 SESTAMIBI SCAN 1989 Coakley used it for cardiac function studies O’Doherty & associates compared radionuclide uptake in parathyroid and noted a greater uptake per gm 1992 : Taillefor : dual phase scan Solitary adenomas sensitivity 100 % False + : thyroid nodules , hurthle cell ca ,LN mets , False – ve : smaller adenomas , sub-optimal dosing of Tc 99 sestamibi With iodine 123 and then subtraction With SPECT

USG:

USG High resolution USG : edis and evans in 1979 Well tolerated Performed rapidly Intrathyroid parathyroid adenoma Color doppler : discrete blood supply to a mass within the thyroid parenchyma

CT , MRI:

CT , MRI MRI > CT Ectopic Reoperation

LOCALISATION STUDIES: INVASIVE:

LOCALISATION STUDIES: INVASIVE PRE-OP FNA Selective venous sampling DSA INTRA- OP Intra- op USG Methylene blue Intra op PTH monitoring GAMMA PROBE

SELECTIVE VENOUS SAMPLING :

SELECTIVE VENOUS SAMPLING Expensive Technically difficult Sampling must be obtained as selectively as possible from the smallest venous branch However IJV , innominate vein , SVC may yeild optimal results Two fold gradient in the peripheral sample and selective venous sampling establishes the site Most sensitive Mediastinal glands

IPM:

IPM INTRODUCED IN 1990 BY IRVIN TO PREDICT POSTOP EU CA++ TO ALERT INCOMPLETE REMOVAL TO CONFIRM COMPLETE EXCISION

IPM:

IPM > 50 % DROP 10 MIN AFTER COMPLETE EXCISION PRE-INCISION LEVEL PRE- EXCISION LEVEL 5-MIN LEVEL 10- MIN LEVEL

TREATMENT:

TREATMENT MEDICAL SURGICAL BISPHOSPHONATES CALCIMIMETIC AGENTS AVOID DEHYDRATION PERCUT ETHANOL ABLATION GOLD STD : COMPREHENSIVE PARATHYROIDECTOMY ; B/L NECK EXPLORATION FOCAL / UNILATERAL EXPLORATION GUIDED BY ITRA OP PTH RADIO GUIDED PARATHYROID SURGERY VIDEOSCOPIC ROBOTICALLY ASSISTED

Indications for Surgery:

Indications for Surgery Symptomatic Hyperparathyroidism Acute Primary Hyperparathyroidism (Parathyroid Crisis) Asymptomatic Patients

Asymptomatic Hyperparathyroidism:

Asymptomatic Hyperparathyroidism < 50 yrs Cannot F/U Sr Ca ++ > 1 mg/dl above normal range Ur Ca ++ > 400 mg /dl 30 % ↓ RFT Systemic complications : Nephro-calcinosis , Osteoporosis , Psycho-neurological disorder

Bilateral Vs Selective (Focused or Minimally Invasive):

Bilateral Vs Selective ( Focused or Minimally Invasive ) b/l neck exploration selective Has excellent results Successful > 95% Always an option for surgical treatment of PHPT About 85 % – 90 % of PHPT is due to solitary adenoma. Possibility of identifying diseased parathyroid by preoperative imaging Best results are obtained when Ultrasound and Sestamibi are concordant and localise the adenoma in same position.

INDICATIONS FOR COMPREHENSIVE PARATHYROIDECTOMY ; B/L NECK EXPLORATION:

INDICATIONS FOR COMPREHENSIVE PARATHYROIDECTOMY ; B/L NECK EXPLORATION absolute relative Suspected MEN Intra- Op PTH fails to drop Failed to find diseased glan d Neg Imaging Co-existing Thyroid Ca Discordant Imaging Unavailability of intra-op PTH Li induced Non MEN familial Surg preference

SURGICAL STRATEGY:

SURGICAL STRATEGY Individualized acc to pt and disease entity Routine B/L neck exploration to more directed U/L approach Traditionally : B/L exploration has high success rate > 95 % , Single gland disease : directed U /L approach after localising with Tc 999 sestamibi and intra op PTH monitoring Mulitple gland disease,MEN : standard B/ L exploration Routine biopsy of normal looking parathyroids are not recommended

MINIMALLY INVASIVE:

MINIMALLY INVASIVE Scan directed surgery under LA Improved comfort postop Ambulatory procedure Radio guided para -thyroidectomy : 18-20 mCi of Tc 99 sestamibi 2 hrs before surgery Endoscopic parathyroid : G agner 1996 under GA ; Video assisted parathyroidectomy : Miccoli ; with limited insufflation, least invasive most focused , extensive time Better cosmetic, negligible discomfort

TECHNIQUE:

TECHNIQUE SKIN CREASE INCISION ABOVE SUPRA STERNAL NOTCH SUBPLATYSMAL PLANE THYROID IS MEDIALLY ROTATED MIDDLE THRYOID VEIN LIGATED AND DIVIDED BLOODLESS FIELD LOWER PARATHYROID FIRST THEN UPPER EXPLORE ALL 4 PARATHYROIDS ASSESS DISEASE PROCESS REMOVE DISEASED

PEARLS:

PEARLS Upper parathyroid dissection should be initiated at the outermost tip Lower parathyroid dissection should be initiated at the caudal end Suspected devitalisation : auto transplantation Sharp fragmentation to prevent bleeding Failure to identify a missing gland mandates a thorough dissection in an effort to locate abnormally located or ectopic parathyroid tissue

SURGICAL OPTIONS:

SURGICAL OPTIONS SINGLE ADENOMA : EXCISION MULTIPLE GLAND HYPERPLASA : SUB –TOTAL PARATHYROIDECTOMY ( 3 ½ OR 25 MG REMNANT ) Recurrent Hyperparathyroidism in 30 % TOTAL PARATHYROIDECTOMY + AUTO TRANSPLANTATION OR CRYO PRESERVATION Permanent Hypoparathyroidism in about 30%

CANT FIND PARATHYROID ! :

CANT FIND PARATHYROID ! EXPLORE CERVICAL REGION FOR ECTOPICS RETRO- ESOPHAGEAL THYMUS MOBILISE SUPERIOR POLE OF THYROID THYROID LOBECTOMY ON THE SIDE OF MISSING CAROTIDS, JUGULAR GENERALLY SYMMETRICAL

POST-OP:

POST-OP Postop hypo Ca ++ maybe seen in pts with severe skeletal depletion of Ca ++ resulting in “ bone hunger “ In some pts symptoms on hypo Ca ++ may occur while the Sr Ca ++ is normal . This phenomenon is due to the rapid fall of in Sr . Ca ++ Monitoring of Ca ++ and PTH 2 weeks after surgery , then 6 months , then annual Adequate Ca ++ & Vit D suppl to prevet Vit D defi Ca ++ upto 500 mg BD 800-2000 IU Vit D3 ( chole calciferol ) Sometimes symptoms persists after Ca replacement , bcoz of accompanying hypo Mg ++

COMPLICATIONS:

COMPLICATIONS INFECTION HEMATOMA HOARSENESS HYPO Ca ++ ( can be prevented by cryo preservation and later auto- transplantation )

RE EXPLORATION:

RE EXPLORATION PERSISTENT : hyper Ca ++ > 6 months after Surg RECURRENT : Hyper Ca ++ after 6 months of normo Ca ++ 2-10 % of surgical failure is due to wrong diagnosis Most common finding is a missed single adenoma In subtotal PT : principle cause for recurrence is hypertrophy of remnant RLN injury risk higher Risk of permanent hypo Ca ++ Strategy : remove a single gland without extensive dissection Difficult & tedious due to fibrosis Thyroid lobectomy if intra thyroidal gland is suspected Thoracic approach : if mediastinal location

RE EXPLORATION:

RE EXPLORATION Most problematic scenario : localization fails to identify Reoperative surgery is least successful and most morbid Mandates B/L exploration and address all potential sites Approach : explore the vertibro visceral angle lateral to medial Ant sup mediastinum ….. thyro thymic lig ….. tracheo esophageal groove Cervical thymectomy Retropharyngeal and retro esophageal Thyroid lobe Carotid sheath All maneuvers unsuccessful then procedure is terminated Mediastinal exploration should not be performed with no localisation

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