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Medical Interventions in Puberty Menorrhagia
Sanjay Rao , Vijay Pawar, VR Badhwar, MN Fonseca

Puberty menorrhagia can pose a significant challenge to the gynaecologist when associated with serious systemic complications like anaemia and hypoproteinaemia. The present ongoing study analyses 35 cases at a multidisciplinary tertiary institute of severe puberty menorrhagia which needed medical management.

There were 35 indoor admissions in the gynaecology ward at LTMG Hospital (2001-2002) for critical puberty menorrhagia over a span of two years. The leading cause was anovulatory dysfunctional uterine bleeding. Other systemic associations included hypothyroidism, idiopathic thrombocytopenic purpura, genital tuberculosis, and PCOD. Each case was analyzed for demographic profile, duration of menorrhagia, severity of symptoms, degree of anaemia, final diagnosis, requirement of blood and component therapy and response to conservative management. Early diagnosis and treatment with individualization of each and every case is the keystone in the management of puberty menorrhagia. Exclusion of pregnancy is mandatory in every case, irrespective of the history, reassurance, counselling, regular follow-up along with a balanced nutritional diet and long term iron therapy go a long way in successful management of such cases.


Menarche is a hallmark event in the life of most adolescent girls. It marks the transition from childhood to puberty. Although mechanisms triggering puberty and menarche remain uncertain, they are dependent on genetics, nutrition, body weight and maturation of the hypothalamic pituitary- ovarian axis. The complete maturation of the axis may take up to 2 years. During this time, it is common for adolescents to present with complaints of menstrual irregularities.

Abnormal bleeding accounts for approximately 50% of gynaecological visits in adolescent girls.1 These complaints encompass disorders ranging from minimal spotting to profuse bleeding. Puberty menorrhagia is defined as excessive bleeding occurring between menarche and 19 years. In 80% of cases puberty menorrhagia is caused by anovulatory cycles.2 There is an immaturity of the hypothalamus and inadequate positive feedback resulting in sustained high levels of oestrogen. An organic disease or malignancy in particular is very rare.

In all cases of puberty menorrhagia it is mandatory to exclude pregnancy, especially an incomplete abortion or ectopic pregnancy. In persistent abnormal bleeding coagulation disorders and leukaemia should be ruled out. Occasionally menorrhagia is the only presenting symptom in a patient of coagulation disorders. In general the prognosis is better when dysfunctional uterine bleeding starts after a period of regular menstruation than when it starts at menarche.4

Material and Methods

The present ongoing study evaluates 35 cases of critical puberty menorrhagia managed by domiciliary care at a multidisciplinary tertiary care institute, over a span of 2 years. Data was collected from medical case records in each of these cases.

Each case was evaluated for the demographic profile, severity of symptoms, degree of anaemia, final diagnosis, requirement of blood and component therapy and response to conservative management. The baseline investigations in all the cases included exclusion of pregnancy by urine testing, complete blood count, peripheral smear for RBC and WBC morphology, coagulation profile, blood grouping and Rh typing and transabdominal USG. In selected cases thyroid function test (T3, T4, TSH) and hormonal assays including (LH, FSH, Prolactin) and chest X-ray were done.


Analysis of data (Table 1) showed that 50% of patients were in the age group of 13-15 years.

Socioeconomic status

Majority of the patients belonged to the lower socioeconomic status.

As shown in Table 2 almost 62% of patients had onset of menorrhagia since less than 6 months. Of these 33% of patients had haemoglobin less than 6 gms%.

As shown in Table 3 anovulatory dysfunctional uterine bleeding occurred in 27 cases (80%). Two patients of secondary DUB had a final diagnosis of idiopathic thrombocytopenic purpura, 2 patients were diagnosed to have hypothyroidism. Genital tuberculosis was detected in another 2 cases. One patient was found to have a rare cause - Glanzmanns thromboasthenia that is discussed later.

Analysis of data showed that 37% of patients received fresh blood transfusion, 8% required component therapy in the form of fresh frozen plasma, platelets and cryoprecipitates. Majority of patients received a combination medical therapy as shown in the following Table:

Combination medical therapy regimes

Majority of patients received OCPills + ethamsylate (20%). Six patients received i.v. oestrogens plus progesterone while ethamsylate along with progestogens was used in 5 patients. Tranexamic acid was used with Biphasic OCPills in 17.1% of cases and with progestogens in 8.5% cases.


Puberty menorrhagia is excessive bleeding occurring between menarche and 19 years of age. It severely affects the quality of life.5 The main causes of abnormal uterine bleeding adolescent are shown in the Table.

In the present study series in 80% of cases of puberty menorrhagia the cause was found to be anovulatory dysfunctional uterine bleeding. A review of literature shows that during puberty, maturation of the hypothalamic pituitary - ovarian axis is characterised by an increase in the frequency and amplitude of pulsatile GnRH, which initiates and regulates secretion of pituitary gonadotropins.9 During the prepubertal years, LH is secreted primarily at night in an episodic fashion. With the progression to puberty, LH peaks increase in a pattern similar to that seen at night. The timing of these LH pulses is crucial in establishing normal ovulatory cycles. Increases in basal LH as well as immature timing of pulses result in anovulatory cycles. These cycles are characterized by levels of LH and FSH secretion that are sufficient to induce follicular development and oestrogen production but inadequate to induce follicular maturation and ovulation. Thus unopposed oestrogen stimulates endometrial growth. This ultimately outgrows its blood supply and architectural support, resulting in partial breakdown and shedding in an irregular manner.

In the proliferative phase the endometrium synthesizes equal amounts of (Vasoconstrictor and weak platelet aggregator) and PGE2 (Vasodilator with weak platelet antiaggregatory effect). However in the luteal phase the levels of progressively increase under the influence of estradiol and progesterone. In normal menstruation the ratio of so that it is the vasoconstrictor and platelet aggregator action that predominates. In anovulatory DUB the lack of progesterone results in decrease in the : PGE2 ratio and relative increase in the vasodilator and antiplatelet aggregatory PGE2 which would account for the increased mean menstrual blood loss. It could also account for the absence of uterine contractions and painless periods characteristics of anovulatory menstruation.

In the present series of patients, majority were administered a combination medical regime, to control the acute phase of bleeding. The primary management of anovulatory bleeding should be directed at controlling symptoms and prevention of anaemia. In adolescents with mild bleeding, reassurance and prophylactic iron treatment are suitable. However in patients who are sexually active or symptomatic for 3 to 6 months with anaemia (Hb 9-12 mg/dl) require cyclical medroxy progesterone acetate or a monophasic oral contraceptive pill in addition to iron. If the patient is actively bleeding, but haemodynamically stable, the acute phase is managed with one oral contraceptive pill three times daily for 3 days followed by two oral contraceptive pills twice daily for 2 days; this is followed by one oral contraceptive pills until completion of the packet. The cycles are further stabilized by a course of oral contraceptive for 3 to 6 months. If the patient continues to bleed heavily after the first 3 days, treatment is extended to three times daily for 7 days, twice daily for 7 day and then daily as mentioned previously. In patient with severe bleeding associated with haemodynamic changes, blood transfusions are indicated with administration of intravenous conjugated oestrogens (e.g. Premarin) in a dose of 25 mg every 4 to 6 hours until bleeding stops for 24 hours.13 Once bleeding is controlled, the patient is started on a regimen of strong androgenic progestogen or oral contraceptive pills.

The occurrence of excessively heavy irregular menses should prompt an evaluation of haematological status to rule out blood dyscrasias. In the present study group 3 patients (8.5%) had blood dyscrasias manifesting as DUB. Claessens and Cowell reported 19% of adolescents with menorrhagia requiring hospitalization had an underlying coagulation disorder in their study.6 A more recent retrospective study by Falcone et al in 1994 found that 4.9% of admissions over a 10 year period were secondary to a coagulopathy.9

The most common coagulation disorders were idiopathic thrombocytopenic purpura, Von Willebrands disease, leukaemia and platelet dysfunction like Glanzmanns thromboasthenia. Young girls with blood coagulopathies are at a high risk for abnormal bleeding with the onset of menarche,9 and must be treated appropriately at the time of puberty. Laboratory evaluation, including a complete blood count, platelets, prothrombin time, partial thromboplastin time and bleeding time provides an adequate screen for coagulation disorders.

In our study there were 2 patients diagnosed to have idiopathic thrombocytopenic purpura. 80% patients of idiopathic thrombocytopenic purpura have menorrhagia.4 Acute Idiopathic thrombocytopenic purpura is most commonly seen in young and is immunological thrombocytopenia, caused by immuno complexes containing viral antigens that bind to the platelet, Fc receptors, or, by antibodies produced against viral antigens that cross react with platelets. It can be associated with infectious mononucleosis, acute toxoplasmosis, CMV infections, viral hepatitis and HIV.11

In the present study group there was one rare case of Glanzmanns thromboasthenia. This is a disorder in which the IIb-IIIa complex glycoprotein on the platelet surface is defective and platelets cannot form aggregates. Our case required multiple platelet transfusions. All haematological disorders underlying dysfunctional uterine bleeding cases are best treated in liaison with the haematologist. They require adequate blood transfusion, component therapy and platelet transfusion.

Hypothyroidism can be associated with pubertal DUB. The reported incidence of subjective menorrhagia in myxoedema varies from 32-80% and menorrhagia may not infrequently be the presenting complaint (Scoot and Massey 1964). The menorrhagia associated with hypothyroidism responds promptly to the thyroid replacements, often in doses insufficient to correct the other manifestations of the condition. This suggests that thyroxine does have a direct effect on the spiral arterioles and on haemostasis at menstruation.4

In our study there were two cases of genital TB which were treated with Anti-Kochs therapy along with OCPs. Of these one case presented initially with idiopathic thrombocytopenic purpura and was detected to have genital tuberculosis on further evaluation. The incidence of genital TB is about 1% amongst the gynaecological patients attending the ODP in developing countries.10 Menorrhagia or irregular bleeding in genital TB is probably due to ovarian involvement, pelvic congestion or endometrial lesions.

Polycystic ovarian disease can be infrequently associated with irregular heavy bleeding in 30% of cases, as reported by Goldzeiher et al. Chronic anovulation may result from an increased pulsatility of GnRH. This results in elevated LH levels and increased ovarian androgen production. These hormone increases result in menstrual irregularity and oily skin. Ovaries typically have multiple follicular cysts less than 10 mm in size and increased stroma. This condition may be temporary in adolescent or may eventually progress to advanced polycystic ovarian disease with hirsuitism. Peripheral conversion of androstenedione to oestrone causes a hyperoestrogenic effect that perpetuates menstrual irregularity.

The goals of treatment in adolescents are to regulate menstruation and decrease hirsuitism and acne. The best treatment modality is an oral contraceptive pill because of the inhibition of LH and decrease in circulating testosterone levels. Sex hormone -binding globulin is increased and available to bind and inactivate testosterone in the circulation.7 Oral contraceptive pills do not seem to aggravate the underlying insulin resistance significantly and may attenuate some of the lipid derangement’s induced by sustained excess androgen exposure.8 Another treatment option to control abnormal bleeding is cyclic medroxyprogesterone acetate 10 mg orally for 10 days of each month. However this regimen does not alleviate the associated androgenic effects of polycystic ovaries.9

To summarize, Blood and component therapy along with hormones constitute the main medical therapy in the treatment of critical puberty menorrhagia. In the present study 6 patients required intravenous conjugated oestrogen. Various studies suggest that these are of value in arresting profuse haemorrhage4 and are usually given with antiemetics. Oral contraceptive pills were administered to 19 patients in our study group. These form an effective hormonal therapy to restore the balance between prostaglandins and thromboxane A2 and reduce the mean menstrual blood loss with additional cycle stabilization. 45.7% patients in our study series had received progestogens for medical curettage. Androgenic progestogens alone may be used to arrest uterine haemorrhage or administered cyclically throughout the menstrual cycle (5th to 25th day) Norethisterone acetate (primolut N) 20-30 mg daily is given to arrest haemorrhage and not more than 3 days. The progestogen may then be continued at a lower dose for upto 21 days. The patient should be warned that a withdrawal bleeding will occur on stopping treatment that will cease in 4-5 days. Norethisterone acetate can also be given from 5th to 25th day in a dose of 5 mg once a day.

Androgens like Danazol are less favoured because of their masculinizing side effects in adolescent girls.

Antifibrinolytic like tranexamic acid are a newer form of treatment in puberty menorrhagia. Plasminogen activator are a group of enzymes that cause fibrinolysis. An increase in the levels of plasminogen activators has been found in the endometrium of patients with heavy menstrual bleeding compared to those with normal menstrual loss. Plasminogen activators have been therefore been prompted as a treatment in heavy menstrual bleeding.3

There has been reluctance to prescribe tranexamic acid due to possible side effects of the drugs such as thrombogenic disease (DVT). Long term studies in Sweden, however have shown that the rate of incidence of thrombosis in women treated with tranexamic acid is comparable with the spontaneous frequency of thrombosis in women.3
Ethamsylate was used in 8 of our patients. It reduces capillary bleeding when the platelets are adquate; probably it corrects abnormal platelet function. It is not an antifibrinolytic. It does not stabilize fibrin.
Majority of patients in the study group received a combination therapy with OCPs with androgens or with progesterone or with antifibrinolytic agents.12


In conclusion, most abnormal bleeding in adolescents is caused by immaturity of the hypothalamic - pituitary ovarian axis resulting in anovulation. Approximately 20% of adolescents have an underlying endocrine or haematological disorder requiring targeted diagnostic testing.

Individualizing every case, excluding pregnancy, timely hospitalization, a thorough history, physical examination and base line workup are crucial in the management of every case. Reassurance, counselling of adolescent girls about reproductive physiology, regular follow-up, balanced diet and long term iron therapy go a long way in treatment of puberty menorrhagia.


We thank the Dean, LTMG Hospital, Dr. ME Yeolekar for permitting us to use hospital data.


1. Caufriez A. Menstrual disorders in adolescence: Pathophysiology and treatment. Horm Res 1991; 36 : 156.

2. Devore GR, Owens O, Kase N. Use of intravenous premarin in the treatment of dysfunctional uterine bleeding: A double blind randomized control study. Obstet Gynecol 1982; 59 : 285.

3. Lethaby A, Farquhar C, Cooke I. Antifibrinolytics for heavy menstrual bleeding. The Cochrane Library, Issue 1, 2003.

4. Davey DA. Dewhurst’s textbook of Obstetrics and Gynaecology for postgraduates. 5th edition, pages 591-607.

5. RCOG guideline for management of menorrhagia after referral to secondary care.

6. Claessens EA, Cowell CA. Acute adolescent menorrhagia, Am J Obstet Gynecol 1981; 139 : 277.

7. Raj SG, Raj MHG, Talbert LM, et al. Normalization of
testosterone levels using a low estrogen containing oral contraceptive in women with polycystic ovary syndrome. Obstet Gynecol 1983; 60 : 15.

8. Kory Kowski MT, Molan M, Horwitz MJ, et al. Metabolic effects of oral contraceptives in women with polycystic ovary syndrome. J Clin Endocrinal Metab 1996; 80 : 517.

9. Debra A, Minjarez MD, Karen D, Bradshaw MD. Abnormal uterine bleeding in adolescents. Obstetrics and Gynecology Clinics of North America. Vol. 27 no. 1 march 2000 WB Saunders Company, Orlando, FL 32887-4800.

10. Dutta DC. Pelvic infections: Genital tuberculosis - Textbook of gynecology- 2nd edition pages 128-134, New central book agency (P) Ltd.

11. Robert I Handin. Disorders of the platelet and vessel wall -Harrisons Principles of internal medicine 15th edition 745-750.

12. Tripathi KD. Drugs affecting coagulation, bleeding and thrombosis. Essentials of medical pharmacology KD Tripathi 4th edition 599.

13. Duflos-Cohade C, Amandruz M, Thibaud E. Pubertal menorrhagia. J Pediatr Adolesc Gynaecol 1996; 9 : 16.


National programmes of mammographic screening can lead to one in three breast cancers being overdiagnosed. Zahl and colleagues report that the incidence of breast cancer among women 50-69 years of age increased by 50% when Norway and Sweden introduced mammographic screening. They also found no compensating fall in incidence over age 69, when women are no longer invited for screening. In the absence of screening, the authors say, one of three women in the 50-69 age group who were diagnosed with invasive breast cancer would not have been diagnosed as having breast cancer in her lifetime. The authors conclude that women cannot make an informed choice on screening unless the level of overdiagnosis is properly explained to them.

BMJ, 2004; 328 : 921.

Department of Obstetrics and Gynaecology, LT Medical College, Sion, Mumbai - 22.

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