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Maternal hydramnios and congenital anomalies of the central nervous system
“poor risk.” ful pregnancy pregnant.
Patients in the “favorable” group ‘~l~nfavorable” as normal women.
I'd.
14,
lmvc almost as good a prognosis or “poor risk” patients should DOUWAS
2?!2?, .vo.
*Prindle,
4pil
Richard Hydramnios
t’r~r- >ucc*s>,* nor lwcom~’
$1. RAYNFX,
M.!).
7, 1955.
A., Ingalls, Theodore H., and Congenital Anomalies
Maternal Prindle, Ingalls, and Kirkwood: of the Central Nervous System, p. 555.
and Kirkwood, of the Central
Hydramnios
Samuel Nervous
13.: Systenr!
and Congenital
brnttxrd p. 55.5.
Anomalies
The authors analyze the records of 145 patients with diagnoses of hgdramnios in the Boston Lying-in Hospital, delivered from Jan. I, 1935, through June 30, 1950. l)uring each of the last three decades at the Boston Lying-in Hospital, some 3.6 cases of hydramnios have been observed for each 1,000 live births. This rate compares very closelyFrom their data, the authors support the conwith figures reported from other countries. clusion that hydramnios, anencephaly, fetal death, and abnormalities associated with them are all interrelated components of materrlal-placental-fetnl disease. IIydramnil,.~ usuall> The frecllleut association of II>-~lranrnios begins during the first trimester of pregnancy. with anomalous development of 110th placenta and fetus suggests thct both abnormalities Since the laboratory evidence for may be manifestations of the same maternal disease. such a concept is incomplete and inclusive, the authors suggest that correlation sl~ould btb sought in maternal history, physical findings, the course IIf pregnancy, chamcieri.:tic~ :,f the placenta and physical findings in the child. I )oLor..w N. Hn~sw, bI.1).
The Medical
Journal
of Australia
Vol. 8, No. 3, J,uly 16, 1955. ,Simmons, R. T., and Albrey, J. A,: Rho (l-j’,) Variants Coomhs Antiglobulin Test, and Their Signiilcauw, Vol.
8, No. 4, Shelton, Campbell, Krieger,
l)etected
(Guly
1,~ thr~
July 33, 1955. J. Grantley: The Problem of the Iso-immunized Kate I.: Foetal Erythroblastosis, p. 116. Vera I.: Rh Antibodies, p. 1 IS.
Nederlandsch Pal.
in Blood 1’. 47.
tijdschrift
55, No. 1, January-Pebrzcary,
Rh-Negative
voor verloskunde
1). 1 I::.
en gynaecologie
1955.
J. C.: Premature Separation of the Normally implanted p. 1. *van Eps, L. W. St.: On Labor Pain, p. 9. Yo Bwan Hie: Vulvovaginitis Mycotica in Pregnancy, p. 23. van Gelderen, H. II.? Posthuma, J. H., and deHaas, .T. H.: maturity in the Netherlands, p. 35.
“Beker,
Beker : Premature
Mother,
Separation
of the Normally
Implanted
This paper suggests the infiuence of the premature ment, supporting the author’s opinion that the primary of resistance in the area of the uterus.
Placenta
Birthweight,
Placenta
separation cause of
and
Tvscmia,
aurl
and Toxemia,
Prr-
p. 1.
as a natural esperitoxemia is an incrra+>
The hemodynamic balance can be disturbed either b.y insuficient hypertrophy of the supplying arteries or uterine musculature (primipara) and abnormal increase of the uterine capacity (hydramnion, twins, mole) or by insufficient peripheral compensation by VZLSOCO~striction (low-reserve circulation).
Patients in the “favorable” group ‘~l~nfavorable” as normal women.
I'd.
14,
lmvc almost as good a prognosis or “poor risk” patients should DOUWAS
2?!2?, .vo.
*Prindle,
4pil
Richard Hydramnios
t’r~r- >ucc*s>,* nor lwcom~’
$1. RAYNFX,
M.!).
7, 1955.
A., Ingalls, Theodore H., and Congenital Anomalies
Maternal Prindle, Ingalls, and Kirkwood: of the Central Nervous System, p. 555.
and Kirkwood, of the Central
Hydramnios
Samuel Nervous
13.: Systenr!
and Congenital
brnttxrd p. 55.5.
Anomalies
The authors analyze the records of 145 patients with diagnoses of hgdramnios in the Boston Lying-in Hospital, delivered from Jan. I, 1935, through June 30, 1950. l)uring each of the last three decades at the Boston Lying-in Hospital, some 3.6 cases of hydramnios have been observed for each 1,000 live births. This rate compares very closelyFrom their data, the authors support the conwith figures reported from other countries. clusion that hydramnios, anencephaly, fetal death, and abnormalities associated with them are all interrelated components of materrlal-placental-fetnl disease. IIydramnil,.~ usuall> The frecllleut association of II>-~lranrnios begins during the first trimester of pregnancy. with anomalous development of 110th placenta and fetus suggests thct both abnormalities Since the laboratory evidence for may be manifestations of the same maternal disease. such a concept is incomplete and inclusive, the authors suggest that correlation sl~ould btb sought in maternal history, physical findings, the course IIf pregnancy, chamcieri.:tic~ :,f the placenta and physical findings in the child. I )oLor..w N. Hn~sw, bI.1).
The Medical
Journal
of Australia
Vol. 8, No. 3, J,uly 16, 1955. ,Simmons, R. T., and Albrey, J. A,: Rho (l-j’,) Variants Coomhs Antiglobulin Test, and Their Signiilcauw, Vol.
8, No. 4, Shelton, Campbell, Krieger,
l)etected
(Guly
1,~ thr~
July 33, 1955. J. Grantley: The Problem of the Iso-immunized Kate I.: Foetal Erythroblastosis, p. 116. Vera I.: Rh Antibodies, p. 1 IS.
Nederlandsch Pal.
in Blood 1’. 47.
tijdschrift
55, No. 1, January-Pebrzcary,
Rh-Negative
voor verloskunde
1). 1 I::.
en gynaecologie
1955.
J. C.: Premature Separation of the Normally implanted p. 1. *van Eps, L. W. St.: On Labor Pain, p. 9. Yo Bwan Hie: Vulvovaginitis Mycotica in Pregnancy, p. 23. van Gelderen, H. II.? Posthuma, J. H., and deHaas, .T. H.: maturity in the Netherlands, p. 35.
“Beker,
Beker : Premature
Mother,
Separation
of the Normally
Implanted
This paper suggests the infiuence of the premature ment, supporting the author’s opinion that the primary of resistance in the area of the uterus.
Placenta
Birthweight,
Placenta
separation cause of
and
Tvscmia,
aurl
and Toxemia,
Prr-
p. 1.
as a natural esperitoxemia is an incrra+>
The hemodynamic balance can be disturbed either b.y insuficient hypertrophy of the supplying arteries or uterine musculature (primipara) and abnormal increase of the uterine capacity (hydramnion, twins, mole) or by insufficient peripheral compensation by VZLSOCO~striction (low-reserve circulation).