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    Case Discussion

     A 63-year-old woman was seen because of sudden onset of headache about one month ago. The pain was intermittent and could be partially relieved by analgesics. It was dull and full sensation in character, lasted about 2 to 3 hours in duration, and was located at the right temporal and occipital regions. There was no radiation, provocative factors or prodrome. In recent two days before this admission, she had severe headache, nausea, vomiting and dizziness despite medications, and she visited ER for help. There was no cough, fever, weight loss, visual or mental disturbance. She did not consume alcohol, tobacco or medicine. She had no history of animal contact, travel or trauma recently. She had three children, and no complications related to the three pregnancies and deliveries were known to herself.

     On examination, she had clear consciousness. Her body height was 160 cm and weight was 58 kg. The body temperature was 37¢XC, the pulse rate 84 per minute and the respiratory rate 20 per minute. Her blood pressure in supine position was 101/60 mmHg. Her conjunctivae were pink and the sclerae were anicteric. The pupils were isocoric with prompt light reflexes. The neck was supple without lymphadenopathy, engorged jugular veins, palpable thyroid gland or carotid bruit. The chest was symmetric expansion and breath sounds were bilaterally clear. The heart beats were regular without audible murmur. The abdomen was soft without purple striae. Normoactive bowel sounds and impalpable liver and spleen were noticed. Her extremities were freely movable without edema. There was no cyanosis, petechiae, purpura or pigmentation. Neurological examinations were unremarkable.

< Laboratory data >

1.CBC

WBC

RBC

HB

HCT

MCV

MCHC

PLT

K/£gL

M/£gL

g/dL

¢H

fL

g/dL

K/£gL

5.62

3.77

11.3

32.2

85.4

35.1

270

2. BCS+e-

ALB

TP

T-Bil

AST

ALT

ALP

£^-GT

LDH

g/dL

g/dL

mg/dL

U/L

U/L

U/L

U/L

U/L

4.4

7.1

0.5

24

25

165

23

210

UN

CRE

Na+

K+

 Mg2+

Ca2+

Glucose

mg/dL

mg/dL

mmol/L

mmol/L

mmol/L

mmol/L

mg/dL

8.4

0.4

120.8

4.0

0.88

2.29

87

3. Other tests 

hsTSH

free T4

T3

ACTH*

Cortisol*

0.1- 4.5 ƒÝ£gIU/mL

0.60-1.75 ng/dL

80-180 ng/dL

10-65 pg/mL

5-25 ƒÝ£gg/dL

1.34

1.11

107

10.2

4.8

hGH

DHEA-SO4

MA

Osmolality (urine)*

0.06-5 ng/mL

4.6-15.4 £gmol/L

 

mOsm/Kg

3.7

1.1

1¡G40(-)

379


**high sensitivity thyroid-stimulating hormone¡×hsTSH, free thyroxine¡×free T4, triiodothyronine¡×T3, corticotropin¡×ACTH, *¡×random, growth hormone¡×hGH, DHEA-SO4¡×dehydroepiandrosterone sulfate, MA¡×microsomal antibodies.

< Course and treatment >

     Computerized tomography of the head without administration of contrast medium revealed negative finding. A lumbar puncture was performed and analysis of the cerebrospinal fluid specimen disclosed a few red blood cells. Because subarachnoid hemorrhage could not be ruled out, magnetic resonance imaging (MRI) of the head was performed which showed a mass lesion with bleeding in the pituitary fossa (Fig 1). Pituitary apoplexy with acute secondary adrenal insufficiency was diagnosed. No significant neurological or visual field defect was noted. She began to receive acetaminophen (500 mg Q.I.D), hydration and adrenal corticosteroids supplement with hydrocortisone 100 mg q12h. The symptoms, including headache, nausea, vomiting, and dizziness, resolved gradually. Follow-up serum sodium concentration gradually elevated to 132 mmol/L and corticosteroids was reduced in dose, which was subsequently discontinued 2 weeks later. Blood tests after she received luteinizing hormone-releasing hormone (GnRH) (100 £gg) and thyrotropin-releasing hormone (TRH) (400 £gg) were carried out to investigate pituitary function. Both FSH and LH levels rose following GnRH challenge. Prolactin and hsTSH responded normally to TRH challenge. She was followed regularly at OPD without any hormone supplement.

< °Q½× >

      ¸£¤U««Å餤­·(pituitary apoplexy)¡A¦³§O©ó¤@¯ëªº¸£¤¤­·¡A³q±`¬O¦]¬°¸£¤U««Å骺¸~½Fµo¥Í¥X¦å®ê¶ë©ÎÃa¦º¡A¨Ï±o½º¾b¤ºÀ£¤OÁت@¡A¾É­PÁ{§É¯gª¬«æÁØ´c¤Æ¡CµM¦Ó¡A¦³¨Ç¯f±wªº¸£¤U««Åé«o¬O¥¿±`ªº¡A¸£¤U««Å餤­·µo¥Í¦b¥Í²£®É©Î¥Í²£«á¡B¸£¥~¶Ë©Î¨Ï¥Î§Ü¾®¦å¾¯±wªÌ¡F¤]¥i¯à©M¿}§¿¯f¡B©ñ®g½uªvÀø©Î¶}¤ß¤â³N¦³Ãö¡C¯f±w³Ì±`¥X²{ÄY­«ÀYµh¡Bµø¤O¨ü·l(³q±`¬OÀ£¨ìµø¥æ¤e¦Ó¾É­PÂùù®°¼¥bª¼)¡A©Î³æ°¼©ÎÂù°¼²´²y¹B°Ê¯Ê·l¡A³q±`·|¦³¸£½¤ª¢¯gª¬¦p²ä¤l»øµw¤Î¯«´¼¤£²M¡A©Ò¥H¥²¶·©Mµïºô½¤¤UµÄ¥X¦å(subarachnoid hemorrhage, SAH)¡B¸£½¤ª¢¤Î¸£½F§@Ų§O¶EÂ_¡A¤]¦³¥i¯à¥X²{«æ©ÊÄòµo©ÊµÇ¤W¸¢¥\¯à¤£¨¬(acute secondary adrenal insufficiency)ªº¯gª¬¡A¥]¬Aäú¤ß¡B¹Ã¦R¡B§C¦åÀ£¡B¥ð§J©Î¦º¤`¡C

      ¸£¤U««Å餤­·ªº24¦Ü48¤p®É¤º³Ì¦nªº¶EÂ_ªº¤u¨ã¬°¥]§t¸£¤U««Å骺ÀY³¡¹q¸£Â_¼h¡A¨å«¬¥i¥H¬Ý¨ì¸£¤U««ÅéÅܤj¥B¦³¥X¦åªºªí¼x¡C4¤Ñ«á¦Ü30¤Ñ®É¥i¥H§Q¥Î®ÖºÏ¦@®¶·Ó¼v¡C

      ªvÀø¥]¬A²üº¸»X¸É¥R¤Î¯«¸g¥~¬ìªvÀø¡C«æ©Ê´Á¥u¶·¦Ò¼{¬O§_µ¹¤©µÇ¤W¸¢²üº¸»XªvÀø«æ©ÊÄòµo©ÊµÇ¤W¸¢¥\¯à¤£¨¬¤Î¦³®Ä´î»´¸£¤ô¸~¡A¤£»Ý¸É¥R¨ä¥Lªº²üº¸»X¡C¸g½ºÄu¸£¤U««Åé´îÀ£³N´£¨Ñ«D±`ºò«æ¤Î¦³®ÄªºªvÀø¡A¥i¥H«O¯d¤@¨Ç¸£¤U««Åé¥\¯à¡CµM¦Ó¡A«æ©Ê´Á¹L«á¡AÀ³¸Óµû¦ô¸£¤U««Åé¥\¯à¡A¦]¬°«Ü¦h¯f±w³£¥i¯à¥X²{¥Ã¤[©Êªº¸£¤U««Åé²üº¸»X¯Ê¤Ö¡C

< References >

  1. Biousse V, Newman NJ, Oyesiku NM: Precipitating factors in pituitary apoplexy. J Neurol Neurosurg Psychiatry 2001;71:542.
  2. da Motta LA, et al: Pituitary apoplexy. Clinical course, endocrine evaluations and treatment analysis. J Neurosurg Sci 1999; 43:25.

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(B)
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4.
(B)
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AÀY³¡®ÖºÏ¦@®¶
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5.
(A)
¸£¤U««Å餤­·®É³Ì±`¨£ªºµø³¥¯Ê·l¬°¡H
ABitemporal hemianopia
BBi-horizontal defect
CLeft homonymous hemianopsia
DHomonymous left upper quadrantic defect
ERight homonymous hemianopsia
6.
(D)
¤U¦C¦óªÌ«D¸£¤U««Å餤­·«æ©Ê´Á©Ò»ÝªºªvÀø¡H
ADexamethasone
BHydration
CElectrolyte replacement
DThyroid hormone
ETranssphenoidal decompression

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  5. ¡iA¡j¸£¤U««Å餤­·®É³Ì±`¨£ªºµø³¥¯Ê·l¬°Âùù®°¼¥bª¼(bitemporal hemianopia)¡C
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