U.S. patent application number 10/292338 was filed with the patent office on 2004-01-29 for use of digoxin immune fab (ovine) for the regulation of sodium/potassium atpase activity in preeclamptic and eclamptic patients.
Invention is credited to Adair, Charles David.
Application Number | 20040018202 10/292338 |
Document ID | / |
Family ID | 30769950 |
Filed Date | 2004-01-29 |
United States Patent
Application |
20040018202 |
Kind Code |
A1 |
Adair, Charles David |
January 29, 2004 |
Use of digoxin immune Fab (ovine) for the regulation of
sodium/potassium ATPase activity in preeclamptic and eclamptic
patients
Abstract
A method of regulating a preeclamptic/eclamptic patient's
sodium/potassium ATPase activity includes the administration of
digoxin immune Fab (ovine). It is theorized that an endogenous
digitalis-like factor present in preeclamptic and eclamptic
patients inhibits the functioning of sodium/potassium ATPase,
resulting in elevated level of intracellular sodium and calcium
levels. These elevated intracellular sodium and calcium levels lead
to intravascular volume contraction and vasoconstriction. Digoxin
immune Fab (ovine) binds with the endogenous digitalis-like factor
to prevent it from interfering with the functioning of the
sodium/potassium ATPase, thereby allowing the patient's
intracellular sodium and calcium to return to a more normal
level.
Inventors: |
Adair, Charles David;
(Signal Mountain, TN) |
Correspondence
Address: |
HUSCH & EPPENBERGER, LLC
190 CARONDELET PLAZA
SUITE 600
ST. LOUIS
MO
63105-3441
US
|
Family ID: |
30769950 |
Appl. No.: |
10/292338 |
Filed: |
November 12, 2002 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
10292338 |
Nov 12, 2002 |
|
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|
10202957 |
Jul 25, 2002 |
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Current U.S.
Class: |
424/178.1 ;
514/26 |
Current CPC
Class: |
A61P 9/12 20180101; A61K
2039/505 20130101; A61K 2039/545 20130101; C07K 16/44 20130101;
A61K 31/7048 20130101 |
Class at
Publication: |
424/178.1 ;
514/26 |
International
Class: |
A61K 039/395; A61K
031/704 |
Claims
What is claimed is:
1. The use of a digoxin immune Fab (ovine) for administration to a
human patient exhibiting symptoms of preeclampsia/eclampsia in
order to reverse at least one preeclamptic/eclamptic symptom in the
group including intravascular volume contraction, vasoconstriction
and exaggerated myocardial function.
2. The use of a digoxin immune Fab (ovine) as set forth in claim 1,
wherein the digoxin immune Fab (ovine) is administered according to
a formula of an endogenous digitalis-like factor level times the
patient's body weight in kilograms divided by 100.
3. The use of a digoxin immune Fab (ovine) as set forth in claim 2,
wherein the endogenous digitalis-like factor level is between
approximately 3.0 and 5.0 ng/mL.
4. The use of a digoxin immune Fab (ovine) as set forth in claim 2,
wherein the endogenous digitalis-like factor level is approximately
4.0 ng/mL.
5. The use of a digoxin immune Fab (ovine) as set forth in claim 2,
wherein the digoxin immune Fab (ovine) is administered via an
intravenous bolus and wherein the administration of the digoxin
immune Fab (ovine) is repeated on a fixed schedule.
6. The use of a digoxin immune Fab (ovine) as set forth in claim 5,
wherein the fixed schedule is approximately every five to eight
hours.
7. The use of a digoxin immune Fab (ovine) as set forth in claim 5,
wherein the fixed schedule is approximately every six hours.
8. The use of digoxin immune Fab (ovine) for the regulation of
sodium/potassium ATPase activity in a human patient exhibiting
symptoms of preeclampsia.
9. The use of a digoxin immune Fab (ovine) as set forth in claim 8,
wherein the digoxin immune Fab (ovine) is administered according to
a formula of an endogenous digitalis-like factor level times the
patient's body weight divided by 100.
10. The use of a digoxin immune Fab (ovine) as set forth in claim
9, wherein the endogenous digitalis-like factor level is between
approximately 3.0 and 5.0 ng/mL.
11. The use of a digoxin immune Fab (ovine) as set forth in claim
9, wherein the endogenous digitalis-like factor level is
approximately 4.0 ng/mL.
12. The use of a digoxin immune Fab (ovine) as set forth in claim
8, wherein the digoxin immune Fab (ovine) is administered via an
intravenous bolus and wherein the administration of the digoxin
immune Fab (ovine) is repeated on a fixed schedule.
13. The use of a digoxin immune Fab (ovine) as set forth in claim
12, wherein the fixed schedule is approximately every five to eight
hours.
14. The use of a digoxin immune Fab (ovine) as set forth in claim
12, wherein the fixed schedule is approximately every six
hours.
15. The use of digoxin immune Fab (ovine) to prevent the binding of
an endogenous digitalis-like factor with a receptor site in a human
patient exhibiting symptoms of preeclampsia/eclampsia.
16. The use of digoxin immune Fab (ovine) as set forth in claim 15,
wherein the receptor site is sodium/potassium ATPase.
17. The use of a digoxin immune Fab (ovine) as set forth in claim
15, wherein the digoxin immune Fab (ovine) is administered
according to a formula of an endogenous digitalis-like factor level
times the patient's body weight divided by 100.
18. The use of a digoxin immune Fab (ovine) as set forth in claim
17, wherein the endogenous digitalis-like factor level is between
approximately 3.0 and 5.0 ng/mL.
19. The use of a digoxin immune Fab (ovine) as set forth in claim
17, wherein the endogenous digitalis-like factor level is
approximately 4.0 ng/mL.
20. The use of a digoxin immune Fab (ovine) as set forth in claim
15, wherein the digoxin immune Fab (ovine) is administered via an
intravenous bolus and wherein the administration of the digoxin
immune Fab (ovine) is repeated on a fixed schedule.
21. The use of a digoxin immune Fab (ovine) as set forth in claim
20, wherein the fixed schedule is approximately every five to eight
hours.
22. The use of a digoxin immune Fab (ovine) as set forth in claim
20, wherein the fixed schedule is approximately every six
hours.
23. The use of a digoxin immune Fab (ovine) to control
preeclampsia/eclampsia in a human patient.
24. The use of a digoxin immune Fab (ovine) for administration to a
human patient exhibiting symptoms of preeclampsia/eclampsia in
order to improve the flow of blood between the patient and a fetus
and placenta.
25. The use of a digoxin immune Fab (ovine) for administration to a
human patient exhibiting symptoms of preeclampsia/eclampsia to
treat prevent growth restriction of a fetus.
26. The use of a digoxin immune Fab (ovine) for administration to a
human patient to treat the symptoms of preeclampsia/eclampsia.
27. The use of a digoxin immune Fab (ovine) as set forth in claim
26, wherein the digoxin immune Fab (ovine) is administered to
alleviate the patient's hypertension.
28. The use of a digoxin immune Fab (ovine) as set forth in claim
26, wherein the digoxin immune Fab (ovine) is administered to
reduce the patient's proteinuria.
29. The use of digoxin immune Fab (ovine) as set forth in claim 26,
wherein the digoxin immune Fab (ovine) is administered to improve
and stabilize the patient's urinary output.
30. The use of digoxin immune Fab (ovine) as set forth in claim 26,
wherein the digoxin immune Fab (ovine) is administered to improve
and stabilize the patient's neurologic functions.
Description
CROSS-REFERENCES
[0001] This application is a continuation-in-part of co-pending
application Ser. No. 10/202,957, filed Jul. 25, 2002.
TECHNICAL FIELD OF THE INVENTION
[0002] The present invention relates generally to the field of
medicine and, more particularly, to a method of regulating
sodium/potassium ATPase activity in obstetric patients exhibiting
symptoms of preeclampsia and eclampsia by the administration of
digoxin immune Fab (ovine).
DESCRIPTION OF THE RELATED ART
[0003] Preeclampsia is a rapidly progressive condition occurring
during pregnancy characterized by high blood pressure, swelling and
protein in the urine. It is specifically defined as the presence of
hypertension or pregnancy-induced hypertension ("PIH") accompanied
by proteinuria, edema, or both after 20 weeks gestation.
Preeclampsia occurs in 5 to 10 percent of all pregnancies and is
most common in first-time pregnancies or in first pregnancies with
a new partner or husband. Typically, preeclampsia occurs in the
late second or third trimesters of pregnancy. Complications of
preeclampsia include eclamptic seizures, hemolysis, elevated liver
function tests, low platelet count (HELLP) syndrome, hepatic
rupture, DIC pulmonary edema, acute renal failure, placental
abruption, intrauterine fetal demise (IUFD), cerebral hemorrhage,
cortical blindness, and retinal detachment.
[0004] Preeclampsia causes vasospasm, which constricts and damages
the smooth lining of the blood vessels. This leads to the
accumulation of platelets in the damaged blood vessels, which form
small clots along the blood vessel wall and further narrow the
blood vessel. This damage to blood vessels can also lead to edema,
including cerebral edema. Vasospasm can occur throughout the body,
damaging the heart, kidneys and liver. Vasospasm can also develop
in the placenta, decreasing the blood supply to the fetus and/or
placenta.
[0005] Preeclampsia is divided into mild and severe forms. Mild
preeclampsia is indicated where the patient exhibits hypertension,
a proteinuria level of greater than 300 mg per 24 hour period, mild
edema signaled by weight gain of greater than 2 pounds per week or
6 pounds per month, and urine output of less than 500 ml per 24
hour period. Severe preeclampsia is indicated where the patient's
blood pressure is greater than 160/110 on two occasions at least
six hours apart while on bed rest or a systolic blood pressure
increase of greater than 60 over a baseline value or a diastolic
increase of greater than 30. In addition, a proteinuria level of
greater than 5 g per 24 hour period or a reading of 31 or 41 on a
urine dipstick, massive edema, oliguria (less than 400 ml per 24
hour period), presence of fetal growth retardation (IUGR), or
systemic symptoms including pulmonary edema, headaches, visual
changes, right upper quadrant pain, elevated liver enzymes or
thrombocytopenia.
[0006] After a diagnosis of preeclampsia, the baby is generally
induced and delivered if it is near term, i.e., after 36 weeks.
However, if preeclampsia occurs earlier in the pregnancy, its
impact is more profound. The only "cure" for the disease is
delivery of the baby, which is generally contrary to the best
interests of the baby if it is not near term. However, if the
condition does not respond to traditional management options, early
delivery may be the only option remaining. Traditional management
includes bed rest, antihypertensive therapy, including methyldopa
(Aldomet.RTM.), atenolol, and labetalol. If pregnancy from the
diagnosis of preeclampsia to delivery could be extended relatively
safely for both the fetus and mother, then significant improvement
in perinatal outcomes may be achieved.
[0007] The present invention is directed to overcoming one or more
of the problems set forth above.
SUMMARY OF THE INVENTION
[0008] An aspect of the present invention is to provide a means of
regulating a preeclamptic/eclamptic patient's sodium/potassium
ATPase activity to extend pregnancy and allow further development
of the patient's fetus.
[0009] Another aspect of the present invention is to provide a
means to reverse intravascular volume contraction, vasoconstriction
and exaggerated myocardial function in preeclamptic/eclamptic
patients.
[0010] In accordance with the above aspect of the invention, there
is provided a method of regulating a preeclamptic/eclamptic
patient's sodium/potassium ATPase activity through the
administration of digoxin immune Fab (ovine). It is theorized that
an endogenous digitalis-like factor present in preeclamptic and
eclamptic patients inhibits the functioning of sodium/potassium
ATPase, resulting in elevated level of intracellular sodium and
calcium levels. These elevated intracellular sodium and calcium
levels lead to intravascular volume contraction and
vasoconstriction. Digoxin immune Fab (ovine) binds with the
endogenous digitalis-like factor to prevent it from interfering
with the functioning of the sodium/potassium ATPase, thereby
allowing the patient's intracellular sodium and calcium to return
to a more normal level.
[0011] These aspects are merely illustrative of the innumerable
aspects associated with the present invention and should not be
deemed as limiting in any manner. These and other aspects, features
and advantages of the present invention will become apparent from
the following detailed description when taken in conjunction with
the drawings.
BRIEF DESCRIPTION OF THE DRAWINGS
[0012] Reference is now made more particularly to the drawings
which illustrate the best presently known mode of carrying out the
invention and wherein similar reference characters indicate the
same parts throughout the views.
[0013] FIG. 1 is a flow chart illustrating the steps and sequence
of a method for controlling preeclampsia according to an embodiment
of the present invention.
[0014] FIG. 2A is a chart of the blood flow velocity through a
patient's umbilical artery in a normal pregnancy.
[0015] FIG. 2B is a chart of the blood flow velocity through a
pre-eclamptic patient's umbilical artery.
DETAILED DESCRIPTION
[0016] Patients suffering from preeclampsia and eclampsia
experience vascular contraction, retention of cellular sodium (Na),
and expansion of intracellular volume. It is theorized that these
conditions in preeclamptic and eclamptic patients are related to
the occurrence of faulty invasion of the placenta into the uterine
wall and a corresponding reaction by the fetus and/or placenta to
that faulty invasion. In the early stages of pregnancy, the
placenta has a "loose" connection with the uterine wall. Around the
fourteenth to sixteenth week of pregnancy, the placenta develops a
"tight" attachment to the uterine wall in order to tap more fully
into the maternal blood supply. This tighter connection between the
placenta and uterine wall allows for the exchange of larger and
more complex nutrients that are required for the continued
development of the fetus at that stage of the pregnancy. In certain
instances, the placenta is unable to fully develop the necessary
tight connection with the uterine wall. This faulty connection
makes the exchange of the required nutrients between the mother and
fetus and/or placenta more difficult and places stress on the
fetus. The reaction of the fetus to this stress is the generation
of a compensatory mechanism. As part of this compensatory
mechanism, the fetus and/or placenta produces and transfers to the
mother an endogenous digitalis-like factor(s).
[0017] It is further theorized that the endogenous digitalis-like
factor(s) binds to the mother's sodium/potassium ATPase in a manner
similar to digoxin or digitoxin. Digoxin is a toxin that binds to
and inhibits the activity of sodium/potassium ATPase pumps in cells
of the human body. The resulting inhibition of these ATPase pumps
produces an imbalance of sodium and potassium in the intra and
extra cellular space. In cases of severe digitalis intoxication, a
patient's serum potassium concentration can be elevated to
life-threatening levels, due to the shifting of potassium from
inside to outside of the patient's cells. This leads to increased
renal excretion of potassium and, possibly, to hyperkalemia with a
total body deficit of potassium. Other symptoms of severe digitalis
intoxication include severe ventricular arrhythmias, such as
ventricular tachycardia or ventricular fibrillation, or progressive
bradyarrhythmias, such as severe sinus bradycardia or second or
third degree heart block not responsive to atropine.
[0018] According to the theory, the endogenous digitalis-like
factor(s) produced by the fetus and/or placenta creates a similar
effect on the cells of a preeclamptic patient. The endogenous
digitalis-like factor(s) binds to and inhibits the activity of the
patient's sodium/potassium ATPase. The inhibition of
sodium/potassium ATPase results in elevated intracellular sodium
and, consequently, elevated intracellular calcium. The elevated
levels of intracellular sodium lead to intravascular volume
contraction and vasoconstriction in the patient. The
vasoconstriction experienced by the patient can produce exaggerated
myocardial function due to the increased effort required by the
heart to pump blood through the patient's narrowed vascular system.
It is also possible that this exaggerated myocardial function is
produced by the endogenous digitalis-like factor(s) binding to
cells in the patient's heart.
[0019] Due to the similarity of effects of digoxin and the
endogenous digitalis-like factor(s), it is theorized that the drug
used for treatment of digitalis intoxication may prove effective
for the treatment of preeclampsia and eclampsia. Digitalis
intoxication is treated through the administration of digoxin
immune Fab (ovine). Digoxin immune Fab (ovine), which is marketed
in the United States as DIGIBIND.RTM. by GlaxoSmithKline and
DIGIFAB.TM. by Protherics, Inc., is a sterile lyophilized powder of
antigen binding fragments (FAB) derived from specific antidigoxin
antibodies raised in sheep. Digoxin immune Fab (ovine) is indicated
for treatment of digoxin or digitoxin overdose manifested by severe
ventricular arrhythmias such as ventricular tachycardia or
ventricular fibrillation, or progressive bradyarrhythmias such as
severe sinus bradycardia or second or third degree heart block not
responsive to atropine. DIGIBIND.RTM. is distributed in vials, with
each vial containing 38 mg of digoxin-specific Fab fragments plus
75 mg of sorbitol as a stabilizer and 28 mg of sodium chloride and
capable of binding approximately 0.5 mg of digoxin. DIGIBIND.RTM.
is generally administered by intravenous injection after
reconstitution with 4 mL/vial of sterile water for injection.
DIGIFAB.TM. is distributed in 40 mg vials and contains no
preservatives. DIGIFAB.TM. is generally administered by intravenous
infusion over at least thirty minutes after reconstitution with 4
mL/vial of sterile water for injection. Digoxin immune Fab (ovine)
binds to molecules of digoxin, thereby preventing them from binding
to and inhibiting the activity of the body's sodium/potassium
ATPase pumps. This is due to the fact that the affinity of digoxin
immune Fab (ovine) is significantly greater than the affinity for
sodium/potassium ATPase. The Fab fragment-digoxin combined molecule
then accumulates in the blood and is excreted by the kidneys.
[0020] It is theorized that administration of digoxin immune Fab
(ovine) to preeclamptic and eclamptic patients will result in the
digoxin immune Fab (ovine) binding to the endogenous digitalis-like
factor(s), thereby preventing the endogenous digitalis-like
factor(s) from binding to and inhibiting the activity of the
patient's sodium/potassium ATPase pumps and leading to the eventual
excretion of the endogenous digitalis-like factor(s) through the
kidneys. This, in turn, should allow the patient's levels of
intracellular sodium and calcium to normalize and ease any
intravascular volume contraction and vasoconstriction, further
leading to normal myocardial function.
[0021] The vasoconstriction and exaggerated myocardial function
experienced by preeclamptic and eclamptic patients also negatively
impacts the flow of blood to the fetus and/or placenta. FIG. 2A
illustrates the blood flow velocity in the umbilical artery of a
normal pregnancy. "A" refers to the blood flow velocity during
systole, while "B" refers to the blood flow velocity in the
umbilical artery during diastole. FIG. 2A illustrates that even
during diastole, there is a significant flow velocity through the
umbilical artery. This is in contrast to the flow velocity in a
pre-eclamptic patient as shown in FIG. 2B. Pre-eclamptic
vasoconstriction reduces the blood flow velocity through the
umbilical artery and results in the flow velocity "bottoming out"
during diastole, indicated by "C". During diastole, little or no
blood is flowing to the fetus and/or placenta, placing further
stress on the fetus and restricting oxygenation, fluid exchange and
nutrition, potentially resulting in growth restriction of the
fetus. It is theorized that administration of digoxin immune (Fab)
ovine to an obstetric patient suffering from preeclampsia or
eclampsia eases vasoconstriction, thereby allowing the fetal blood
flow to improve.
[0022] According to one example, a patient is first evaluated for
preeclampsia or eclampsia. Once a diagnosis of preeclampsia is
confirmed, a suitable dosage of digoxin immune Fab (ovine), such as
DIGIBIND.RTM. or DIGIFAB.TM., is calculated. A typical
manufacturer's recommended dosage formula for a known digitalis
toxicity level (E) is: 1 D .times. W 100
[0023] where (D) is the serum digoxin concentration in ng/mL and W
is the patient's weight in kilograms. However, in preeclampsia and
eclampsia cases there is no known digitalis toxicity level.
Therefore, according to the method, a measured or assumed
endogenous digitalis factor(s) level is utilized for the
calculation. In one embodiment, the endogenous digitalis-like
factor(s) level (E) is between approximately 3.0 and 5.0 ng/mL. In
a preferred embodiment, the endogenous digitalis-like factor(s)
level is approximately 4.0 ng/mL. The endogenous digitalis-like
factor(s) level is then used in the following equation: 2 E .times.
W 100
[0024] where E is the endogenous digitalis-like factor(s) level.
Use of the preferred endogenous digitalis-like factor(s) level
results in an equation of: 3 4.0 ng / mL .times. ( W ) 100
[0025] which in turn produces the suitable dosage of digoxin immune
Fab (ovine). While the above formulas have been provided, slight
deviations therefrom may be used.
[0026] Once the dosage is calculated, it is administered to the
patient via an intravenous bolus. Administration of the calculated
dosage via intravenous bolus is then repeated on a fixed schedule
of every five to eight hours, preferably every six hours.
[0027] In another embodiment, the administration of digoxin immune
Fab (ovine) is accompanied by an administration of corticosteroids,
such as betamethasone, to stimulate the cells in the lungs of the
fetus in preparation for breathing air and decrease the risk of
brain hemorrhage and intestinal problems in the fetus. The
corticosteroids are administered once at the time of admission and
again in twenty-four hours.
[0028] The method will now be further illustrated with reference to
the following non-limiting example.
BIOLOGICAL EXAMPLE
[0029] A 16-year-old 70 Kg primigravida at 29 weeks {fraction
(5/7)} days presented with a presumed diagnosis of eclampsia. Her
prenatal course had been uncomplicated until the day of admission.
Her past medical history was negative for chronic illness. The
patient had complaints of scotomata, persistent headache, and
reported seizure activity for two episodes prior to hospital
arrival and one on the labor deck. Initial evaluation revealed an
alert patient with obvious postictal behavior. Her blood pressure
was elevated at 160/110's and otherwise stable vital signs.
Physical examination revealed A-V nicking on funduscopic exam, 4+
edema of the lower extremities and obvious facial and upper
extremity edema. Deep tendon reflexes were 3 plus with 2 beats of
clonus. The remainder of the exam was within normal limits. Lab
evaluation of the urine noted proteinuria on qualitative analysis
of 2+ and a urine specific gravity of 1.025. Serum chemistry
revealed hyperuricacidemia at 8.2, elevated creatinine of 1.0, BUN
of 6, and otherwise normal electrolytes and liver enzymes. The
complete blood count revealed a platelet count of 429,000, white
count of 10.4 and a hemoglobin/hematocrit of 12.0 and 35.6
respectively. The ammonia level was 3 and coagulation studies were
normal. Urine drug screening was negative for substances of abuse
including cocaine and methamphetamines. CT scanning of the maternal
head failed to reveal any pathological abnormalities.
[0030] Ultrasound examination revealed a singleton gestation with a
breech presentation. The estimated gestational age was consistent
with the previously determined age of 29 weeks with an estimated
fetal weight of 1331 grams. The amniotic fluid index was 5.42 cm
and fetal breathing, movement, and tone were noted to be present.
Doppler flow studies of the umbilical artery revealed an elevated
S/D ratio of 5.6, RI of 0.82, and minimal diastolic flow. No
anatomical abnormalities were noted on exam. Fetal cardiotocograph
revealed a baseline of 135 with minimal beat-to-beat variability.
Occasional non-repetitive decelerations were noted with good
recovery. They were deemed to be non-ominous.
[0031] The patient was placed on intravenous magnesium sulfate.
Central venous access and arterial line placement were performed.
After informed discussion with the immediate family including the
option to stabilize with compassionate off label use of fragmented
antibody to digoxin and to administer corticosteroids for fetal
benefit, the patient's mother provided consent.
[0032] Standard preeclampsia monitoring every hour was followed
with intensive care unit one on one nursing. Using an endogenous
digitalis like factor(s) level of 4.0 ng/mL and a dosage formula of
4.0 ng/mL x patient's body weight divided by 100 resulted in a
dosage of 3 vials. This dosage was administered via an intravenous
bolus and was repeated every 6 hours.
[0033] Intravenously administered fluids were standardized to 125
cc/hr. Urine output from admission to time of digoxin immune Fab
(ovine) infusion was 300 cc. Over the first 6 hours post infusion
of digoxin immune Fab (ovine), the average urinary output increased
to 100 cc/hr with blood pressure readings of 148 to 162 systolic
and 104 to 111 diastolic. At the next dosing interval the drug was
doubled to 6 vials every six hours until 12 hours prior to
delivery. Over the next 36 hours a diuresis followed over 5,840 cc
of urine for an average hourly output of 162 cc. The total intake
of intravenous fluids during the same time period was 3409 cc. The
urine qualitative exam revealed negative proteinuria with a
specific gravity of 1.011 and osmolality of 125, normal 500 to 800
mosm. Her creatinine decreased to 0.7 with the remainder of
electrolytes remaining normal. Serial blood pressure measurements
during the 36-hour period from the doubling of the dose ranged from
131 to 160 systolic (mean 140's) and diastolic 58 to 111 (mean
90's). The edema resolved in face and upper extremities with
significant decreases in lower extremities as well to 1+. Deep
tendon reflexes became 1+ with no clonus.
[0034] Fetal assessment during this time showed no changes in the
cardiotocograph. Ultrasound examination every 6 hours revealed a
reassuring biophysical score of 8 of 10. Doppler flow assessment of
the umbilical artery every 6 hours revealed a decreasing
systolic/diastolic ratio with an increasing diastolic component.
The S/D ratio 6 hours prior to delivery was 3.7 with a RI of 0.75
suggesting improved fetal hemodynamics albeit still abnormally
elevated.
[0035] Cesarean delivery was performed at 48 hours post
administration of corticosteroids secondary to a breech
presentation. The delivery was attended by NICU and resulted in a
livebirth of a female child. Apgars were 7 & 8 at one and five
minutes respectively. The neonate did not require any oxygen
support and was admitted to the neonatal intensive care unit
secondary to prematurity size of 1290 grams.
[0036] The maternal postoperative course was complicated by
elevated blood pressures of 140 to 160's systolic and diastolic
readings in the 100's. The patient was started on metoprolol 100 mg
twice daily. She was discharged home on postoperative day # 4 with
stable blood pressures controlled with metoprolol. All follow up
laboratory tests remained within normal limits. The neonate had no
adverse sequelae and was discharged home on day of life # 31.
[0037] Other objects, features and advantages of the present
invention will be apparent to those skilled in the art. While
preferred examples and steps of the present invention have been
illustrated and described, this has been by way of illustration and
the invention should not be limited except as required by the scope
of the appended claims and their equivalents.
* * * * *