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Pituitary Apoplexy

Summary

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  • Acute clinical syndrome due to sudden haemorrhage or infarction of the pituitary gland
  • Often occurs in patients with pre-existing pituitary adenomas
  • Characterised by sudden onset of headache, visual disturbances, and hormonal dysfunction

Pathophysiology

  • Rapid expansion of pituitary gland due to:
    • Haemorrhage within a pituitary tumour
    • Infarction of pituitary tissue
  • Leads to:
    • Compression of surrounding structures
    • Potential ischaemia of normal pituitary tissue
  • Risk factors:
    • Anticoagulation therapy
    • Major surgery
    • Pregnancy
    • Head trauma
    • Hypertension

Demographics

  • Incidence: 0.6-9.1% of all pituitary tumours
  • Mean age at presentation: 50-60 years
  • Male to female ratio: 1.5:1
  • Most common in patients with macroadenomas (>10mm)

Diagnosis

  • Clinical presentation:
    • Sudden severe headache (95%)
    • Visual disturbances (62%)
    • Decreased visual acuity
    • Visual field defects
    • Ocular palsies (40%)
    • Nausea and vomiting (69%)
    • Altered mental status (19%)
  • Laboratory findings:
    • Hypopituitarism (80%)
    • Hyponatremia
    • Mild hyperprolactinemia

Imaging

  • CT:
    • Acute phase: Hyperdense lesion within pituitary fossa
    • Subacute phase: Mixed density lesion
    • Limited sensitivity (21-28%)
  • MRI (preferred modality):
    • T1-weighted:
    • Acute: Isointense to hyperintense
    • Subacute: Hyperintense due to methaemoglobin
    • T2-weighted:
    • Variable signal intensity
    • Contrast-enhanced:
    • Rim enhancement of the lesion
    • Fluid-fluid levels may be present
    • Sensitivity: 88-90%

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  • 45-year-old patient presented with sudden onset headache and vomitting.
  • CT showed subtle hyperdensity within an enlarged pituitary gland and dehisence of the floor of the fossa.
  • MRI showed a heterogenously enlarged pituitary gland with T1-shortening, consistent with haemorrhage.

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  • A 40-year-old patient presented with sudden onset headache and vomitting.
  • CT showed an increased soft tissue within the pituitary fossa with hyperdense acute blood product.
  • MRI showed T1-hyperintense and T2-hypointense blood product with peripheral enhancement of normal pituitary tissue.
  • There was contact, without compression, of the optic chiasm.
  • One year later, without surgery, the volume of soft tissue within the fossa significantly decreased.

Treatment

  • Initial management:
    • Haemodynamic stabilization
    • Corticosteroid replacement
    • Correction of electrolyte imbalances
  • Surgical intervention:
    • Transsphenoidal surgery for:
    • Severe visual impairment
    • Altered mental status
    • Progressive neurological deterioration
  • Conservative management:
    • For patients with mild symptoms and stable condition
    • Close monitoring and hormonal replacement therapy
  • Long-term follow-up:
    • Regular endocrine evaluation
    • Imaging surveillance
    • Hormone replacement as needed

Differential diagnosis

Differential Diagnosis Differentiating Feature
Aneurysm (thrombosed parasellar) Layered haemorrhage with peripheral flow void; arterial origin on MRA/CTA
Rathke cleft cyst haemorrhage Non-enhancing T1 hyperintense sellar collection without solid component
Craniopharyngioma (haemorrhagic) Suprasellar cystic/solid mass with calcifications on CT
Pituitary macroadenoma (non-haemorrhagic) Enhancing sellar mass without blood products on T1/GRE