Disorders of Parathyroid Gland
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This document provides information on disorders of the parathyroid gland. It discusses the anatomy and histology of the parathyroid glands. It describes how parathyroid hormone is synthesized and its role in calcium regulation. It covers different types of hyperparathyroidism including primary, secondary, and tertiary. Primary hyperparathyroidism can be caused by adenomas, hyperplasia, or carcinoma. It discusses clinical manifestations, diagnosis, and differential diagnosis of primary hyperparathyroidism. It also covers hypercalcemia associated with other conditions like malignancy, immobilization, and familial hypocalciuric hypercalcemia.
Disorders of Parathyroid Gland
- 1. DISORDERS OF PARATHYROID GLAND GUIDE – Dr. Kalinga.B.E Student – Dr. Prashanth Gajula
- 2. Anatomy
- 3. Anatomy • Arterial supply usually from inferior thyroid artery • Superior glands usually imbedded in fat on posterior surface of middle or upper portion of thyroid lobe • Lower glands near the lower pole of thyroid gland • In 1-5% pts, inferior gland in deep mediastinum
- 5. Histology • 50/50 parenchymal cells, stromal fat • Chief cells – secrete PTH • Oxyphil cells - have the potential to produce additional autocrine/paracrine factors, such as Parathyroid hormone- related protein (PTHrP) and calcitriol.
- 6. PTH Physiology • Synthesized in chief cells as large precursor – pre-proparathyroid hormone Cleaved intracellularly into proparathyroid hormone then to final 84 AA PTH • PTH then metabolized by liver into hormonally active N-term and inactive C- term
- 12. CALCIUM Calcium is a important micronutrient .
- 17. Test Specimen ConventionalUnits Calcium serum 8.9-10.1 mg/dL Ionised calcium plasma 4-5.2 mg/dL Calcium urine M <300mg/d F<250 mg/d Phosphorus serum 2.5-4.5 mg/dL PTH(intact) serum 11-67 pg/mL Normal laboratoryvalues
- 18. Major mediators of calcium and phosphate balance Serum Parathormone (PTH) Cas Ps • increases the release of calcium and phosphate from bones • stimulates the formation of active vitamin D in the kidneys (activation of 1 α hydroxylase) • reduces calciuria and increases phosphaturia Vitamin D • increases the uptake of Ca and P in the gastrointestinal tract Calcitonin (low physiological importance) • decreases the uptake of Ca in the gastrointestinal tract • increases calciuria • reduces bone resorption FGF 23 (Fibroblast Growth Factor 23) • increases phosphaturia
- 19. Classification of Causes of Hypercalcemia Parathyroid-ReIated A. Primary hyperparathyroidism 1. Adenoma(s) 2. Multiple endocrine neoplasia 3. Carcinoma B. Lithium therapy C. Familial hypocalciuric hypercalcemia Malignancy-Related A- Solid tumor with metastases (breast) B. Solid tumor With humoral mediation Of hypercalcemia (lung, kidney) C. Hematologic malignancies (multiple myeloma, lymphoma. leukemia)
- 20. Vitamin D—Related A. Vitamin D intoxication B. 1,25(OH)2 D ; sarcoidosis and other granulomatous diseases C. 1,25(OH)2 D ; impaired metabolism due to 24-hydroxylase deficiency Associated with High Bone Turnover • Hyperthyroidism • Immobilization • Thiazides • Vitamin A intoxication • Fat necrosis Associated with Renal Failure • severe secondary hyperparathyroidism • Alluminum intoxication • Milk-alkali syndrome
- 21. Hyperparathyroidism Primary - PTHsecretion isdisproportionately high in relation to the serum calciumconcentration. Secondaryto kidney failure, severevitamin D andcalcium deficiency.Reversible, after removing the causeof thedisorder. Tertiary - isexcessiveautonomous secretion of parathyroid hormone after along period of secondary hyperparathyroidism.
- 22. Primaryhyperparathyroidism(PHPT) • Primary hyperparathyroidism ischaracterised by secretionof PTH that isexcessivelydisproportionate to serum calcium levels, resulting from aprimary defect ofparathyroid cells. • one or moreadenomas • hyperplasia of all parathyroid glands • parathyroid carcinoma (75-80% of cases) (20%) (fewer than 1%)
- 23. • Theaetiology of 4-glandparathyroid hyperplasia ismulti-factorial. • It may be associatedwith afamilial hereditary syndrome(5-10%),suchas multiple endocrine neoplasia(MEN),types 1(90%)and 2a(30%)or 2b (4%). • In the caseof parathyroid adenomas,molecular mechanismsare heterogeneous.
- 24. PHPT- familial hereditarysyndromes Hereditary forms of PHPTaccount for 5–10% of cases: • Multiple endocrine neoplasia(MEN) • Hereditary hyperparathyroidism – jaw tumor syndrome
- 25. Primaryhyperparathyroidism (PHPT) PHPTis the endocrinopathy which occurs in 3rd to 5th decade and it affects: 0.3 -1.0% 1-3% of the generalpopulation of postmenopausalwomen. women to menratio is 3-4 : 1 Epidemiology
- 26. Classicalclinical consequencesof PHPT Bonedestruction Hypercalcemia Hypercalciuria Osteopenia Peptic ulcer disease Urolithiasis Osteoporosis Pancreatitis Nephrocalcinosis Bone deformities and fractures Constipation, nausea, vomiting or lossof appetite Nephrogenic diabetes insipidus Osteitis fibrosa cystica, brown tumors Polydipsia and polyuria Renal failure Cardiovascular features: hypertension, arrhythmia, ventricular hypertrophy, and vascular and valvular calcification Tiring easily or weakness Neuropsychiatric disorders Parathyroid crisis
- 27. Theclassicalmanifestations ofPHPT: "bones, stones, abdominal groans and psychic moans”
- 28. Primary hyperparathyroidism –clinical forms • Themost common clinical presentation of PHPT is asymptomatic or low symptomatic disease. • Symptomatic primary hyperparathyroidism nowadays tends to reduce the incidence in highly developed countries (20%). • Atypical occurences include normocalcemic PHPTand parathyroid crisis.
- 29. The incidence of clinical consequences PHPT* (n=63) Percentageof patients Osteoporosis (DXA) 76 96 Osteopenia 20 Urolithiasis 67 Bone fractures 16 Gastritis, peptic ulcer disease 22 Cholelithiasis 28 Pancretitis 2 persons *Dept. ED& IT,Wrocław Med.Univ. J.Szymczak
- 30. PHPT-skeletal changes • Parathyroid hormone causes reductionin bonemineral density (BMD) • In more severe cases,the cortex is grossly thinned, and the marrow contains increased amounts of fibrous tissue accompanied by foci of hemorrhage and cyst formation(osteitis fibrosa cystica). • Aggregates of osteoclasts, reactive giant cells, andhemorrhagic debris occasionally form massesthat may be mistaken for neoplasms (brown tumorsof hyperparathyroidism).
- 31. Primaryhyperparathyroidism –bone destruction Brown tumor of the skull ofayoung woman (CT)
- 32. Normocalcemicprimaryhyperparathyroidism (a variant ofPHPT) • ↑PTH • Normal serum total and ionized calcium concentration. • Thefeatures of PHPTmay be present (e.g. lowBMD) • All secondary causesfor hyperparathyroidism mustbe ruled out Normocalcemic PHPTis considered to be an early form of asymptomatic PHPT.
- 33. Primaryhyperparathyroidism –bone fracturerisk PHPT ,even when appearing asan asymptomatic disorder, is characterised by compromised cortical and trabecular compartments and increased fracture risk.
- 34. Parathyroid crisis Severe hypercalcemia : above 15 mg/dl with features of hypercalcemia : • Dehydration (hypercalciuria) • Central nervous systemdysfunction (confusion, dizziness,nauseaand vomiting) • GI dysfunction (constipation, paralytic ileus) • Bradycardia (ECG- QTshortening)
- 35. Diagnosisof primaryhyperparathyroidism Thediagnosis of primary hyperparathyroidism is established by appropriate biochemical testing. PHPT is associated with hypercalcemia and elevated levels of parathyroidhormone.
- 36. Diagnosisof Primary Hyperparathyroidism Laboratory tests Results Blood tests ↑ Calcium ↑ PTH ↓, N Inorganic phosphate N, ↓ Vitamin 25(OH)D (but 1,25(OH)2D - ↑ or N) ↑ ALP (alkaline phosphatase) N (↑) Creatinine 24 hour urine collection ↑ (N) Calciuria N Creatinine excretion
- 37. Diagnosisof primary Hyperparathyroidism Bone densitometry (DXA) • lumbar spine • hip (total or femoralneck) • radius (distal 1/3 site) Ultrasoundabdominal examination renal imaging X-rayof painful ordeformed parts of theskeleton Vertebral FractureAssessment (VFA)by DXAor x-ray* In order to diagnose asymptomatic vertebral compression fractures in asymptomatic patients who do not have osteoporosis in DXA Detection of geneticdisease * optional
- 38. Primary hyperparathyroidism - Differential Diagnostics PTH excess PTH independent bone resorption Vitamin D excess Excessive dietary intake of calcium Thiazides Hyperparathyroidism: PTHrP secreting ↑ intake of Vit. D Milk alkali • primary malignancy syndrome • secondary • tertiary (calcium-alkali syndrome - ↑ intake of CaCO3) Familial hypocalciuric Osteolytic bone Ectopic hypercalcemia (FHH) - (inactivating mutation in the calcium sensing receptor gene) metastases 1,25(OH)2D production (lymphoma, granuloma) Lithium (reduces sensitivity of PTH secretion to inhibition by calcium) Paget’s disease Immobilisation Hyperthyroidism
- 39. Secondary hyperparathyroidism Disorder Comment Chronic kidney disease (CKD) (GFR below 60 ml/min) Impaired 1,25(OH)2D production, hyperphosphatemia Decreased calcium intake Calcium malabsorption Vitamin D deficiency, celiac disease, chronic pancreatitis, post gastrectomy syndrome, bariatric surgery Renal calcium loss Renal hypercalciuria Drugs Bisphosphonates (inhibiton of bone resorption), anticonvulsants, furosemide, phosphorus
- 40. Hypercalcemia associated with high bone turnover Disorder Comment Hyperthyroidism TSH has bone protective effect, suppressed TSH levels play role in hypercalcemia. Immobilization Patients after spinal cord injury and paraplegia or quadriplegia Thiazides Chronic administration leads to reduction in urinary calcium Vitamin A intoxication Leads to bone resorption when consumed more than 10-20 times of RDA.
- 41. Familial Hypocalciuric Hypercalcemia (FHH) ↑Serum calcium and↑PTH but • Urine calcium is low (<100mg/24H) • Calcium-creatinine clearance ratio =<0.01 (24 Hurine Ca/serum Caxserum Cr/24 Hurine Cr) Thereason of FHHis inactivating mutation of thecalcium sensingreceptor in parathyroid glands. FHHis arare, lifelong, benigncondition.
- 42. FHH • The hypercalcaemia of FHH is always asymptomatic and complications do not occur. • The main risk of FHH is pt being subjected to an unnecessary parathyroidectomy if misdiagnosed as having primary hyperparathyroidism. • Testing of family members for hypercalcaemia is helpful in confirming the diagnosis and it is also possible to perform genetic testing. • No treatment is necessary.
- 43. Hypercalcemia in neoplastic disorders massive bone resorption humoral factors metastases +/- •1,25 (OH)2V D (granulomatous diseases) •TNF α, prostaglandins 1% local osteolysis ++++ sporadically ectopic secretion of PTH PTH 20% 80% PTHrP - PTH relatedprotein
- 44. Humoral hypercalcemia of Malignancy • Mediated by the production of PTHrP • PTHrP acts on osteoblasts, leading to enhanced synthesis of RANKL, with subsequent activation of osteoclasts and bone resorption with calcium release into the blood. • Increases renal calcium reabsorption.
- 45. • Squamous cell carcinoma of Lung • Urinary tract cancers (renal cell carcinoma and bladder carcinoma) • Breast cancer • Non hodgkins lymphoma • Ovarian cancers
- 46. PHPT (Primary hyperpara- thyroidism) FHH (Familial Hypocalciuric Hypercalcemia) Secondary hyperparathyroidism Malignancy Chronic renal failure Malabsorption, Ca & Vit.D deficiency PTH ↑ ↑ ↑ ↑ ↑ ↑ ↑, N ↓ Cas ↑↑ ↑ ↓, N ↓, N ↑ Cau24h ↑↑ ↓ ↓ ↓ ↑↑ Phosphates ↓ N ↑ ↓, N ↓, N BMD (DXA) ↓ ↓ N ↓ ↓ ↓, N Primary hyperparathyroidism - differential diagnostics
- 47. Primaryhyperparathyroidism -treatment 1. Selective parathyroidectomy • Thetreatment of choice for symptomatic diseaseis surgical removal ofthe hyperactive parathyroid glands along with intraoperative PTH monitoring. • Surgery maybe also recommended in some asymptomatic or low symptomatic patients. 2. Pharmacotheraphy
- 49. Localisation studies They should be done after a decision for surgery has been made. Localisation studies, in conjunction with intraoperative parathyroid hormone testing, can help minimise the extent of surgical dissection, and can help detect ectopic parathyroid tissue. Localisation studies should not be used to establish the diagnosis of PHPT or to determine management.
- 50. PHPT - localisation tests The type of imaging Comments Sensitivity* Ultrasonography Usually a hypoechoic parathyroid adenoma posterior to the thyroid parenchyma with peripheral vascularity seen on colour Doppler. US provides additional anatomic informationabout the thyroid gland. up to 80% Technetium-99m sestamibi scintigraphy Planar image 60-90% SPECT — Sestamibi-single photon emission computed tomography Is a three-dimensional sestamibi scan. The multidimensional images illustrate the depth of the parathyroid gland or glands in relation to thethyroid. ~ 90% SPECT-CT SPECT and CT fusion. Adds the ability to discriminate parathyroid adenomas fromother anatomic landmarks. Computed tomography (CT) Low sensitivity Magnetic resonance imaging (MRI) For reoperative surgery. Provides a non-invasive imaging to localise abnormal parathyroidtissue 40-85% * Sensivity for detecting solitary adenoma. No imaging technique accurately predicts multiglandular disase
- 51. Parathyroid scintigraphy (Tc99 + MIBI) Adenoma of left inferior parathyroid gland 99mTc-sestamibiis taken up by the mitochondria in thyroid and parathyroid tissue; however, the radiotracer is retained by the mitochondria-rich oxyphil cells in parathyroid glands longer than in thyroid tissue. Radionuclid usually washes out of normal thyroid tissue in under an hour. It persists in abnormal parathyroid tissue.
- 53. Surgicaltechniquesapplied inPHPT Minimally invasive technique : • Require adequate imaging, experienced surgeons,and an intraoperative PTHassay* • Not appropriate for apatients who havemultigland disease especially those who havefamilial forms ofPHPT . Bilateral cervical exploration is the ideal operation for most patients with multigland disease,including those with genetic disease. • Recommended operation for MEN1 patients with is asubtotal PTX removing 31/2 glands and leaving aviable 30 to 50 mgremnant from the most normal- appearing gland.
- 54. Theeffect of successfulparathyroidectomy in PHPT 1.Normalisation of biochemical disorders 2.Reduction of nephrolithiasis 3.Improvement in bone mineral density, bone reconstruction
- 55. PHPT - postoperative hypocalcemia Hypocalcemia The cause of hypocalcemia Transient and mild Suppression of the remaining normal parathyroid tissue Prolonged and accompanied by hypo- or euphosphatemia and high PTH levels (hungry bone syndrome) Rapid deposition of serum calcium into demineralised bone Accompanied by hyperphosphatemia and low PTH levels Hypoparathyroidism
- 56. Medical Management ofPrimary Hyperparathyroidism Pharmacotherapy may be used in mild or asymptomatic PHPTand in in patients after an unsuccessful parathyroidectomy (PTX),or inthose who are unwilling to undergo or considered unsuitable forsurgery. Pharmacological treatment should be reserved for those patients in whom it is desirable to lower the serum calcium or increaseBMD.
- 57. Medical Management ofPrimary Hyperparathyroidism Medicine Effect Calcimimetics (cinacalcet) • Decrease calcemia and calciuria • Reduce, but not normalise PTH • Do not affect BMD Bisphosphonates (alendronate) • Improve BMD • Do not alter serum calcium Denosumab • RANKL antagonist - decrases bone resorption Patients with low serum 25-hydroxyvitamin D should be repeatedely administered with doses of vitamin D that bring its serum levels to 20 ng/ml at a minimum (with caution, so as not to aggravate hypercalcemia).
- 58. Treatmentof ParathyroidCrisis • Hydration with normalsaline • Furosemide (after hydration) • Bisphosphonates iv. (pamidronate, zoledronic acid) • Glucocorticoids (prednisone 40-60mg/d) • Calcitonin sc.,im. • Calcimimetics (cinacalcet) – 10-80mg/d
- 64. A. Aplasia/Hypoplasia of Parathyroid Glands • DiGeorge/velocardiofacial syndrome (1/4000) • In 90% of patients, the condition is caused by a deletion of chromosome 22q11.2. – Approximately 25% of these patients inherit the chromosomal abnormality from a parent. HEREDITARY HYPOPARATHYROIDISM
- 66. B.HDR Syndrome • Hypoparathyroidism, • sensorineural Deafness, and • Renal anomaly • The GATA3 gene is located at chromosome 10p14.
- 67. C.Autoimmune Hypoparathyroidism • Parathyroid antibodies • Autoimmune polyglandular disease type I autoimmune polyendocrinopathy, candidiasis, and ectodermal dystrophy (APCED). • Autosomal recessive • AIRE gene (autoimmune regulator); chromosome 21q22 • One third of patients with this syndrome have all 3 components; 66% have only 2 of 3 conditions.
- 68. • The candidiasis almost always precedes the other disorders (70% of cases occur in children <5 yr of age); • The hypoparathyroidism (90% after 3 yr of age) usually occurs before Addison disease (90% after 6 yr of age). • Alopecia areata or totalis, malabsorption disorder, pernicious anemia, gonadal failure, chronic active hepatitis, vitiligo, and insulin dependent diabetes.
- 69. D.Autosomal Dominant Hypoparathyroidism • Activating (gain-of-function) mutation of the Ca2+ sensing receptor, • The patients have hypercalciuria. • The hypocalcemia is usually mild and might not require treatment beyond childhood.
- 70. Surgical Hypoparathyroidism • Removal or damage of the parathyroid glands can complicate thyroidectomy. tetany can occur abruptly and may be temporary or • Symptoms of postoperatively permanent.
- 71. Pseudohypoparathyroidism Definition: Peripheral resistance to parathyroid hormone rather than a deficiency. Hypocalcaemia, hyperphosphataemia, raised serum PTH Three Types: 1a, 1b, 2 Epidemiology: F:M ratio – 2:1 Any age can be affected
- 72. Etiology • Collection of Autosomal Dominant inherited genetic conditions. • All heterozygous • Haploinsufficiency of GNAS1 – only 1 copy of the normal protein. It is not fatal but cannot continue normal functioning.
- 73. Pseudohypoparathyroidism: Type 1a Signs and Symptoms • Short 4th and 5th metacarpals • Round face • Short stature • Calcium deposits under the skin • Stocky habitus, developmental delay • Dental hypoplasia • Soft tissue calcification/ossification Associated with TSH resistance, hypogonadism, females often suffer impaired fertility, oligomenorrhea, delayed puberty, male – infertility
- 75. Type 1b Pathophysiology of Type 1b is by the same mechanism (GNAS1) leading to Gsa defect. Characterised by only renal resistance to parathyroid hormone, otherwise endocrinologically normal. Paternal imprinting.
- 76. Type II • Type II is characterised by a low calcium andhigh phosphate levels. • Type II is not characterised by any skeletal changes or the phenotypic appearance of Type 1a. • All different physiologies are due to differences in the imprinting defect.
- 77. Pseudopseudohypoparathyroidism Phenotypic appearance mimicking those of pseudoparathyroidism type 1a. No lack of parathyroid hormone, no peripheral resistance to PTH – biochemically normal. Also caused by a defect in the GNAS1. First described by Fuller Albright in 1952.
- 79. The symptoms of hypoparathyroidism result from: Hypocalcemia: Tetany, paresthesias, neurological disorders, epileptic seizures Deposits of calcium phosphate in soft tissues: due to an excess of phosphate (basal ganglia, joint capsules, subcutaneous tissue, vitreous humor of the eye, muscles, bones).
- 80. Themajor clinical manifestations of hypoparathyroidism are referable to hypocalcemia and are related tothe severity and chronicity of thehypocalcemia. A. Subjects who develop severe hypoparathyroidism quickly (for example, after neck surgery) can feel tired, irritable, anxious or depressed and demonstrate spontaneous or latent tetany.
- 81. Tetany Tetanyis asyndrome of increasedneuromuscular excitability usually associatedwith hypocalcemia. Three subtypes of tetany can appear in isolation, but all three can occur simultaneously in the same subject. Theseare: • Tetanicattack o Sensory symptoms: paresthesias of the lips, tongue, fingers andfeet o Carpopedal spasm o Spasmof facial musculature o Generalised muscle aching and spasm
- 82. • Latent tetany (Chvostek’sand Trousseau’s signs are easily performed to elicid latent tetany). • Tetanicequivalents The involvement of autonomic nervous system may be present as: diplopia, blepharospasmus, laryngospasms, spasm of the bronchi, cardia and sphincter of the bladder. In similar manner blood vessels may be affected causing migraine, angina pectoris, abdominal angina or Raynaud syndrome.
- 83. B. Patients with gradually developing hypoparathyroidism and long standing hypocalcemia associated with hyperphosphatemia may also exhibit: • Calcification of the basal ganglia (Fahr’s syndrome) with symptoms suchas deterioration of motor functions and speech, seizures, headaches, dementia, and vision impairment. • Ocular cataracts (mineral deposits in the lens) • Dry and thick skin, coarse breaking hair, brittle nails • Defects of the tooth enamel
- 84. Hypoparathyroidismus- differential diagnostics (Hypocalcemia - etiologiesbymechanism) Hypoparathyroidism Vitamin Ddeficiency Lowdietary intake of Ca+2 PTH ↓ , N PTH ↑ Thyroidectomy or otherneck surgery Lowcalcitriol: • ↓ intake of dietary Vit. D • Inadequate sunlight exposure • Malabsorption syndrome I 131 therapy for thyroid cancer Autoimmune hypoparathyroidism ↓ conversion of 25OHDto 1,25(OH)2D • Renalfailure • Hyperphosphatemia • Vitamin Ddependent rickets, type 1 Infiltration ofparathyroids Hypomagnesemia Calcitriol resistance • Vitamin Dresistantrickets Congenital /genetic PTHresistance(pseudo hypoparathyroidism) PTH ↑ ) ↑ inactivation of vit. D(e.g. carbamazepine,phenytoin )
- 85. Diagnosticsof hypoparathyroidism 1.Blood tests: ↓ calciumlevels ↑ phosphorus levels ↓ PTHlevels(but normal or elevated in pseudohypoparathyroidism) ↔ ALP ↔ magnesium ↔ creatinine ↓ 1,25(OH)2D
- 86. 2.24 urine low calciumexcretion 3.Imagingtests if necessary: • X-ray and CTmay reveal calcifications in the basal ganglia of the brain and other soft tissue and the density of the bone structure • Renal ultrasoud 4.Consultationswith an ophthalmologist (cataract) and neurologist. 5.ECG:prolonged QTinterval
- 87. Themethods of treatmentof hypoparathyroidism: • A high-calcium and low-phosphorous diet. • Calcium carbonate 1000 - 1500 mg/d orally, during and in between meals. • Activated vitamin Danalogues e.g. alfacalcidol 1-3 µg/d. • Vitamin Dsupplementation 25,000–1,00,000 IU/d to patients treated with activated vitamin Danalogues.
- 88. • In a patient with hypercalciuria, consider a reduction in calcium intake, a sodium-restricted diet, and/or treatment with athiazide diuretic. • Magnesium supplementation in case of deficiency. • Recombinant human parathyroid hormone (rhPTH, Natpara) is commercially available in the United States and is indicated asan adjunct to calcium and vitamin D(caution! may causeosteosercoma) • Implants of stem cells (trials are inprogress).
- 89. Tumour lysis syndrome • It is characterised by hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia, and is caused by destruction of large no. of rapidly proliferating neoplastic cells. • Associated with treatment of Burkitt’s lymphoma, ALL and some chronic leukemias like CLL. • Incidence - 6% among these pts.
- 91. Tetanyattack should betreated withiv infusion of calciumsalts. Calciumgluconate maybegiven as10ml of 10%solution in 50ml NS over5min, andif hypocalcemia continues, next infusion with 10 ampoules or 900 mg of 10%calcium gluconatein 1 litre of 5%glucoseor0.9%NS over24hrs.
- 92. References • Guyton and Hall Textbook of Medical Physiology. • Harrisons Principles Of Internal Medicine 20th Edition. • Williams Textbook Of Endocrinology.
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