Harvey's Garden

Pituitary adenoma

3 min read

Epidemiology

Etiology

Pathophysiology

  • Tumor classification according to ability to secrete hormones
    • Nonsecretory pituitary adenomas
      • Nonfunctioning tumors account for 15–45% of all pituitary adenomas.
      • Gonadotroph adenomas
      • Null cell adenomas
      • Plurihormonal adenomas
      • Silent somatotroph and corticotroph adenomas
    • Secretory pituitary adenomas: hormone secretion → hyperpituitarism
      • Most exclusively proliferate in only one type of endocrine cell and therefore secrete only one pituitary hormone.

Tip

Prolactinomas are the most common pituitary adenomas.

Clinical features

  • Mass Effect (especially Macroadenomas >1 cm):
    • Headaches are a common symptom.
    • Bitemporal hemianopsia: Classic visual field defect due to compression of the optic chiasm.
    • Cranial nerve palsies from invasion of the cavernous sinus (CN III, IV, V1, V2, VI).
    • Hypopituitarism: Compression of normal pituitary tissue leading to hormone deficiencies (e.g., hypothyroidism, hypogonadism).
  • Hormone Hypersecretion (Functional Adenomas):
    • Prolactinoma (Most common type, ~40%):
    • Somatotroph (GH-secreting) Adenoma:
      • Acromegaly (Adults): Coarsening of facial features, large hands/feet, frontal bossing, prognathism, glucose intolerance/DM, HTN.
      • Gigantism (Children/Adolescents with open epiphyseal plates): Increased linear growth.
    • Corticotroph (ACTH-secreting) Adenoma (Cushing Disease):
      • Causes about 70% of endogenous Cushing’s syndrome.
      • Features: Central obesity, moon facies, buffalo hump, purple striae, proximal muscle weakness, HTN, hyperglycemia, osteoporosis.

Diagnostics

Treatment

  • Prolactinoma:
    • Dopamine agonists (e.g., Cabergoline, Bromocriptine) are first-line therapy. They decrease prolactin levels and shrink the tumor.
    • Transsphenoidal surgery is reserved for patients who do not respond to or cannot tolerate medical therapy.
  • Acromegaly & Cushing’s Disease:
    • Transsphenoidal surgery is the primary treatment.
    • Medical therapy can be used adjunctively. For acromegaly, options include somatostatin analogs (e.g., Octreotide) or GH receptor antagonists (e.g., Pegvisomant). For Cushing’s, adrenal enzyme inhibitors (e.g., Ketoconazole) can be used.
    • Radiation therapy may be used for residual or recurrent tumors.
  • Non-functioning Adenoma:
    • Observation for small, asymptomatic tumors.
    • Transsphenoidal surgery if mass effect symptoms (e.g., vision changes) are present.

Complications

Pituitary apoplexy

  • Etiology/Pathophysiology
    • Sudden hemorrhage or infarction of a pre-existing pituitary adenoma.
    • Often the first clinical presentation of a previously undiagnosed adenoma.
    • The rapid expansion of the sellar mass leads to compression of surrounding structures (optic chiasm, cavernous sinus) and acute pituitary dysfunction.
  • Clinical Features
    • Classic Triad:
      • Sudden, severe headache (“thunderclap headache”).
      • Visual field defects (classically bitemporal hemianopsia from optic chiasm compression).
      • Ophthalmoplegia (diplopia due to CN III, IV, VI palsies from cavernous sinus invasion).
    • Signs of meningeal irritation (nuchal rigidity) due to blood in the subarachnoid space.
    • Altered mental status, nausea/vomiting.
    • Features of acute panhypopituitarism, which is the most life-threatening aspect:
      • Acute adrenal insufficiency (secondary): Hypotension, shock, hypoglycemia, fever. This is a medical emergency.
      • Central hypothyroidism: Can contribute to altered mental status.
  • Diagnostics
    • Initial Imaging: Non-contrast head CT is often done first to rule out subarachnoid hemorrhage. May show a hyperdense sellar mass.
    • Definitive Imaging: MRI of the pituitary is the gold standard; shows hemorrhage and necrosis within the adenoma.
    • Labs (Urgent):
      • Assess for acute adrenal insufficiency: ↓ cortisol, ↓ ACTH.
      • Evaluate other pituitary axes: TSH, free T4, prolactin, LH, FSH.
      • Check electrolytes: Hyponatremia is common due to cortisol deficiency (impaired free water excretion) or SIADH.
  • Treatment
    • This is a NEUROENDOCRINE EMERGENCY.
    • 1st Step: Administer high-dose glucocorticoids (e.g., IV hydrocortisone or dexamethasone) immediately. Do NOT wait for imaging or lab confirmation if clinically suspected. This treats the life-threatening adrenal crisis.
    • Supportive Care: IV fluids, electrolyte correction.
    • Neurosurgical Consultation: Urgent decompression via transsphenoidal surgery is indicated for:
      • Progressive visual deterioration.
      • Severe or persistent ophthalmoplegia.
      • Declining level of consciousness.
  • Complications & Prognosis
    • Permanent hypopituitarism is common, requiring lifelong hormone replacement (e.g., levothyroxine, cortisol, sex steroids).
    • Mortality is high if acute adrenal insufficiency is not promptly treated.
    • Vision may not fully recover.

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