Pituitary Apoplexy 

Introduction

Pituitary apoplexy is a life-threatening endocrine and neurosurgical emergency caused by acute hemorrhage or infarction of the pituitary gland, usually occurring within a pituitary adenoma.

Acute ischemic or hemorrhagic infarction of the pituitary gland, most commonly in a pre-existing pituitary tumor, leading to sudden expansion and compression of surrounding structures.


Epidemiology

  • Occurs in:
    • 2–12% of pituitary adenomas
  • Often first presentation of undiagnosed adenoma
  • Mean age:
    • 40–60 years


Anatomy & Pathophysiology

Why Pituitary is Vulnerable?

The pituitary gland has:

  1. High metabolic demand
  2. Unique portal vascular supply
  3. Limited space inside sella turcica

Blood Supply

  • Superior hypophyseal arteries → portal circulation → anterior pituitary
  • Inferior hypophyseal arteries → posterior pituitary

👉 Tumors outgrow blood supply → ischemia
👉 Fragile tumor vessels → hemorrhage


Pathophysiology Cascade

Step 1 – Tumor Enlargement

  • Adenoma increases metabolic and oxygen demand

Step 2 – Vascular Compromise

  • Infarction or hemorrhage occurs

Step 3 – Rapid Expansion

Leads to:

  • Sellar pressure rise
  • Optic chiasm compression
  • Cavernous sinus involvement
  • Pituitary hormone failure


Risk Factors & Precipitating Events

Tumor-Related

  • Pituitary macroadenoma (>1 cm)
  • Non-functioning adenomas (most common)
  • Prolactinomas
  • ACTH-secreting tumors


Systemic Triggers

Hemodynamic

  • Hypotension
  • Major surgery
  • Shock
  • Cardiac arrest

Hormonal

  • Pregnancy
  • Dynamic pituitary testing
  • Dopamine agonist therapy

Hematologic

  • Anticoagulation
  • Thrombocytopenia
  • Coagulopathy

Others

  • Head trauma
  • Radiation therapy


Clinical Presentation

Classic Presentation (Sudden Catastrophic Onset)

1️⃣ Severe Headache

  • Most common symptom
  • Retro-orbital or frontal
  • Thunderclap type possible


2️⃣ Visual Disturbances

Mechanisms:

  • Optic chiasm compression
  • Cavernous sinus involvement

Manifestations:

  • Bitemporal hemianopia
  • Visual acuity loss
  • Diplopia
  • Ophthalmoplegia (CN III, IV, VI)

👉 CN III palsy is common → ptosis + mydriasis


3️⃣ Altered Sensorium

  • From raised ICP
  • Subarachnoid hemorrhage mimic
  • Electrolyte disturbances
  • Acute adrenal crisis


4️⃣ Acute Endocrine Failure

MOST DANGEROUS:

Acute Secondary Adrenal Insufficiency

Symptoms:

  • Hypotension
  • Shock
  • Hyponatremia
  • Hypoglycemia


5️⃣ Meningeal Irritation

  • Neck stiffness
  • Photophobia
  • Due to blood in subarachnoid space


Hormonal Deficits in Pituitary Apoplexy

Frequency Order 

  1. ACTH deficiency (most life-threatening)
  2. TSH deficiency
  3. Gonadotropin deficiency
  4. GH deficiency
  5. Prolactin variable
  6. ADH abnormalities (DI or SIADH)


Differential Diagnosis

Neurocritical Mimics

  • Subarachnoid hemorrhage
  • Meningitis
  • Cavernous sinus thrombosis
  • Intracranial tumor bleed
  • Aneurysmal rupture


Diagnostic Evaluation

1️⃣ Laboratory Evaluation

Essential Emergency Labs

  • Serum cortisol
  • ACTH
  • TSH + free T4
  • Prolactin
  • Electrolytes
  • Glucose
  • Gonadotropins

👉 Never delay steroid therapy for labs


2️⃣ Imaging

MRI – GOLD STANDARD

MRI findings:

  • Sellar mass
  • Hemorrhagic signal changes
  • Optic chiasm compression
  • Cavernous sinus invasion


CT Scan Useful if:

  • MRI unavailable
  • Detects acute hemorrhage

But:

  • Lower sensitivity than MRI


Emergency Management (ICU Perspective)


STEP 1 – Stabilization

ABC Approach

  • Airway protection if ↓ GCS
  • Hemodynamic stabilization
  • Correct electrolytes
  • Glucose control


STEP 2 – Immediate Steroid Therapy

 LIFE-SAVING THERAPY

Recommended Regimen:

  • Hydrocortisone 100 mg IV stat
  • Followed by:
    • 50–100 mg IV every 6 hours
      OR
    • 200 mg/day infusion

👉 Prevents adrenal crisis
👉 Improves hemodynamics


STEP 3 – Fluid & Electrolyte Correction

  • Treat hyponatremia
  • Manage DI if present
  • Monitor sodium closely


STEP 4 – Neurosurgical Evaluation

Indications for Urgent Decompression:

  • Severe visual loss
  • Progressive neurological deficit
  • Reduced consciousness
  • Radiological optic chiasm compression


Surgical Management

Transsphenoidal Decompression

Preferred approach:

  • Minimally invasive
  • Reduces optic pressure
  • Improves visual outcome


Timing of Surgery

Strong Indications for Early Surgery:

  • Severe visual loss
  • Cranial nerve palsy progression
  • Deteriorating consciousness

Conservative Management Possible If:

  • Mild symptoms
  • Stable neurology
  • No visual deficit


Conservative (Non-Surgical) Management

Includes:

  • High-dose steroids
  • Hormone replacement
  • Close neuro-ophthalmologic monitoring


Endocrine Replacement Therapy

Acute Phase

ALWAYS Replace:

  • Glucocorticoids first

Q: Why steroids before thyroxine?

Thyroxine increases metabolic demand → worsens cortisol deficiency → shock.


Then Replace:

  • Thyroxine (after steroid coverage)
  • Desmopressin if DI
  • Sex hormones later
  • GH replacement delayed


Complications

Acute

  • Adrenal crisis
  • Permanent visual loss
  • Stroke
  • Hydrocephalus

Long Term

  • Permanent hypopituitarism (common)
  • Tumor recurrence