Spontaneous uterine rupture caused by placenta percreta.
- [Show abstract] [Hide abstract]
ABSTRACT: Two cases of placenta pecreta confirmed histologically were treated conservatively with retention of the uterus. Both later went on to have successful pregnancies.European Journal of Obstetrics & Gynecology and Reproductive Biology 01/2002; 100(1):112-5. · 1.84 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: A case of placenta percreta invading the posterior wall of the bladder caused dysuria, frequency and hematuria. The patient had had four previous Caesarean sections.The Journal of obstetrics and gynaecology of the British Commonwealth 01/1971; 77(12):1142-3.
- British Journal of Obstetrics and Gynaecology 06/1983; 90(5):491-3.
13 April 1968
Considerable variation was found from case to case in the pro-
portion of cells containing glycogen.
Weak P.A.S. positivity was significantly related to short first
tained remission and survival, high initial peripheral blood
blast count, and short duration of symptoms at the time of
diagnosis. The results suggest that P.A.S. positivity is inversely
related to the rate of progression of lymphoblastic leukaea.
Furthr work is being carried out to elucidate this finding.
I would like to thank Dr. M. L. N. Willoughby, consultant
haeatologist, Royal Hospital for Sick Children, Glasgow, for his
advice in the preparation of this paper and Dr. F. G. J. Hayhoe,
Department of Medicine, University of Cambridge, for critiism
and useful suggestions.
of Professor J. H. Hutchison and Drs. R. A. Shanks, D. H. Wallace,
G. C. Ameil, J. 0. Craig, E. N. Coleman, W. Hamilton, and
J. A. Inall, under whose care these patients were admitted.
cytochemical tests were performed by Mr. F. G. Jewell. This work
I also wish to acknowledge the co-operation
has been supported by a grant from the Leukaemia Research Fund
H. C. LAURIE, M.B., GCHD.
Department of Haematology,
Royal Hospital for Sick Children,
Acute Leukaemia Group B (1963). Blood, 21, 699.
Astaldi, G., and Verga, L. (1957). Acta haemat. (Basel), 17, 129.
Bjornberg, 0. (1963). Acaa med. scand., 173, 451.
Hardisty, R. MA, and Norman, P. M. (1967).
Hayhoe, P. G.I.,Quaglino
med. Res. Coun. (LoM)4 No. 304.
Nagao, T. (1966). Acta paediau. 7ap. overseas ed., 8, No. 16, 86.
Quaglino, D., and Hayhoc, P. G.J. (1959). 7. Path. Bact., 78, 521.
Saunders, E. F., Lampkin, B. C., and Mauer, A. M. (1967).
Invest., 46, 1356.
Willoughby, MA L. N., and Laurie, H. C. (1968). Arch. Dis. Childh.,
Zuelzer, W. W. (1964). Blood, 24, 477.
Arch. Dis. Childh., 42,
D., and Doll, R. (1964). Spec. Rep. Ser.
Spontaneous Uterine Rupture Caused
by Placenta Percreta
Brit, med.J., 1968,2, 97-98
Placenta accreta is the abnormal adherenge of the chorionic
vili to the myometrium, and is associated with partial or com-
plete absence of the decidua basalis, and in particular the
stratum spongiosum (Phaneuf, 1933; Kistner et a., 1952).
Three degrees are recognized, according to the extent of tropho-
Placenta accreta vera is the term applied
when villi are in juxtaposition with the myomeium.
placenta increta the villi partially penetrate the myomium.
Placenta percreta indicates that the villi have invaded the full
hickess of myometnum to or through the serosa of the
uterus, causing incomplete or complete uterine rupture respec-
Spontaneous rupture of the uterus due to placenta percreta
is one of the most urgent obstetrical catastrophes, resulting
in rapid exsanguination and high mortality in spite of prompt
anti-shock therapy and massive blood transfusion.
Sumawong et al. (1966) found 30 cases of rupture caused by
placenta percreta and added three cases of their own. A search
of the literature has revealed only three previous reports of
spontaneous rupture due to placenta accreta concomitant with
placenta praevia (Bakanow, 1928; Callender and King, 1949;
Malkasian and Welch, 1964). The last of these was a case of
placenta praevia percreta.
This paper describes two cases of spontaneous uterine
rupture due to placenta percreta, one of which was associated
with placenta praevia. As pointed out by Rotton and Friedman
(1957), the necessity for expeditious therapy when this condi-
tion is encountered makes imperative its clinical recoiion
In a review
A 36-year-old multipara was admitted to hospital as an emer-
gency case on 14 July 1966 in a state of collapse.
stated that she had her last menstrual period six months previously.
She had been well until five hours before admission, when she experi-
enced a continuous pain in her right shoulder while in bed.
soon developed a lancinating pain under the left costal margin and
fainting attacks. No vaginal bleeding or discharge occurred.
Her three previous pregnancies, labours, and puerperia were
Her youngest child was 2* years old.
had no previous illnesses or operations.
General examination revealed a state of shock.
was 97.6° F. (36.4° C.), pulse barely perceptible at 136 a minute,
and respiration was sighing and shallow; the blood pressure was
Gross pallor of the mucous membrane was present.
On abdominal examination there was marked distension with free
fluid.Generalized tenderness and guarding were elicited, and, apart
from uterine enlargement consistent with a 26-week gestation, no
other abnormality was detected.
Vaginal examination was not contributory.
Intraperitoneal haemorrhage due to rupture of the uterus, rupture
of the spleen or its blood vessels, and extrauterine pregnancy, in
that order, were considered in the differential diagnosis.
Investigations.-Full blood count showed a haemoglobin of 28%
Haldane, and an acute pot-haemorrhagic anaemia.
fibrinogen level was 285 mg./100 ml.
On admission resuscitation was begun with intravenous fluids,
morphine hydrochloride, metaraminol
cortisone, oxygen, and compatible group B rhesus-positive blood
as soon as the latter became available.
After an infusion of 2.500 ml. of blood the systolic pressure was
audible at 80 mm. Hg and the pulse improved to about 110 a
While she was being transferred to the operating-theatre
the blood pressure dropped to nil.
were simultaneously given under pressure and the necessary calcium
gluconate was administered.
Some improvement in the patient's
condition occurred and it was decided to proceed with immediate
The peritoneal cavity contained about 2,000 ml. of blood and
The uterus was consistent with a 26-week gestation.
uterine fundus was perforated by placental tissue (see Fig.) and
bleeding was occurring from that site.
Both Fallopian tubes and ovaries were normal
Haemostasis was secured and the abdomen sutured
The eighth litre of blood was being given at the con-
clusion of the operation when cardiac arrest suddenly occurred.
With the endotracheal tube still in situ the lungs were ventilated
and immediate external cardiac massage was performed.
failed to maintain an adequate circulation, left anterior thoracotomy
through the fourth intercostal space was performed and direct cardiac
massage resulted in the return of a regular heart beat.
and respiration were maintained for two and a quarter hours, when
arrest of the heart again occurred.
were of no avail.
This was followed by progressive weakness and
The foetal heart was not audible.
tartrate (Aramine), hydro-
The next two bottles of blood
Total hysterectomy was
All measures at resuscitation
13 April 1968Medical Memoranda
Post-mortem examination showed pallor of the organs.
was due to haemorrhage caused by complete rupture of the uterus.
histological section of the uterus confirmed a complete placenta
accreta and a 3-cm. fundal rupture due to placenta percreta.
stidlbirth was normal in all other respects and corresponded to its
reriod of gestation.
There was no evidence of any other uterine
Abnormality or amniotic fluid embolism.
CASE 1-Postoperative specimen showing perforation of the
placenta in situ.
A 30-year-old multipara was first seen at the antenatal clinic
when 16 weeks pregnant.
She had had four previous normal con-
finements followed by a lower segment caesarean section for central
placenta praevia at 37 weeks in November 1965.
Pregnancy progressed satisfactorily until the 37th week.
was advised to enter hospital at the 38th week to await the onset
of labour.Five days later, on 8 August 1967, however, she was
admitted to the labour ward with a history of severe lower abdominal
pain for nine hours followed by vaginal bleeding five hours later.
On examination there were no signs of circulatory collapse.
uterine fundus corresponded to a 38-week gestation, with the non-
engaged vertex presenting at the pelvic brim.
rate was 168 per minute.There was pronounced tenderness over
the lower uterine segment.
Rupture of a previous caesarean scar
was diagnosed and immediate preparations for laparotomy were
Investigations.-The haemoglobin was 67% Haldane and the
differential blood count was within normal limits.
was 155 mg./100 ml. Her blood group was 0 rhesus-positive;
Wassermann reaction and Kahn test were negative.
Profuse vaginal bleeding occurred prior to laparotomy.
blood was not present in the peritoneal cavity.
evident beneath the intact uterovesical peritoneum and into the left
broad ligament. The uterovesical fold was opened.
presented through a 4-cm. rupture of the previous caesarean scar.
The lower segment was opened by extending the rupture with scissors.
The placenta was firmly adherent to the region of the scar and
could not be digitally separated.
asphyxiated male infant delivered.
the placental margin and the torn uterine vessels on the
Manual removal failed owing to morbid adherence of half of the
Total hysterectomy with conservation of both Fallopian
tubes and ovaries was carried out. A total of 4 litres of blood was
given before, during, and after the operation.
period was complicated by ileus, complete recovery from which
Regular respiration was established in the infant in four minutes
Mother and baby were discharged on the 10th day.
Histopathological Report.-The operation specimen showed a
rupture in relation to a transverse lower segment caesarean scar.
The foetal heart
The placenta was incised and an
Bleeding occurred freely from
The myometrium underlying the placenta was half
The greater part of the placenta was intertwined with
the myometrium and at the rupture site penetrated its entire thick-
The microscopical features confirmed placenta percreta.
The incidence of placenta accreta is variously reported from
At this hospital five microscopically proved
cases occurred among 11,532 deliveries over two years, an
incidence of 1 in 2,306.
In Case 1 the condition probably resulted as a consequence
of chronic hypoxia, because all other known associated factors
were excluded clinically and pathologically.
fibrinoid transformation is a striking feature of hydatidiform
mole and chorionepithelioma (BidirAu and Gavrilii, 1967).
The diagnosis of placenta accreta may be suspected during
the third stage of labour when manual removal is attempted,
or before the third stage in the case of placenta percreta.
definitive diagnosis can be made only on microscopical evidence.
Placenta accreta may be complicated by severe haemorrhage,
sepsis, inversion of the uterus, placenta praevia (Kistner et at.,
1952), or rupture of the uterus and hypofibrinogenaemia
(Koren et al., 1961).
The association between rupture of the
uterus and hypofibrinogenaemia has been previously reported
The mortality after attempted manual removal of an accretic
placenta is 64.5% (Irving and Hertig, 1937), as a consequence
of uncontrollable haemorrhage, traumatic rupture, and inver-
sion of the uterus caused by such attempts.
removal and hysterectomy showed a 20%
hysterectomy with no attempt at manual removal resulted in
When the adherent placenta was left in situ
hysterectomy with no attempt at manual removal.
exception is the primipara with a focal placenta accreta, when
conservative treatment is followed.
1,956 (Irving and Hertig, 1937) to none in 80,000
In Case 2 the
Clearly, the treatment of choice is total
ABu M. HASSIM, M.B., B.CH., B.SC., M.R.C.O.G.,
Consultant Obstetrician and Gynaecologist.
CYNTHIA LUCAS, M.B., B.S., M.R.C.O.G.,
Assistant Obstetrician and Gynaecologist.
S. A. M. ELKABBANI, M.B., CH.B.,
Lusaka Central Hospital, Zambia.
Bfdlriu, L., and GavrilitA, L. (1967). Amer. 7. Obstet. Gynec., 98, 252.
Bakanow (1928). Zbl. Gynak., 52, 2159.
Callender, C. G., and King, E. L. (1949). Amer. 7. Obstet. Gynec., 57,
Eastman, N. J. (1954).
Hassim, A. M. (1967).
Irving, F. C., and Hertig, A. T. (1937). Surg. Gynec. Obstet., 64, 178.
Kismer, R. W., Herdg, A. T., and Reid, D. E. (1952).
Obstez., 94, 141.
Koren, Z., Zuckerman, H., and Brzezinski, A. (1961). Obstet. and Gynec.,
Malkasian, G. D., and Welch, J. S. (1964). Obstet. and Gynec., 24, 298.
Phaneuf, L. E. (1933). Surg. Gynec. Obstet., 57, 343.
Rotton, W. N., and Friedman, E. A. (1957). Obstet. and Gynec., 9, 580.
Sumawong, V., Nondasuta, A., Thanapath, S., and Budthimedhee, V.
Obstet. gynec. Surv., 9, 514.
7. Obstet. Gynaec. Brit. Cwlth, 74, 303.
Obstet. and Gynec., 27, 511.