32 year G2 P1+0 35+3 BY SCAN .

BOOKED
TRIPLET TRI/TRI
ADMITTED ON 19 / 1 /14
C/O LOWER AB. PAIN
NO PV LOSS
+FM
NO OTHER COMPLAIN
CX 1 CM DILATED WITH CERCLAGE
INSITU,NOT IN TENSION

MEDICALLY AND SURGICALLY FREE
ONE NSVD ( IVF ), MALE FACTOR
SECOND (CURRENT) PREGNANY IVF HAD CX
AT 4 MONTHS
VS STABLE
ADMITTED FOR OBSERVATION AND
ELECTIVE CS AT 36 WEEKS.
ANALGESICS .
IF INCREASE PAIN FOR CS.
NEXT DAY PT HAD INCREASED LABOR PAIN
WITH CHANGES IN CX .
CTG REACTIVE WITH CONTRACTION
NICU INFORMED,AGREED
CS DONE 20 1 14

OUTCOME
T1 FEMALE 2120 GM 8/9
T2 MALE 2270 6/8
T3 MALE 1790 7/8
DAY 0 , PT NOTED TO HAVE HIGH BP
(2) READING 17O- 90
PROTEIN NIL
PLT 63 FROM 143
ALT 412
URIC ACID 392
ADEQUATE URINE OUTPUT
ASYMPTOMATIC
IMPRRESION -POSTPARTUM PRECLAMSIA
WITH HELLP. STARETED ON MGSO4 (D/C
AFTER 24 HRS)
DAY O (MIDNIGHT )
C/O SEVERE HEADACH ( FRONTAL AND BITEMPORAL )
DIPLOPIA
NO VERTIGO , NO LOC
NO VOMITING OR MUCLE WEAKNESS
NO NECK STIFNEES OR FEVER . NO FACIAL AYMMETRY
VS BP 120/ 70 P 66
PET WORKUP
ALT 475
AST 450
PLT 70
URGENT NEUROLOGY CONSULTATION DONE
IMPRESSION :POSTPATUM HEADACH



GOAL :TO RULE OUT PRESS , CVT,
INTRACEREBRAL HEAMORHAGE ,INFARCTION
URGENT CT RESULT
NO INFARCTION
NO HEAMORRHAGE
NO SPACE OCUPYING LESION
NO INCREASE ICP

DAY 2 STILL SAME COMPLAIN
BP IN NORMAL RANGE (120-70),DID
NOT REQUIRE ATI HTN MEDICATION
URIN PROTEIN NIL
PLT 158
PET WORKUP NORMALIZED.
THOUGH PT SYMPTOMS NOT EXPLIANED ?
PRECLAMPSIA (MODEST INCREASE IN BP)


FUNDUS :NORMAL
OPTIC DISC :HEALTHY
NO PAPPILEDEMA
Pituitary gland enlarged in size 1.2 cm ,abuts
the optic chaisma.
Optic chaisma slightly streched over the
pituitary gland
No infarct no thrombosis,
Mri pituitary protocol study suggsted.

PT SEEN BY ENDOCRINOLOGIST
ACTH3.2
CORTISOL 66
CORTISOL 817
TSH 1.31
T4 15
PROLACTIN 10874
FSH LH ,< O.1
E21298
SST ( SHORT SYNECTHEN TEST)

30 MIN -CORTISOL 866
60 MIN -CORTISOL 1144
PITIUTATRY MACROADENOMA IN
POSTPARTUM PERIOD (PROLACTINOMA)

HYPOPHYSITIS

NONFUNCTIONING ADENOMA

COULD BE PHYSIOLOGICAL (DEPENDS ON
FOLLOW UP)


REPEAT PROLACTIN
ANA
ESR , CRP
PITUITARY ANTIBODIES
THRIOD ANTIBODIES
DYNAMIC PITUATRY MRI

High probability of hyophysitis
Appereance not typical for macroadenoma
Repeat mri pituitary or evaluation by
histopathology suggested.
HIGH PROLACTIN DT LACTATION OR
SECONDARY TO STALK EFFECT
NO CLINAL OR BIOCHEMCAL EVIDENCE
OF ENDOCRINE DISORDER
PT ASYMPTOMATIC
PET WORK UP NORMAL
D/ C HOME
HORMONAL PROFILE TO BE REPETED IN 6
WEEKS
PITUITARY MRI IN 3 MONTHS

HYPPPHYSITIS
PROLACTINOMA
SHHEHAN SYNDROME
Pregnancy is a normal altered physiological
state in which profound anatomic and
physiological changes occur in almost every
organ.
.Anterior pituitary undergoes two- to
three-fold enlargement during pregnancy,
because of hyperplasia and hypertrophy of
lactotroph cells.
In contrast to lactotrophs, the size of other
anterior pituitary cells remains unchanged
or decrease
There is considerable evidence regarding the
enlargement of the pituitary gland during
pregnancy.


increase in three dimensions with an overall
increase of 136%.
This increment was 45% in the first
trimester.


highest pituitary volumes and widths of
the infundibulum were observed during
the first three postpartum days
height of the normal pituitary gland was
suggested as 9.610 mm for the
gestational period and as 10.212 mm
for the immediate postpartum period

The height of the gland correlated best with
the gestational age.
The pituitary glands were demonstrated to
gain their normal size, shape, and volume
within 6 months postpartum.
The differential diagnosis of pituitary gland
enlargement is difficult in pregnant women
since magnetic resonance imaging (MRI) is not
specific enough.
Previous pituitary adenoma,
pituitary apoplexy or hemorrhagic necrosis of
an adenoma,
acute Sheehans syndrome (SS),
and lymphocytic hypophysitis (LyH)
should be kept in mind in a differential
diagnosis
pituitary gland lesions should be evaluated
carefully in pregnant women with headaches
and visual problems.
Surgical intervention is usually not required
unless there is a suspicion of pituitary
adenoma or apoplexy on MRI causing
compressive signs.
MRI without i.v. contrast injection seems to
be safe during pregnancy, but all FDA-
approved Gd chelates belong to Pregnancy
Category C.
The rational approach for pregnant patients
is to consider postponing MRI after birth.
If not possible, MRI without a contrast agent
should be the choice.

The weight of the gland increases by
approximately one-third during pregnancy.

During pregnancy, the maternal pituitary gland
undergoes remarkable hemodynamic changes.

Pituitary height that is higher than 910 mm
during pregnancy may arouse suspicion of a
pathological reason .
diagnosis of any pituitary disorder
becomes challenging and requires special
consideration in pregnancy bc of alter
the hormonal enviornment.


During pregnancy, the percentage of
lactotrophs increases up to 40% in response to
elevated maternal estrogen and at the end of
pregnancy, prolactin (PRL)mean level 200
ng/ml.

Role of progesterone on PRL secretion has
also been suggested
Prolactin begins to rise at 5-8 weeks.

first trimester 20-40 ng/ml

Second trimester 50-150

Third trimester 100-400

Rapidly decline after delivery if non
lactating,reaching to baseline in 1_3 weeks .


High levels of estrogen increase the binding
proteins and the bound form of thyroid
hormone .
There is almost 50% physiological increase in
total thyroxine (T4) although the free form
remains unchanged
renal iodine clearance and metabolism of
thyroid hormones by placenta increse.


thyroid gland size and vascularity increases.



Gonadotrophs(FSH.LH) constitute 7 to 15% of
anterior pituitary cells and are located in the lateral
portion of the gland.

Gonadotroph cells decrease during pregnancy and
normalize at one year after delivery.

Basal level of gonadotropins decrease starting from
6-7 weeks and remain undetectable thereafter.
During pregnancy there is decrease in the
number of somatotroph cells_Decreased GH
levels


pseudo-acromegaloid state -production of
placental GH from syncytiotrophoblast
increase in
(ACTH)
cortisol (both free and total)
urinary free cortisol
ACTH level progressively increases followed
by final surge during labor
Lymphocytic hypophysitis or autoimmune
hypophysitis is the most common among
inflammations affecting pituitary gland.

six times more common in women and shows
a striking association with pregnancy.
patients present in last month of pregnancy
or immediately after delivery;
although, it can rarely occur in men as well
as in children.
can involve predominantly anterior pituitary
(lymphocytic adenohypophysis) or posterior
pituitary (infundibuloneurohypophysitis
associated with other autoimmune
disorders especially Hashimoto's
thyroiditis. (30_50%).

Though many autoimmune diseases go
into remission during pregnancy, LH
manifests during pregnancy.

The cause of this paradox is not completely
understood but there are some
explanations. First pituitary enlarges
during pregnancy, which may lead to
release of pituitary antibodies.
During pregnancy, pattern of pituitary
blood-flow changes such that it derives
more blood from systemic circulation
and less from hypothalamic-pituitary
portal system; it is thus possible that
pituitary becomes more accessible to the
immune system.
Clinical picture of LH is variable and may
present either symptoms related to
sellar compression,(visual disturbance)
headach
hypopituitarism,
diabetes insipidus and
hyperprolactinemia(may b increased or
decreased)
Adrenal insufficiany (fatal in 25% cases if not
treated)

It is important to differentiate both
conditions , because both occur in
postpartum period.
Common differentiating features between LH
and Sheehan's syndrome (SS)
hypophysitis should be suspected if following
three features are present:
1) Symptoms occur during or soon after
pregnancy;
2) ACTH and/or TSH deficiency is present
with normal gonadotropin and GH secretion
and
3) diffuse contrast enhancement following
gadolinium on MR imaging
LH can sometimes be confused with pituitary
adenoma on imaging; some differentiating
features between the two are
The pituitary gland is firm and gritty after
sectioning.
initially enlarged, and is later atrophied.
infiltration by lymphocytes and plasma cells.
Later, fibrosis is present, with scanty pituitary
cells
The literature is unclear on the correct
treatment modality
Multiple reports showed improvement with
glucocorticoid administration alone.

exact dosage not been determined but 60
mg of prednisone per day for a period of 1
month to a year, followed by a gradual
tapering,.
often resolves sellar mass and improves
endocrine dysfunction




The natural history is often to regress, so in
the absence of a controlled trial, the true
response to glucocorticoids remains
speculative, and the role of this treatment is
unproven.
Surgery should be opted if patient has visual
impairment.
Transsphenoidal surgery may require to
confirm diagnosis and to relieve symptoms of
compression.

Hyperprolactinemia cause infirtility due to
inhibitory effect on gonadotrophin.

Adenoma growth in pregnancy
Risk of exposure to dopamine agonist to
fetus
Bromocriptine and cebergoline can be used
in first half of pregnancy but insufficient
data regarding safety in second half of
pregnancy.
NONPREGNANT
If microadenoma :to lower prolactin level to
achieve spontaneous ovulation
Macroadenoma:medical treatment by
dopamine agonist or surgery to reduce the
size before attempting to conceive
PREGNANT :
MICROADENOMA:risk of enlargement is
small.
MACROADENOMA:high risk of enlargement
Surveillance to monitor possible growth and
visual symptoms.
Treatment by dopamine agonist or
surgery(ideally in second trimester)
Postpartum pituitary necrosis leading to
hypopiturism
RISK FACTOR
Type 1 DM e vasculopathy
Previous pituitary mass
PPH
Breast atrophy
Failure to lactate
Amenrrehea
Lack of regrowth of pubic n axillary hair
Hypotension
Acute adrenal crisis
hypothyriodism
Rx: hormone replacement , ovulation
induction