eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic
Hypopituitarism: Treatment & Medication
Updated: Aug 14, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Prehospital Care
Vital sign abnormalities and life-threatening concerns should be managed according to prehospital protocols, such as those for hypoglycemia, altered mental status, bradycardia, hypothermia, or seizures.
Emergency Department Care
The ED treatment of hypopituitarism is 3-fold. Missing hormones must be replaced coincidentally with treatment of electrolyte and cardiovascular effects of the missing hormones being treated. In addition, the stressor that caused decompensation should be treated. For instance, administer antibiotics in a patient with coincident urosepsis or pneumonia.
Standard acute resuscitation principles apply to patients who have hypotension or cardiovascular instability. Intravenous saline boluses are the first-line therapy. Vasopressors are used according to standard recommendations.
Electrolyte disorders are common. The combination of hypovolemia and hyponatremia are addressed with normal saline boluses. Hyperkalemia is usually mild and does not require acute intervention. It corrects with replacement of aldosterone.
Test for hypoglycemia and treat. Retest glucose level frequently. Begin continuous intravenous dextrose infusions in a patient with a single episode of recurrent hypoglycemia during the ED stay.
The supportive measures above are standard for all patients. If the emergency physician suspects hypopituitarism based on clinical presentation or knows that the patient has a prior diagnosis of hypopituitarism, emergent intervention is warranted.
Hormone replacement in hypopituitarism varies with the patient's diagnosis. In the emergency department, the single most important agent to replace emergently is the glucocorticoid. Hydrocortisone in a stress dose is the standard choice for replacement. Early thyroxine replacement is the second most important treatment. Intravenous levothyroxine is the preferential thyroid hormone to administer. Triiodothyroxine is associated with cardiovascular complications.
Consultations
- Patients with a hypopituitarism crisis will be admitted to the intensive care unit.
- In the setting of a newly diagnosed brain mass, a neurosurgeon may need to be emergently consulted.
- Other consultants who may be involved in the case, but are not emergently consulted from the ED, include an endocrinologist, oncologist, and radiation oncologist.
- Patients in whom the emergency physician suspects nondecompensated, undiagnosed hypopituitarism can be referred to an endocrinologist on an outpatient basis.
Medication
Medications used in hypopituitarism vary depending on the specific hormone deficiency that exists.
Agents for hormone replacement
These drugs are either synthetic or natural agents used to supplement hormone deficiencies resulting from hypopituitarism.
Hydrocortisone (Solu-Cortef, Westcort)
Used as steroid replacement in patients who have adrenal insufficiency. For hypotensive patients and acute management, use IV preparation.
Adult
Outpatient: 10 mg PO qam, 5 mg PO qpm
Inpatient: 100-250 mg IV initial bolus, followed by 100 mg IV q8h until patient is hemodynamically stable and able to take PO
Pediatric
0.5-0.75 mg/kg/d or 20-25 mg/m2/d PO divided q8h
Clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia
Documented hypersensitivity; viral, fungal, or tubercular skin infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis
Prednisone (Deltasone, Orasone, Sterapred)
Alternative to hydrocortisone in patients with adrenal insufficiency. Medication of choice for maintenance therapy.
Adult
5 mg PO divided bid
Pediatric
4-5 mg/m2/d PO
Alternatively, administer 1-2 mg/kg PO qd
Estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with concurrent diuretics
Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; connective tissue infections; GI disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur
Thyroxine products
These agents are used for the treatment of hypothyroidism.
Levothyroxine (Synthroid, Levoxyl)
Thyroid supplement whose active form influences tissue growth and maturation. Involved in normal growth, metabolism, and development. Endocrinologists can monitor and adjust doses to optimal effect.
Adult
12.5-50 mcg/d PO initially; increase by 25-50 mcg/d q2-4wk; not to exceed 100-200 mcg/d
Pediatric
Neonate to 6 months: 25 mcg/d PO
6-12 months: 50 mcg/d PO
1-5 years: 75 mcg/d PO
6-12 years: 100 mcg/d PO
>12 years: 150 mcg/d PO
Cholestyramine may decrease absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; increases effects of anticoagulants; activity of some beta-blockers may decrease when hypothyroid patient is converted to a euthyroid state
Documented hypersensitivity; uncorrected adrenal insufficiency
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in angina pectoris or cardiovascular disease; monitor thyroid status periodically
Antidiuretic hormone replacement
These agents are used for the replacement of vasopressin.
Vasopressin (Pitressin)
IM or SC injection of ADH analog that has vasopressor and ADH activity. Increases water resorption at distal renal tubular epithelium (ADH effect). Promotes smooth-muscle contraction throughout vascular bed of renal tubular epithelium (vasopressor effects).
Adult
5-10 U IM/SC q6h
Pediatric
2.5-10 U IM/SC bid/qid
Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects
Documented hypersensitivity; coronary artery disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia
Desmopressin acetate (DDAVP, Stimate)
Longer-acting ADH derivative that can be used intranasally; increases cellular permeability of collecting ducts, resulting in resorption of water by kidneys.
Adult
150 mcg intranasally q12-24h; endocrinologist should follow effects to adjust dose and timing
Pediatric
<3 months: Not established
3 months to 12 years: 5-30 mcg/d intranasally qd or divided bid
>12 years: Administer as in adults
Demeclocycline and lithium decrease effects; fludrocortisone and chlorpropamide increase effects
Documented hypersensitivity; patients with platelet-type von Willebrand disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Avoid overhydration in patients using desmopressin to benefit from its hemostatic effects
More on Hypopituitarism |
| Overview: Hypopituitarism |
| Differential Diagnoses & Workup: Hypopituitarism |
Treatment & Medication: Hypopituitarism |
| Follow-up: Hypopituitarism |
| References |
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References
Schneider HJ, Schneider M, Saller B, et al. Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury. Eur J Endocrinol. Feb 2006;154(2):259-65. [Medline].
Bülow B, Hagmar L, Eskilsson J, et al. Hypopituitary females have a high incidence of cardiovascular morbidity and an increased prevalence of cardiovascular risk factors. J Clin Endocrinol Metab. Feb 2000;85(2):574-84. [Medline].
Abboud CF. Hypopituitarism. In: Conn RB, ed. Current Diagnosis. 8th ed. 1991:811-19.
Abboud CF. Anterior pituitary failure. In: The Pituitary. 2nd ed. 2002:349-404.
Arafah BM, Nasrallah MP. Pituitary tumors: pathophysiology, clinical manifestations and management. Endocr Relat Cancer. Dec 2001;8(4):287-305. [Medline].
Baldelli R, Bellone S, Corneli G, et al. Traumatic brain injury-induced hypopituitarism in adolescence. Pituitary. 2005;8(3-4):255-7. [Medline].
Benvenga S. Brain injury and hypopituitarism: the historical background. Pituitary. 2005;8(3-4):193-5. [Medline].
Blondell RD. Hypopituitarism. Am Fam Physician. Jun 1991;43(6):2029-36. [Medline].
Chang YC, Tsai JC, Tseng FY. Neuropsychiatric disturbances and hypopituitarism after traumatic brain injury in an elderly man. J Formos Med Assoc. Feb 2006;105(2):172-6. [Medline].
Darzy KH, Shalet SM. Hypopituitarism as a consequence of brain tumours and radiotherapy. Pituitary. 2005;8(3-4):203-11. [Medline].
Giordano G, Aimaretti G, Ghigo E. Variations of pituitary function over time after brain injuries: the lesson from a prospective study. Pituitary. 2005;8(3-4):227-31. [Medline].
Guyton AC, Hall JE. The pituitary hormones and their control by the hypothalamus. In: Textbook of Medical Physiology. 11th ed. 2005:846-856.
Insel JR, Dhanjal N. Pituitary infarction resulting from intranasal cocaine abuse. Endocr Pract. Nov-Dec 2004;10(6):478-82. [Medline].
Kreitschmann-Andermahr I. Subarachnoid hemorrhage as a cause of hypopituitarism. Pituitary. 2005;8(3-4):219-25. [Medline].
Landman RE, Wardlaw SL, McConnell RJ, et al. Pituitary lymphoma presenting as fever of unknown origin. J Clin Endocrinol Metab. Apr 2001;86(4):1470-6. [Medline].
Lanes R. Metabolic abnormalities in growth hormone deficiency. Pediatr Endocrinol Rev. Dec 2004;2(2):209-15. [Medline].
Lin SH, Hung YH, Lin YF. Severe hyponatremia as the presenting feature of clinically non-functional pituitary adenoma with hypopituitarism. Clin Nephrol. Jan 2002;57(1):85-8. [Medline].
Masel BE. Traumatic brain injury induced hypopituitarism: the need and hope of rehabilitation. Pituitary. 2005;8(3-4):263-6. [Medline].
McArthur RG, Morgan K, Phillips JA 3rd, et al. The natural history of familial hypopituitarism. Am J Med Genet. Nov 1985;22(3):553-66. [Medline].
Minniti G, Esposito V, Piccirilli M, et al. Diagnosis and management of pituitary tumours in the elderly: a review based on personal experience and evidence of literature. Eur J Endocrinol. Dec 2005;153(6):723-35. [Medline].
Moll GW, Bock HG. Two tumors detected by thyroid assessment in two children. Endocr Pract. Nov-Dec 2001;7(6):467-73. [Medline].
Ozkan Y, Colak R. Sheehan syndrome: clinical and laboratory evaluation of 20 cases. Neuro Endocrinol Lett. Jun 2005;26(3):257-60. [Medline].
Pivnick EK, Burstein S, Wilroy RS. Hallermann-Streiff syndrome with hypopituitarism contributing to growth failure. Am J Med Genet. Dec 15 1991;41(4):503-7. [Medline].
Popovic V. GH deficiency as the most common pituitary defect after TBI: clinical implications. Pituitary. 2005;8(3-4):239-43. [Medline].
Reynaud R, Chadli-Chaieb M, Vallette-Kasic S, et al. A familial form of congenital hypopituitarism due to a PROP1 mutation in a large kindred: phenotypic and in vitro functional studies. J Clin Endocrinol Metab. Nov 2004;89(11):5779-86. [Medline].
Schneider HJ, Aimaretti G, Kreitschmann-Andermahr I, et al. Hypopituitarism. Lancet. Apr 28 2007;369(9571):1461-70. [Medline].
Sert M, Tetiker T, Kirim S, et al. Clinical report of 28 patients with Sheehan's syndrome. Endocr J. Jun 2003;50(3):297-301. [Medline].
Somali MH, Anastasiou AL, Goulis DG, et al. Pituitary abscess presenting with cranial nerve paresis. Case report and review of literature. J Endocrinol Invest. Jan 2001;24(1):45-50. [Medline].
Tanriverdi F, Senyurek H, Unluhizarci K, et al. High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma. J Clin Endocrinol Metab. Jun 2006;91(6):2105-11. [Medline].
Tindall GT, Barrow DL. Pituitary deficiency states. In: Disorders of the Pituitary. Vol 1. 1986:451-72.
van Aken MO, Lamberts SW. Diagnosis and treatment of hypopituitarism: an update. Pituitary. 2005;8(3-4):183-91. [Medline].
Vance ML. Hypopituitarism. N Engl J Med. Jun 9 1994;330(23):1651-62. [Medline].
Wass JAH, Besser GM, DeGroot LJ. Tests of Pituitary Function. Endocrinology. 1989;1:491-7.
Williams HR, Oliver NS, Murphy F, et al. The role of the biochemistry department in the diagnosis of pituitary apoplexy. Ann Clin Biochem. Mar 2004;41:162-5. [Medline].
Further Reading
Keywords
hypopituitarism, pituitary apoplexy, Sheehan's syndrome, Sheehan syndrome, pituitary hormone deficiencies, thyrotropin, thyroid-stimulating hormone, TSH, gonadotropins, follicle-stimulating hormone, FSH, luteinizing hormone, LH, growth hormone, GH, corticotropin, adrenocorticotropic hormone, ACTH, prolactin hormone, PRL, traumatic brain injury, TBI, cocaine snorting, subarachnoid hemorrhage, postpartum hypotension, pituitary insufficiency
Treatment & Medication: Hypopituitarism