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SPOTTER PRESENTATION
24-8-24
Dr. P.Anil Kumar Reddy
Senior Resident- Neurosurgery.
Moderator- Dr. V. V. Ramesh Chandra (Professor & HOD)
IDENTIFY THE SPOTTER
IDENTIFY THE SPOTTER
 A 22 years old male patient with no comorbidities, presented with
 H/o facial puffiness for 6 years associated with abdominal distension,
easy fatigability, weight gain.
 H/o acne/hyperpigmentation over face, chest, feet from 6 years not
associated with usage of any drugs.
 H/o weight gain from 5 years, gained 20 kg in the last 5 years.
 H/o trauma( lifting heavy weights) 4yrs back followed by severe low
backache with no weakness of lower limbs.
BRIEF HISTORY
Endocrinology Workup
Hormone Value Normal range
T3 0.6 0.5-5.0
T4 74 54-142
TSH 0.6 0.8-1.7
HbA1c 8.7
FBS 175
Baseline cortisol 8 am 43.5 6.7-22.6
Baseline cortisol 11 pm 30.5 6.7-22.6
ACTH 60 6.17-58.2
Testosterone 0.76
 Over Night Dexamethasone suppression test(ONDST) : 1mg dexa @11pm
8 am serum cortisol- 35.31 (6.7-22.6)
 Low dose dexamethasone test (LDDST)-0.5 mg of dexa every 6th
hrly for 48hrs
8am serum cortisol -27.7 (6.7-22.6)
 High dose dexa suppression test(HDDST)- 2mg of dexa 6th
hrly for 48hrs
8am serum cortisol- 17.7 (6.7-22.6)
more than 50 % suppressed pituitary as cause.
On admission midnight cortisol done, it showed no diurnal drop in
cortisol hence proceeded with LDDST, it was not suppressed, ACTH
was elevated indicating ACTH as cause
hence HDDST was done which showed >50% suppression from
baseline indicating pituitary as cause (Cushings disease)
SPOTTER PRESENTATION CUSHING DISEASE 24-8-24.pptx
X ray dorsal spine- BMD-osteoporosis
1) COLLAPSED D12 VERTEBRA
2) ANTERIOR WEDGING OF D11, D10, L1,L2 VERTEBRAL BODIES
D12
 PROVISIONAL DIAGNOSIS- Endogenous Cushing Disease with Pituitary Macrodenoma
with Vertebral Fractures due to Secondary Osteoporosis.
 Surgery  Endoscopic Transnasal Trans-sphenoidal Excision of
Macroadenoma.
 Biopsy:-
ASPECT CUSHING DISEASE CUSHING SYNDROME
DEFINITION Specific type of Cushing syndrome caused by a pituitary
adenoma
General condition of chronic cortisol excess
CAUSES Endogenous: Adrenal tumors, ectopic ACTH syndrome,
pituitary adenomas (Cushing disease)
- Exogenous: Use of corticosteroids
Pituitary adenoma secreting ACTH
CLINICAL
FEATURES
Similar features as Cushing syndrome
- Additional pituitary mass effects like headache, visual
disturbances
- Central obesity
- Hypertension
- Diabetes
- Osteoporosis
- Mood change
DIAGNOSIS - High-dose dexamethasone suppression test
- CRH stimulation test
- MRI of the pituitary gland
Screening tests: 24-hour urinary free cortisol, late-night
salivary cortisol, low-dose dexamethasone suppression
- Imaging: CT/MRI of adrenal glands and/or pituitary
TREATMENT Primary treatment: Transsphenoidal surgery to remove
pituitary adenoma
- Pharmacological management: Cabergoline, pasireotide
- Radiotherapy if surgery is incomplete
Depends on cause: Surgical resection of tumors,
discontinuation of corticosteroids, or pharmacological
management
- Medications: Ketoconazole, metyrapone
PROGNOSIS Varies based on underlying cause; treatment success depends
on the etiology and extent of disease
Generally good prognosis with successful pituitary
adenoma removal; some may require additional
treatments
 Pituitary Macroadenomas- greater than 10mm in diameter.
 80-90% of cases of Cushing disease are caused by pituitary macroadenomas.
 Macroadenomas secrete excessive amounts of adrenocorticotropic hormone (ACTH), leading
to overproduction of cortisol by the adrenal glands.
 Often cause symptoms due to mass effect, such as headaches, visual disturbances, and
hypopituitarism
 Microadenomas also secrete ACTH but often do so in a less pronounced manner compared to
macroadenomas.
 Cushing disease remission is defined as achieving adrenal insufficiency
with glucocorticoid dependency postoperatively
 Criteria for post op cure 
1. Morning cortisol <5ug/dl (0.43ug/dl on 27-6-24)
2. Undetectable serum ACTH
3. Return of low dose dexamethasone suppression
Assessing Post-operative Remission
Osteoporosis recovery post treatment.
Untreated Cushing syndrome- 4-6 times risk of osteoporotic fractures
Recovery Post-Surgery: Bone density often improves over time, usually slow.
Pharmacotherapy:
Bisphosphonates (e.g., alendronate),
Selective estrogen receptor modulators (SERMs), denosumab are commonly used to improve
bone density.
Calcium and Vitamin D Supplementation:
Lifestyle Modifications: Weight-bearing exercises and fall prevention strategies.
 Cochrane Library(2018) reported a systematic review regarding of
percutaneous vertebroplasty for osteoporotic vertebral compression
fracture, and showed no demonstrable important clinical benefits
compared with the placebo, and did not support a role for
vertebroplasty to treat acute or subacute osteoporotic vertebral
fractures.
Osteoporotic vertebral compression fractures caused by Cushings syndrome in young women: case report and literature
review
 Cheng et al. BMC Musculoskeletal Disorders (2023) 24:167 https://doi.org/10.1186/s12891-023-06253-9
 Preop  Post op (6 months)

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SPOTTER PRESENTATION CUSHING DISEASE 24-8-24.pptx

  • 1. SPOTTER PRESENTATION 24-8-24 Dr. P.Anil Kumar Reddy Senior Resident- Neurosurgery. Moderator- Dr. V. V. Ramesh Chandra (Professor & HOD)
  • 4. A 22 years old male patient with no comorbidities, presented with H/o facial puffiness for 6 years associated with abdominal distension, easy fatigability, weight gain. H/o acne/hyperpigmentation over face, chest, feet from 6 years not associated with usage of any drugs. H/o weight gain from 5 years, gained 20 kg in the last 5 years. H/o trauma( lifting heavy weights) 4yrs back followed by severe low backache with no weakness of lower limbs. BRIEF HISTORY
  • 5. Endocrinology Workup Hormone Value Normal range T3 0.6 0.5-5.0 T4 74 54-142 TSH 0.6 0.8-1.7 HbA1c 8.7 FBS 175 Baseline cortisol 8 am 43.5 6.7-22.6 Baseline cortisol 11 pm 30.5 6.7-22.6 ACTH 60 6.17-58.2 Testosterone 0.76
  • 6. Over Night Dexamethasone suppression test(ONDST) : 1mg dexa @11pm 8 am serum cortisol- 35.31 (6.7-22.6) Low dose dexamethasone test (LDDST)-0.5 mg of dexa every 6th hrly for 48hrs 8am serum cortisol -27.7 (6.7-22.6) High dose dexa suppression test(HDDST)- 2mg of dexa 6th hrly for 48hrs 8am serum cortisol- 17.7 (6.7-22.6) more than 50 % suppressed pituitary as cause. On admission midnight cortisol done, it showed no diurnal drop in cortisol hence proceeded with LDDST, it was not suppressed, ACTH was elevated indicating ACTH as cause hence HDDST was done which showed >50% suppression from baseline indicating pituitary as cause (Cushings disease)
  • 8. X ray dorsal spine- BMD-osteoporosis 1) COLLAPSED D12 VERTEBRA 2) ANTERIOR WEDGING OF D11, D10, L1,L2 VERTEBRAL BODIES D12
  • 9. PROVISIONAL DIAGNOSIS- Endogenous Cushing Disease with Pituitary Macrodenoma with Vertebral Fractures due to Secondary Osteoporosis. Surgery Endoscopic Transnasal Trans-sphenoidal Excision of Macroadenoma. Biopsy:-
  • 10. ASPECT CUSHING DISEASE CUSHING SYNDROME DEFINITION Specific type of Cushing syndrome caused by a pituitary adenoma General condition of chronic cortisol excess CAUSES Endogenous: Adrenal tumors, ectopic ACTH syndrome, pituitary adenomas (Cushing disease) - Exogenous: Use of corticosteroids Pituitary adenoma secreting ACTH CLINICAL FEATURES Similar features as Cushing syndrome - Additional pituitary mass effects like headache, visual disturbances - Central obesity - Hypertension - Diabetes - Osteoporosis - Mood change DIAGNOSIS - High-dose dexamethasone suppression test - CRH stimulation test - MRI of the pituitary gland Screening tests: 24-hour urinary free cortisol, late-night salivary cortisol, low-dose dexamethasone suppression - Imaging: CT/MRI of adrenal glands and/or pituitary TREATMENT Primary treatment: Transsphenoidal surgery to remove pituitary adenoma - Pharmacological management: Cabergoline, pasireotide - Radiotherapy if surgery is incomplete Depends on cause: Surgical resection of tumors, discontinuation of corticosteroids, or pharmacological management - Medications: Ketoconazole, metyrapone PROGNOSIS Varies based on underlying cause; treatment success depends on the etiology and extent of disease Generally good prognosis with successful pituitary adenoma removal; some may require additional treatments
  • 11. Pituitary Macroadenomas- greater than 10mm in diameter. 80-90% of cases of Cushing disease are caused by pituitary macroadenomas. Macroadenomas secrete excessive amounts of adrenocorticotropic hormone (ACTH), leading to overproduction of cortisol by the adrenal glands. Often cause symptoms due to mass effect, such as headaches, visual disturbances, and hypopituitarism Microadenomas also secrete ACTH but often do so in a less pronounced manner compared to macroadenomas.
  • 12. Cushing disease remission is defined as achieving adrenal insufficiency with glucocorticoid dependency postoperatively Criteria for post op cure 1. Morning cortisol <5ug/dl (0.43ug/dl on 27-6-24) 2. Undetectable serum ACTH 3. Return of low dose dexamethasone suppression Assessing Post-operative Remission
  • 13. Osteoporosis recovery post treatment. Untreated Cushing syndrome- 4-6 times risk of osteoporotic fractures Recovery Post-Surgery: Bone density often improves over time, usually slow. Pharmacotherapy: Bisphosphonates (e.g., alendronate), Selective estrogen receptor modulators (SERMs), denosumab are commonly used to improve bone density. Calcium and Vitamin D Supplementation: Lifestyle Modifications: Weight-bearing exercises and fall prevention strategies.
  • 14. Cochrane Library(2018) reported a systematic review regarding of percutaneous vertebroplasty for osteoporotic vertebral compression fracture, and showed no demonstrable important clinical benefits compared with the placebo, and did not support a role for vertebroplasty to treat acute or subacute osteoporotic vertebral fractures. Osteoporotic vertebral compression fractures caused by Cushings syndrome in young women: case report and literature review Cheng et al. BMC Musculoskeletal Disorders (2023) 24:167 https://doi.org/10.1186/s12891-023-06253-9
  • 15. Preop Post op (6 months)