Book of Medical Disorders in Pregnancy - Tintash

Renal function: In normal pregnant
patients, the urea clearance is 102 to 104
percent of normal in contrast to an
average range of 50 to 70 per cent for
patient with pre eclampsia. In severe
cases, there is decrease in renal blood
flow and glomerular filtration rate.
Glomerular filtration fraction is also
lowered. The resistance of the afferent
glomerular arteries is increased. The
tubular capacity for reabsorption of
sodium appears to be increased. Unless
there is tubular or cortical necrosis
which may occur in very severe cases.
The azotemia is mild and regresses quite
rapidly after delivery. Nitrogen retention
occurs only when there is oliguria or
anuria.
Renal changes: During normal
pregnancy, both glomerular filtration
rate and renal perfusion are elevated above
normal non pregnant levels. In preeclamptic
toxemia, the levels are reduced
proportional to the severity of 'the
disease. Usually creatinine and uric acid
are slightly elevated. Blood Urea levels
are not much affected and have been
reported to be of no prognostic or
diagnostic value in this disease. How
ever uric acid concentrations have been
found to relate better than B.P. level to
fetal prognosis.
Sheehan in (1950) described the
histology of renal lesion, he reported,
"that the glomeruli are 20 per cent
enlarged and pointing into tubules. The
capillary loops are variably dilated or
swollen endothelial cells are swollen
with fibrinous deposits. On Electron
Microscopy, there is marked vascularizetion
and swelling of capillary
endothelial cells without changes else
where. Occasional small subendothelial
deposits of fibrinoid material may be
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seen. IgG and IgM are thought to be
present in these deposits along with
fibrin and complement material. This is
similar to deposits elsewhere e.g.
placenta and liver. Tubular lesions are
either due to degeneration or precipitation
of escaped protein in the
tubules. These changes are common but
not diagnostic of preeclam-psia. Casts
and haemoglobin in urine are also seen
in this disorder.
Hepatic changes: What happens to
blood flow pattern is not known, but
definite changes occur in hepatic function
especially with pre-eclampsia and
eclampsia. There is delay in brom-sulphthalein
(BSP) excretion, and S GOT.
Levels are elevated. Hyperbilirubinemia
is uncommon. Alkaline phos phatase is
elevated but this is placental in origin
and does not signify liver damage.
Hemorrhagic necrosis in the periphery of
liver lobule is characteristic lesion in
fatal cases but biopsy of non fatal cases
has also shown the lesion to be present.
The lesion is characteristically variable
in extent and severity "Periportal
necrosis" and subcapsular hemorrhage
may occur and are associated with high
mortality.
Brain:
There is no general blood flow reduction
but there may be focal hypoperfusion or
hyper perfusion. EEG. Shows
nonspecific abnormalities for some time
following eclampsia. There is a higher
familial incidence of EEG abnormalities
suggesting a congenital predisposition to
eclampsia. Autopsy findings reported in
fatal cases include edema, hyperemia,
focal anaemia, thrombosis and
hemorrhage.