Hypermenorrhea and/or Menorrhagia
(Prolonged and/or Excessive Menstrual Bleeding)
Dr. Nelson Soucasaux, Brazilian gynecologist
While in clinical practice the normal duration of the menstrual flow
is easy to establish, taking about 3 to 5-6 days, unfortunately the same
cannot be said regarding the average amount of the normal menstrual blood
loss. This means that, in the daily gynecologic practice, it is the patient
who actually tells and "establishes" if the volume of her menstrual
flow has increased or is less, and this is done by comparing it with her
usual own personal standard. Sometimes there is a rough comparison
with the menstrual bleeding of relatives or friends. Thus, there is
often a considerable subjectivity in this evaluation. Unfortunately, gynecology
has failed to establish a reliable parameter for daily or total blood loss
that could be easily applicable to clinical practice. (Maybe an experiment
carried out with women who make use of the menstrual cup can help us.)
[See also a terrific site to estimate your blood loss: http://www.menstrual-blood-loss.com
and read the creator's amusing comments
about the site.]
Prolonged and/or excessive menstrual bleedings comprise basically two
main groups: the functional and the organic
ones. The functional (or dysfunctional) uterine bleedings
have their main cause in hormonal or congestive disorders, while the organic ones are mostly caused by fibroid tumors
(uterine leiomyomata), polyps and cancer. The association between some excessive
and/or prolonged uterine bleedings with some pre-carcinogenic lesions and
cancer obliges us to pay attention to all cases of hypermenorrhea and menorrhagia
though fortunately most of them are due to entirely benign causes.
Most functional (or dysfunctional) uterine bleeding
is caused by hormonal disorders characterized by absolute or relative
hyperestrogenism [too much estrogen] due to a deficiency of progesterone.
Remember that, in the first phase of the normal ovulatory cycles, the estrogens
produce remarkable proliferative effects in the endometrium that are,
after ovulation and in the second phase, counterbalanced and opposed by
the anti-proliferative and secretory actions of progesterone upon this
tissue. As a result, the proliferative estrogenic endometrium is turned
into the secretory progesteronic endometrium. Nevertheless, if there is
a deficiency of progesterone due to luteal insufficiency or mostly persistent
anovulatory cycles (in which there is no progesterone, except in clinically
non-significant minimal basal levels), the proliferative and unopposed effect
of the estrogens alone will take place along the entire cycle, being able
to cause excessive thickening of the endometrium named endometrial hyperplasia.
(For luteal insufficiency, see Note 1, below.
As to the anovulatory cycles, in which there is no ovulation and no corpus
luteum formation, resulting in the absence of progesterone, see my article with the same title published here at the MUM.)
The hyperplastic and excessively thickened endometrium does not desquamate
[shed its lining] easily (or even completely) at the end of the cycle, resulting
in prolonged and/or excessive menstrual bleedings. In a simplified and didactical
way, we can say that, in these hyperplasias, there is "too much endometrium
to desquamate" and, therefore, to bleed. In this way, most of the dysfunctional
menstrual bleedings are due to endometrial hyperplasias resulting from a
persistent estrogenic action upon the endometrium, and this happens mostly
as a consequence of anovulation. And, if the anovulatory cycles last longer
than the normal duration of the menstrual cycle and the estrogenic production
is normal or heightened, the possibility of the development of endometrial
hyperplasias becomes greater, together with the occurrence of hypermenorrhea
and menorrhagia.
In spite of the frequent occurrence of dysfunctional uterine
bleedings throughout the entire women's fertile years, their frequency is
greater immediately after menarche and mostly along the years that
precede menopause. This is due to the higher incidence of anovulatory cycles
(as well as luteal insufficiency) in puberty and pre-menopause. In
puberty, anovulatory cycles and the defective luteal phase result from the
normal process of maturation of the hypothalamus-pituitary-ovaries
axis, whereas in pre-menopause their main cause is just the aging and progressive
depletion of the ovaries.
Almost all functional uterine bleeding due to non-complicated endometrial
hyperplasias cease with the administration of progestins (synthetic progesterones)
alone or associated with estrogens. (Estrogens alone must never be given
because they aggravate the hyperplasia, and this must be quite clear.)
The use of a progestin like norethysterone in an adequate dose for approximately
10 days usually stops the dysfunctional bleeding in a few days, promoting
the secretory transformation of the hyperplastic endometrium and its normal
desquamation 3 to 4 days after the end of the series. For preventing the
occurrence of further episodes of hypermenorrhea or menorrhagia, the use
of almost all progestins (or even natural micronized progesterone) also
for approximately 10 days during the second half of the cycle (from the
16th to the 25th day, for instance) is advisable. The use of a combined
hormonal oral contraceptive is also indicated, since their balanced synthetic
progestin-estrogen association taken in series of 21 days with a 7 days
interval between the series prevents the development of endometrial hyperplasias.
That's why the use of the combined "Pill" reduces the incidence
of endometrial cancer, since some special kinds of endometrial hyperplasias
are precursors of this neoplasia.
Conversely, prolonged and/or excessive uterine bleedings due to organic
causes, like fibroids, polyps and cancer do not respond to hormones.
That means that they do not cease or diminish with hormonal therapy,
and this is also a very important test in clinical practice, allowing us
to know with a considerable degree of certainty if an abnormal uterine bleeding
is due to a functional or an organic cause. Of course, there are exceptions
and "in-between" situations.
There are several kinds of hyperplasias of the endometrium, as well
as several classifications for them. These endometrial alterations are studied
based not only on the histological architecture of the endometrial glands
but also on the features of their cells. Basically, for a didactic and practical
purpose, endometrial hyperplasia can be typical or atypical. The typical
endometrial hyperplasias are the most frequent ones and, fortunately,
are histologically benign. They comprehend the simple
and the cystic endometrial hyperplasias. On the other hand, the atypical - or adenomatous - endometrial hyperplasias
do have an important relationship with the genesis of endometrial cancer.
For a long time they were classified in slight, moderate and accentuated
atypical hyperplasias of the endometrium. Among them, the accentuated type
basically corresponds to the adenocarcinoma in situ of the endometrium
(the first stage of endometrial cancer). In this way, the management of
typical or atypical endometrial hyperplasias differs a lot. Nevertheless,
to speak of the treatment of the atypical endometrial hyperplasias is not
the purpose of this article. Endometrial cancer or adenocarcinoma of the
uterine corpus is more frequent in women above the age of 50, but also may
occur earlier. For that reason, any uterine bleeding in post-menopausal
women who are not on hormonal replacement therapy requires immediate and
careful investigation.
As to the aforementioned functional congestive disorders that also may
cause increased menstrual bleedings, they are related to the pelvic
congestion syndrome, characterized by variable degrees of vascular
stasis resulting on a persistent engorgement in the female genitals, ligaments
and near organs and tissues. There are also other symptoms like pelvic and
lumbo-sacral pain and discomfort, and the condition may be due to sexual
and psychosomatic problems. The main sexual problem that may cause pelvic
congestion seems to be persistent sexual excitement without orgasmic response.
I also must emphasize the great importance of psychosomatic
factors in the origin or aggravation of almost all kinds of functional uterine
bleedings, hormonal and functional disorders in gynecology. Here,
the psychosomatic influences are exerted mostly through the neuroendocrine
and neurovegetative pathways, the neuroendocrine being the most important
one. As to this subject, see my articles "Psychosomatic
Gynecology" and "Psychosomatic and Symbolic
Aspects of Menstruation," published here at the MUM.
As to the organic causes for prolonged and/or
excessive menstrual bleedings, the most frequent ones are the widely
known uterine leiomyomatas or fibroids. Nevertheless,
not all kinds of fibroids cause uterine bleedings. In order to cause hypermenorrhea
and/or menorrhagia, fibroids must grow towards the uterine cavity, protruding
inside it, distorting its shape and/or increasing its size. This causes
compressive and congestive alterations in the endometrium, leading to the
excessive bleedings. Basically, there are three kinds of fibroids, according
to their position in the uterus: the submucous, intramural and subserous
ones. Submucous fibroids are the ones that more easily cause uterine abnormal
bleedings, because they grow close and towards the uterine cavity, protruding
inside it and exerting a direct pressure upon the endometrium. Some of them
are even pedunculated [growing on stalks]. Intramural fibroids grow in the
middle of the uterine wall and, therefore, need to reach a considerable
size in order to protrude inside the uterine cavity and cause the bleedings.
Nevertheless, the growth of multiple intramural fibroids may cause a diffuse
uterine enlargement accompanied by several distortions and alterations in
the shape of the uterine cavity, also resulting in hypermenorrhea and/or
menorrhagia. Subserous fibroids are those that grow close and towards the
uterine surface, distant from the uterine cavity. For that reason, they
do not cause menstrual alterations.
As in all cases of hypermenorrhea and/or menorrhagia due to organic
pathologies, abnormal uterine bleedings caused by fibroids do not respond
to the use of progestins or progestin-estrogen associations. Nevertheless,
there is an exception: cases in which the presence of the fibroids coexist
with endometrial hyperplasias due to hyperestrogenism. Cases like these
are relatively frequent and, in this way, the intensity of the abnormal
bleedings can, at least, be reduced with the use of progestins. This means
that, sometimes, cases of excessive menstrual bleeding whose main cause
is attributed to existing fibroids actually may have their main origin
in hormonal disorders and resulting simple endometrial hyperplasias, which
can be treated with progestins.
The treatment of uterine fibroids that
undoubtedly are causing abnormal menstrual bleedings (or even other problems,
depending on their position and size) unfortunately remains surgical (see
Note 2, below. Even so, with the present-day
great development of endoscopic surgery (especially the hysteroscopic
ones), the operation treatment of fibroids became much more conservative
and less invasive and aggressive than in the past. Submucous fibroids, for
instance, presently are easily removed with a hysteroscopic surgery, performed
by introducing a highly sophisticated endoscopic-surgical-optical device
inside the uterine cavity through the vagina. Endometrial polyps, another
organic cause of abnormal bleedings, are also easily removed by the same
procedure. (As to hysteroscopy, it is also an excellent way of establishing
the exact cause of abnormal uterine bleedings, since it allows the observation
of the entire uterine cavity at high magnification and, if necessary, to
perform a biopsy with precision. Nevertheless, as it is an invasive procedure,
in my opinion, as a clinical gynecologist, we only must order
a hysteroscopy when it is absolutely necessary.)
Fibroids (or uterine leiomyomata) are very frequent and fortunately
benign tumors of the myometrium (the uterine muscular layer). They are formed
by a mixture of smooth muscle fibers and fibrous connective tissue and grow
into nodules. Their possibility of malignant transformation is extremely
low and, for that reason, usually is not considered in clinical practice.
Before finishing I would like to remark that this is only an introductory
and very brief article about the extremely complex and intricate subject
of the prolonged and/or excessive menstrual bleedings. Because of this and
considering not only the limitations of an article written for the Web but
also the unimaginable extent and complexity of the subject, this article
cannot be regarded as a truly specialized approach to menstrual disorders
like hypermenorrhea, menorrhagia and other abnormal kinds of uterine bleeding.
Thus, this article is inevitably too, too far from being complete,
and I think (and hope) that this is quite obvious to the readers.
Note 1: Luteal
insufficiency is a condition in which the production of progesterone by
the corpus luteum is deficient. A deficient corpus luteum, though producing
low progesterone levels, may last the usual 12 to 14 days or less (7 to
10 days). In the last case, there is a luteal insufficiency due to a short
luteal phase.
Note 2: Sadly,
the recent attempts at developing a medicinal treatment for uterine fibroids
have proved to be disappointing at least on a long-term basis and
mostly considering its side-effects. As everybody knows, the growth
of fibroids depends on the estrogens, since these hormones are the main
responsible factors for the appearance and development of these tumors.
That's why the size of fibroids is naturally greatly reduced (and some
of them even disappear) after menopause in women who are not on hormonal
replacement therapy. Based on this, a medicine named Gn-RH analog was
developed in order to promote an intense blockage of the ovarian function
resulting in very low estrogen levels (like those existing in natural
menopause) and, consequently, in a considerable reduction in the size of
fibroids during the treatment. Nevertheless (and obviously), the use of
this medicine also produces great genital atrophy and almost all the signs
and symptoms of menopause (including even some degree of osteoporosis).
For that reason, the treatment with the Gn-RH analog cannot be used for
periods of time longer than six months. Despite the great reduction in the
fibroids' size obtained during the treatment, a few months after its interruption
and due to the subsequent return of the ovarian function to normal,
the fibroids grow up again. Because of this, the treatment is only used
in a few situations.
Copyright Nelson Soucasaux 2005
______________________________________________
Nelson Soucasaux is a gynecologist dedicated to clinical, preventive
and psychosomatic gynecology. Graduated in 1974 by Faculdade de Medicina
da Universidade Federal do Rio de Janeiro, Brazil, he is the author of several
articles published in medical journals and of the books "Novas Perspectivas
em Ginecologia" ("New Perspectives in Gynecology") and "Os
Órgãos Sexuais Femininos: Forma, Função, Símbolo
e Arquétipo" ("The Female Sexual Organs: Shape, Function,
Symbol and Archetype"), published by Imago Editora, Rio de Janeiro,
1990, 1993. He has been working in his private clinic since 1975.
Web site ( Portuguese-English ): www.nelsonginecologia.med.br
Email: nelsons@nelsonginecologia.med.br