eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Hypopituitarism: Differential Diagnoses & Workup

Author: Lisa Diane Mills, MD, Assistant Professor of Emergency Medicine, Director, Section of Emergency Medicine Ultrasound, Louisiana State University at New Orleans
Contributor Information and Disclosures

Updated: Aug 14, 2008

Differential Diagnoses

Adrenal Insufficiency and Adrenal Crisis
Hypothyroidism and Myxedema Coma
Shock, Cardiogenic
Shock, Septic

Other Problems to Be Considered

Chronic liver disease
Myotonia dystrophica
Primary psychosis
Primary hypogonadism

Workup

Laboratory Studies

In the emergency department, routine laboratory results will not diagnose hypopituitarism. The diagnosis of decompensated hypopituitarism is clinical. In patients in whom nondecompensated hypopituitarism is suspected, the laboratory testing is not part of emergency care.

Laboratory and radiographic tests are necessary to confirm the diagnosis. A variety of diagnostic laboratory tests can be used, but significant controversy exists regarding which tests are ideal. Because many specific endocrine tests are not rapidly available in the ED setting, immediate confirmation of hypopituitarism may not be practical. Clinical suspicion by history and clinical examination may be the only tools to reveal the etiology and to guide appropriate endocrine follow-up care. Expensive, time-consuming tests, which may be performed and interpreted upon follow-up by endocrinologists, are listed below.

  • Corticotropin deficiency may be evident with the finding of a decreased serum cortisol level.  
    • A low cortisol level may not help to distinguish primary adrenal insufficiency from secondary adrenal insufficiency due to hypopituitarism. The conditions can be differentiated on clinical grounds. A patient with secondary causes due to pituitary dysfunction will have a relatively pale complexion, a normal aldosterone response, and low ACTH level.
    • The opposite is true for primary adrenal insufficiency. Hyperpigmentation in primary adrenal insufficiency is due to increased ACTH production with concomitant overproduction of melanocyte-stimulating hormone, which is coupled ACTH in a mutual precursor.
    • ACTH deficiency in the morning during its highest circadian levels suggests a pituitary/hypothalamic etiology.
  • The corticotropin stimulation test, which evaluates the hypothalamic-pituitary-adrenal axis, is a superior tool in distinguishing hypopituitarism from primary adrenal insufficiency.  
    • This dynamic test measures serum cortisol level before and after a 250-mcg dose of ACTH.
    • The cortisol level should at least double 30-60 minutes after ACTH administration in those with normal adrenal function.
    • A low cortisol level that fails to rise after ACTH administration represents an abnormal cortisol response, a response seen in primary adrenal insufficiency. However, because of adrenal atrophy, cortisol response is often slightly blunted in patients with hypopituitarism.
  • Assessment of thyroid function is important in the evaluation of ACTH deficiency.  
    • In a hypothyroid state, cortisol clearance decreases, causing an increase in serum cortisol level.
    • If thyroid replacement is initiated, cortisol level drops acutely, initiating an adrenocortical crisis.
  • In suspected thyrotropin deficiency, measure serum thyrotropin (TSH) and thyroxine (T4).  
    • A normal level of total free T4 rules out hypothyroidism.
    • Low serum TSH and a small, atrophic thyroid gland confirm the diagnosis of thyrotropin deficiency.
  • LH and FSH deficiencies may indicate secondary hypogonadism.  
    • Measuring LH and FSH is possible, but values range widely throughout the day and are therefore unreliable. Measure multiple samples, and calculate a mean value before establishing gonadotropin deficiency.
    • In men, measuring serum testosterone levels is useful.
        • Decreased testosterone level should be associated with an increase in FSH and LH levels if pituitary function is normal. Low or normal FSH or LH levels in the face of low testosterone indicates hypopituitarism.
        • Semen analysis also may be performed. A normal semen sample excludes hypogonadism of a primary or secondary source.
    • Elevated FSH and LH levels differentiate primary hypogonadism from secondary hypogonadism.
  • GH deficiency can be confirmed by directly measuring serum levels. 
    • Given that GH secretion is pulsatile, a single low serum level must be repeated for confirmation, whereas a single elevated or normal serum GH level can exclude the diagnosis of GH deficiency.
  • PRL deficiency can also be verified by directly measuring serum levels.  
    • As with most other pituitary hormones, secretion of PRL is episodic; more than one value is necessary for diagnosis.
    • Testing is rarely necessary since most patients are asymptomatic.
  • A water deprivation test can help differentiate psychogenic polydipsia from diabetes insipidus.  
    • Supervise patients constantly to calculate water intake, as patients with psychogenic polydipsia often use any means possible to consume water (eg, drinking from a toilet bowl).
    • While withholding water, take blood and urine samples hourly to measure serum and urine osmolalities.
    • If the cause is psychogenic, urine osmolality increases while serum osmolality remains normal.
  • If urinary concentrations do not increase in a water deprivation test, the diagnosis of diabetes insipidus is established. Subsequently, an aqueous vasopressin stimulation test may assist in discriminating between central and nephrogenic diabetes insipidus.  
    • Administer either 5 units of aqueous vasopressin or 1-2 mcg of desmopressin (DDAVP) subcutaneously.
    • After 1 hour, acquire an additional set of serum and urine specimens and record the results.
    • An increase in urine osmolality and a decrease in serum osmolality support a central cause of diabetes insipidus and a lack of ADH.
    • If osmolalities remain unchanged, the patient has nephrogenic diabetes insipidus.

Imaging Studies

  • Radiographic studies of the head (eg, MRI, CT scan) can be performed for patients with a history and physical examination suggestive of an intracranial lesion. Both MRI and CT scans should be obtained with intravenous contrast to increase sensitivity of the tests.
  • MRI is superior in localizing and characterizing intracranial lesions; however, CT scan may be more readily accessible.
  • A lateral skull film can delineate contours of the sella turcica but are otherwise very unlikely to provide any beneficial information.

Procedures

  • There is no emergent procedure to diagnose hypopituitarism.

More on Hypopituitarism

Overview: Hypopituitarism
Differential Diagnoses & Workup: Hypopituitarism
Treatment & Medication: Hypopituitarism
Follow-up: Hypopituitarism
References
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References

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Further Reading

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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

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Contributor Information and Disclosures

Author

Lisa Diane Mills, MD, Assistant Professor of Emergency Medicine, Director, Section of Emergency Medicine Ultrasound, Louisiana State University at New Orleans
Lisa Diane Mills, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Southern Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Howard A Bessen, MD, Professor of Medicine, Department of Emergency Medicine, UCLA School of Medicine; Program Director, Harbor-UCLA Medical Center
Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

 
 
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