Acute Hypopituitarism
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Causes of pituitary insufficiency include pituitary adenomas or other intrasellar and parasellar tumors, inflammatory and infectious destruction, surgical removal, radiation-induced destruction of pituitary tissue, traumatic brain injury (TBI), subarachnoid hemorrhage, and postpartum pituitary necrosis (Sheehan syndrome). [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15]
Pituitary tumors, or adenomas, are the most common cause of hypopituitarism in adults. [16] Depletion of pituitary function by tumors occurs via the following mechanisms: primary pituitary destruction and destruction of the hypothalamus.
In primary pituitary destruction, the anterior pituitary is destroyed. The result is deficiency in some or all pituitary hormones. Pituitary tumors, or adenomas, can be secretory or nonsecretory. Approximately 30% of all macroadenomas larger than 10 mm will produce at least 1 hormone. Hypothalamic disease involves destruction of the hypothalamus. This causes a deficiency or loss of hypothalamic regulatory hormone input to the pituitary, resulting in loss of anterior pituitary hormone secretion.
Hypopituitarism may present in an acutely decompensated patient or in a patient who is stable but with symptoms of the disorder. The diagnosis of hypopituitarism is easily overlooked, as the symptoms and signs are frequently protean and nonspecific, including abnormalities in electrolyte levels, mental status, glucose levels, body temperature, and heart rate. The setting is not uncommon in which an emergency physician is evaluating a patient with complaints of weakness, fatigue, or altered mental status without a clear diagnosis. Subtle, but still abnormal, vital signs, such as slightly reduced blood pressure or heart rate, may be the only initial clues to suggest a pituitary deficiency rather than a relatively benign etiology.
Emergency physicians frequently provide care to patients at risk of developing hypopituitarism. Risk factors include, but are not limited to, TBI, cocaine use, subarachnoid hemorrhage, and postpartum hypotension (a sign that Sheehan syndrome may be present). [1, 2, 3, 5, 6, 7, 8] Establish a broad differential diagnosis in the initial evaluation of patients with abnormal vital signs, and include hypopituitarism as a cause of these abnormalities. Also consider hypopituitarism as the cause of abnormal laboratory values.
In its initial presentation, hypopituitarism is difficult to diagnosis in the acutely decompensated or the stable patient. 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 emergency department (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. In the acutely decompensated patient with hypopituitarism, for example, expect to find an ill-appearing patient with hypotension and signs of dehydration.
The history in an acutely decompensated patient with hypopituitarism should be aimed at identifying the stressor that caused decompensation. Most commonly, trauma or infectious disease cause the change from compensated to decompensated disease. Patients may also have discontinued medication or have emotional stressors. These conditions should be evaluated and treated concurrently with the pituitary emergency.
Symptom presence and severity depend on the amount of and rapidity of hormone depletion. Clinical manifestations closely match those of primary deficiency or hypofunctioning of target glands. Hypopituitarism is usually a combination of several hormonal deficiencies and rarely involves all pituitary hormones. End-organ hormonal insufficiencies are referred to as secondary deficiencies of the target organ (eg, hypothyroidism caused by a decrease in thyroid-stimulating hormone [TSH] is termed secondary hypothyroidism).
The presence of an antecedent closed-head injury may be elicited. Patients with TBI can have some degree of hypopituitarism as soon as 3 months, and typically by 12 months, following the injury. Nearly all patients with resultant pituitary deficiency will have experienced loss of consciousness following the trauma, and approximately half have a skull fracture. A study by Taheri et al found that altered expression of circulating microRNAs may play a part in the progression of traumatic brain injury-induced hypopituitarism. [17]
The onset of hypopituitarism is often gradual over a period of years, but in some conditions, rapid onset is seen. The insidious decline in health is often attributed to other medical conditions prior to recognition.
A deficiency of adrenocorticotropic hormone (ACTH), or corticotropin, is characterized by a decrease in adrenal androgens and production of cortisol. Acute loss of adrenal function is a medical emergency and may lead to hypotension and death if not treated.
Signs and symptoms of ACTH deficiency may be profound and potentially fatal; they include myalgias, arthralgias, fatigue, headache, weight loss, anorexia, nausea, vomiting, abdominal pain, altered mentation or altered consciousness, dry wrinkled skin, decreased axillary and pubic hair, anemia of chronic disease, dilutional hyponatremia, hypoglycemia, hypotension, and shock.
Symptoms are nearly identical to those of primary adrenal insufficiency but can be differentiated by lack of hyperpigmentation. Hyperpigmentation occurs in a long feedback loop in which a cortisol deficiency results in increased production of ACTH by the pituitary. The ACTH precursor coupled to melanocyte-stimulating hormone is not produced in patients with pituitary disease, and therefore, hyperpigmentation does not take place.
Patients with secondary adrenal insufficiency usually are eukalemic. This differs from primary adrenal insufficiency, in which patients develop hyponatremia and hyperkalemia. Aldosterone secretion is not affected, as it does not depend on corticotropin but instead on the renin-angiotensin axis.
Secondary hypothyroidism due to decreased TSH (also known as thyrotropin) exhibits symptoms identical to those of primary thyroid disease, only typically less severe. Signs and symptoms of secondary hypothyroidism include fatigue, weakness, weight gain, thickened subcutaneous tissues, constipation, cold intolerance, altered mental status, impaired memory, and anemia. Physical examination of the patient may reveal bradycardia, delayed relaxation of the deep tendon reflexes, and periorbital edema.
Low levels of the gonadotropins–follicle-stimulating hormone (FSH) and luteinizing hormone (LH) –increase the risk of osteoporosis due to decreased bone density and result in hypogonadism in men and women. In men, symptoms include decreased libido, varying degrees of erectile dysfunction, decreased ejaculate, muscle weakness, and fatigue. Men with long-standing hypogonadism have decreased hair growth, soft testes, and gynecomastia.
Patients may be anemic due to decreased erythropoietin production, which causes a normochromic, normocytic anemia. Pubic and axillary hair growth is usually normal unless a concomitant ACTH deficiency exists.
Premenopausal women present with altered menstrual function, ranging from regular anovulatory periods to amenorrhea, as well as hot flashes, decreased libido, breast atrophy, vaginal dryness, and dyspareunia. Postmenopausal women usually present with headache or visual abnormalities due to other hormonal deficiencies or mass lesions.
In children, FSH and LH deficiency can cause eunuchoidism and lack of sexual development. FSH and LH have an indirect effect on bone growth by causing closure of the epiphysis. Characteristics of eunuchoidism are due to delay in closure of the epiphysis, resulting in long extremities.
In children, growth hormone (GH) deficiency presents as growth retardation and delayed sexual maturation. Patients may present with fasting hypoglycemia due to loss of the gluconeogenic effect of GH, which counteracts the effect of insulin. In adults, GH deficiency presents as weakness, poor wound healing, decreased exercise tolerance, and decreased social functioning.
Tumor growth that decreases prolactin (PRL) production affects the process of lactation; these tumors become evident only in the postpartum state. PRL deficiency is very rare; any process that affects the hypothalamus and the pituitary stalk decreases the normal inhibitory effect of dopamine from the hypothalamus on the pituitary, causing a rebound increase in PRL.
Antidiuretic hormone (ADH) deficiency causes polyuria and polydipsia (diabetes insipidus). When deficient in ADH (also known as vasopressin), the distal tubules of the kidney are unable to absorb water, producing very dilute urine and increasing serum osmolality. If water excretion exceeds oral intake, a patient may become hypotensive and hypovolemic, with hypernatremia and elevated serum osmolality. If fluid intake matches fluid output, serum sodium and osmolality may remain normal.
Central diabetes insipidus is caused by a decrease in ADH secretion, in contrast to nephrogenic diabetes insipidus, in which the kidney is ADH resistant.
Deficiency in oxytocin is characterized by a decrease in milk ejection during lactation. Interestingly, women with known oxytocin deficiency undergo normal labor and delivery despite the lack of hormone. One of the initial clues to the presence of Sheehan syndrome should be the lack of lactation secondary to oxytocin deficiency.
Radiographic studies of the head (eg, magnetic resonance imaging [MRI], computed tomography [CT] scanning) can be performed for patients with a history and physical examination suggestive of an intracranial lesion. MRI and CT scans should be obtained with intravenous contrast to increase the sensitivity of the tests. MRI is superior in localizing and characterizing intracranial lesions; however, CT scanning 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.
Prior to the patient reaching the ED, 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.
The ED treatment of hypopituitarism is 3-fold. Missing hormones must be replaced coincidentally with the treatment of the electrolyte and cardiovascular effects of the missing hormones. 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 the 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 ED, 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. Triiodothyronine is associated with cardiovascular complications.
Acutely decompensated hypopituitarism requires admission. Patients with a hypopituitarism crisis will be admitted to the intensive care unit.
Once diagnosed, hypopituitarism due to a pituitary adenoma may be entirely reversible by shrinking the tumor with pharmacologic therapy or radiation. Pituitary surgery is an option, depending on the size of the tumor, the degree of destruction of adjacent tissue, and the ability of the neurosurgeon to remove the tumor without disturbing the normal pituitary tissue. If the tumor can be removed selectively, hormone secretion may return to normal.
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 who 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.
Patients with hypopituitarism who are seen in the ED for nonendocrinologic reasons should be reminded to increase their baseline steroids in response to the stress. They should follow up with their primary doctor or endocrinologist as previously directed by the physician. Outpatient evaluation for hypopituitarism in a well-appearing patient can be orchestrated by the primary doctor in consultation with appropriate specialists.
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Lisa Diane Mills, MD Associate Professor of Emergency Medicine, University of California, Davis, School of Medicine
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, Southern Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen 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.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
The authors and editors gratefully acknowledge the contributions of previous authors Jerome FX Naradzay, MD, and Stuart A Brilliant, MD, to the development and writing of the source article.
Acute Hypopituitarism
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