• 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 :NORMALOPTIC DISC :HEALTHYNO 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 PROLACTINANAESR , CRPPITUITARY ANTIBODIESTHRIOD ANTIBODIESDYNAMIC 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

HYPPPHYSITISPROLACTINOMA

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 9.6–10 mm for the gestational period and as 10.2–12 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 Sheehan’s 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 9–10 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