The word apoplexy is defined as a sudden neurologic impairment, usually due to a vascular process. Pituitary apoplexy is characterized by a sudden onset of headache, visual symptoms, altered mental status, and hormonal dysfunction due to acute hemorrhage or infarction of a pituitary gland.Pituitary apoplexy is bleeding into or impaired blood supply of the pituitary gland. This usually occurs in the presence of a tumor of the pituitary, although in 80% of cases this has not been diagnosed previously. this study details about almost all the aspects of pituitary apoplexy.such as clinical manifestations , pathophysiology , sheehan syndrome , predisposing factors , imaging studies , cases etc please comment thank u

1. PITUITARY APOPLEXY
( MEDICAL INFORMATION )
PRESENTED BY
MARTIN SHAJI
PHARM D

2. Introduction
The word “apoplexy” comes from the Greek “apoplexia”
meaning a seizure, in the sense of being struck down. In
Greek “plexe” is “a stroke.”
The ancients believed that someone suffering a stroke had
been struck down by the gods
apoplexy :a sudden neurologic impairment,‘ Love usually due
to a vascular process.

3. •:• Pituitary apoplexy:
--sudden onset of headache-
-visual symptoms(‘F&VC: optic nerve or chiasm Ocular motility:
cranial nerves in cavernous sinus)
--altered mental status
--hormonal dysfunction
•:•There ¡s usually an existing pituitary adenoma present.

4. Pathophysiology-
- stems from an acute expansion of a pituitary adenoma or, less
commonly, in a no adenomatous gland, from infarction or
hemorrhage.-
- - Some postulate:
- gradual enlarging pituitary tumor -)compressing and distorting the
hypophyseal stalk and its vascular supply4causing ischemia and
subsequent necrosis
- -- Another theory :rapid expansion of the tumor outstrips its vascular
supply-) resulting in ischemia and necrosis(doubtful?4 tumors that
undergo apoplexy are slow growing

5. •:• Frequency:
This condition results ¡n an estimated 1.5-27.7% of cases of
pituitary adenoma
•:• Sex: Male-to-female predominance ¡s 2:1.
•:• Age:The age range is 37-57 years.

6. Clinical manifestations
•:• headache ¡n 95% of cases.
The headache ¡s sudden .Frequently, ¡t ¡s retro orbital ¡n
location and may be unilateral at onset, then becomes
generalized.
•:•Vomiting occurs ¡n 69% of patients and often accompanies
the headache.

7. Clinical manifestations
•:•The classic visual field defect is a bitemporal superior quadratic
defect.
•:• Ocular paresis (78%) results from compression of the cavernous
sinus, which make cranial nerves Ill ,IV,VI vulnerable to
compression.
diplopia may be present.
Of the cranial nerves, the occulomotor nerve is involved most
commonly- uniIateral dilated pupil, ptosis
Less commonly, cranial nerve IV is involved

8. Clinical manifestations
•:• Homer syndrome may develop from damage to the
sympathetic fibres.
•:• Involvement of the hypothalamus may alter thermal regulation.
•:• Destruction of adenohypophyseal tissue may lead to
endocrinologic deficiencies.

9. Predisposing factors
•:• Predisposing factors :endocrine stimulation tests,
bromocriptine treatment, head trauma, pregnancy, and pituitary
irradiation.
•:• Some believe :more prevalent in patients who produce excess
pituitary hormones (eg, acromegaly, Cushing syndrome)
— because the tumour is fuelled by the hormones.
-Others :most pituitary tumours that undergo Love apoplexy are
endocrinologically silent.

10. Sheehan syndrome
•:• Sheehan syndrome refers to pituitary apoplexy of anon
tumorous gland, presumably due to postpartum arterial spasm of
arterioles supplying the anterior pituitary and its stalk.
•:• In 1937, Sheehan reported 11 cases of women who died in the
puerperium
-- 11/11 necrosis of the anterior pituitary gland
-- 9/11 severe hemorrhage at delivery.
-- 2/11 no haemorrhage but were gravely ill prior to delivery.

11. •:•The pituitary gland hypertrophies in pregnancy.This
hypertrophy combined with locally released factors.
meditvascular spasm -) more susceptible to infraction from
compromised blood flow .

12. Sheehan syndrome
•:• inability to lactate (prolactin deficiency)
amenorrhea (gonadotropin deficiency),
skin depigmentation.
•:• hypothyroidism
hypoadrenalism
diabetes insipidus (posterior pituitary involvement)

13. Imaging Studies
•:• CT scan and MRI.
MRl is the most sensitive imaging study for evaluating the pituitary
gland, possibly visualizing hemorrhage not seen on CT scan.
ln the first 3-5 days, hemorrhage within the sella is isointense or
hypointense onTI-weighted images. OnT2-weighted sequences,
the blood appears hypointense.

14. Imaging findings
•:• CT:
CT(-):
-acute: seller/suprasellar mass with patchy or confluent
hyperdensity,may associated with SAH
-chronic: ”empty sella”(filled withCSF)CT(+):minimal or no
enhancement (rim pattern suggestive of PA).

15. Imaging findings
•:• MR:
Ti :early acute, enlarged gland, iso /hypointense with brain late
acute/subacute: hyperintensechronic :hypointense
T2:
acute: enlarged, hypointense (haemorrhagic) or hyperintense
(nonhemorrhagic)
pituitarysubacute:hyperintenseChronic:hyperintense
T1+:
rim enhancement

16. •:• 69 y/o male
•:• Headache, vomiting
•:• L’t ptosis, L’t EOM limitation(medial)
•:• Fever—)antibiotics , subsided after steroid usage
•:• Ptosis persistent-transfer to NS for operation
•:• Pathology report: pituitary adenoma
cases

17. •:• CT(-):a sellar lesion with slight
high density
•:.CT(+):without obvious intra-
lesion enhancement
case

18. •:• mixed signal intensity onT1W,T2W images. Hematoma
content is suspected. Mild , stud contrast enhancement.

19. •:• 46-year-old man,- sudden onset of severe headache- no
projectile vomiting,- followed by high fever and cranial nerve palsies
•:• a large heterogeneous mass, highly consistent with hemorrhagic
macroadenoma

20. •:• PrecontrastTI :a heterogeneous mass in the sella,

21. •:•T2 and FLAIR :heterogeneity of signal, consistent with
hemorrhage and or proteinaceous debris.

22. •:• Post contrastTI: no detectable enhancement.
•:•The normal calibler left cavernous carotid (first image)
•:• narrowed right cavernous carotid (following 3 images w/
arrows).

23. Treatment
•:• Administer high-dose corticosteroids (most patients have
hypopituitarism). Hydrocortisone lOOmg IV initially, then q6-8h
until surgery
•:• evaluate electrolytes, glucose, and pituitary hormones
•:• Administer appropriate endocrinologic replacement therapy
alone or combined with transsphenoidal surgicaldecompression of
the tumour ,

24. THANK UU……