Book of Medical Disorders in Pregnancy - Tintash

lood flow to adapt to the requirements
of the uterus and the products of conception.
Reduced uterine blood flow
provides a situation which favors increase
in production of pressor polypeptides,
such as thromboplastin or
thromboplastin like substances. These
are produced by the ischemic placenta or
by ischemia induced degeneration of
decidual tissue. These substances are responsible
for the clinical manifestations
of preeclampsia.
Factors which have been implicated to
increase uterine ischemia include the
following. Increased Myometrial Tension
in multiple pregnancies or in the
course of labour and excessive amounts
of trophoblast as seen in the presence of
hydatidiform mole.
In primi gravidas, deficient vascular
hypertrophy and hyperplasia have been
reported as causes of the failure of
circulatory adaptation. It is also believed
that arteriolar sclerosis depresses adequate
circulatory adjustment in patients
with acute preeclampsia super imposed
on chronic hypertensive disease.
These hypothetical changes are
suggested as the basis for exacerbation
of chronic renal and vascular diseases
during gestation, the high incidence of
pre-eclampsia in primi gravidas and in
patients with twins and with hydatidiform
moles, and for the failure of the
disorders to recur in subsequent pregnancies
after the first. A decrease of 40
per cent in uterine blood flow has been
measured in hypertensive patients by
Assail and his colleagues. Hunter and
Howard reported finding of pressor
polypeptides in blood, amniotic fluid and
decidua of patients with acute preeclampsia.
42
Theory of disseminated intravascular
coagulation - MacKay, on reviewing the
evidence supported the contention that
disseminated intravascular coagula-tion
is a major mechanism in eclampsia. He
reported that Pathologic evidence is
available in the form of platelet fibrin
thrombi in the microcirculation of
various organs, including the brain,
kidney, heart, lung and placenta. Clinical
signs and symptoms of consumptive
coagulopathy has been shown to be quite
similar to the manifestations of eclampsia,
including secondary hypertension,
bleeding tendency, oliguria, anuria, hematuria,
convulsions, coma, abdomi-nal
pain, dyspnea and cyanosis, which further
supports that DIC may be the causative
factor in some cases.
The immunological theory:
According to this theory some immuno
active substances in the primigravida
patient produce these changes. Scott and
Beer in (1976) reviewed the immunological
aspects of pregnancy and suggested
that the increase in the number of
antigenic cells transferred to the maternal
circulation during pregnancy are
increased in size along with the size of
placenta (hyperalimentosis) in diabetes,
Twins and molar pregnancy. This alters
the maternal immune state and produces
the problem.
Nutritional or metabolic theory:
There is little evidence confirming this
theory. There is evidence that good nutriation
prevents Pre eclamptic toxemia.
Good nutrition implies adequate caloric
intake and adequate protein intake.
Renin angiotensin IL theory: Speraff
in 1975 summarized the theory con-