Which statement about pituitary microadenomas is true?
(A) By definition, they are less than 1.0 cm in size.
(B) They are best seen on coronal T2 gadolinium-enhanced magnetic resonance scans.
(C) They are rarely found at autopsy in asymptomatic individuals.
(D) Fifteen percent will enlarge to macroadenomas.
(A) The “gold standard” for classifying pituitary adenomas is based on immunohistochemistry and electron microscopy. However, from a surgical standpoint, they can be classified by size and growth characteristics. In the simplest form, adenomas are divided into two groups: microadenomas (<10 mm in diameter) and macroadenomas (≥10 mm in diameter). To further classify macroadenomas, it can be useful to use a system that takes into account grade, degree, and direction of extrasellar extension (stage). Microadenomas of the pituitary are best visualized with a coronal T1 MRI. Eighty to 95% of such studies will show a focal hypointense lesion within an otherwise homogenous adenohypophysis. The excellent sensitivity of unenhanced T1-weighted spin echo (SE) MRI for microadenomas has made it the primary sequence for imaging the pituitary gland. Contrast is reserved for those cases in which there is good clinical or biochemical evidence of a pituitary adenoma with a negative or equivocal plain MRI. In most cases, the best imaging routine is to perform a plain scan followed by a repeat T1-weighted coronal sequence immediately after intravenous injection of contrast (gadolinium). Autopsy studies have repeatedly shown that 20–25% of the general population harbor small pituitary microadenomas. Microadenomas are usually clinically silent and occur in patients without apparent endocrine symptoms. Whereas very few microadenomas will show interval growth, more than one-third of macroadenomas will increase in size.
Atlas S. Magnetic Resonance Imaging of the Brain and Spine, 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.
Jane J, Thapar K, Laws E. Pituitary tumors. In: Winn HR (ed.), Youmans Neurological Surgery, 6th ed. Philadelphia, PA: W. B. Saunders; 2011:1476–1510.
A 19-year-old woman has had amenorrhea and galactorrhea for 13 months. Her prolactin level is 100 ng/mL (normal 4–23 ng/mL for nonpregnant women). She brought a recent magnetic resonance image (MRI) with her (see Fig. 14-1). After other causes of hyperprolactinemia have been ruled out, she should
FIGURE 14-1. Coronal magnetic resonance scan (T1 with contrast).
(A) Begin medical therapy with dopamine agonists
(B) Begin medical therapy with oral contraceptives
(C) Begin calcium supplementation
(D) Undergo transsphenoidal resection of the lesion
(A) The MRI shown in Fig. 14-1 shows a microadenoma on the right side of the sella. Regardless of cause, the classic features of prolactin excess in women are galactorrhea and amenorrhea. In men, decreased libido and impotence are common. The elevated prolactin level, combined with the findings on MRI, makes prolactinoma a likely diagnosis. However, pituitary incidentalomas are very common, and other possible etiologies must be excluded. Other common causes of increased prolactin secretion include pregnancy, hypothalamic-pituitary disorders, primary hypothyroidism, and drug ingestion (estrogen therapy, oral contraceptives, dopamine antagonists, monoamine oxidase inhibitors [MAOIs], intravenous cimetidine, and verapamil). Other causes can include nipple stimulation, chest wall lesions, spinal cord lesions, chronic renal failure, or severe liver disease. Prolactin secretion from the pituitary is primarily under inhibitory control by dopamine, which is secreted by the hypothalamus. Increased production of prolactin will suppress luteinizing hormone (LH) and follicle-stimulating hormone (FSH) production, leading to decreased estrogen production. In the short term, these abnormalities can lead to galactorrhea and hypogonadism. In the long term, osteoporosis can become a concern. Although most microadenomas do not progress, control of prolactin hypersecretion is recommended for cessation of galactorrhea and return to normal gonadal function. This can usually be achieved with dopamine agonists such as cabergoline or bromocriptine. Of these, cabergoline is the usual therapy of choice due to its more favorable side effect profile and success rate of 90% in treating microadenomas. Once prolactin levels have been restored to normal levels, fertility will also be restored. Therefore, women not wishing to become pregnant should be counseled about use of birth control. The risk of major expansion of an existing adenoma during pregnancy is less than 2%, and although no late toxicity from dopamine agonists taken during pregnancy has been reported, studies are limited at this time. Women are advised to discontinue their medication and obtain a pregnancy test if they miss a period. Transsphenoidal resection is an option for patients who do not respond to medical therapy.
Javorsky BR, Aron DC, Findling JW, Tyrrell J. Hypothalamus and pituitary gland. In: Gardner DG, Shoback D (eds.), Greenspan’s Basic & Clinical Endocrinology, 9th ed. New York, NY: McGraw-Hill; 2011.
A 45-year-old truck driver presents to your office reporting painless loss of vision. On exam, you discover bitemporal hemianopsia and decreased visual acuity. He also states that he has put on “a lot of weight,” feels tired, and has decreased libido. An MRI scan is obtained as shown in Fig. 14-2. The most important diagnostic test in this situation is
FIGURE 14-2. Magnetic resonance imaging scan. From McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS. Principles and Practice of Hospital Medicine. New York, NY: McGraw-Hill; 2012:Fig. 152-2.
(B) Thyroid function tests
(D) Computed tomography (CT) scan
(C) The image shown in Fig. 14-2 is a coronal MRI demonstrating a pituitary macroadenoma (solid arrow) with superior extension and compression of the optic chiasm (dashed arrow). Superior extension of such an adenoma can compress the optic chiasm, leading to visual disturbances, as seen in this patient. A classic finding is bitemporal hemianopsia. In addition, the mass effect on native pituitary tissue can lead to hypopituitarism. Extension of such tumors into the cavernous sinus may result in diplopia, ophthalmoplegia, and involvement of the cranial nerves, especially the third nerve. Prolactinomas compose 30–40% of all pituitary tumors; therefore, a prolactin level should be drawn for diagnostic purposes. Given this patient’s severe visual deficits, urgent medical therapy should be initiated including dopamine agonist therapy and steroids; this therapy should not be delayed while waiting for lab tests to return. Dopamine agonists will suppress prolactin secretion and cause the adenoma to shrink, which should improve or restore visual and neurologic deficits. In addition, steroids reduce tumor edema and treat a potential adrenal crisis. If the patient had presented with more severe vision loss, had more sudden onset of symptoms, or had headache and change in mental status, a CT scan would be useful to differentiate subarachnoid hemorrhage from pituitary apoplexy.
Jain SH, Katznelson L. Pituitary disease. In: McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS (eds.), Principles and Practice of Hospital Medicine. New York, NY: McGraw-Hill; 2012.
Nelson BK. Pituitary apoplexy. In: Adams JG (ed.), Emergency Medicine, 2nd ed. Philadelphia, PA: W. B. Saunders; 2013:1439–1441.e1.
Parker KL, Schimmer BP. Introduction to endocrinology: the hypothalamic-pituitary axis. In: Brunton LL, Chabner BA, Knollmann BC (eds.), Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12th ed. New York, NY: McGraw-Hill; 2011.
A 30-year-old woman presents with signs of fulminant Cushing syndrome that have developed over the past 4 months. She does not take any medications. Which of the following would be a fairly specific finding in her case?
(B) Peripheral neuropathy
(C) The term Cushing syndrome encompasses a constellation of clinical features. Truncal obesity and thin frail skin resulting in reddish purple striae across the abdomen can be common findings (see Fig. 14-4).
FIGURE 14-4. Truncal obesity and reddish purple striae across the abdomen in Cushing syndrome. From Kantarjian HM, Wolff RA, Koller CA. The MD Anderson Manual of Medical Oncology, 2nd ed. New York, NY: McGraw-Hill; 2011:Fig. 38-21.
In addition, hirsutism, balding, ecchymosis, hypertension, glucose intolerance, development of a supraclavicular fat pad, rounding of the facies, proximal muscle weakness, and thin extremities may also be present. Cushing syndrome is a term used to describe the clinical abnormalities associated with excess glucocorticoid circulation when the etiology is identified outside the pituitary gland. Cushing disease is the term reserved for clinical findings caused by pituitary adrenocorticotropic hormone (ACTH) excess from a tumor within the pituitary itself. In Cushing disease, there is hyperplasia of pituitary cells that produce ACTH, which stimulates the adrenal glands, resulting in the common clinical findings listed earlier. In patients with clinical features suggesting Cushing syndrome, the initial screening test is the overnight dexamethasone suppression test. If Cushing disease is suspected after initial screening, an MRI of the pituitary gland is useful for localization. Treatment of an ACTH-secreting pituitary adenoma usually requires transsphenoidal resection of the lesion, with a cure rate approaching 80%. After surgery, roughly 10% of patients will experience complications such as cerebrospinal fluid (CSF) leak, transient diabetes insipidus, visual abnormalities, or meningitis. Twenty percent of patients will have incomplete excision of the lesion and experience recurrence or persistence of symptoms.
Ferri FF. Cushing’s disease and syndrome. In: Ferri FF (ed.), Ferri’s Clinical Advisor 2014. Maryland Heights, MO: Mosby; 2014:308–308.
Ropper AH, Samuels MA. The hypothalamus and neuroendocrine disorders. In: Ropper AH, Samuels MA (eds.), Adams and Victor’s Principles of Neurology, 9th ed. New York, NY: McGraw-Hill; 2009.
If the patient from Question 4 had a negative MRI for pituitary abnormality, with and without contrast, what is the most likely etiology of her Cushing syndrome?
(B) Adenocarcinoma of the lung
(C) Exogenous steroid use
(D) Even with negative imaging, the most likely etiology of this patient’s Cushing syndrome is a pituitary tumor. In fact, only 70% of microadenomas, some as small as 3 mm in diameter, can be detected with high-resolution, gadolinium-enhanced MRI. Although iatrogenic causes account for most cases of Cushing syndrome due to widespread use of therapeutic high-dose glucocorticoids, the question stem clearly states she is not taking any medications. Of the spontaneous causes of Cushing syndrome, Cushing disease is the most common cause in adults, accounting for 70% of cases. Cushing syndrome can be divided into two groups: ACTH dependent and ACTH independent. The ACTH-dependent forms include pituitary-dependent Cushing syndrome (Cushing disease), ectopic tumor source, ectopic CRH production (rarely), and exogenous ACTH administration. ACTH-independent causes include adrenal adenoma, adrenal carcinoma, and primary pigmented nodular adrenal disease (PPNAD). Of these other causes of Cushing syndrome, adrenal adenomas account for 8–19%, adrenal carcinomas account for 6–7%, and ectopic ACTH syndrome accounts for 6–15% of cases.
Bertagna X, Guignat L, Raux-Demay MC, Guilhaume B, Girard F. Cushing’s disease. In: Melmed S (ed.), The Pituitary, 3rd ed. Philadelphia, PA: Elsevier; 2011:533–617.
Morris DG, Grossman A, Nieman LK. Cushing’s syndrome. In: Jameson JL, De Groot LJ (eds.), Endocrinology, 6th ed. Philadelphia, PA: W. B. Saunders; 2010:282–311.
Winn HR. Pituitary tumors. In: Winn HR (ed.), Youmans Neurological Surgery, 3rd ed. Philadelphia, PA: W. B. Saunders; 2011:1476–1510.
After excluding exogenous glucocorticoid use, what diagnostic test should be ordered if you suspect Cushing syndrome?
(A) Insulin tolerance test
(B) Early morning salivary cortisol
(C) 48-hour dexamethasone suppression test
(D) Random serum cortisol or plasma adrenocorticotropic hormone (ACTH) level
(C) The current guidelines released by the Endocrine Society in 2008 state that patients with multiple and progressive features compatible with Cushing syndrome should undergo one test with high diagnostic accuracy to aid in diagnosis. Acceptable tests include a urine free cortisol (UFC; at least two measurements), late-night salivary cortisol (two measurements), 1-mg overnight dexamethasone suppression test (DST), or longer low-dose DST (2 mg/d for 48 hours). The test chosen depends on the individual patient’s preference. The guidelines specifically recommend against using a random serum cortisol, plasma ACTH level, urinary 17-ketosteroid, insulin tolerance test, loperamide test, or tests designed to determine etiology of Cushing syndrome (e.g., pituitary or adrenal imaging). In individuals with an abnormal test, referral to an endocrinologist is warranted.
Nieman LK, Biller BMK, Findling JW, et al. The diagnosis of Cushing’s syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2008;93(5):1526–1540.
A corticotropin-releasing hormone (CRH) stimulation test is conducted in a patient with Cushing syndrome who had an intermediate ACTH level. The results show no response of ACTH to CRH. This result is most consistent with
(A) ACTH-dependent Cushing
(B) ACTH-independent Cushing
(B) Normally CRH is released from the hypothalamus in response to stress. It is secreted at the median eminence into the hypothalamo-hypophyseal portal system where it travels to the anterior lobe of the pituitary to stimulate the release of ACTH. ACTH, in turn, acts to stimulate the adrenal glands to produce cortisol, glucocorticoids, mineralocorticoids, and dehydroepiandrosterone (DHEA). Therefore, a normal physiologic response to a bolus of CRH, whether from the hypothalamus or given exogenously, as in this test, would be to increase ACTH release from the pituitary. In ACTH-dependent Cushing (i.e., Cushing disease or an ectopic tumor), excess CRH will also stimulate increased release of ACTH. A patient with an ACTH-independent cause of Cushing (i.e., adrenal tumor) would be expected to have low levels of ACTH at baseline due to the negative feedback of cortisol on the pituitary and hypothalamus. This can be useful in diagnosing these patients without conducting a CRH stimulation test. However, if a patient with ACTH-independent Cushing initially had an intermediate ACTH level and a CRH stimulation test were conducted, there would be little or no effect on the level of ACTH measured because the pituitary is already suppressed.
Molina PE. Chapter 6. Adrenal Gland. In: Molina PE. eds. Endocrine Physiology, 4e. New York, NY: McGraw-Hill; 2013. http://accessmedicine.mhmedical.com.ezproxy2.library.arizona.edu/content.aspx?bookid=507&Sectionid=42540506.
Javorsky BR, Aron DC, Findling JW, Tyrrell J. Chapter 4. Hypothalamus and Pituitary Gland. In: Gardner DG, Shoback D. eds. Greenspan’s Basic & Clinical Endocrinology, 9e. New York, NY: McGraw-Hill; 2011. http://accessmedicine.mhmedical.com.ezproxy2.library.arizona.edu/content.aspx?bookid=380&Sectionid=39744044.
The best test to distinguish between pituitary and ectopic secretion of corticotropin is
(A) High-dose dexamethasone suppression test
(B) High-resolution CT of the head
(D) Selective inferior petrosal sinus sampling
(D) Dexamethasone suppresses ACTH through feedback inhibition in both pituitary and ectopic sources, but pituitary tumors are much more responsive, with ACTH levels dropping much lower in a high-dose dexamethasone test. However, a more sensitive and specific method for distinguishing between the two is the use of inferior petrosal sinus sampling (IPSS). This is done by simultaneous sampling of the peripheral blood and the inferior petrosal sinuses bilaterally after a dose of CRH is given. A significant rise in ACTH in the petrosal blood, but not the peripheral, is consistent with a pituitary source. The bilateral sampling can be helpful for lateralization of the tumor as well, especially if not visualized on MRI. In several studies, IPSS has been demonstrated to have 95% sensitivity and 93% specificity.
Invitti C, Pecori Giraldi F, de Martin M, Cavagnini F. Diagnosis and management of Cushing’s syndrome: results of an Italian multicentre study. Study Group of the Italian Society of Endocrinology on the Pathophysiology of the Hypothalamic-Pituitary-Adrenal Axis. J Clin Endocrinol Metab 1999;84(2):440–448.
Kaltsas GA, Giannulis MG, Newell-Price JD, et al. A critical analysis of the value of simultaneous inferior petrosal sinus sampling in Cushing’s disease and the occult ectopic adrenocorticotropin syndrome. J Clin Endocrinol Metab 1999;84(2):487–492.
A 46-year-old man with Cushing syndrome and history of low back pain presents to the emergency department with progressive lower extremity weakness in all muscle groups and new-onset radicular symptoms. What is the most likely diagnosis?
(A) Vertebral body compression fracture with cord injury
(B) Thoracic disk herniation
(C) Epidural lipomatosis is nonneoplastic accumulation of fatty tissue in the epidural space of the thoracic or lumbar spine. It is most commonly associated with chronic corticosteroid excess, obesity, or hypothyroidism. Seventy-five percent of cases are associated with exogenous steroid use. Patients typically have been on corticosteroids for greater than 6 months, are obese, and cushingoid. With removal of corticosteroids, the fatty tissue can regress, but severe neurologic symptoms warrant laminectomy. A spinal MRI will be highly suggestive of the diagnosis with findings of epidural fat thickness greater than 7 mm (see Fig. 14-5).
FIGURE 14-5. T1-weighted magnetic resonance imaging axial view of L5-S1. Hyperintense tissue (indicated by arrows), consistent with adipose tissue, is circumferentially compressing the spinal cord.
This patient’s presentation is classic, with low back pain being present long before other symptoms. Vertebral body compression is not a common cause of radicular symptoms but can be a source of back pain. Disk herniation could explain this patient’s symptoms; however, he has involvement of multiple spinal cord levels, which argues against disk herniation as a cause. Although spinal stenosis is associated with back and leg pain, this type of pain is often worse with movement and relieved with sitting or spine flexion. Spinal stenosis is also more prevalent in the sixth or seventh decades of life.
Fenton DS. Epidural lipomatosis. In: Czervionke LF, Fenton DS (eds.), Imaging Painful Spine Disorders. Philadelphia, PA: W. B. Saunders; 2011:222–227.
Rosenbaum RB, Kula RW. Disorders of bones, joints, ligaments, and meninges. In: Daroff RB, Fenichel GM, Jankovic J, Mazziotta JC (eds.), Bradley’s Neurology in Clinical Practice, 6th ed. Philadelphia, PA: W. B. Saunders; 2012:1824–1854.e2
The treatment for compression fracture of the thoracic spine, when associated with the osteoporosis that accompanies Cushing disease, is
(A) Prolonged bed rest and narcotics
(B) Polymethyl methacrylate injection
(C) Endoscopic transthoracic stabilization
(D) Bracing and medical therapy for osteoporosis
(B) Percutaneous treatment of painful osteoporotic vertebral compression fractures can be accomplished with injection with polymethyl methacrylate (PMMA), bone cement used in orthopedic surgeries. This is a minimally invasive, radiologically guided procedure that can serve to decrease pain and increase function for symptomatic patients. In retrospective case studies, immediate pain relief was achieved in 70–90% of cases, with complications occurring less than 1% of the time (see Fig. 14-6).
FIGURE 14-6. Images obtained in a 78-year-old woman with a history of T12 fracture. A. Sagittal fast spin echo T1-weighted magnetic resonance image (MRI) shows low signal intensity in the bone marrow and a loss of vertebral body height at the T11 vertebra. A fluid-filled vacuum cleft was noted (arrow). B. Sagittal MRI obtained with fat saturation shows high signal intensity within the T11 vertebra. A fluid-filled vacuum cleft was noted (arrow). C. Lateral radiograph obtained after vertebroplasty shows restoration of the vertebral height and correction of spinal kyphosis. D. Radiograph obtained 3 months after vertebroplasty, after the patient returned with a new onset of back pain, shows a new deformity of the T10 vertebra. From Lin W, Cheng T, Lee Y, et al. New vertebral osteoporotic compression fractures after percutaneous vertebroplasty: retrospective analysis of risk factors. J Vasc Interv Radiol 2008;19:225–232.
Lin W, Cheng T, Lee Y, et al. New vertebral osteoporotic compression fractures after percutaneous vertebroplasty: retrospective analysis of risk factors. J Vasc Interv Radiol 2008;19:225–232.
Rowland L. Merritt’s Neurology, 12th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.
The best test to confirm suspected acromegaly is
(A) Growth hormone (GH) level >5 ng/mL
(C) Failure of GH to suppress with 75 mg of glucose
(D) Elevated insulin-like growth factor (IGF)-1 level
(C) Growth hormone is secreted in a pulsatile manner; therefore, a random level would not be helpful in the diagnosis of acromegaly. The gold standard for diagnosis is measurement of GH after 75 g of oral glucose. Suppression to less than 0.4 ng/mL excludes the diagnosis. Lack of suppression establishes the diagnosis. Other situations that can lead to decreased suppression are pregnancy, puberty, oral contraceptive pill use, poorly controlled diabetes, and hepatic or renal insufficiency. IGF-1 levels are reflective of the 24-hour GH concentration and correlate well with clinical activity of the hormone.
Bope ET, Kellerman RD. Section 11. In: Bope ET, Kellerman RD (eds.), Conn’s Current Therapy. Philadelphia, PA: W. B. Saunders; 2014:687–774.
Patients with acromegaly are at increased risk of
(A) Atrophy of the thyroid gland
(B) Carcinoma of the colon
(C) Coronary artery disease
(B) Overgrowth of bone is the classic feature associated with acromegaly, particularly of the face and skull. Long term, this increases the risk for disabling degenerative arthritis. Hypersecretion of GH leads to excessive IGF-1 production by the liver, which is the mediator of many other systemic effects. GH excess leads to generalized organ hypertrophy, clinically evident as thyromegaly and enlargement of the submandibular glands. Cardiomyopathy, hypertension, and cardiomegaly are a significant cause of morbidity and mortality in acromegaly. Obstructive and central sleep apnea are also common. In addition, glucose intolerance occurs in 50–70% of patients. Patients with acromegaly are also at increased risk for development of colon polyps and colon cancer, with recent estimates suggesting they are at double the risk of the general population.
Javorsky BR, Aron DC, Findling JW, Tyrrell J. Hypothalamus and pituitary gland. In: Gardner DG, Shoback D (eds.), Greenspan’s Basic & Clinical Endocrinology, 9th ed. New York, NY: McGraw-Hill; 2011.
Melmed S. Acromegaly. In: Jameson J, De Groot L (eds.), Endocrinology, 6th ed. Philadelphia, PA: W. B. Saunders; 2010:262–281.
A 60-year-old man presents with acromegaly. An MRI demonstrates a mass in the pituitary with superior extension above the sella (see Fig. 14-3). The patient’s GH, prolactin, and IGF-1 are grossly elevated. He is not currently having visual deficits. The best immediate treatment option would be
FIGURE 14-3. Magnetic resonance imaging scan. From Doherty GM (ed.). Current Diagnosis & Treatment: Surgery, 13th ed. New York, NY: McGraw-Hill; 2010:Fig. 36-17.
(A) Transsphenoidal excision
(C) Long-acting octreotide
(C) This patient has a macroadenoma with extrasellar extension, which is not causing compressive symptoms. Therefore, there is no need for urgent surgical decompression. In fact, 40–60% of macroadenomas are unlikely to be controlled with surgery alone. Transsphenoidal surgery is the treatment of choice for intrasellar microadenomas (<10 mm), noninvasive macroadenomas, and tumors causing compressive symptoms. For other situations, including this patient, there are currently three drug classes available to treat acromegaly: dopamine agonists, somatostatin receptor ligands, and GH receptor antagonists. Of these, serotonin receptor ligands are most appropriate for first-line therapy in tumors that have low probability for surgical cure. Radiosurgery should be considered a third-line therapy, usually reserved for patients who cannot achieve tumor growth control or normalization of hormone levels with surgery or medical therapy.
Melmed S, Colao A, Barkan A, et al. Guidelines for acromegaly management: an update. J Clin Endocrinol Metab 2009;94(5):1509–1517.
Your patient with acromegaly must have a cholecystectomy. The safest method for intubating this patient for his surgery is
(A) Awake fiberoptic intubation
(D) Extra-large endotracheal tube
(A) Patients with acromegaly characteristically will have difficult airways. This is due to a number of factors. First, the increased size of facial bones, particularly the mandible, makes face mask sealing difficult. This can become particularly dangerous with attempted ventilation after the induction of anesthesia. Enlargement of the tongue and other soft tissues of the pharynx not only makes laryngoscopy difficult, but these changes also predispose to sleep apnea and further complicate ventilation. In addition, tracheal intubation may be challenging because the glottis can be narrowed due to enlargement of the vocal cords. Second, enlargement of the thyroid can compress the trachea, further complicating intubation. As with obese patients and those with obstructive sleep apnea, the safest technique for intubation is with the awake fiberoptic technique. Additionally, the use of a small endotracheal tube can facilitate easier passage through the cords. Patients with acromegaly may also have enlarged nasal turbinates, making nasal intubation a less viable option.
Flint PW, Haughey BH, Lund VJ, et al. Surgical management of the difficult adult airway. In: Bhatti NI (ed.), Cummings Otolaryngology Head & Neck Surgery. New York, NY: Elsevier; 2010:121–129.
Walters TL. Acromegaly. In: Bready LL, Dillman D, Noorily SH (eds.), Decision Making in Anesthesiology, 4th ed. Philadelphia, PA: Elsevier; 2007:200–202.
A 40-year-old women is admitted for deep vein thrombosis (DVT). The following morning, she begins to experience retro-orbital headache, visual field deficits and vomiting. She has no medical conditions but is currently in her second cycle of in vitro fertilization (IVF) treatments. On exam, she has ptosis of the left eyelid and is unable to move her left eye up, down, or inward. She is most likely suffering from
(A) Subarachnoid hemorrhage
(D) Medication-related oculomotor neuropathy
(B) The patient has findings consistent with pituitary apoplexy (see Fig. 14-7), which is due to hemorrhage or infarct within the pituitary gland. Although pituitary tumors are common, apoplexy is a rare but serious complication. Factors that may precipitate this complication include endocrine stimulation (in the form of diagnostic studies), head trauma, pregnancy (Sheehan syndrome), anticoagulation, hypertension, recent cardiac surgery, diabetic ketoacidosis, and ovarian stimulation medications. The combination of anticoagulation and ovarian stimulation medications in this patient likely triggered a hemorrhage into an undiagnosed pituitary macroadenoma. The visual disturbances she is experiencing are likely due to the tumor’s proximity to the optic chiasm. Additionally, nerves passing through the cavernous sinus can also be affected (CN III, IV, V1, and V2). Acute hypopituitarism is a major concern in these patients who may develop adrenal crisis. In addition, delay in diagnosis and treatment can lead to permanent blindness, nerve palsies, or death. She should be treated with parenteral corticosteroids immediately. There is currently controversy regarding surgical intervention rather than conservative medical management. However, definitive therapy involves transsphenoidal decompression of the pituitary.
FIGURE 14-7. Axial computed tomography demonstrating evidence of hemorrhage within the pituitary gland, seen as areas of patchy enhancement.
Nelson BK. Pituitary apoplexy. In: Adams JG (ed.), Emergency Medicine, 2nd ed. Philadelphia, PA: Saunders; 2013:1439–1441.e1431.
Tan T, Caputo C, Mehta A, Hatfield E, Martin N, Meeran K. Pituitary macroadenomas: are combination antiplatelet and anticoagulant therapy contraindicated? A case report. J Med Case Rep. 2007;1:74.