PATIENT’S DATA:

Madam Laili Asniza Binti Mastor, a 30 year old Malay lady, gravida 2 para 1,
currently at 36 weeks of gestation. She couldn’t remember her last menstrual period
(LMP), the cycle has been irregular and she was not on any form of hormonal
contraception. Given revised date of delivery (REDD) is at 10 January 2010, based on
scan at 33 weeks of gestation.
Date of Admission: 5 January 2010
Date of Clerking: 6 January 2010
Source of information: Patient

PRESENTING COMPLAINT:
She was admitted from Antenatal Clinic Hospital Sultan Ahmad Shah for further
management of symptoms of Impending Eclampsia and high blood pressure
(160/110mmHg).

HISTORY OF PRESENTING COMPLAINT:

She suspected the pregnancy when her distended abdomen was noted by her
friends. She had her pregnancy confirmed at nearby clinic by ultrasound scanning. She
was told that her pregnancy is about 33 weeks of gestation. Then she had her booking at
KK Triang. She underwent several blood test, urine test and ultrasound. However she did
not know the result except that she was told the result was normal. Unfortunately, her
booking blood pressure was 140/90 mmHg and her haemoglobin level was 11.4 g/dL.
She also had pedal oedema. She on rountine hematinic and antihypertensive drug T.
Labetolol since that. She was asked to come every other day (EOD) for blood pressure
reading, urine test, ultrasound scanning and weight measurement. All results came to be
normal.
She had history of admission to this hospital referred from Hospital Jengka at 34
weeks of gestation due to high blood pressure 160/110 mmHg. She was given T.
Labetolol and intravenous Hydralazine while she was at Hospital Jengka. She also
completed the Dexamethasone course. At 36 weeks of gestation during antenatal check
up at this hospital, she had high blood pressure 160/110mmHg. She also had symptoms

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of impending eclampsia such as headache, dizziness and nausea. However there was no
blurring of vision, no vomiting, and no epigastric pain. There were no signs and
symptoms of labour such as uterine contraction, leaking liquor and show. Fetal
movement is good. She was given MgSO4 stat and admitted to High Dependency Unit for
close monitoring.
Since admission, her blood pressure is being monitored and she had PE profile
done and also ultrasound. Her baby was monitored with CTG. She was given intravenous
Hydralazine and MgSO4 regime to control her blood pressure. Modified oral glucose
tolerance test (MOGTT) was done due to family history of Diabetes mellitus and the
result was normal. So far, she had no complications and not in labour. According to her,
she will be induced to deliver the baby as soon as her blood pressure is normal.

SYSTEMIC REVIEW:
Cardiovascular system: There is no chest pain, palpitation, orthopnea and paroxysmal
nocturnal dyspnoea.
Respiratory system: She had no cough, shortness of breath. No heamoptysis.
Gastrointestinal system: There is no alteration bowel habit, no nausea and vomiting,
diarrhea and hematemesis.
Genitourinary system: There was no dysuria and hematuria, no polydypsia, urgency,
swollen ankle or urinary incontinence.
Central Nervous System: There was no headache, blurred vision

PAST OBSTETRIC HISTORY:

She delivered a baby boy in year 2000 from her first marriage via lower segment
cesarean section (LSCS) due to fetal distress; currently her child is alive and well. In
previous pregnancy she also had late diagnosed PIH. The birth weight of her child was
2.8 kg. The operation was uncomplicated. There is no history of premature labour. She
breastfed her child for 5 months and took traditional medication after she had her first
child.

PAST GYNAECOLOGY HISTORY:

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 This is her second marriage. They have been married since 2005. She attained
menarche at 12 years old, irregular cycle but good flow lasting for 5 days. There is no
menorrhagia, dyspareunia and intermenstrual bleeding. No Pap smear and past
gynaecological surgical history were done.

PAST MEDICAL/SURGICAL HISTORY:

She had no history of diabetes mellitus, hypertension, heart diseases, asthma or
bleeding tendencies however she had history of cesarean section in 2000. There is no
known drug or anaesthetic allergies.

MEDICATION/DRUG HISTORY:

As far as she knows, she is on antihypertensive drug. She did not take any
traditional medication during her pregnancy. She also took the routine haematinic given
by the doctor and she is not allergic to any drug.

FAMILY HISTORY:
Her mother had Diabetes mellitus but there was no family history of other
medical illnesses such as hypertension, heart diseases, and asthma, bleeding tendencies,
breech and congenital abnormalities.

SOCIAL HISTORY:
She is a housewife while her husband did village works. Her family income is
RM 300 monthly indicates that she from low socioeconomic class. She does not smoke or
consume alcohol however she is a passive smoker.

PHYSICAL EXAMINATION:
General Examination
On inspection, the patient is alert, conscious with GCS 15/15 not in pain and not
in respiratory distress at that time lying on her bed. She is fairly hydrated and has
moderate body built. Her vital signs were:
Blood Pressure – 150/90 mmHg

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 Pulse Rate - 80 beats/ minute, good volume and regular rhythm,
Temperature - 37 ˚C
There were no facies abnormalities, muscle wasting, scars or any other abnormalities.
There were also no signs of jaundice, pallor or cyanosis. Reflexes are normal.
Hand: Warm, no excessive sweating, capillary filling time was less than 2 seconds, no
finger clubbing, no Dupuytren contracture, no palmar erythema,
Eye: There are no signs of pallor on the conjunctiva and jaundice on the sclera.
Mouth: No central cyanosis, no gum bleeding and hydration was fair.
Neck: No anterior neck swelling was palpable, JVP not elevated
Lower limb: There is pedal edema, but no calf tenderness and visible dilated vein.
Lymph nodes: No palpable lymph nodes detected.

Specific physical examination

[Abdomen]
Inspection: Abdomen is distended by gravis uterus as evidence by linea nigra and striae
gravidarum. There is suprapubic tranverse incision scar. The umbilicus is centrally
located and inverted.
Palpation: On light palpation, the abdomen is soft, non tender. No scar tenderness. No
uterine contraction felt. On deep palpation, the fundal height correspondence to 36 weeks
of gestation. It measures 36 cm. There is singleton fetus in longitudinal lie with the fetal
back on left side of the mother. The presentation is cephalic. The head is not engage yet
and it is about 5/5 palpable. The amount of liquor is adequate for this period. The
estimated fetal weight is about 3.0-3.2kg.
Auscultation: The fetal heart is heard and regular at 140 beats per minute.
Vaginal examination should be done to complete this examination.

[Breast]
Both breast are symmetrical bilaterally, no visible or palpable mass and dilated veins, no
nipple discharge.

Systemic examination

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[Cardiovascular system]
The first and second heart sounds were present and normal. There were no murmur and
added heart sound.

[Respiratory system]
Air entry equal bilaterally with vesicular breath sound. Vocal resonance was equal on
both sides.

CASE SUMMARY:
Madam LA, a 30 year old Malay lady gravida 2 para 1 currently at 36 weeks of
gestation admitted from Antenatal Clinic for further management of symptoms of
Impending Eclampsia and high blood pressure (160/110mmHg). On examination, there is
no scar tenderness, fetal in longitudinal lie with the fetal back at left side of the mother.
The presentation is cephalic. Currently, her blood pressure is stable no uterine contraction
felt and the plan to induce her is carried out as planned.

PROVISIONAL DIAGNOSIS:
Pregnancy induced hypertension
Reason for: Blood pressure more than 140/90 mmHg occurring after 20 weeks of
gestation in previously normotensive woman,can be associated with proteinuria
and after the pregnancy is over the blood pressure should return to normal.

LABORATORY INVESTIGATIONS:
Date/Time Event Value: 5/1/2010
Full Blood Count (FBC)
To assess hemoglobin and platelet count in this patient.
Haemoglobin – 12 x 103 / mm3 (11.5- 16)
Platelet – 459 x 103 / mm3 (140-440)
White Blood Cells - 6.6 x 103 / mm3 (4-10)
Interpretation: All parameters show no abnormalities.

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Liver Function Test (LFT)
To assess the level of aminotransferases and protein level especially albumin level
Total protein – 64 g/L (55-82) Albumin – 36 g/L (27-46) Globulin – 28 g/L (28-
36) A/G ratio – 1.3 (0.9-1.8) ALP – 139 u/L (20-95) ALT – 18 u/L (0-30) Total
bilirubin – 3 umol/L (3.4-17.1)
Interpretation: All parameters show no abnormalities.

Renal Profile (RP)

To assess glomerular and tubular function of the kidney.
Urea – 1.3 mmol/L (2.5-7.5) Sodium – 138 mmol/L (135-148) Potassium – 4.2
mmol/L (3.5-5.2) Chloride – 105 mmol/L (95-108) Uric acid – 412 umol/L (120-
420) Creatinine – 27 umol/L (44-80)
Interpretation: All parameters show no abnormalities.

Urine Analysis (24 Hr Urine Protein)

To look any presence of protein in the urine to exclude pre-eclampsia and to assess
the severity of the proteinuria quantitatively.
Result : 100 mg/dl
Interpretation : The proteinuria is not severe because significant proteinuria is more
than 300 mg/dl.

Urine FEME
To rule out urinary tract infection
RBC/uL – 5 WBC/uL – 25

Coagulation Profile
Prothrombin tine (PT) – 12.4 s (10-14)
Activated Partial Thromboplastin Time (APTT) – 31.6 s (35-45)
International Normalized Ratio (INR) – 0.94 s (0.9-1.2)
Interpretation: All parameters show no abnormalities.

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Date/Time Event Value: 6/1/2010
MOGTT
Fasting blood sugar – 4.1 mmol (3.9-6.1)
2 hours postprandial – 5.7 mmol

MANAGEMENTS:
Antepartum management

Since admitted to HDU, CTG was done before intravenous MgSO4 was given.
Close blood pressure monitoring was done and intravenous Hydralazine and MgSO4
regime was given to reduce and maintain her blood pressure at least at 140/90 mmHg.
Patient was asked to record fetal movements (FKC) and continued patient with T.
Labetolol. PE profile was done on day of admission but the result came back to be
normal. MOGTT was done afterwards due to history of Diabetes mellitus in her family
and the result was normal. She will be induced to deliver the baby as soon as her blood
pressure is normal.

Intrapartum management

However while she was in labour, the CTG showed sign of fetal distress and
emergency Cesarean section was done. A baby boy was delivered with cord round neck
x1 and thick meconium stained liquor. The birth weight of the baby is 2.8 kg and Apgar
scores 8 and 9 respectively in first and 5 minutes after delivery. Estimated blood loss is
1000 cc.
Postpartum management

1. Allow discharge
2. Discharge with hematinics and analgesic
3. EOD blood pressure reading at KK
4. TCA 6 weeks at local clinic for post natal review/pap smear and contraceptive advice
5. TCA stat if experience excessive per vaginal bleeding/fever or abdominal pain
6. Advice patient for LSCS and bitubal ligation (BTL) for next pregnancy

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 DISCUSSION:

There are three classifications of Hypertensive Disorders in Pregnancy:Chronic

Hypertension – Known hypertension before pregnancy or rise in blood pressure to >
140/90 mmHg before 20 weeks. Pre-eclampsia/Eclampsia – Rise of blood pressure of >15
mmHg diastolic or >30 mmHg systolic from measurement in early pregnancy or to >
140/90 mmHg in late pregnancy if no early reading available; plus proteinuria (>3gm per
24hours and/or Edema). Transient hypertension – Rise in blood pressure as for
preeclampsia/eclampsia; NO proteinuria (>3gm per 24 hours). [2]
The initiating event in PIH appears to be reduced uteroplacental perfusion as a
result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is
thought to lead to widespread activation/dysfunction of the maternal vascular endothelium
that results in enhanced formation of endothelin and thromboxane, increased vascular
sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide
and prostacyclin. The quantitative importance of the various endothelial and humoral
factors in mediating the reduction in renal hemodynamic and excretory function and
elevation in arterial pressure during PIH is still unclear. [1]
Symptoms of preeclampsia: Visual disturbances typical of preeclampsia are
scintillations and scotomata. These disturbances are presumed to be due to cerebral
vasospasm. Headache is of new onset and may be described as frontal, throbbing, or
similar to a migraine headache. Epigastric pain is due to hepatic swelling and
inflammation, with stretch of the liver capsule. Pain may be of sudden onset, is typically
constant, and may be moderate to severe in intensity. While mild lower extremity edema is
common in normal pregnancy, rapidly increasing or nondependent edema may be a signal
of developing preeclampsia. Edema is no longer included among the criteria for diagnosis
of preeclampsia. Rapid weight gain is a result of edema due to capillary leak as well as
renal sodium and fluid retention. [3]

Maternal personal risk factors for preeclampsia: First pregnancy, New

partner/paternity, Age younger than 18 years or older than 35 years, History of

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preeclampsia, Family history of preeclampsia in a first-degree relative, Obesity (BMI 
30). Maternal medical risk factors for preeclampsia: Chronic hypertension, especially when
secondary to such disorders as hypercortisolism, hyperaldosteronism, pheochromocytoma,
or renal artery stenosis, Preexisting diabetes (type 1 or type 2), especially with
microvascular disease, Renal disease and Systemic lupus erythematosus. Placental/fetal
risk factors for preeclampsia: Multiple gestations, Hydrops fetalis, Gestational
trophoblastic disease and Triploidy. [3]
The risk of pre-eclampsia is higher in first pregnancies (4.1%) than in subsequent
ones (1.7%). The lower overall risk of pre-eclampsia among parous women is not explained
by fewer pregnancies among women who experienced pre-eclampsia in a previous
gestation. The risk of recurrence is around 15% for women who had pre-eclampsia in one
previous pregnancy and around 30% when two consecutive previous pregnancies were
affected. Recurrence is higher for pre-eclampsias associated with very preterm delivery. [4]

REFERENCES:

1. Joey P. Grange, Barbara T. Alexander, William A. Bennett and Raouf A. Khalil

Pathophysiology of pregnancy-induced hypertension Am J Hypertens (2001) 14, 178S–
185S; doi: S0895-7061(01)02086-6

2. Roberts, James M.; Redman, Christopher W. G. Preeclampsia: More Than Pregnancy-

Induced Hypertension Obstetrical & Gynecological Survey: January 1994 - Volume 49 -
Issue 1 - pg 6-7

3. Paul Gibson, Michael P Carson Hypertension and Pregnancy eMedicine Specialities

> Obstetrics and Gynaecology > Medical Problems in Pregnancy

4. Sonia Hernández-Díaz, Sengwee Toh, Sven Cnattingius Risk of pre-eclampsia in

first and subsequent pregnancies: prospective cohort study BMJ 2009; 338:b2255