acute puerperal uterine inversion

3
IMAGES IN FORENSICS Acute puerperal uterine inversion Yoko Ihama Maki Fukasawa Kenji Ninomiya Tetsuji Miyazaki Accepted: 21 November 2013 Ó Springer Science+Business Media New York 2013 Case Report A gravida 3, para 2, 42-year-old woman was admitted to a hospital for induced labor at 38 weeks and 3 days gesta- tion. Twelve hours after an intravenous infusion of pros- taglandin E2 as an oxytocic agent, a healthy female baby weighing 3.41 kg was spontaneously delivered. Placental delivery was prolonged; therefore, an obstetrician manually removed the placenta 1 h after childbirth. Blood loss was estimated to be 700 ml at the time of placental delivery. Vaginal bleeding continued, and the patient’s blood pres- sure was noted to be 60/48 mmHg with a heart rate of 144 beats/min 30 min after the placental delivery. Although a vasopressor and volume expander fluid (Hespander Ò ) were administered intravenously, the patient’s state of shock persisted. Blood transfusion was initiated 9 h after child- birth when the total blood loss exceeded 2,500 ml. Nev- ertheless, the patient gradually lost consciousness as vaginal bleeding persisted. Uterine inversion was detected by ultrasonography and the total blood loss was estimated to be 3,550 ml 12 h after childbirth. She was immediately transferred to an emergency department, but experienced cardiopulmonary arrest in the ambulance. The patient died of hemorrhagic shock 15 h after childbirth. The decedent was 170 cm tall and weighed 63 kg. At the medico-legal autopsy, there was very slight postmortem hypostasis on the back. Abdominal palpation revealed that the uterine fundus was approximately 5 cm below the umbilicus, but the crater-like depression of the fundus was not clear. The external genitalia had some edema from the vaginal birth, but there was no injury to the perineum or birth canal. A large number of blood clots were present in the vagina. Vaginal palpation revealed that the fundal endometrium was exposed through the cervix. External examination revealed no injuries except those from clinical procedures. There was 700 ml of reddish ascites but no bleeding in the abdominal and pelvic cavity. The uterine fundus had a crater-like depression, which was 9.5 cm in depth (Fig. 1). The bilateral fallopian tubes and right ovarian artery were caught in this depression. The removed uterus weighed 1,080 g. The cervix was extended by the inverted fundus, and the fundal endometrium was exposed widely through the cervix (Fig. 2). The uterine cavity had 730 ml of clots and had become narrow because of fundus inversion. The endometrium showed no sign of placental retention or injury. The heart weighed 350 g, and slight bleeding was noted on the outflow tract of the left ventricle. The left and right lungs weighed 960 and 1,030 g, respectively, and severe edema was seen in the bilateral lungs. Macroscopic and microscopic examination of the lungs did not reveal pulmonary thromboembolism or amniotic fluid embolism. We concluded that the patient died of puerperal bleeding caused by uterine inversion after vaginal childbirth. Discussion Uterine inversion occurs when the uterus inverts and the uterine fundus prolapses to or through the dilated cervix. Although the precise cause is unknown, the cause of acute uterine inversion is usually reported as mismanagement of the third stage of labor, with premature traction on the umbilical cord and/or the buildup of fundal pressure before Y. Ihama (&) Á M. Fukasawa Á K. Ninomiya Á T. Miyazaki Department of Legal Medicine, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan e-mail: [email protected] 123 Forensic Sci Med Pathol DOI 10.1007/s12024-013-9517-4

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Page 1: Acute puerperal uterine inversion

IMAGES IN FORENSICS

Acute puerperal uterine inversion

Yoko Ihama • Maki Fukasawa • Kenji Ninomiya •

Tetsuji Miyazaki

Accepted: 21 November 2013

� Springer Science+Business Media New York 2013

Case Report

A gravida 3, para 2, 42-year-old woman was admitted to a

hospital for induced labor at 38 weeks and 3 days gesta-

tion. Twelve hours after an intravenous infusion of pros-

taglandin E2 as an oxytocic agent, a healthy female baby

weighing 3.41 kg was spontaneously delivered. Placental

delivery was prolonged; therefore, an obstetrician manually

removed the placenta 1 h after childbirth. Blood loss was

estimated to be 700 ml at the time of placental delivery.

Vaginal bleeding continued, and the patient’s blood pres-

sure was noted to be 60/48 mmHg with a heart rate of 144

beats/min 30 min after the placental delivery. Although a

vasopressor and volume expander fluid (Hespander�) were

administered intravenously, the patient’s state of shock

persisted. Blood transfusion was initiated 9 h after child-

birth when the total blood loss exceeded 2,500 ml. Nev-

ertheless, the patient gradually lost consciousness as

vaginal bleeding persisted. Uterine inversion was detected

by ultrasonography and the total blood loss was estimated

to be 3,550 ml 12 h after childbirth. She was immediately

transferred to an emergency department, but experienced

cardiopulmonary arrest in the ambulance. The patient died

of hemorrhagic shock 15 h after childbirth.

The decedent was 170 cm tall and weighed 63 kg. At

the medico-legal autopsy, there was very slight postmortem

hypostasis on the back. Abdominal palpation revealed that

the uterine fundus was approximately 5 cm below the

umbilicus, but the crater-like depression of the fundus was

not clear. The external genitalia had some edema from the

vaginal birth, but there was no injury to the perineum or

birth canal. A large number of blood clots were present in

the vagina. Vaginal palpation revealed that the fundal

endometrium was exposed through the cervix. External

examination revealed no injuries except those from clinical

procedures. There was 700 ml of reddish ascites but no

bleeding in the abdominal and pelvic cavity. The uterine

fundus had a crater-like depression, which was 9.5 cm in

depth (Fig. 1). The bilateral fallopian tubes and right

ovarian artery were caught in this depression. The removed

uterus weighed 1,080 g. The cervix was extended by the

inverted fundus, and the fundal endometrium was exposed

widely through the cervix (Fig. 2). The uterine cavity had

730 ml of clots and had become narrow because of fundus

inversion. The endometrium showed no sign of placental

retention or injury. The heart weighed 350 g, and slight

bleeding was noted on the outflow tract of the left ventricle.

The left and right lungs weighed 960 and 1,030 g,

respectively, and severe edema was seen in the bilateral

lungs. Macroscopic and microscopic examination of the

lungs did not reveal pulmonary thromboembolism or

amniotic fluid embolism. We concluded that the patient

died of puerperal bleeding caused by uterine inversion after

vaginal childbirth.

Discussion

Uterine inversion occurs when the uterus inverts and the

uterine fundus prolapses to or through the dilated cervix.

Although the precise cause is unknown, the cause of acute

uterine inversion is usually reported as mismanagement of

the third stage of labor, with premature traction on the

umbilical cord and/or the buildup of fundal pressure before

Y. Ihama (&) � M. Fukasawa � K. Ninomiya � T. Miyazaki

Department of Legal Medicine, Graduate School of Medicine,

University of the Ryukyus, 207 Uehara, Nishihara,

Okinawa 903-0215, Japan

e-mail: [email protected]

123

Forensic Sci Med Pathol

DOI 10.1007/s12024-013-9517-4

Page 2: Acute puerperal uterine inversion

separation of the placenta [1, 2]. Uterine inversion is rare,

but it is a life-threatening and unpredictable obstetric

emergency. If acute uterine inversion goes unrecognized

and is not appropriately managed, it results in severe

hemorrhage and shock leading to maternal death. Mortality

from uterine inversion has been reported to be as high as

15 % [3]. Uterine inversions can be classified according to

the period between onset and delivery: acute inversion

occurs within 24 h of delivery; subacute inversion occurs

between 24 h and 1 month after delivery; and chronic

inversion occurs [1 month after delivery [1, 4, 5]. Fur-

thermore, uterine inversions can be classified by severity as

(1) incomplete, in which the fundus descends but does not

extend through the cervix; (2) complete, where the fundus

descends through the external cervical os but not to the

vaginal introitus; and (3) prolapsed, where the fundus

extends to or through the vaginal atony [4]. Puerperal

uterine inversion leads to severe postpartum bleeding

because the invaginated fundus in the uterine cavity

obstructs uterine contraction after delivery. Furthermore,

the inverted endometrium is stretched, which exacerbates

the bleeding from the mucosa site of placental separation.

This decedent had an acute and complete uterine

inversion. We assumed that manual placental delivery was

the primary cause of uterine inversion. Although an

autopsy revealed no placenta accreta, prolongation of pla-

cental delivery might indicate abnormal placental separa-

tion. This potential defect in placental separation may have

led to excess traction on the fundus at the time of manual

removal of the placenta. We do not believe that there was

serious fault in the placental delivery procedure even if the

manual placental delivery led to the patient’s uterine

inversion, because there are always some risks of uterine

inversion during vaginal delivery. On the other hand, in

this case uterine inversion was not diagnosed until 12 h

after childbirth, in spite of obvious massive vaginal

bleeding and shock. The patient’s life may have been saved

if a basic inspection, such as vaginal examination or vag-

inal ultrasonography, had been performed at an early stage.

The first treatment priorities for uterine inversion are

rapid diagnosis and adequate treatment [4]. Diagnosis is

made by abdominal and vaginal palpation; further colpos-

copy and vaginal ultrasonography are also effective [6].

The standard treatment for uterine inversion is rapid fundal

repositioning and management of postpartum hemorrhage.

The primary approach immediately after uterine inversion

is manual repositioning by vaginal manipulation, which

involves resetting uterine inversion by pushing up on the

fundus with the palm and fingers [6]. If initial attempts fail,

surgical intervention is required. The most commonly

described abdominal procedure is the Huntington tech-

nique. If these approaches are unsuccessful, lifesaving total

hysterectomy is the final option [1].

Obstetric hemorrhage is considered the leading cause of

maternal mortality worldwide, accounting for 25–30 % of

all maternal deaths, with an estimated 140,000 women

dying annually from this complication [7, 8]. In Japan,

obstetric hemorrhage is the highest cause of maternal death

and accounts for 22–40 % of all maternal deaths [9].

Consequently, the prevention of death by obstetric bleeding

is a key factor in reducing overall maternal mortality.

Puerperal bleeding often leads to massive hemorrhage

caused by the increased blood flow around the uterus,

which can cause hemorrhagic shock. Furthermore, patients

in obstetric shock immediately develop disseminated

intravascular coagulation because of the excessive activa-

tion of the coagulation system. In terms of maternal

bleeding, it is essential to recognize abnormal bleeding

Fig. 1 A crater-like depression in the uterine fundus 9.5 cm in depth,

viewed from above. Bilateral fallopian tubes and the left ovarian

artery were dragged into the depression (arrows)

Fig. 2 Inverted endometrium of the fundus was exposed through the

external cervical os

Forensic Sci Med Pathol

123

Page 3: Acute puerperal uterine inversion

during the early stages to promptly diagnose the cause of

bleeding and administer appropriate treatment. Clarifying

the causes of maternal death should be the focus of forensic

pathologists and, therefore, it is desirable for forensic

pathologists to have knowledge of all lethal obstetric

diseases.

References

1. Achanna S, Mohamed Z, Krishnan M. Puerperal uterine inversion:

a report of four cases. J Obstet Gynaecol Res. 2006;32:341–5.

2. Baskett TF. Acute uterine inversion: a review of 40 cases. J Obstet

Gynaecol Can. 2002;24:953–6.

3. Mondal PC, Ghosh D, Santra D, Majhi AK, Mondal A, Dasgupta

S. Role of Hayman technique and its modification in recurrent

puerperal uterine inversion. J Obstet Gynaecol Res. 2012;38:

438–41.

4. Mirza FG, Gaddipati S. Obstetric emergencies. Semin Perinatol.

2009;33:97–103.

5. Shirota K, Ota T, Tsujioka H, Miyamoto S. Uterine inversion due

to a leiomyoma on postpartum day 41: a case report. J Obstet

Gynaecol Res. 2011;37:897–900.

6. Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Gilstrap L,

Wenstrom KD (2005) Inversion of the uterus: Section VII

Obstetrical complications 35. Obstetrical hemorrhage. In: Wil-

liams Obstetrics. 22nd ed. New York: Mc-Graw-Hill, pp 833–834.

7. Oyelese Y, Ananth CV. Postpartum hemorrhage: epidemiology,

risk factors, and causes. Clin Obstet Gynecol. 2010;53:147–56.

8. Walfish M, Neuman A, Wlody D. Maternal haemorrhage. Br J

Anaesth. 2009;103:i47–56.

9. Suzuki Y, Ikeda T. Current situation of maternal deaths. Obstet

Gynecol. 2011;78:155–61 (in Japanese).

Forensic Sci Med Pathol

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