Follow-up
Further Inpatient Care
- Care of patients is primarily on an outpatient basis. Only patients who are undergoing surgery are inpatients. Additionally, a small percentage of patients with pituitary apoplexy present with a clinical picture similar to that of subarachnoid hemorrhage.
- Transsphenoidal surgery
- Careful hormonal control of these patients under the direction of an endocrinologist is essential.
- A syndrome of inappropriate antidiuretic hormone secretion (SIADH) may be seen transiently, followed by diabetes insipidus.
- Postoperative hypoadrenalism is a possibility that requires careful monitoring.
- Hormonal levels should be assessed and replacements provided when appropriate.
- In most cases, CSF rhinorrhea should be diagnosed and addressed promptly.
- In most cases, transsphenoidal hypophysectomy involves low risk and has a good prognosis.
- Pituitary apoplexy
- As its name indicates, the apoplectic onset of hemorrhage within a pituitary adenoma may lead to hypothalamic, chiasmal, cavernous sinus, and brainstem compression.
- Meningeal irritation results from blood in the subarachnoid space. On occasion, the degree of subarachnoid hemorrhage is significant, and a spinal tap may show evidence of acute or subacute bleeding. The acute panhypopituitarism is associated with shock and hypothalamic-brainstem compression, which could lead to coma and even death.
- Headache, vomiting, visual loss, blindness, ophthalmoplegia, and altered consciousness may be present. In a series involving 62 patients, Semple et al found headache was the most common symptom in 87% of their cases, visual loss occurred in 56% of the patients, ophthalmoplegia in 45%, and altered level of consciousness in 13%. Hypopituitarism was present in 73% of patients and diabetes insipidus in 8%.3
In most cases, surgical intervention is required with excellent results. Candidates for emergency surgery include patients with rapidly deteriorating vision, altered mental status, and hypothalamic compression. Pituitary apoplexy may be fatal in a few instances. Conservative treatment is an option in stable cases, particularly if they are prolactinomas. - Factors leading to hemorrhage within a pituitary adenoma identified by Biousse et al include the following: reduced blood flow to the gland, sudden increment of blood flow, stimulation of the gland by endocrine mechanisms, anticoagulation, and trauma.4 An upper respiratory tract infection with frequent coughing and sneezing also may trigger an apoplectic event. The best method to make the diagnosis of pituitary apoplexy is cerebral imaging. MRI preferentially but CT scan is an acceptable option if MRI is not available.
Further Outpatient Care
- Adjustment of hormonal therapy is necessary following transsphenoidal resection of the adenoma. This may be accomplished in the weeks following surgery by the consulting endocrinologist.
- Assess the need for replacement of cortisol 4 weeks after the resection. This is done by measuring the cortisol levels following an IV injection of 250 mcg of tetracosactin. Cortisol levels greater than 500 nmol/L indicate sufficient endogenous steroid production.
- Low thyroid levels are an indication for replacement. The same is true for low testosterone levels in symptomatic males and low estrogen/progesterone levels in females.
- Periodic neuro-ophthalmologist follow-up is essential, particularly when residual tumor is present. Visual fields and fundus photographs should be obtained before and immediately after tumor resection. These parameters provide a baseline for follow-up examinations.
- Radiation therapy (RT) is often necessary for managing local mass effects of large macroadenomas. The indications for RT at this time are controversial. In a recent study, Alameda et al followed 51 patients with pituitary tumor who underwent surgery; 22 with complete macroscopic resections, judged by imaging, were tumor-free 3-6 years postoperatively. Twenty-seven patients with residual tumors after surgical resection were treated with RT. Fourteen residual tumors decreased in size, 11 remained stable, 1 increased in size, and 1 patient was lost to follow-up. RT is a useful treatment alternative among patients with residual tumors after surgery. Fractionated stereotactic radiotherapy (FSR) was found to be safe and effective by Colin et al in 110 consecutive patients. Moreover, it may reduce the possibility of postradiation optic neuropathy.
Inpatient & Outpatient Medications
- Initial hormonal deficiencies may improve over time. Therefore, frequent endocrine re-evaluation is necessary.
- Perform preradiation and postradiation endocrinologic and neuro-ophthalmologic evaluations. A postoperative cerebral imaging study is important to determine the possibility of residual tumor. If residual tumor is present, serial imaging is required.
- Adverse radiation effects on the hypothalamus, pituitary, and visual pathways require close monitoring.
Transfer
- Pituitary apoplexy
- Patients with a diagnosis of pituitary apoplexy should be transferred immediately to a tertiary care center intensive care unit.
- IV fluids and IV steroid replacement should be initiated.
- Urgent decompression surgery is indicated.
- Patients with other pituitary lesions are investigated as outpatients and admitted for transsphenoidal resection.
- Inferior petrosal sinus corticotrophin levels also can be obtained on an outpatient basis.
Complications
- Treatment of pituitary tumors, particularly those resected via a transsphenoidal approach, has an excellent outcome with successful decompression of the visual pathways, cavernous sinus, and hypothalamus.
- Transfrontal resections are associated with more complications.
- In cases handled by a skilled surgeon, surgical complications are minimal but can include any of the following:
- Incomplete resection of large adenomas
- Transient or permanent diabetes insipidus
- CSF rhinorrhea
- Monohormonal or polyhormonal deficiencies
- Residual permanent visual field defects
- Empty sella syndrome: An empty sella may occur after transsphenoidal surgery and is generally benign. Generally, herniation of the chiasm inside the sella typically does not cause visual field defects.
- Radiation toxicity may occur as a rare complication in the treatment of pituitary adenomas, resulting in hypothalamic and chiasmal necrosis.
Prognosis
- Prolactin-secreting microadenomas
- Surgical resection is curative.
- Dopamine agonists provide symptom control.
- Prolactin-secreting macroadenomas: Dopamine agonists provide symptom control.
- Acromegaly
- Surgical resection is curative in 60% of patients.
- Octreotide therapy controls symptoms.
- Cushing disease: Surgical resection is curative.
- Rarely, invasive tumors produce metastatic deposits within the neuraxis via CSF pathways.
- Rarely, distant metastases may occur.
Patient Education
- The successful management of pituitary adenomas requires a highly motivated and compliant patient.
- Hormone-replacement therapy is demanding, and a noncompliant patient is at risk for complications due to misuse of these agents.
- Interaction of a team of specialists is required to manage these lesions. One of the specialists should serve as team leader and coordinate the patient's care.
- Prompt reporting of new symptoms is important in addition to routine follow-up visits.
- If the patient has no new symptoms or problems beyond about 5 years after beginning treatment, follow-up visits can be less frequent.
- The frequency of follow-up visits depends on the presence of residual tumor, visual deficit, hormonal needs, history of radiation therapy, or other complicating circumstances.
- Visual prognosis is excellent with transsphenoidal surgery. Ninety-five percent of patients studied by Gnanalingham et al experienced visual improvement.5 The extent of the visual field recovery is mainly dependent on the preoperative visual field defect. These authors also found that visual recovery may occur in a rapid fashion (3-6 mo) but may also take place slowly over several months and even a few years.
More on Pituitary Tumors |
| Overview: Pituitary Tumors |
| Differential Diagnoses & Workup: Pituitary Tumors |
| Treatment & Medication: Pituitary Tumors |
 Follow-up: Pituitary Tumors |
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References
Vlotides G, Eigler T, Melmed S. Pituitary tumor-transforming gene: physiology and implications for tumorigenesis. Endocr Rev. Apr 2007;28(2):165-86. [Medline].
Talkad AV, Kattah JC, Xu MY, et al. Prolactinoma presenting as painful postganglionic Horner syndrome. Neurology. Apr 27 2004;62(8):1440-1. [Medline].
Semple PL, Webb MK, de Villiers JC, Laws ER Jr. Pituitary apoplexy. Neurosurgery. 2005;56(1):65-72; discussion 72-3. [Medline].
Biousse V, Newman NJ, Oyesiku NM. Precipitating factors in pituitary apoplexy. J Neurol Neurosurg Psychiatry. Oct 2001;71(4):542-5. [Medline].
Gnanalingham KK, Bhattacharjee S, Pennington R, et al. The time course of visual field recovery following transphenoidal surgery for pituitary adenomas: predictive factors for a good outcome. J Neurol Neurosurg Psychiatry. Mar 2005;76(3):415-9. [Medline].
Alameda C, Lucas T, Pineda E, et al. Experience in management of 51 non-functioning pituitary adenomas: indications for post-operative radiotherapy. J Endocrinol Invest. Jan 2005;28(1):18-22. [Medline].
Colin P, Jovenin N, Delemer B, et al. Treatment of pituitary adenomas by fractionated stereotactic radiotherapy: a prospective study of 110 patients. Int J Radiat Oncol Biol Phys. Jun 1 2005;62(2):333-41. [Medline].
Conomy JP, Ferguson JH, Brodkey JS, Mitsumoto H. Spontaneous infarction in pituitary tumors: neurologic and therapeutic aspects. Neurology. Jun 1975;25(6):580-7. [Medline].
David, NJ, Gargano FP, Glaser JS. Pituitary apoplexy in clinical perspective. In: Neurophthalmology Symposium. Vol 8. St Louis: CV Mosby; 1975:140-165.
Dawson BH, Kothandaram P. Acute massive infarction of pituitary adenomas. A study of five patients. J Neurosurg. Sep 1972;37(3):275-9. [Medline].
Gharib H, Frey HM, Laws ER, et al. Coexistent primary empty sella syndrome and hyperprolactinemia. Report of 11 cases. Arch Intern Med. Jul 1983;143(7):1383-6. [Medline].
Greenberg HS, Chandler WF, Ensminger WD. Radiosensitization with carotid intra-arterial bromodeoxyuridine +/- 5-fluorouracil biomodulation for malignant gliomas. Neurology. Sep 1994;44(9):1715-20. [Medline].
Jho HD. Endoscopic endonasal pituitary surgery: Technical aspects. Contemporary Neurosurgery. 1997;19:1-8.
Jho HD, Carrau RL, Ko Y, Daly MA. Endoscopic pituitary surgery: an early experience. Surg Neurol. Mar 1997;47(3):213-22; discussion 222-3. [Medline].
Levy A, Lightman SL. Diagnosis and management of pituitary tumours. BMJ. Apr 23 1994;308(6936):1087-91. [Medline].
Melmed S. Acromegaly. N Engl J Med. Apr 5 1990;322(14):966-77. [Medline].
Molitch ME. Pregnancy and the hyperprolactinemic woman. N Engl J Med. May 23 1985;312(21):1364-70. [Medline].
Oldfield EH, Doppman JL, Nieman LK, Chrousos GP, Miller DL, Katz DA, et al. Petrosal sinus sampling with and without corticotropin-releasing hormone for the differential diagnosis of Cushing's syndrome. N Engl J Med. Sep 26 1991;325(13):897-905. [Medline].
Orth DN. Cushing's syndrome. N Engl J Med. Mar 23 1995;332(12):791-803. [Medline].
Thorner MO, Vance ML, Laws ER. The anterior pituitary. In: Williams, ed. Textbook of Endocrinology. Philadelphia: WB Saunders; 1998:249-340.
Zhang X, Horwitz GA, Heaney AP, Nakashima M, Prezant TR, Bronstein MD, et al. Pituitary tumor transforming gene (PTTG) expression in pituitary adenomas. J Clin Endocrinol Metab. Feb 1999;84(2):761-7. [Medline].
Further Reading
Keywords
pituitary adenoma, pituitary tumor, hormone deficiencies, hormone overproduction, prolactinoma, acromegaly, Cushing disease, Cushing syndrome, hormone therapy, pituitary mass
