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Management quandary
J Pediatr Adolesc Gynecol (1999) 12:233-235
Management Quandary Edited by Elisabeth H. Quint, MO University of Michigan Health Systems. Ann Arbor. Michigan
Case Contributor: Yolanda R. Smith, MO University of Michigan Health Systems. Ann Arbor. Michigan
Comments: Lesley L. Breech, Mot and Sue Ellen Carpenter, M02 'Washington University School of Medicine. St. Louis, Missouri, and 2Emory University School of Medicine, Atlanta, Georg ia
Case 4-1999 Persistent Vaginal Bleeding at Menarche Case Presentation. The patientis a 15-year-old girl with a history of autism and developmental delay, who presented to the Emergency Department with a history of 7 to 10 days of vaginal bleeding, increasing in flow and with moderate clots at the time of the visit. She had prior to this visitnever had a menstrual cycle. The motherwas unable to quantify the bleeding but stated she soaked through adult diapers. She denied any fever, chills, nausea, vomiting, lightheadedness, or dizziness. Her past medical history revealed autism. She had a work-up for delayedonsetof puberty 2 yearsprior to this visit, which showed an advanced bone age and mildly enlarged muIticystic ovaries on ultrasound, but no other abnormalities. She uses no medications. Her physical examination revealed a weight of 221 pounds, blood pressure 116/62, pulse54, respirations 20. Head and neck exam was normal. Breastexam was Tanner stage III-IV. Abdomen was obese and non-tender with normal bowel sounds. Pelvic examination revealed normal external genitalia. Speculum showed some blood in the vault. Cervix was normal, bimanual exam showed a normal size uterus with no adnexal tenderness. Drs. Breech and Carpenter's comments:
multicystic ovaries, and the history of delayed puberty with an advanced bone age may be suggestive of hyperandrogenism. Hyperandrogenism can lead to anovulation and possible abnormal uterine bleeding . Obesity alone, as in this patient of 221 pounds, can be associated with anovulation. Congenital anomalies of the female reproductive tract may initially present with heavy vaginal bleeding due to trauma. Other uterine disorders may include malignant cervical lesions, which are extremely rare, or cervicitis from a sexually transmitted disease. which is quite common in a sexually active teenager. Pregnancy and pregnancy complications may be the cause of acute and heavy bleeding. Sexual abuse may also present with vaginal trauma and bleeding. An attempt should be made to ascertain the degree of blood loss. Pad counts, descriptions of pad saturation, the number of days of bleeding, and a history of lightheadedness or dizziness are all helpful. The physical exam should focus on vital signs, including orthostatic vital signs, dry mucous membranes. a pale hue to the skin, and decreased capillary refill in the extremities. Other clues include: petechiae or ecchymoses may indicate a coagulation disorder: hirsutism. virilization, or striae may suggest an endocrinopathy; visual changes may be present with central nervous system (CNS) tumors; or low body weight with villous hair growth may suggest an eating disorder. A thorough pelvic exam is imperative . An ultrasound can be performed if the examination is not adequate. Endocervical cultures for sexually transtnitted diseases (SID) may be obta ined during this exam . Rarely will an exam under anesthesia be necessary. Laboratory evaluation for acute menorrhagia in an adolescent should include a complete blood count. platelet count. prothrombin time, thromboplastin time, bleeding time, and a urine pregnancy test. Thyroid function may also be assessed with a TSH level. Clinical circumstances may dictate further evaluation with STD screening. a prolactin level, or serum androgen levels.
The most likely cause of abnormal uterine bleeding in adolescents is anovulation . Coagulation disorders should certainly be considered when abnormal bleeding occurs with the first menses. Previous retrospective reviews report that 19%-33% of young women admitted for dysfunctional uterine bleeding had a hematologic disease. 1.2 The studies also note the presence of numerous other chronic medical conditions in young women with abnormal bleeding. These disorders include thyroid disease, diabetes mellitus and endocrinopathies. Delayed puberty and menstrual disturbances may be seen in hypothyroidism: however, a delayed bone age is generally expected. The ultrasound, which demonstrated
Laboratory values revealed hemoglobin of 11.6 g1dl and a hematocrit of 34.6%, with similar values 6 hours later.
CI 1999North American Society for Pediatric and Adolescent Gynecology Published by Elsevier ScienceInc.
1083-3t881991$20.00 PII SI038·3188(99)OOO18·2
234
Management Quandary
Urine pregnancy test was negative. TSH, prolactin, PT, and PTT were in the normal range. Drs. Breech and Carpenter 's comments: At this time, there is no evidence of hypovolemia (hypotension or tachycardia) and no evidence of active hemorrhage on physical exam. Since the hematologic studies did not reveal any gross abnormalities, an outpatient regimen is appropriate. As demonstrated in a retrospectivereview of dysfunctionaluterine bleeding in adolescents by Falcone and others, most patients (72%) were started on an initial treatment plan consisting of combinationoral contraceptivepills (OCP) containing at least 35 meg of ethinyl estradiol administered several times daily.' A smaller percentage (37%) of patients received intravenousconjugated estrogens (25 mg every 4 hours) and hospitalization. In that review, vaginal bleeding stopped or decreased in 93% of patients regardless of which steroid therapy was utilized. Oral progesterone agents have also been utilized; however, they do not routinely abate the bleeding in acute menorrhagiaas quickly as estrogen containing agents.
The patient was started on an OCP taper but represented 24 hours later with severe bleeding. Her initial hemoglobin was 10.2 and a bleeding time was 5 minutes. The patient was admitted for Premarin I.V. treatment. Initially her bleeding slowed down and her blood values were stable for 12 hours. She then started to bleed heavier again. Drs. Breech and Carpenter's comments: The initial treatment plan appeared to have failed in this young woman. When she presentedthe second time with severe bleeding resistant to OCP's, the hemoglobinlevel had already decreased by more than one gmldl. Because of worsening anemia and bleeding resistant to medical therapy, immediate hospitalization is indicated. Intravenous hydration may be provided in addition to other medical therapy. A trial of intravenous conjugated estrogen is a reasonable next step. The patient's initial stabilization is certainly reassuring; however, the increase in vaginal bleeding some 12 hours later raises concerns regarding worsening anemia and adequate tissue perfusion. On initial exam, a normal pelvic exam is documented. In the setting of persistent resistance to hormonal management, a pelvic ultrasound is merited to rule out any intrauterine or adnexal pathology. Fluid management should be followed closely with hemoglobin, hematocrit, platelet, and coagulation studies. Levels of coagulationfactors may substantiallydrop, further compounding the bleeding situation. Packed red cells or blood product replacement may be necessary in emergent circumstances.
An ultrasound was performed. This revealed an endometrial lining of 5 mm and a 4-cm clear ovarian cyst. The patient continued to bleed heavily and her hemoglobin
dropped from 7.3 gldl to 4.0 gldl in the next 12 hours, despite Premarin and later added progesterone treatment. The patient received 2 units of packed red cells and she was taken to the operating room for evaluation and a dilation and curettage. Exam under anesthesia revealed a mobile small uterus that sounded to 6 em. Curettage revealed a moderate amount of tissue and the bleeding slowed down after that but did not stop. A Foley catheter was then placed in the uterus and inflated with 10 cc of saline. This slowed the bleeding down significantly . The catheter was left in place for two days and then slowly deflated and removed. The patient received a total of 4 units of packed red cells and a 6-pack of platelets. The patient was discharged after that in stable condition with hemoglobin of 10 gld!. Her discharge medications included Premarin and Provera. The pathology evaluation of the endometrium revealed proliferative phase endometrium. Drs. Breech and Carpenter 's comments: The acute menorrhagiain this adolescent was resistantto several hormonal regimens. In adolescents, a dilation and uterine curettage (D&C) has more recently been reserved for vaginal bleeding unresponsive to medical therapy. Smith and others reported 0/9 adolescents admitted for menorrhagia required a D&C from 1991 to 1995; however, 8/46 (17%) adolescent women underwent a D&C from 1979 to 1991 .2 In this case, the young woman continued to bleed with falling hemoglobin levels despite medical therapies. This situation became more serious, even life threatening, and required aggressive measures. Even uterine curettage did not produce adequate hemostasisand a mechanical measure, a Foley catheter, was necessary to achieve hemostasis. This may have been due to a secondary coagulopathy from acute blood loss and depletion of platelets and coagulation factors. This patient's history and later histology of the endometrium did not suggest an infectious component; however, some authors suggest empiric antibiotic therapy, especially in menorrhagiaresistant to hormonal therapy." A recent paper by Creatsas and others suggests an alternative therapy for menorrhagia in adolescents requiring hospitalization.P Forty-eight patients were randomized to receive 20 mg orally of tenoxicarn, a prostaglandin synthetase inhibitor, daily, or I tablet of lynestrenol-ethinyl estradiol (0.05 mg and 2.5 mg respectively). Twenty-three patients received tenoxicam and the remainder received the Iynestrenol-ethinyl estradiol combination. Less hospitalization and higher hemoglobin and hematocrit levels were seen in the tenoxicam group. Also, three D&C procedures and seven blood transfusions were necessary in the Iynestrenol-ethinyl estradiol group versus none in the tenoxicam group. The early data from this small group is promising for alternative treatment modalities that may avoid surgical instrumentation, especially in patients resistant to hormonal therapy. The pathology report from the endometrial curetting
Management Quandary showed proliferative endometrium consistent with anovulation. which is the most common cause of menorrhagia in adolescents," Some authors suggest that the risk of developing menorrhagia may be highest during the first few years after menarche because maturation of the hypothalamic pituitary ovarian (HPO) axis occurs slowly during adolescence.l" It is unknown at this time which adolescents may have slower maturation of the HPO axis. In this patient, the history of autism and developmental delay may suggest CNS problems that may affect the HPO axis. Continuation of hormonal management of the menstrual cycle would be advisable in this young woman. Cyclic progesterone withdrawal or OCp's would eliminate the risk of a persistent proliferative endometrium and acute menorrhagia.
Editor's Comments An unusual case of persistent anovulatory bleeding is presented. Two interesting points can be made. In the first place the use of ultrasound to measure endometrial thickness can guide our management. If the lining is thin. which is often the case after prolonged bleeding. estrogen therapy is usually successful. If the lining is thick and the patient does not respond to treatment. then adding early on a progestational agent may be very helpful. A second point about this case is the use of the foley catheter for the continued bleeding. In the literature this has been described mostly in obstetrics," but it can be
235
used in gynecology as well for tamponade of the uterine wall.
References I. Claessens EA. Cowell CA: Acute adolescent menorrhagia. Am J Obstet Gyncol 1981; 139:277 2. Smith YR. Quint EH, Hertzberg RB: Menorrhagia in adolescents requiring hospitalization. J Pediatr Adolesc Gynecol 1998; II: 13 3. Falcone T, Desjardins C, Bourque J, Granger L. Hemmings R. Quiros E: Dysfunctional uterine bleeding in adolescents. J Reprod Med 1994; 39:761 4. Pittaway DE, Deaton JL: Abnormal uterine bleeding. In: Pediatric and Adolescent Gynecology. Edited by SEK Carpenter, JA Rock. New York. Raven Press. Ltd., 1992: pp 189-204 5. Creatsas G. Cardamakis E. Deligeoroglou E, Hassan E. Tzingounis V: Tenoxicam versus Iynestrenol-ethinyl estradiol treatment of dysfunctional uterine bleeding cases during adolescence. J Pediatr Adolesc Gynecol 1998; II: 177 6. LeMarchand-Beraud T, Zufferey M, Reymond M, et al: Maturation of the hypothalarnic-pituitary-ovarian axis in adolescent girls. J Clin Endocrinol Metab 1982; 54:241 7. De Loor JA. van Dam PA: Foley catheters for uncontrollable obstetric or gynecologic hemorrhage. Ob Gyn 1996; 88:737
Management Quandary Edited by Elisabeth H. Quint, MO University of Michigan Health Systems. Ann Arbor. Michigan
Case Contributor: Yolanda R. Smith, MO University of Michigan Health Systems. Ann Arbor. Michigan
Comments: Lesley L. Breech, Mot and Sue Ellen Carpenter, M02 'Washington University School of Medicine. St. Louis, Missouri, and 2Emory University School of Medicine, Atlanta, Georg ia
Case 4-1999 Persistent Vaginal Bleeding at Menarche Case Presentation. The patientis a 15-year-old girl with a history of autism and developmental delay, who presented to the Emergency Department with a history of 7 to 10 days of vaginal bleeding, increasing in flow and with moderate clots at the time of the visit. She had prior to this visitnever had a menstrual cycle. The motherwas unable to quantify the bleeding but stated she soaked through adult diapers. She denied any fever, chills, nausea, vomiting, lightheadedness, or dizziness. Her past medical history revealed autism. She had a work-up for delayedonsetof puberty 2 yearsprior to this visit, which showed an advanced bone age and mildly enlarged muIticystic ovaries on ultrasound, but no other abnormalities. She uses no medications. Her physical examination revealed a weight of 221 pounds, blood pressure 116/62, pulse54, respirations 20. Head and neck exam was normal. Breastexam was Tanner stage III-IV. Abdomen was obese and non-tender with normal bowel sounds. Pelvic examination revealed normal external genitalia. Speculum showed some blood in the vault. Cervix was normal, bimanual exam showed a normal size uterus with no adnexal tenderness. Drs. Breech and Carpenter's comments:
multicystic ovaries, and the history of delayed puberty with an advanced bone age may be suggestive of hyperandrogenism. Hyperandrogenism can lead to anovulation and possible abnormal uterine bleeding . Obesity alone, as in this patient of 221 pounds, can be associated with anovulation. Congenital anomalies of the female reproductive tract may initially present with heavy vaginal bleeding due to trauma. Other uterine disorders may include malignant cervical lesions, which are extremely rare, or cervicitis from a sexually transmitted disease. which is quite common in a sexually active teenager. Pregnancy and pregnancy complications may be the cause of acute and heavy bleeding. Sexual abuse may also present with vaginal trauma and bleeding. An attempt should be made to ascertain the degree of blood loss. Pad counts, descriptions of pad saturation, the number of days of bleeding, and a history of lightheadedness or dizziness are all helpful. The physical exam should focus on vital signs, including orthostatic vital signs, dry mucous membranes. a pale hue to the skin, and decreased capillary refill in the extremities. Other clues include: petechiae or ecchymoses may indicate a coagulation disorder: hirsutism. virilization, or striae may suggest an endocrinopathy; visual changes may be present with central nervous system (CNS) tumors; or low body weight with villous hair growth may suggest an eating disorder. A thorough pelvic exam is imperative . An ultrasound can be performed if the examination is not adequate. Endocervical cultures for sexually transtnitted diseases (SID) may be obta ined during this exam . Rarely will an exam under anesthesia be necessary. Laboratory evaluation for acute menorrhagia in an adolescent should include a complete blood count. platelet count. prothrombin time, thromboplastin time, bleeding time, and a urine pregnancy test. Thyroid function may also be assessed with a TSH level. Clinical circumstances may dictate further evaluation with STD screening. a prolactin level, or serum androgen levels.
The most likely cause of abnormal uterine bleeding in adolescents is anovulation . Coagulation disorders should certainly be considered when abnormal bleeding occurs with the first menses. Previous retrospective reviews report that 19%-33% of young women admitted for dysfunctional uterine bleeding had a hematologic disease. 1.2 The studies also note the presence of numerous other chronic medical conditions in young women with abnormal bleeding. These disorders include thyroid disease, diabetes mellitus and endocrinopathies. Delayed puberty and menstrual disturbances may be seen in hypothyroidism: however, a delayed bone age is generally expected. The ultrasound, which demonstrated
Laboratory values revealed hemoglobin of 11.6 g1dl and a hematocrit of 34.6%, with similar values 6 hours later.
CI 1999North American Society for Pediatric and Adolescent Gynecology Published by Elsevier ScienceInc.
1083-3t881991$20.00 PII SI038·3188(99)OOO18·2
234
Management Quandary
Urine pregnancy test was negative. TSH, prolactin, PT, and PTT were in the normal range. Drs. Breech and Carpenter 's comments: At this time, there is no evidence of hypovolemia (hypotension or tachycardia) and no evidence of active hemorrhage on physical exam. Since the hematologic studies did not reveal any gross abnormalities, an outpatient regimen is appropriate. As demonstrated in a retrospectivereview of dysfunctionaluterine bleeding in adolescents by Falcone and others, most patients (72%) were started on an initial treatment plan consisting of combinationoral contraceptivepills (OCP) containing at least 35 meg of ethinyl estradiol administered several times daily.' A smaller percentage (37%) of patients received intravenousconjugated estrogens (25 mg every 4 hours) and hospitalization. In that review, vaginal bleeding stopped or decreased in 93% of patients regardless of which steroid therapy was utilized. Oral progesterone agents have also been utilized; however, they do not routinely abate the bleeding in acute menorrhagiaas quickly as estrogen containing agents.
The patient was started on an OCP taper but represented 24 hours later with severe bleeding. Her initial hemoglobin was 10.2 and a bleeding time was 5 minutes. The patient was admitted for Premarin I.V. treatment. Initially her bleeding slowed down and her blood values were stable for 12 hours. She then started to bleed heavier again. Drs. Breech and Carpenter's comments: The initial treatment plan appeared to have failed in this young woman. When she presentedthe second time with severe bleeding resistant to OCP's, the hemoglobinlevel had already decreased by more than one gmldl. Because of worsening anemia and bleeding resistant to medical therapy, immediate hospitalization is indicated. Intravenous hydration may be provided in addition to other medical therapy. A trial of intravenous conjugated estrogen is a reasonable next step. The patient's initial stabilization is certainly reassuring; however, the increase in vaginal bleeding some 12 hours later raises concerns regarding worsening anemia and adequate tissue perfusion. On initial exam, a normal pelvic exam is documented. In the setting of persistent resistance to hormonal management, a pelvic ultrasound is merited to rule out any intrauterine or adnexal pathology. Fluid management should be followed closely with hemoglobin, hematocrit, platelet, and coagulation studies. Levels of coagulationfactors may substantiallydrop, further compounding the bleeding situation. Packed red cells or blood product replacement may be necessary in emergent circumstances.
An ultrasound was performed. This revealed an endometrial lining of 5 mm and a 4-cm clear ovarian cyst. The patient continued to bleed heavily and her hemoglobin
dropped from 7.3 gldl to 4.0 gldl in the next 12 hours, despite Premarin and later added progesterone treatment. The patient received 2 units of packed red cells and she was taken to the operating room for evaluation and a dilation and curettage. Exam under anesthesia revealed a mobile small uterus that sounded to 6 em. Curettage revealed a moderate amount of tissue and the bleeding slowed down after that but did not stop. A Foley catheter was then placed in the uterus and inflated with 10 cc of saline. This slowed the bleeding down significantly . The catheter was left in place for two days and then slowly deflated and removed. The patient received a total of 4 units of packed red cells and a 6-pack of platelets. The patient was discharged after that in stable condition with hemoglobin of 10 gld!. Her discharge medications included Premarin and Provera. The pathology evaluation of the endometrium revealed proliferative phase endometrium. Drs. Breech and Carpenter 's comments: The acute menorrhagiain this adolescent was resistantto several hormonal regimens. In adolescents, a dilation and uterine curettage (D&C) has more recently been reserved for vaginal bleeding unresponsive to medical therapy. Smith and others reported 0/9 adolescents admitted for menorrhagia required a D&C from 1991 to 1995; however, 8/46 (17%) adolescent women underwent a D&C from 1979 to 1991 .2 In this case, the young woman continued to bleed with falling hemoglobin levels despite medical therapies. This situation became more serious, even life threatening, and required aggressive measures. Even uterine curettage did not produce adequate hemostasisand a mechanical measure, a Foley catheter, was necessary to achieve hemostasis. This may have been due to a secondary coagulopathy from acute blood loss and depletion of platelets and coagulation factors. This patient's history and later histology of the endometrium did not suggest an infectious component; however, some authors suggest empiric antibiotic therapy, especially in menorrhagiaresistant to hormonal therapy." A recent paper by Creatsas and others suggests an alternative therapy for menorrhagia in adolescents requiring hospitalization.P Forty-eight patients were randomized to receive 20 mg orally of tenoxicarn, a prostaglandin synthetase inhibitor, daily, or I tablet of lynestrenol-ethinyl estradiol (0.05 mg and 2.5 mg respectively). Twenty-three patients received tenoxicam and the remainder received the Iynestrenol-ethinyl estradiol combination. Less hospitalization and higher hemoglobin and hematocrit levels were seen in the tenoxicam group. Also, three D&C procedures and seven blood transfusions were necessary in the Iynestrenol-ethinyl estradiol group versus none in the tenoxicam group. The early data from this small group is promising for alternative treatment modalities that may avoid surgical instrumentation, especially in patients resistant to hormonal therapy. The pathology report from the endometrial curetting
Management Quandary showed proliferative endometrium consistent with anovulation. which is the most common cause of menorrhagia in adolescents," Some authors suggest that the risk of developing menorrhagia may be highest during the first few years after menarche because maturation of the hypothalamic pituitary ovarian (HPO) axis occurs slowly during adolescence.l" It is unknown at this time which adolescents may have slower maturation of the HPO axis. In this patient, the history of autism and developmental delay may suggest CNS problems that may affect the HPO axis. Continuation of hormonal management of the menstrual cycle would be advisable in this young woman. Cyclic progesterone withdrawal or OCp's would eliminate the risk of a persistent proliferative endometrium and acute menorrhagia.
Editor's Comments An unusual case of persistent anovulatory bleeding is presented. Two interesting points can be made. In the first place the use of ultrasound to measure endometrial thickness can guide our management. If the lining is thin. which is often the case after prolonged bleeding. estrogen therapy is usually successful. If the lining is thick and the patient does not respond to treatment. then adding early on a progestational agent may be very helpful. A second point about this case is the use of the foley catheter for the continued bleeding. In the literature this has been described mostly in obstetrics," but it can be
235
used in gynecology as well for tamponade of the uterine wall.
References I. Claessens EA. Cowell CA: Acute adolescent menorrhagia. Am J Obstet Gyncol 1981; 139:277 2. Smith YR. Quint EH, Hertzberg RB: Menorrhagia in adolescents requiring hospitalization. J Pediatr Adolesc Gynecol 1998; II: 13 3. Falcone T, Desjardins C, Bourque J, Granger L. Hemmings R. Quiros E: Dysfunctional uterine bleeding in adolescents. J Reprod Med 1994; 39:761 4. Pittaway DE, Deaton JL: Abnormal uterine bleeding. In: Pediatric and Adolescent Gynecology. Edited by SEK Carpenter, JA Rock. New York. Raven Press. Ltd., 1992: pp 189-204 5. Creatsas G. Cardamakis E. Deligeoroglou E, Hassan E. Tzingounis V: Tenoxicam versus Iynestrenol-ethinyl estradiol treatment of dysfunctional uterine bleeding cases during adolescence. J Pediatr Adolesc Gynecol 1998; II: 177 6. LeMarchand-Beraud T, Zufferey M, Reymond M, et al: Maturation of the hypothalarnic-pituitary-ovarian axis in adolescent girls. J Clin Endocrinol Metab 1982; 54:241 7. De Loor JA. van Dam PA: Foley catheters for uncontrollable obstetric or gynecologic hemorrhage. Ob Gyn 1996; 88:737