Pituitary apoplexy - medical information / with case studies

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 on TI-weighted images . On T2-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 with CSF)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 on T1W, 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. •:• Precontrast TI :a heterogeneous mass in the sella ,

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

22. •:• Post contrast TI: 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……