This document discusses hypertensive disorders in pregnancy, which remain a leading cause of maternal mortality in Uganda. It defines various hypertensive disorders including chronic hypertension, gestational hypertension, preeclampsia, and HELLP syndrome. Risk factors, pathogenesis, clinical features, investigations, and management are described. Severe preeclampsia is treated with antihypertensive drugs like hydralazine to control blood pressure and delivery of the baby to resolve the condition. Hypertensive disorders continue to have high mortality and morbidity rates in Uganda.

1. HYPERTENSIVE DISORDERS IN
PREGNANCY
PRESENTED BY
DR. MATOVU RICHARD
AND
SR. NANDITTA SARAH

2. INTRODUCTION
 Is one of the most frequent cause of maternal morbidity and mortality.
 Black women are 3 time as likely to die from preeclampsia as white women
 Remains among the most significant and intriguing unsolved problems in
obstetrics. Complicating about 5-10% of all pregnancies.
 Majority of preeclampic pts are nulliparous patients.
 Increased mortality risk in older gravidas.
 Increased risk in first pregnancy with new partner
 Preeclampsia is a leading cause of direct maternal mortality

3. • In Uganda hypertensive disorders remain among the top 3 causes of maternal
mortality.(Heamorrhage, infection and HTN disorders)
• With a case-specific maternal mortality ratio of 780/100,000 live
births.(MOH,2018)
• Case- fatality ratio for all hypertensive conditions in pregnancy was 5.1%
according to the 2018 reports.
(http//bmcpregnancychildbirth.biomedcentral.co.ug)

4. RISK FACTORS
 Parity: PGs
 Maternal Age: Extreme Age (<18 & > 35 years old) some sources considered
older than 40.
 Genetic Predisposition. (You have a family history of preeclampsia)
 Poor socioeconomically status.
 Multifetal gestation. ( pregnant mothers with multiple babies (such as twins
or triplets).)
 Mothers who become pregnant using in vitro fertilization.

5.  Obesity: BMI > 35 OR have type 1 or type 2 diabetes.
 Molar Pregnancy
 Race: African-American
 Chronic disease: Hypertension, diabetes.
 Mothers who had preeclampsia during a previous pregnancy.
 Mothers having a history of thrombophilia (a condition that increases risk
of blood clots).
 Mothers having lupus (an autoimmune disease).
 Mothers with new partners

6. Classification of Hypertensive Disorders of
Pregnancy
1. Chronic Hypertension
2. Gestational Hypertension
3. Preeclampsia- eclampsia syndrome.
4. Preeclampsia superimposed on chronic hypertension

7. Chronic Hypertension
• History of Hypertension before pregnancy or once before 20 weeks of
pregnancy.
• Causes of chronic hypertension may be Primary (idiopathic; ) or
secondary to a known medical condition like renal disease.
• Up to 25% of patients with chronic hypertension develop preeclampsia.
( Granger JP, Alexander BT,2017)

8. 2. Gestational Hypertension
Hypertension that appears de novo after 20 weeks of gestation and normalizes after pregnancy.
However, some women with gestational hypertension have a higher risk of developing chronic
hypertension in the future. (no proteinuria, BP returns to normal < 12 weeks postpartum)

9. 3. Preeclampsia-eclampsia Syndrome.
De novo hypertension after 20 weeks’ gestation to 6 weeks after delivery,
accompanied by at least one of the following:
A. Proteinuria: 300mg/24 hours or protein: creatinine ratio of 0.3. OR
Dipstick reading of 1+.
B. Other features of maternal organ dysfunction including :
i. Acute kidney injury (creatinine ⩾90 µmol/L; 1 mg/dL),
ii. Liver involvement (elevated alanine aminotransferase or aspartate
aminotransferase >40 IU/L) with or without right upper quadrant pain
or epigastric abdominal pain
iii. Neurological complications (such as fits, altered mental status,
blindness, stroke, clonus, severe headaches, and persistent visual
scotomata)
iv. And hematological complications (decreased platelet count
<100,000/μL, disseminated intravascular coagulation, hemolysis)

10. C . Uteroplacental dysfunction (such as fetal growth restriction,
abnormal umbilical artery Doppler wave form analysis, or stillbirth)
Classified as
• Mild if only preeclampsia only and
• Severe if;
- Eclampsia.
- HELLP Syndrome

11. Eclampsia
• Eclampsia is defined by new-onset tonic-clonic, focal, or multifocal
seizures in the absence of other causative conditions such as epilepsy,
cerebral arterial ischemia and infarction, intracranial hemorrhage, or
drug in pregnant mother or after deliverly.
• Some of these alternative diagnoses may be more likely in cases in
which new-onset seizures occur after 48–72 hours postpartum or
when seizures occur during administration of magnesium sulfate.

12. DDX
ECLAMPSIA PREECLAPSIA
• Epilepsy
• Cerebral Artery Ischemia
• Cerebral Infarction
• Intra Cranial
Heamorrhage
• Uncontrolled
hypertension
• Aneurysms
• Metabolic disorders
• Pancreatic disease
• Immune thrombocytic
purpura
• Anti phospholipid
syndrome
• Hemolytic uremic
syndrome
• NAFL

14. 3. Preeclampsia superimposed on chronic hypertension.
• This is chronic hypertension that develop proteinuria before or after 20
weeks. Usually hypertension or need to change medications to control it.
• They present with altered lab results: reduced platelet count< 100,000,
elevated liver enzymes to twice normal.
• Other symptoms of headache, epigastric pain, pulmonary congestion or
oedema may be present.

15. PATHOPHYSIOLOGY
• Any hypertensive disorder of pregnancy can result in preeclampsia. It occurs in
up to 35% of women with gestational hypertension
• and up to 25% of those with chronic hypertension
• The underlying pathophysiology that upholds this transition to, or
superimposition of, preeclampsia is not well understood; however, it is thought
to be related to a mechanism of reduced placental perfusion, inducing systemic
vascular endothelial dysfunction.
• This arises due to a less effective cytotrophoblastic invasion of the uterine
spiral arteries. The resultant placental hypoxia induces a cascade of
inflammatory events, disrupting the balance of angiogenic factors, and
inducing platelet aggregation, all of which result in endothelial dysfunction
manifested clinically as the preeclampsia syndrome.

16. • Angiogenic imbalances associated with the development of preeclampsia
include;
• decreased concentrations of angiogenic factors such as the vascular
endothelial growth factor (VEGF)and placental growth factor (PIGF)
• and increased concentration of their antagonist( the placental soluble
fms-like tyrosine kinase 1 (sFlt-1). )which acts by impeding the binding of
VEGF and PIGF to their receptors leading to the reduction of nitric oxide
synthesis( a crucial factor in vascular remodeling and vasodilation, which
may otherwise be able to ameliorate placental ischemia.)
• Early-onset preeclampsia (EOPE), occurring before 34 weeks of gestation,
is thought to be primarily caused by the syncytiotrophoblast stress leading
to poor placentation, whereas late-onset preeclampsia (LOPE), occurring
at or after 34 weeks, is understood to be secondary to the placenta
outgrowing its own circulation. It is worth mentioning that EOPE is more

17. Abnormal cytotrophoblast invasion
Reduce uteroplacental perfusion
Endothelial cell activation and dysfunction
Vasospasm Capilar Leak Activation of coagulation
Edema Proteinuria
Hemoconcentration
HTA Oliguria Liver
Ischemia
Seizures Abruptio
Thrombocytopenia
Vasoactive Agents:
-Prostaglandins
TxA2
-Endothelins

18. HELLP SYNDROME
• Heamolysis,
• Elevated Liver Functions( bil>1.2mg/dl,LDH>600U/l,SGOT>70U/l).
• Low platelet count< 100,000

19. HELLP SYNDROME
• A severe form of preeclampsia, has the following lab criteria:
(i) Haemolysis (H).
(ii) Elevated liver functions(H): total bil>1.2mg/dl, lactate
dehydrogenase LDH>600U/L,serum glutamic oxaloacetic
transaminase>70U/L
(iii) Low platelets (LP)< 1,000,000/mm3

20. PREECLAMPSIA AS
A SYNDROME
c/m of Hypertensive disorders in pregnancy
CNS: Headache, cerebral
edema, fits, hemorrhage,
hyper reflexia.
CLOTTING SYSTEM: Increased Platelet
aggregation, fibrinogen consumption,
increased TA2 production
EYES: Blurred vision,
flashes, transient
blindness, retinal
edema, etc.
KIDNEYS:
Proteinuria,
oliguria,renal
failure.
LIVER: sub capsular
hemorrhages, abnormal
enzymes productions, rupture
CVS: Hypertension,
pulmonary edema, heart
failure, endothelial damage
GIT: N&V, RUQ abd pain.
Hemopoioetic system: Hemolysis
, Abnormal platelet function

21. Severity of Preeclampsia
Abnormality Mild Severe
 Diastolic blood pressure < 100 mm Hg 110 mm Hg or higher
 Proteinuria Trace to 1+ Persistent 2+ or more
 Headache Absent Present
 Visual disturbances Absent Present
 Upper abdominal pain Absent Present
 Oliguria Absent Present
 Convulsion (eclampsia) Absent Present
 Serum creatinine Normal Elevated
 Thrombocytopenia Absent Present
 Liver enzyme elevation Minimal Marked
 Fetal growth restriction Absent Obvious
 Pulmonary edema Absent Present

23. Goals in the managements of hypertension
1. Control of BP.
2. Prevent fits.
3. Deliver the baby

24. General
Admit women with onset hypertension or development
proteinuria.
Diet: reduce salt intake.
Monitoring body weight weekly.
Monitoring and manage Blood pressure.
Investigations.
Steroid if the GA is between (28 – 34 weeks)
Assessment of the fetus.

25. Investigations
Hematologic
• Hemoglobin, platelets, blood film
• Clotting profile: PT, PTT, BT, CT.
 Hepatic (Liver function test)
• ALT, AST (serum hepatic transaminasa level)
• Bilirrubin .
Renal (renal function test)
• Proteinuria in 24 hours.
• Creatinine, Urea, Uric Acid
Cardiovascular: EKG
Abdominal US scan.

26. Assessment of Fetus
Fetal movement
Fetal heart rate assessment (CTG)
Ultrasound for growth (fetal Biometric)
Biophysical profile
Amniotic fluid volume (AFI)
Doppler flow studies

28. Criteria to start antihypertensive treatment:
I. Oral treatment: 150/100 mm/hg
(Maintenance Therapy)
I. IV treatment: 160/ 105-110 mm/hg.
(Acute Therapy)

29. Anti-hypertensive Agents
A) Acute Therapy
Arteriolar Dilators
• Hydralazine
ß-Blockers
• Labetalol
Calcium Channel Blockers
• Nifedipine

30. Anti-hypertensive Agents
B) Maintenance Therapy
Centrally Acting Sympatholytic Agents
• Methyl-dopa
ß-Blockers
• Atenolol
• Labetalol
Calcium Channel Blockers
• Nifedipine

31. Acute Therapy BP: 160/110 mm/hg
Hydralazine (20 mg): ( Peripheral vasodilator)
Is the best option for under developing countries, due to
safety, efficacy, cheap and availability.
Doses IV.
Bolus: 5mg IV over 1 to 2 min, followed by repeated bolus at
20 min intervals up to 30 mg, BP’s fall usually appear within
10 to 30 min.
Inf: 60 to 80 mg in 500 ml of water for injection or normal
saline. 10 drops x mits “control”. Mornitor bp closely.

32. Acute Therapy BP: 160/110 mm/hg
LABETALOL (100 mg/20ml). Combined 1 and ß-blocker
Doses IV
Bolus: start with 20 mg IV followed at 10 minute
intervals by doses of 20 to 80 mg up to a
maximum total cumulative dose of 300 mg.
Inf: 1-2 mg/min can be used maximum 160 mg/hr.

33. Acute Therapy BP: 160/110 mm/hg
Nifedipine: (tbs 10 -20mg) every 30min, 3 doses

34. Maintenance Therapy
Methyldopa: tbs 250 mg (centrally acting a2-receptor agonist)
Dosage: 750 - 2000 mg/day, in 3 - 4 divided doses
 Hydralazine: tbs 25 mg (Arteriolar Dilators)
Dosage: 50 – 100 mg/day. Max 100mg
 Atenolol: tbs 50-100 mg (ß1-receptor antagonist)
Dosage: 50 – 150 mg/day, od-tid max 150mg.
Nifedipine: tbs 10 – 20 mg (Calcium Channel Blockers)
Dosage: 30 – 120 mg/day. Bd-qid max 180mg/day.
NB: 1) Some patient need combine drugs to control Bp
2) plasma volume expansion not required.

35. INDICATIONS FOR CONSERVATIVE MANAGEMENT IN PRETERM PREGNANCY
• Elevated bp BP.
• Proteinuria < 2 g.
• Liver enzymes normal
• No fetal compromise.
• Pregnancy is < 36weeks of amenorrhea.

36. Deliver the Baby
• When to Deliver
–  37 weeks with gestational hypertension
–  34 weeks with severe gestational hypertension
– < 34 weeks with any of:
• poorly controlled dBP
• lab evidence of worsening end-organ involvement
• suspected fetal compromise
• uncontrolled seizures
• symptoms unresponsive to appropriate therapy

37. Stop convulsions and prevent recurrence, continue
with mgso4 until 24 hours after the last convulsion.
Prompt delivery, at any gestational age.
Lower diastolic blood pressure to 90-100mmhg.
Eclampsia basic principles of management

38. To control and prevent FIT recurrences.
• MgSO4
• Diazepam
• Phenobarbital
• Phenytoin

39. MgSO4 To control and prevent FIT recurrences.
Prichard Method Doses.
Initially:
4 g of 20 % given as a bolus followed by;
5g of 50 %in each buttock.
Maintenance:
5g of 50 % given IM 4 hourly alternating each buttock for
24 hours.

40. Zuspan’s method.
6 g of MgSO4, 20 % given as a bolus iv 20 min.
Followed by an infusion of 20 g within 24 hours.

41. Side effects and surveillance.
• Magnesium toxicity is related to serum concentration:
• Loss of deep tendon reflexes occurs at 8 to 10 mEq/L,
• Respiratory paralysis at 10 to 15 mEq/L,
• Cardiac arrest at 20 to 25 mEq/L.
Magnesium therapy also results in transient reduction of
total and ionized serum calcium concentration due to
inhibition of parathyroid hormone and increased calcium
excretion

42. Side effects and surveillance.
• Respiratory rate <than 12/min.
• Urine out put < than 30 ml/h.
• Loss ofTendon reflexes ( patellar)
So always check for these signs before furthur
administration.
Antidote
Calcium gluconate 1g IV should be given in case of
overdose or intoxication.

43. Major points in the Mngt of HELLP syndrome.
• Correction of coagulopathy if DIC is present.
• IV magnesium sulphate to prevent convulsions( even if HTN is not
severe).
• Lower dBP to 90-100mmHg. Use hydralazine or labetalol.
• High steroid doses to the mother, 10mg every 12 hours to promote
normal liver function test and platelet count.
• Induce labour, if mother and fetus are stable
• computed tomography of the abdomen, if subscapular hematoma of
the liver is suspected ( ind. For massive blood transfusion-
FFP/platelets as well as immediate laparotomy)

46. Our REFs
• Redman CW, Staff AC. Preeclampsia, biomarkers, syncytiotrophoblast stress, and placental capacity. Am J
Obstet Gynecol 2015; 213(4 Suppl.): S9.e1, S9–S11. [PubMed] [Google Scholar]
• . Osol G, Ko NL, Mandala M. Altered endothelial nitric oxide signaling as a paradigm for maternal vascular
maladaptation in preeclampsia. Curr Hypertens Rep 2017; 19(10): 82. [PubMed] [Google Scholar]
• . Granger JP, Alexander BT, Bennett WA, et al. Pathophysiology of pregnancy-induced hypertension. Am J
Hypertens 2001; 14: 178S–185S. [PubMed] [Google Scholar] Ngene NC, Moodley J. Physiology of blood
pressure relevant to managing hypertension in pregnancy. J Matern Fetal Neonatal Med. Epub ahead of print
27 November 2017. DOI: 10.1080/14767058.2017.1404569. [PubMed] [CrossRef] [Google Scholar]