Volume Number
Communications
128 6
P. C.. a 26-year-old white woman, had menarche at 11 years of age and normal development of secondary sexual characteristics. She had two consecutive menses and then no spontaneous flows until the present time. At 14 years of age she developed galactorrhea; otherwise, her health was fine. We initially saw her at 20 years of age. General physical examination was within normal limits. Neurological examination was normal with intact sense of smell. The pelvis was normal except for a hypoplastic uterus. Bilateral galactorrhea was present. Vaginal hormonal smear showed a moderate estrogen deficiency. Plasma luteinizing hormone (LH) was 4.0 m1.U. per milliliter, and serum thyroxine was in the normal range. A 24 hour urine determination of 17-ketosteroids and 17-hydroxycorticosteroids revealed both to be normal at 10.8 and 4.4 mg., respectively. Total urinary gonadotropins were less than 6 rat units per 24 hours. The karyotype was 46, XX. Tomograms ol‘ the sella turcica revealed the volume to be normal at 1.8 c.c., but the width of the pituitary fossa was definitely increased (22 mm.). Anteroposterior diameter was 16 mm., while depth was 11 mm. Pneumoencephalogram failed to reveal a mass lesion, but herniation of the subarachnoid cystern into the pituitary fossa was demonstrated, indicative of an empty sella. Electroencephalogram revealed a generalized grade II dysrhythmia. The patient was examined annually. At 24 years of age a repeat skull x-ray showed the pituitary fossa to be slightly larger with the suggestion of a double floor. Plasma LH was now nondemonstrable. The patient elected not to have a second pneumoencephalogram. She still has amenorrheagalactorrhea, and there has been no further change in the sella turcica. P. A. C., a 29-year-old woman with a history of postpartum amenorrhea-galactorrhea since 19 years of age, developed a thyroid adenoma at 21 years of age. This was removed and she was subsequently found to be hypothyroid. With Synthroid, 0.2 mg. daily, amenorrhea persisted and the spontaneous galactorrhea ceased, but milk was still expressable. Skull x-ray at 24 years of age revealed deepening of the floor of the sella turcica without detectable erosion. Four years later, a repeat skull x-ray showed demineralization of the posterior floor and posterior clinoids of the sella turcica, with an apparent double floor on the lateral view. Tomograms confirmed asymmetric enlargement of the pituitary fossa. Because of this change in x-ray findings, the patient was admitted for further studies. No abnormalities were found on physical examination. Endocrine studies revealed normal triiodothyronine uptake of 37.8 and thyroxine of 6.8 with 0.2 mg. of Synthroicl daily. Plasma cortisol levels at 8 A.M. and 4 P.M. were subnormal at 5.5 and 3.0 pg per cent, respectively. 17-Hydroxycorticosteroids were normal at 4.6 mg. per 24 hours of urine while the 17-ketosteroids were top normal at 14.9 mg. per 24 hours of urine. Base-line human growth hormone was 3.8 ng. per milliliter, and this increased to 24 ng. per milliliter following Inderalglucagon stimulation. Base-line LH was undetected but increased to 21 m1.U. per milliliter 30 minutes after a bolus injection of 100 cLg of the gonadotropin-releasing hormone. Serum prolactin was increased at 62.5 pg. per milliliter. Pancerebral arteriogram failed to reveal any space-occupying lesions. Pneumoencephalogram was negative for intrasellar or suprasellar mass. but the hanging-head tomogram revealed a collection of air in the pituitary fossa, indica-
in brief
689
tive of an empty sella or intrasellar extension of the subarachnoid space. Once again, a double floor of sella due to depression of the pituitary fossa was noted. Significant
endocrinopathy
associated
with
the
pri-
mary empty-sella syndrome is uncommon. Minor abnormalities of growth hormone and adrenocorticotropic hormone have been rep0rted.l There is a case report of empty sella with persistent lactation following pregnancy with normal base-line prolactin but a subnormal prolactin response to thyrotropin-releasing hormone.* However, amenorrhea-galactorrhea associated with the empty-sella syndrome is not a well-known clinical entity. We have seen this association in several patients, but the question arises as to whether this is a chance association or a cause-and-effect relationship. The two cases presented here were selected because they demonstrated progressive sellar enlargement and clinoid erosion with an irregular sella floor, thus being very suggestive of a pituitary tumor. In Case 2, serum prolactin was also elevated. Nevertheless, no tumor was demonstrated, and an empty sella was found. These cases emphasize that despite significant endocrine dysfunction and demonstration of progressive sellar pathology one still cannot rule out the emptysella syndrome. Therefore, a pneumoencephalogram must always be obtained before treatment with radiation therapy or operation. REFERENCES
1. Caplan, R. H., and Dobben, G. D.: Endocrine studies in patients with the “empty sella syndrome,” Arch. Intern. Med. 123: 611, 1969. 2. Gates, R. B., Friesen, H., and Samaan, N. A.: Inappropriate lactation and amenorrhea: Pathological and diagnostic considerations, Acta Endocrinol. 72: 101, 1973.
Uterine rupture following midtrimester abortion by laminaria, prostaglandin Fza, and oxytocin: Report of two cases DIRK PHILLIP JOAN JAMES
PROPPING, G.
M.D. STUBBLEFIELD,
GOLUB, ZUCKERMAN,
M.D.
M.D. M.D.
Department of Obstetrics and Gynecology, Women, Boston, Massachusetts
Boston Hospital
for
MIDTRIMESTER ABORTION byintra-amnioticprostaglandin Fza (PGF,,)* has become increasingly common in the United States and may supplant hypertonic Reprint requests: Dr. Phillip G. Stubblefield, Boston Hospital for Women, 221 Longwood Ave., Boston, Massachusetts 02115. *Purchased from The Upjohn Co., Kalamazoo, Michigan.
690
Communications
in brief
July 15, 1977 Am. .J. Obstet
saline as a safer method. However, posterior cervical rupture has been reported with abortion by PGF,, in young, primigravid women.’ To reduce the incidence of cervical rupture, we have used laminaria tents to achieve cervical softening and dilatation before prostaglandin abortion.’ Our practice has been to use high-dose oxytocin administered by intravenous infusion pump in those cases where rupture of the membranes is not followed by fetal delivery within a few hours. Recently, we have had two cases of intra-abdominal uterine rupture occurring in older women of high parity while receiving oxytocin infusion many hours after prostaglandin injection. In Case 1, a 37-year-old woman, gravida 6, para 3, abortuses 3, was admitted for elective abortion at 18 weeks’ gestation. One 5 mm. laminaria tent was inserted into the cervix. The next morning, this was removed, and 40 mg. of PGF,, was given by amnioinfusion. At 15 hours after infusion, spontaneous rupture of the membranes occurred. An hour later. oxytocin was begun by intravenous infusion pump (120 mL’. per minute). At 27 hours, the infusion pump was stopped for a two-hour rest, as is our protocol. Oxytocin was again resumed (24 mU. per minute). At 29 hours after PCF,, infusion, the patient began to complain of dyspnea, shoulder pain, and extreme abdominal pain. At laparotomy. the fetus and placenta were found to he lying in the cul-de-sac and extruding through a 5 cm. vertical rupture of the lower posterior wall of the uterus. A total abdominal hysterectomy was performed. In Case 2, a 34-year-old woman, gravida 5, para 4, was
admitted at 18 weeks’ gestation for therapeutic
abortion be-
cause of depression. Laminaria insertion and amnioinfusion of PGF,, were the same as in Case 1. Twenty-five hours after PGF,, infusion, the membranes ruptured and palpable uterine contractions ceased. At 28 hours, intravenous oxytotin was begun by infusion pump, gradually increased to 120 mU. per minute. At 38 hours, the infusion was stopped for a two-hour rest. Inadvertently, the oxytocin was not restarted until 46 hours. At 50 hours, the patient’s temperature was 101 degrees. After blood culture and cervical cultures were obtained. intravenous ampicillin was started. The oxytocin infllsion rate was increased from 120 to 240 mU. per minute with the patient’s physician in constant attendance. At 52 hours, fetal delivery began. The placenta was extracted with ovum forceps in our treatment room, and, when bleeding continued, curettage was performed with the use of general anesthesia. Bleeding continued and laparotomy revealed a large left broad ligament hematoma and a long left lateral tear of the lower uterine segment. Abdominal hysterectomy and left salpingo-oophorectomy were performed. The postoperative course of both patients was uneventful.
Posterior cervical rupture in the young primigravid woman may occur as a result of failure of an inelastic external OS to dilate, while the internal OS has opened and allowed transmission of intrauterine pressure to the cervix.’ In the cases reported here, uterine rupture occurred above the peritoneal reflection as is the usual case with
Gyrxd.
uterine rupture in the third trimester. We suggest that the use of oxytocin after prostaglandin f&r midtrimester abortion mimics the situation at term and that the grand multiparous patient must be considered at significant risk if this treatment is used. Thus, two classes of patients appear to be in jeopardy when abortion is induced by intra-amniotic PGF,,: the young primigravid woman at risk for cervical rupture and the older multiparous woman at risk for uterine rupture whrn high-dose oxytocin is added after prostaglandin rreatment. The risk of cervical rupture can be markedly reduced by pretreatment with laminaria tents placed the night before the PGF,, infusion. In 1.400 consecutive abortions performed with this technique, we have had only three cervical ruptures. This is markedly less than the 1 to IO per cent incidence other> have reported. The management of the second c lass of patient remains problematic. We feel that the safest course continues to be the use of’oxytotin
by irttravc‘nous
infusion
pump
at the
lorvcst
rate
that will produce contractions. When intrauterine sepsis seems to be beginninl: following this regimen, we have been able to empty the uterus safely by extraction and currttagc. REFERENCES
I. WentL,
A. C., Thompson, B. H., and King, ‘I‘. M.: Posterior cervical rupture following prostaglandin-induced midtrimester abortion, Am. ,J. Obstet. Gynecol. 115: 1107, 1973. 2. Stuhblefield. P. G., Naftolin, F.. Frigoletto, F., and Ryan, K. .J.: Laminaria augmentation of intra-amniotic PGF,, for midtrimester pregnancy termination, Prost.aglandins 10: 413, 197.5.
Epidemiologic sweillance during a clinical trial of antibiotic prophylaxis in pelvic surgery JOHN
H.
RUTH
I,.
WALTER Departmrnt and Public Gynecologp Connrctirztt
GROSSMAN ADAMS, J.
III,
M.D.
B.S.
HIERHOLZER,
JR.,
M.D
c~/‘lntrmal M~dicmr, Department of Epidemiology H&h, and Department of Obstetrics and Yak Uui~wGty School of Medicinr, NPW Haven,
CONCERNING intramural useofprophylactic antibiotics in pelvic surgery are being formulated by many gynecologic services. It is becoming apparent that therapeutic decisions in this regard cannot be equated solely with the prevention of febrile morbidity. One must consider the potential risks of cliliicalIy POLICIES
Reprint requests: Dr. Walter of Internal Iowa. Iowa
Medicine, City. Iowa
College 52242.
J.
Hierholzer, Jr., Department of
Medicine.
University
of