surgicaldiseasesofthethyroidglandandparathyroidgland-100606231322-phpapp01

7/27/2019 surgicaldiseasesofthethyroidglandandparathyroidgland-100606231322-phpapp01

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SURGICAL DISEASES OF THE PARATHYROIDGLANDS


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Anatomy / Embryology and Physiology Four parathyroid glands 2

superior and 2 inferiorglands

Flat, ovoid and red-brownto yellow

3 x 3 x 3 mm

30 50 mg

Inferior thyroid artery main blood supply

4th 5th weeks of fetal life pharyngeal pouchesdeveloped

4th pouch + lateral thyroidanlage = superior gland

3rd pouch + thymus =inferior gland


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Primary Function is the ENDOCRINE REGULATION OFCALCIUM AND PHOSPHATE METABOLISM.

Parathyroid Hormone Vitamin D CalcitoninGastrointestinal tract No direct effect Stimulates calcium

and phosphate

absorption

No direct effect

Skeleton Stimulates calciumand phosphate

resorptionStimulates calcium

and phosphate

transport

Inhibits calcium and

phosphate

resorptionKidneys Stimulates calcium

resorption

Inhibits phosphate

resorption

No direct effect

Inhibits calcium and

phosphate

resorption

Hormonal Regulation of Calcium and Phosphate metabolism


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Feedback loops involved in the regulation of serum calcium andphosphorus (PTH parathyroid hormone; CT-calcitonin)


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PRIMARY HYPERPARATHYROIDISM Inappropriately increased amounts of parathyroid

hormone (PTH) relative to the serum calcium level Occurs in 1:1000 population Increased detection due to increase use of serumcalcium determination Three histologic pattern:

SINGLE ADENOMA HYPERPLASIA PARATHYROID CARCINOMA


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Three histologic patterns are seen:(primary hyperparthyroidism)

Single adenoma 90% of cases A rim of normal parathyroid tissue around the

adenoma distinguishes adenoma from hyperplasia Hyperplasia

10% of cases.

No rim of normal parathyroid tissue and lack ofstromal fats All 4 glands are involved. The hyperparathyroidism of MEN syndromes is due to

hyperplasia. Parathyroid carcinoma -


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Clinical presentation primary hyperparathyroidism 70% are asymptomatic

Stones

Nephrolithiasis or nephrocalcinosis (never both).

10-20% of patient

Usually calcium phosphate. Calcium oxalate less

common. Bones

Bone pain, arthralgias, and muscular aches.

20% of symptomatic patients.

Cortical resorption with medullary bone sparing

secondary to increased turnover. Osteitis fibrosa cystica is the condition where

resorption leads to Brown cysts in the bone.Predisposes to fractures.


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Groans

Peptic ulcer disease and pancreatitis

20% of symptomatic patients

Psychic overtones

Fatigue, depression, anxiety, irritability, lack of

concentration, and sleep disturbances. 40% of symptomatic patients.

No relationship of PTH or calcium levels to the severityof symptoms

Surgery improves all symptoms except anxiety.

Clinical presentation primary hyperparathyroidism


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Physical examination primary hyperparathyroidism Usually not helpful in diagnosis. If a mass is palpable, suspect thyroid pathology orparathyroid carcinoma


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Laboratory exam primary hyperparathyroidism Hypercalcemia, hypophosphatemia, and hypercalciuria are the

classic hallmarks of hyperparathyroidism

PTH levels are elevated relative to the serum ionized calciumlevel (normal or upper normal)

Serum phosphorus will be low in primaryhyperparathyroidism, high in secondary hyperparathyroidism.

Chloride will be high secondary to renal HCO3, wasting (directeffect of PTH)

Chloride to phosphorus ratio of >33 is diagnostic of primaryhyperparathyroidism; Poor mans parathyroid hormoneassay

Malignancy with or without bone metastasis is the cause of>50% of hypercalcemia (hematologic, lung, pancreas, bone,ovary, breast, and prostate).


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Other causes of hypercalcemia include: Endocrine disorders - hyperthyroidism, adrenal

insufficiency, pheochromocytoma

Vitamin D toxicity

Lymphomas with ectopic Vitamin D3 production

Granulomatous disease sarcoidosis, tuberculosis,histoplasmosis, Coccidioidomycosis, leprosy.

Drugs thiazides, lithium, milk alkali syndrome.Immobilization


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Radiologic Examinations: Subperiosteal resorption in the classic distribution

on the radial aspect of the 2nd and 3rd phalangealtufts, and distal clavicles.

Solitary bone cysts (Brown tumors) Intravenous pyelogram (IVP) may show urolithiasis

or nephrocalcinosis.


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Medical treatment of hypercalcemic crisis. Symptoms include anorexia, nausea, vomiting, polyuria,

polydipsia, abdominal pain, lethargy, bone pain, and muscularweakness.

If untreated may progress to dehydration, oliguria, acutetubular necrosis and delirium within hours.

Rapid rehydration with normal saline to restore urine output.

Forced diuresis with Furosemide drip (10-20 mg/hr). Steroids

Etidronate Disodium 7.5 mg/kg IV daily for 3 days followed by5-20 mg/kg PO daily inhibits bone metabolism inhypercalcemia of malignancy. This should not be used in renalfailure patients.

Mithramycin may be used as a last resort. If not used properly,can lead to aplastic anemia (25 microgram/kg over 4 hoursIVPB).

Dialysis can be used to lower serum calcium emergently.


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Management primary hyperparathyroidism Surgery is treatment for the hypercalcemia of hyperthyroidism, but

only after hydration with adequate urine output is established.

Surgical indications Parathyroid carcinoma

Asymptomatic patients with:

Persistent calcium elevation 1-1.6 mg/dl above normal

Calciuria >400 mg/day

Decreased bone density > 2 standard deviation points fromnormal for age, sex and race.

Creatinine clearance decrease by 30% below normal for age,sex, and race

Symptomatic patients

Urolithiasis or nephrocalcinosis Peptic ulcer disease

Pancreatitis

Musculoskeletal symptoms


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Surgical options primary hyperparathyroidism With single adenoma, resection is curative.

For hyperplasia,

3 gland resection

4-gland resection with gland reimplanted in theforearm or sternocleidomastoid muscle is indicated.

For parathyroid carcinoma

Wide excision including involved structures isindicated.

Initial exploration is successful in 90-95% of caseswithout pre-op localization studies.

Ectopic locations: Thymic substernal 20%; Posterior

neck 5-10%; Intrathyroid 5%; Carotid sheath 1%;Anterior mediastinum 1-2%.

If initial exploration fails localization studies areindicated.


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Localization techniques Ultrasound 80% accuracy for glands as small as3mm. Will not detect mediastinal tumors. CT scan / MRI will detect mediastinal tumors >2cm. Thallium-technetium subtraction scan 80%accuracy Arteriography 50% accuracy Selective venous sampling for PTH - 70% accuracy


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Post-operative care. Airway management

Hypocalcemia is common and occurs almostimmediately.

Monitor serum calcium

Symptoms anxiety, hyperventilation, Chvosteksand Trousseaus signs, acral and circumoral

paresthesias.

Some advocate treating only symptomatichypocalcemia.

Treat hypocalcemia with oral calcium carbonate 1 g

PO q6h, or IV calcium gluconate for severehypocalcemia (< 7.0).

Vitamin D supplementation may be necessary forrefractory hypocalcemia

Watch out for bleeding and infection


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SECONDARY HYPERPARATHYROIDISM Hyperparathyroidism secondary to malfunction of

another organ system

Usually occurs in patients with chronic renal failure,but may also be due to osteogenesis imperfecta,Pagets disease, or multiple myeloma

Pathophysiology in renal failure

Increased phosphate because of poor renalexcretion Decreased serum calcium, decreasedgut absorption of calcium due to decreased renal

1-hydroxylation of vitamin D2 and decreasedrenal clearance of PTH breakdown products.


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Secondary hyperparathyroidism Clinically manifests as psychiatric disorders, headache,

muscle weakness, weight loss, fatigue, renalosteodystrophy (bone resorption with pathologicfractures) and soft tissue calcifications (vessels, tendonsand joint sheaths)

Treatment is directed at underlying disorder phosphate-binding antacids, oral calcium and vitaminD, increased calcium dialysate for chronic renalinsufficiency patients.

Surgery is indicated for uncontrolled symptoms either

3--gland parathyroidectomy or 4-glandparathyroidectomy with implantation of minced glandsinto sternocleidomastoid or forearm muscles marked bya surgical clip.


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TERTIARY HYPERPARATHYROIDISM Persistent hyperparathyroidism and hypercalcemiafollowing successful renal transplant or resolutionof underlying disorder Up to 30% of patients who have pre-transplanthyperparathyroidismPathophysiology is irreversible Parathyroid gland hyperplasia with autonomousPTH production.


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Tertiary hyperparathyroidism

Surgery is indicated for symptomatic patients orpatients unresponsive to medical management 6months post - transplant either 3 glandparathyroidectomy with implantation of mincedglands into muscle.


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THANK YOU


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surgicaldiseasesofthethyroidglandandparathyroidgland-100606231322-phpapp01

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