Sheehan's syndrome is a condition that affects women who lose a life-threatening

amount of blood in childbirth or who have severe low blood pressure during or after
childbirth, which can deprive the body of oxygen. This lack of oxygen that causes
damage to the pituitary gland is known as Sheehan's syndrome.

Sheehan's syndrome causes the pituitary gland to not produce enough pituitary
hormones (hypopituitarism). Also called postpartum hypopituitarism, Sheehan's
syndrome is rare in industrialized nations, largely because care during pregnancy
and childbirth is better than in developing countries.

Treatment of Sheehan's syndrome involves lifelong hormone replacement therapy.

Sheehan's syndrome is caused by severe blood loss or extremely low blood pressure
during or after childbirth. These factors can be particularly damaging to the
pituitary gland, which enlarges during pregnancy, destroying hormone-producing
tissue so that the gland can't function normally.

Pituitary hormones regulate the rest of your endocrine system, signaling other
glands to increase or decrease production of the hormones that control metabolism,
fertility, blood pressure, breast milk production and many other vital processes. A
lack of any of these hormones can cause problems throughout the body.

summary
Sheehan's syndrome is a known complication, even if postpartum hemorrhage has been
well managed, this complication cannot be excluded. It is necessary to consider
this diagnosis in all patients having presented with cardiovascular collapse during
childbirth, whatever the cause and in the presence of classical signs of pituitary
insufficiency. We provided an extremely rare experience that hypothermia could be
an initial presentation of the Sheehan's syndrome.

Sheehan's syndrome (SS) is postpartum hypopituitarism caused by necrosis of the

pituitary gland. It is usually the result of severe hypotension or shock caused by
massive haemorrhage during or after delivery. Patients with SS have varying degrees
of anterior pituitary hormone deficiency. Its frequency is decreasing worldwide
However; it is still frequent in underdeveloped and developing countries. SS often
evolves slowly and hence is diagnosed late. History of postpartum haemorrhage,
failure to lactate and cessation of menses are important clues to the diagnosis.
Early diagnosis and appropriate treatment are important to reduce morbidity and
mortality of the patients.

abs
Sheehan's syndrome occurs as a result of ischemic pituitary necrosis due to severe
postpartum hemorrhage. It may be rarely seen without massive bleeding or after
normal delivery. Improvement in obstetric care and availability of rapid blood
transfusion coincided with a remarkable reduction in the frequency of Sheehan's
syndrome particularly in western society. But it has recently been reported more
often from well-developed countries. It is one of the most common causes of
hypopituitarism in underdeveloped or developing countries. Enlargement of pituitary
gland, small sella size, disseminated intravascular coagulation and autoimmunity
have been suggested to play a role in the pathogenesis of Sheehan's syndrome in
women who suffer from severe postpartum hemorrhage. The patients may seek medical
advice because of various presentations ranging from non-specific symptoms to coma
and the clinical manifestation may change from one patient to another. Failure of
postpartum lactation and failure to resume menses after delivery are the most
common presenting symptoms. Although a small percentage of patients with Sheehan's
syndrome may cause abrupt onset severe hypopituitarism immediately after delivery,
most patients have a mild disease and go undiagnosed and untreated for a long time.
It may result in partial or panhypopituitarism and GH is one of the hormones lost
earliest. The great majority of the patients has empty sella on CT or MRI.
Lymphocytic hypophysitis should be kept in mind in differential diagnosis. In this
review, the old and recent data regarding Sheehan's syndrome are presented.Although
named after Harold Sheehan, postpartum ischemic pituitary necrosis was reported for
the first time 100 years ago in Przeglad Lekarski by Leon Konrad Gliński. In the
majority of cases, the syndrome is a consequence of severe postpartum bleeding
episode resulting in severe hypotension or hemorrhagic shock. The frequency of
Sheehan's syndrome has decreased in developed countries as a result of improved
obstetrical care, but this clinical entity remains a common cause of
hypopituitarism in developing countries. The syndrome is characterized by varying
degrees of anterior pituitary dysfunction resulting from the deficiency of multiple
pituitary hormones. The order of frequency of hormone loss has generally been found
to be growth hormone and prolactin, gonadotropins, ACTH and thyrotropin. Women with
Sheehan's syndrome exhibit a variety of signs and symptoms including failure to
lactate or resume menses, loss of genital and axillary hair, and often occurring
long after delivery clinical manifestations of central hypothyroidism and secondary
adrenal insufficiency. Diagnosis is based on laboratory studies, including hormone
levels and hormone stimulation tests. Treatment of Sheehan's syndrome involves
hormone replacement therapy. The aim of this study is to review current knowledge
on clinically relevant aspects of this clinical entity and to provide the reader
with recommendations concerning its diagnosis and treatment.

abs

A 40 year old patient, G3P3, with no significant medical or surgical history, was
admitted to the intensive care unit with hemorrhagic shock due to postpartum
hemorrhage following a normal delivery at home. The clinical examination on arrival
confirmed the state of shock: an undetectable blood pressure, a tachycardia of 120
beats/min, cold peripheries, pale conjunctivae and polypnea. Immediate care
involved vascular expansion with colloids via a central venous catheter, followed
by a transfusion of 5 units of cross matched packed red cells since the haemoglobin
level was 5g/dl. The short-term evolution was marked by lactational failure and
hypoglycemic crisis (obnubilation, profuse sweats, agitation and convulsions)
confirmed by glycemias of 0,4g/l and relieved by the administration of hypertonic
glucose solutions. The medium-term evolution was marked by prolonged amenorrhea,
fatigue and apathy. In the light of this clinical picture, Sheehan's syndrome was
suspected and confirmed by a pituitary and cerebral MRI which showed an empty sella
turcica (figure 1). Hormone profiles including cortisol, plasma ACTH, thyroid
hormones, TSH, FSH, LH and prolactin were all low as a result of panhypopituitarism
(cortisol: 40ng/ml, plasma prolactin: 0ng/ml, TSH: 0,05UI/ml, FSH: 0,20mUI/ml, LH:
0,1mUI/ml, T3: 2pmol/l, T4: 4pmol/ml). The treatment is essential hormone
replacement: thyroxin 50mg per day, hydrocortisone 40mg per day. The evolution was
favorable.

stat
It is estimated that postpartum hemorrhage takes place in 1-2% of all live births
[5]. Sheehan’s Syndrome occurs in 1 out of every 100,000 births globally and is the
most common cause of hypopituitarism in underdeveloped or mid-income countries
[4,6]. Lack of access to sophisticated medical procedure, skilled professionals,
and medical resources contribute to higher rates of postpartum hemorrhage and
subsequent Sheehan’s Syndrome in developing nations, where the syndrome is said to
occur in 5 out of every 100,000 births [7,8]. Incidence estimates vary greatly,
with a range of 0-30% of cases reported following postpartum hemorrhage [9]. The
disease is deemed “rare” in industrialized nations, but there has been an increase
in prevalence of the disorder due to the flow of immigrants into these nations from
developing countries, where the disorder is more prevalent [10]. It is reported
that Sheehan’s Syndrome accounts for 0.5% of all known cases of hypopituitarism in
females [11].

Pathophysiology
Hyperplasia of the pituitary gland is a normal pathophysiologic process of
pregnancy. This hyperplasia is attributed to the growth of prolactin-secreting
lactotrophs, as they attempt to prepare the body for breastfeeding [17,18]. The
pituitary gland increases in both volume and physical size, with an estimated 120-
136% growth throughout the course of the pregnancy [3,19]. Increasing size
correlates to increased nutritional and metabolic needs, but the arteries supplying
blood to the gland remain unchanged [7]. The large pituitary gland compresses the
superior hypophysial arteries, which supply the anterior pituitary with rapid, low-
pressure flow [3]. The compression has minimal effect when the body is operating
optimally [6].

After delivery, the gland enlarges slightly, but this hyperplasia stops
approximately three days after delivery. The gland should return to pre-pregnancy
size within six months in an uncomplicated pregnancy [20]. When postpartum
hemorrhage occurs, the resultant hypotension and hypovolemic shock cause a decline
in blood flow to the gland. Superior hypophysis compression impedes adequate
perfusion throughout the hemorrhage process [4,6]. The resulting pituitary gland
ischemia causes necrosis of the adenohypophysis, which can be further complicated
by the hypercoagulable state of pregnancy [17]. The area of necrosis converts to
scar tissue, causing the gland itself to atrophy. The result is physical
destruction and dysfunction of the anterior pituitary lobe [4].

The pituitary gland tissue is not able to regenerate, meaning that these changes
cannot be physically reversed [3,18]. The gland is still considered to be
appropriately functioning if 50% or less is atrophied. Sheehan’s Syndrome is
considered in any presentation in which 70-90% of the gland has experienced
necrosis and subsequent scarring [4]. The severity of the condition is determined
by how many hormones are affected by tissue destruction [6]. It is posited that
tissue destruction continues to occur after the initial infarct. Necrosed tissue
releases antigens, which promote the development of anti-pituitary antibodies.
These antibodies grow in number over time, and they attack the remaining pituitary
tissue. The percentage of available tissue dwindles, which causes increased hormone
interruption and progression of presentation

Excessive blood loss during or after delivery of a baby may affect the function of
the pituitary gland, leading to a form of maternal hypopituitarism known as Sheehan
syndrome (SS). Such extensive bleeding may reduce the blood flow to the pituitary
gland causing the pituitary cells to be damaged or die (necrosis). Thus, the
production of the usual pituitary hormones will be reduced, perhaps by a
significant amount. During pregnancy the pituitary gland will enlarge and may
double in size. At this time the gland is especially vulnerable to a severe drop in
blood pressure (sometimes called "shock") and excessive maternal bleeding may
induce the "shock" and the damage to the cells of the gland. At that time the
amount of hormones produced by the pituitary may be decreased giving rise to the
symptoms associated with hypopituitarism. There appear to be two forms of the
disorder; a chronic form and an acute form, depending on the amount of damage to
the gland's cells. The acute form reflects considerable damage so that symptoms
become apparent soon after delivery. In chronic cases, the volume of damage is much
less and symptoms may not appear for months or years after delivery.