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