Vicente Sotto Memorial Medical Center

Department of Obstetrics & Gynecology

A CASE OF CHRONIC HYPERTENSION

Bunga, Arianne Mae P.

Constantino, Jehesus Jireh C.
Catis, Deean G.
Cueva, Beatrice Isabel B.
Flores, Irah Franz D.
Padin, Janessa Kim C.
Ramos, Herondio L.
Rhudy, Karina Jo C.
Sangre, Hezel Clair C.
Santana, Jaypee M.
Tañagras, Kyra Marj F.
Tawi, Vanessa P.
Teves, Annah S.
Yap, Eunice T.
Tanzo, Leah Nenez T.
Calibugar, Van Lendl T
 CLINICAL DATA

This is a case of E.J. a 35-year-old, female, married, Filipino, Roman Catholic, from Carcar
City Cebu who came in last July 4, 2019 with a chief complaint of elevated BP.

Patient is not a known hypertensive, diabetic, nor asthmatic and has no previous
surgeries. Previous hospitalizations in 2009 and 2014 were both for obstetrical reasons. She has
no known food and drug allergies. No known heredofamilial diseases. She is a housewife.

She is a G3P2(2002). Menarche at 16 years old with a 30-day interval lasting for 3 days,
consuming 2-3 pads per day of moderate flow with no associated dysmenorrhea. She had her
coitarche at 25 years old with one sexual partner. No history of post-coital bleeding, dyspareunia,
or sexually transmitted infections. No papsmears done.

She had her first prenatal checkup at 12 weeks AOG at Carcar District Hospital where she
was seen by an obstetrician. At 17 weeks AOG, her BP was noted to be elevated at 180/110 mmHg
with no associated headache, nape pain, blurring of vision, and vomiting. She was prescribed
with Methyldopa 250mg/tab twice a day as maintenance taken with good compliance as claimed.
BP was maintained at 110-120/70-80mmHg on succeeding prenatal checkups.

She received one dose of tetanus toxoid and was prescribed with folic acid, ferrous
sulfate, and calcium supplements all taken with good compliance. She had 2 prior ultrasounds
taken. The first ultrasound was taken on May 7, 2019 which showed an AOG of 28 5/7 ---37
weeks; 2nd ultrasound taken at June 24, 2019 showed an AOG of 35 5/7---- 37 1/7.

Night prior to admission, patient noted occipital headache and nape pain associated with
irregular uterine contractions with a 15-30 min interval with good fetal movement; condition
tolerated. No medications taken, no consult done.

Six hours prior to admission, patient had her prenatal checkup at Carcar District Hospital
where her BP was elevated at 180/110mmHg. She was diagnosed as a case of severe
preeclampsia and was given venoclysis of D5LR 1L at KVO rate and was given loading dose of
MgSO4 4g slow IVTT, 5g deep IM both buttocks and 2 doses of Hydralazine 5g IVTT. She was
subsequently referred to VSMMC for further management since no obstetrician was available.
No associated headaches, nausea and vomiting, blurring of vision, and epigastric pain.

Upon examination at the admitting section, patient was placed in a wheel chair,
conscious, coherent, cooperative, with vital signs: BP: 160/100 HR: 96 RR: 19 T: 36.7c.
IE done showed 3cm, slightly effaced, ruptured flat membranes, station -3. Fundic height at 36
cm with a fetal heart rate of 133 beats per minute.
 Physical Examination was unremarkable.

Admitting diagnosis was G3P2(2002) Pregnancy Uterine 37 weeks AOG/LUTZ cephalic in

labor, Chronic Hypertension.

Plan of care was termination of pregnancy. Patient delivered via normal spontaneous
delivery with good fetal outcome.

PRIMARY IMPRESSION: Chronic Hypertension with Superimposed Preeclampsia with Severe

Features

Our primary impression is chronic hypertension since the patient had a BP of

180/110mmHg at less than 20 weeks of gestation which classifies her under chronic
hypertension. To be ruled in if there is persistence of elevated BP after 12 weeks’ post-partum.
However, superimposed preeclampsia is strongly considered because of the first BP elevation
documented early in pregnancy. It is with severe feature because of SBP reading more than or
equal to180 and DBP of equal or more than 110 mmHg for at least 2 occasions-first was during
the prenatal checkup at 180/110mmHg at 17 weeks AOG, second was during the latest prenatal
visit at Carcar Provincial Hospital at 180/110mmHg, and the last one was at the VSMMC AS at
SBP of 160mmHg with at least 4hrs interval from the 2nd BP reading (source: Williams, 24th Ed.).
Laboratories such as 24-hour urine, serum transaminases, or platelets were not yet taken which
could confirm the diagnosis

DIFFERENTIAL DIAGNOSIS
1. Gestational Hypertension – This was considered because the patient is a pregnant woman
who came in with complaints of an elevated BP. However, this is ruled out since the
patient’s first BP elevation was at 17 weeks’ gestation. This is noted to be a temporary
diagnosis which has to be confirmed 12 weeks after delivery.
2. Preeclampsia – This was considered since the patient presented with BP elevation and
nape pain, occipital headaches. No other cerebral or visual disturbances, no epigastric
pain. Also noted normal creatinine, platelet and minimal elevation of LDH and
transaminases However, “pure” preeclampsia would have a later onset as opposed to
superimposed preeclampsia which makes pure preeclampsia unlikely.
3. Eclampsia - No documented seizure episode

Course in the Wards

At the ER, patient was admitted under the service of OB department as a case of
G3P2(2002) Pregnancy Uterine 37 weeks AOG/LUTZ cephalic in labor, Chronic Hypertension. The
definite plan was to terminate pregnancy by normal spontaneous delivery, control BP elevation
of the patient, prevent seizure and monitor maternal and fetal well being as labor ensues. Thus
venoclysis was started with D5LR at KVO rate and cardiotocogram was done to assess the fetus.
Furthermore, the following preeclampsia panel were also ordered: CBC, Urinalysis, HbSAg, Blood
Typing, Creatinine, BUN, BUA, SGPT, LDH, Serum electrolytes, Urine protein: Creatinine Ratio,
Clotting time, Bleeding Time, APTT, Protime, Chest Xray PA view.

The patient was also given the following medications MgSO4 loading dose: 4 grams in
20% solution slow IVTT, 5mg in 50% solution deep IM in both buttocks q4 x 6 doses after
parameters are checked. Hydralazine 5mg IVTT q15 mins x 2 doses, then 10mg q15 mins x 2 doses
PRN for SBP>160 mmhg and DBP >110mmhg.

Progress of labor monitored, patient delivered via normal spontaneous delivery a live
female neonate, with AS 89, BS 38 weeks, BW 2810g, AGA. Venoclysis D5LR+ 30 units oxytocin
at 30 gtts/min. Given 10 units oxytocin IM. Postpartum condition stable, monitored q15 mins x 2
hours, then q hourly. Medications given Cefuroxime 500mg 1 tab OD, Tramadol + Paracetamol 1
tab PRN, Vitamin A 50,000 IU cap OD, MV+ FeSO4 1 tab OD, Diphenhydramine 50mg IVTT. MgSO4
and Hydralazine as maintenance were continued.

Hospital Day 1 July 5, 2019 (Postpartum Day 1)

Patient was seen on hospital and postpartum day 1 (July 5, 2019) with complains of dull
pain on episiorrhaphy site PS 5/10, no seizure, no dysuria, no fever, no cough, no difficulty of
breathing, able to pass flatus. No bowel movement noted.

Patient was seen and examined conscious, coherent and oriented with limited
movements related to delivery with the following vital signs- BP: 150/80mmHg, HR-84 bpm, RR-
20 cpm, temp-35.9C, and O2 sat of 98 %. Other PE findings were unremarkable with clear breath
sounds, normoactive bowel sounds, well contracted uterus, no vulvar hematoma, with good
urine output at 45cc/hr and with strong pulses.

Patient’s assessment was Gravida 3 Para 3 (3003) Pregnancy Uterine, delivered cephalic,
term, live birth by NSD to a live female neonate, AS 8,9, BW 2810g, BS 38 weeks, AGA;
Preeclampsia with Severe Features.

BP was monitored every 2 hrs, watched out for signs of active bleeding; continued
maintenance dose of MgSO4 with parameters checked before the next dose was given; vital signs
monitored q4H, I and O q shift, perineal care BID, encouraged breastfeeding; continued the
present medications.

Hospital Day 2 July 6, 2019 (Postpartum Day 2)

Patient still with complains of dull pain on episiorrhaphy site, no seizure noted, no
dysuria, no fever, no cough, no difficulty of breathing, able to pass flatus, still with no bowel
movement. Patient was seen and examined conscious, coherent and oriented with significant
improvement in mobility from delivery with the following vital signs- BP: 160/90mmHg, HR-84
bpm, RR-21 cpm, temp-36.6, and O2 sat of 98%. Still with unremarkable PE findings with well
contracted uterus, no vulvar hematoma noted with adequate urine output at 50cc/hr and with
strong equal peripheral pulses.
Repeat creatinine, CBC, SGPT/ALT, LDH was ordered with the normal levels

Hospital Day 3 July 7, 2019 (Postpartum Day 3)

Hospital and postpartum day 3 (July 7, 2019) was uneventful with stable vital signs, no
BP spikes recorded (150/80mmHg). Still with no bowel movement. Present management was
continued with additional order to increase fiber intake to facilitate bowel movement, and
another repeat of the CBC, Creatinine, SGPT/ALT and LDH. Results showed normal levels of
Creatinine, SGPT/ALT and LDH.

Hospital Day 4 (July 8, 2019)

On hospital and postpartum day 4 (July 8, 2019), patient was ordered a May Go Home
status with stable vital signs and improved condition. Home medications include Multivitamins
+ FeSO4 1 tab OD PO, Cefuroxime 500mg/tab, 1 tab BID PO x 5 days, Celecoxib 200mg/tab , 1
tab OD PO or as needed for pain, Amlodipine 10mg/tab, 1 tab OD PO and follow up checkup at
OPD after 1 week.

Laboratories taken

CBC 7/5 7/6 7/7 Normal Values

WBC Count 11.76 H 14.23 H 9.66 4.4-11
RBC Count 5.73 H 4.92 4.80 4.5-5.1
Hemoglobin 141.00 122.00 117.00 L 123-153
Hematocrit 41.30 36.10 35.50 L 35.9-44.6
MCV 72.10 L 73.40 L 74.00 L 80-96
MCH 24.60 L 24.80 L 24.40 L 27.5-33.2
MCHC 34.10 33.80 33.00 L 33.4-35.5
RDW-CV 14.40 15.00 14.60 H 11.50-14.50
Platelet 197.00 198.00 194.00 150-450

Neutrophil 76.40 H 71.00 H 65.50 H 55-65

Lymphocyte 18.00 L 20.70 L 24.50 L 25-35
Monocyte 4.10 5.30 5.00 3-11
Eosinophil 1.30 2.60 4.70 H 2-4
Basophil 0.20 0.40 0.30 0-1

7/4 7/6 7/7 Normal Values

Creatinine 0.55 0.77 0.75 0.5-0.9
LDH 300.42 H 254.55 256.17 0-247.00
SGPT/ALT 13.61 17.21 19.32 0-34
 BUN 5.82 L 7.87-20.25
BUA 6.09 2.3-6.1
Sodium 139.40 135-145
Potassium 3.83 3.5-5.5
Chloride 109.30 98-108
Protime 7/4
Patient 11.60s
% Activity 102.80
INR 0.96
Control 13.00
% Activity 87.40
Control INR 1.09

7/4 Normal Values

Clotting Time 4’35” 3-6

Bleeding Time 2’10” 1-3

Blood Typing A+

CASE DISCUSSION

Epidemiology
How pregnancy incites or aggravates hypertension remains unsolved despite decades of
intensive research. It complicates 5 to 10 percent of all pregnancies, and together they are one
member of the deadly triad – along with hemorrhage and infection. Of these disorders,
preeclampsia syndrome either alone or superimposed on chronic hypertension, is the most
dangerous.

According to the World Health Organization, 16 percent of maternal deaths were

reported to be due to hypertensive disorders in developed countries. It is important to note that
more than half of these hypertension-related deaths were preventable. The American College of
Obstetricians and Gynecologists identified four types of hypertensive diseases in order to clearly
differentiate preeclampsia syndrome from other hypertensive disorders because it is potentially
more ominous. The four types are as follows:
 1. Gestational Hypertension
2. Preeclampsia and preeclampsia syndrome
3. Chronic hypertension of any etiology
4. Preeclampsia superimposed on chronic hypertension.

Diagnostics

Hypertension is diagnosed empirically when appropriately taken blood pressure exceeds

140 mm Hg systolic or 90 mm Hg diastolic. A woman is diagnosed with gestational hypertension
when blood pressure reach 140/90 mm Hg or greater for the first time midpregnancy, but in
whom proteinuria is not identified. Blood pressure is also noted to return to normal 12 weeks
postpartum.

Although preeclampsia isn’t simply gestational hypertension with proteinuria,

appearance of proteinuria remains an important diagnostic criterion. It is an objective marker
that reflects the system-wide endothelial leak, which characterizes preeclampsia syndrome.
Abnormal protein excretion is defined by a 24-hour urine excretion of more than 300 mg; a urine
protein: creatinine ratio of more than 0.3; or a persistent 30mg/dL (1+ dipstick) protein in random
urine samples. It is now appreciated that overt proteinuria may not be a feature in some women
with the preeclampsia syndrome. Because of this, the Task Force suggested other diagnostic
criteria which are evidence of multi-organ involvement which include thrombocytopenia, renal
dysfunction, hepatocellular necrosis, central nervous system perturbations, or pulmonary
edema.

Eclampsia is diagnosed in a woman who develops generalized convulsions occurring

before, during, and after labor which is not attributed to another cause. It generally occurs within
48 hours of delivery.

Chronic hypertension is diagnosed in a woman who has a documented BP of more than

140/90 mm Hg before pregnancy or before 20 weeks’ gestation or both. Hypertension also
persists more than 12 weeks postpartum.

Preeclampsia superimposed on chronic hypertension is diagnosed in a woman who has

chronic hypertension who has new onset or worsening baseline hypertension accompanied by
new onset proteinuria or other findings suggestive of preeclampsia. Superimposed preeclampsia
also occurs earlier, is more severe, and often accompanied by IUGR.

Risk Factors

Risk factors for hypertensive diseases include primiparity, primipaternity, history of

preeclampsia, obesity (present in the patient), family history of preeclampsia, black ethnicity,
maternal age more than 40 years old, pregnancy interval of less than two years of more than 10
years, previous miscarriage, and lastly, induced abortion. Underlying medical conditions such as
diabetes mellitus, APAS, immunological diseases, and infections also increases the risk. Molar
and multiple pregnancies are also known to increase the likelihood of preeclampsia.

Etiology

There are several identified probable mechanisms that is responsible for preeclampsia.
The important ones include:
1. Placental implantation with abnormal trophoblastic invasion of uterine vessels
2. Immunological maladaptive tolerance between maternal, paternal, and fetal
tissues
3. Maternal maladaptation to cardiovascular or inflammatory changes of normal
pregnancy
4. Genetic factors including inherited predisposing genes and epigenetic influence

Pathogenesis/Pathophysiology and Clinical Manifestations

Although the cause of preeclampsia is unknown, evidence for its manifestation begins
early in pregnancy with covert pathophysiological changes that gain momentum across gestation
and eventually become clinically apparent. Unless delivery supervenes, these changes ultimately
result in multiorgan involvement with a clinical spectrum ranging from an attenuated
manifestation to one of cataclysmic deterioration that is life threatening for both mother and
fetus. These are thought to be consequences of vasospasm, and ischemia.

Several etiologies were identified but there is still really no known cause. But the most
notably known underlying cause is the abnormal trophoblastic invasion of the decidua basalis
and endothelial walls of the spiral arterioles. Normally, these trophoblasts invade the decidua
and extend into the walls of the spiral arteriole to replace the endothelium and muscular wall to
create a dilated low-resistance vessel.

This event is called physiologic remodeling. However, with preeclampsia, defective

implantation is characterized by incomplete invasion of the spiral arteriolar wall by extravillous
trophoblasts leading to failure of physiologic remodelling. This results in a small-caliber vessel
with high resistance to flow. His leads to inability of the arterioles to meet the circulatory
demands and eventually lead to placental ischemia.

The hypoxic placental environment leads to the release of certain factors including
endoglin and sFlt which leads to decreased PGI2 or prostacyclin, and increased thromboxane A2,
a known vasoconstrictor, increased release of procoagulant factors leading to hypercoagulable
state which further leads to formation of thrombi in the arterioles and capillaries in different
body organs including the liver, brain, kidney and pituitary.

This event would lead to ischemia of these organs. Hepatocellular ischemia would
manifest as epigastric pain or right upper quadrant pain as the Glisson’s capsule is stretched due
to edema, as well as increase in the liver enzymes. In the kidney, this is manifested by proteinuria
as the protein can now able to pass through the glomerulus and retention of waste products
including creatinine and BUN. The effects on the brain is headache and visual disturbances and
even seizure that would complicate to eclampsia. There is no known significant effect to the
pituitary.
On the other hand, the endoglin would lead to a decrease in Nitric oxide which lead to
systemic vasoconstriction which is manifested as hypertension. This further leads to tissue
hypoperfusion. This event, together with thrombi formation, ultimately lead to hypertensive
disorder in pregnancy.

Prediction

Mean Arterial Pressure Test taken at 30-33 weeks could effectively identify women at risk
for preeclampsia. Values more than 90 mm Hg in the 2nd trimester and more than 105 mm Hg
in the 3rd trimester has resulted in increased incidence of preeclampsia and perinatal death.

Roll over test taken at 28-32 weeks’ gestation measures the hypertensive response of
women. It is positive if an increase of at least 20 mm Hg diastolic is documented. This predicts a
three-fold risk in developing preeclampsia.

Uterine Artery Doppler Velocimetry can detect faulty trophoblastic invasion of the spiral
arteries by showing decreased placental perfusion and upstream increase in resistance. Presence
of early diastolic notching compared to later diastolic flow in the uterine artery predicts a 50%
chance of developing preeclampsia in 18-24 weeks’ gestation.

Management

1. Control of convulsions using an intravenously administered loading dose of

magnesium sulfate that is followed by a maintenance dose, usually intravenous,
of magnesium sulfate.
2. Intermittent administration of an antihypertensive medication to lower blood
pressure whenever it is considered dangerously high
3. Avoidance of diuretics unless there is obvious pulmonary edema, limitation of
intravenous fluid administration unless fluid loss is excessive, and avoidance of
hyperosmotic agents.
4. Delivery of the fetus to achieve remission of preeclampsia.