ISI KANDUNGAN

INTRODUCTION
LITERATURE REVIEW/FINDINGS
ETIOLOGY
CLINICAL MANIFESTATION/
PRESENTATION
PATHOPHYSIOLOGY
DIFFERENTIAL DIAGNOSTIC
DISSCUSSION
TREATMENT
ASSISTANT MEDICAL OFFICER ROLE
CONCLUSION
REFFERENCE

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INTRODUCTION
A condition in which only occur to a pregnant woman, with the criteria of hypertension,
proteinurea, and systemic dysfunction. This is one of the complication occurred in pregnancy,

which is 5% in normal pregnancy, and 11% for primagravida. PIH is the third causes of
maternal death.

CASE STUDY
NAME: Yuliana Bajri (210/14)
AGE: 35
ETHNIC: Bugis
OCCUPATION: Housewife
COMPLAINT: persistent headache X 3/7
HISTORY:
-Patient came to Mother&Child Health (MCH) Klinik Menggatal with complaints of
persistent headache. Associates with nausea and vomiting , epigastrium pain and oedema in
leg.
-Known case of LSCS in 2003 due to foetal distress .
EXAMINATION:
-B/P 152/90
-UFEME (alb=neg, glu=neg)
-PROTEINUREA +1

LITERATURE REVIEW / FINDINGS

PREGNANCY INDUCED HYPERTENSION (PIH)
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Pregnancy induced hypertension is commonly known in pregnant woman (20/52 weeks and
above). The condition in which raised in the blood pressure (< 140/90), presence of protein in
urea, and oedema in leg.
PIH increases the risk of preterm delivery ,intrauterine growth retardation (IUGR), hepatic
rupture , foetal and maternal death. Occur 10% in every pregnancy, second causesof maternal
death after postpartum haemorrhage. Commonly occur to primigravida or in twins pregnancy
or more.
PIH is classified into 3 stages/conditions;

Gestational hypertension
-No proteinurea
-High blood pressure (PIH)
Pre-eclampsia
-PIH
-Proteinurea
-oedema (leg/hands)
Eclampsia
-PIH
-Convulsion

ETIOLOGY
Unknown, some says it is due to genetic disorder, and some says the immune system in the
maternal body that causes PIH.
In the early stages of pregnancy, it is linked to the abnormalities of the development of
placenta (completed in 18 weeks), the spiral arteries that supply nutrient to placenta became
narrow , and causes vasospasm and ischemic to placenta.

Risk factor for PIH includes:

Not modifiable risk factor

-Extremes age
-Primigravida
-personal or family history of hypertension
Modifiable risk factor
-Multiple Gestations
-Molar Pregnancy
-Diabetes
-Kidney Failure

CLINICAL MANIFESTATION/PRESENTATION

Oedema
Rapid weight gain
Frontal headache
Visual changes (e.g; scotoma)
Oligouria
Loss of consciousness
Seizures
Tinnitus
Tachycardia
Nausea/vomiting
Haematemesis
Hepatomegaly
RUQ or epigastric pain suggest HELLP syndrome

PATHOPHYSIOLOGY

The actual pathogenesis of PIH is not have been fully understands and elucidated yet, despite
of being one of the major causes of maternal death. However, studies during the past decade
show a better understanding of the potential mechanisms responsible for the pathogenesis of
PIH. The initiating event in PIH appears to be reduced ureteroplacental 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 result in
enhanced formation of endothelin and thromboxane , increased vascular sensitivity to
angiotensin II, and decreased formation of vasodilators such as nitric oxide and protacyclin.
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. The investigator are also attempting to elucidate the placental
factors that are responsible for mediating activation/dysfunction of the maternal vascular
endothelium. Microarrays analysis of genes within the ischemic placenta should provide new
insight into the link between placental ischemia and hypertension.
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More effective strategies for the prevention of preeclampsia should be forthcoming once the
underlying pathophysiologic mechanism that are involved in PIH are completely understood.

CHRONIC PIH : Elevated blood pressure prior to pregnancy or occurring before the 20th
week of pregnancy
CHRONIC HTN with PREECLAMPSIA: Patient with hypertension prior to pregnancy who
then develops pre-eclampsia or eclampsia.
TRANSIENT HTN: New onset of HTN without preeclampsia symptoms.
PRE-ECLAMPSIA: HTN, oedema, proteinuria thatoccur during pregnancy; likely secondary
to a placental abnormality causing vasospasm and fluid retention.
ECLAMPSIA: Pre-eclampsia symptoms followed by seizures ; may occur from the 12th week
of gestation through the 10th postpartum day.

DIFFERENTIAL DIAGNOSIS

Chronic hypertension
Secondary hypertension
(e.g; cushing disease, hyperaldosteronism, pheochromocytoma, renovascular)
HELLP syndrome
Hydatidiform mole
Cocaine or amphethamine use
Meningitis/encephalitis
Epilepsy
Physiologic oedema of pregnancy
Central venous thrombosis
Intracranial haemorrhage

DISCUSSION
INVESTIGATION
Criteria of diagnostic PIH/pre-eclampsia (all 3 must present)
Blood pressure >140/90 or rise in systolic BP by 30 mmHg or diastolic BP by 15
mmHg above baseline; diagnosis requires 2 elevated pressure at rest, taken 6 hours
apart.
Oedema resulting in a 5 lb weight gain within 1 week
Proteinurea of 1+ on urine dipstick or 300mg/24 hours
Obtain CBC (TRO hemolysis), liver function test (TRO HELLP syndrome), renal
function test, and coagulation profile (PT/PTT)
Ultrasound may show intrauterine growth retardation , foetal distress , oligohydramnious
or molarpregnancy (multi pregnancy)
Head CT may be used in patients who do not respond to magnesium treatment in order to
rule out other pathologies.

TREATMENT

PRE-ECLAMPSIA

-Bed rest in the left lateral decubitus position

-Acetaminophen for headache
-Continuous foetal monitoring
-Avoid IV fluids (worsen the oedema)
-IV magnesium sulphate infusion decreases blood pressure and the seizures threshold;
frequently check for evidence of magnesium toxicity (e.g,hyporeflexia)

SEVERE PRE-ECLAMPSIA or ECLAMPSIA

-Magnesium for seizures (benzodiazepines are less effective)

-Definitive therapy is delivery of foetus
-Foetal heart rate

B/P control is indicated in chronic HTN or in pre-eclampsia if diastolic B/P remains

>110 mmHg after administration of magnesium

-First line therapy is hydralazine or methyldopa ; labetolol or nipride may be used in

refractory cases
-Contraindicated antihypertensive medications include ACE inhibitors, thiazides and
propanolol.

ASSISTANT MEDICAL OFFICER ROLE INTHIS CASE

Assisting in tracing the pregnant woman during daily examination and refer to Mother
& Child Health (MCH) clinics to do appointment.
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Examine and giving treatment to the cases that referred to them and refer to specialist

or hospital if needed.
Tracing the defaulter cases
Giving appointment for another treatment
Active case detection or passive case detection ,especially for the defaulter and high

risk patient
Teamwork with others paramedics (nurses/doctor) in giving health education and

counselling or promotion for mothers or family

Constant updating of medical information for more effective patient management

CONCLUSION
In a nut shell, PIH appear to be the 3rd causes of the maternal death. It is one of the
complication that happens during pregnancy. Pre-eclampsia may still occur up 10 days after
delivery obstetric/gynecology consultation is mandatory. The majority of pre-eclamptic
patient are admitted; occasionally , reliable patients with good follow up and mild disease
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will be discharge after consultation with OB/Gyn. Eclamptic patient are always admitted for
IV medications. Complications of pre-eclampsia or eclampsia include seizures , placental
abruption, intracerebral haemorrhage, pulmonary oedema, HELLP syndrome, liver
haemorrhage, renal failure .

REFFERENCE

In a page emergency medicine / [edited by Jeffrey M. Caterino, Scott Kahan.

Blackwell publishing.
www.ncbi.nlm.nih.gov/pubmed/11411754
m.hyper.ahajournals.org/content/37/2/232.full
www.scielo.br/scielo.php?pid=s0103-21002008000100008&script=sci_arttext

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