The SA Journal Diabetes & Vascular Disease Vol 16 No 1 (July 2019)

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SA JOURNAL OF DIABETES & VASCULAR DISEASE RESEARCH ARTICLE
VOLUME 16 NUMBER 1 • JULY 2019 9
to sit quietly for five to 10 minutes before each blood pressure
measurement, and blood pressure should be measured in lateral
recumbency with the cuff at the level of the heart. Korotokoff
sounds I and V should be used to define the systolic and diastolic
blood pressure, respectively. In about 5% of pregnant women, an
exaggerated gap exists between the fourth and fifth Korotokoff
sounds with the fifth sound approaching zero. In this type of case,
the fourth sound may more closely approximate the true diastolic
blood pressure.
Signs of secondary hypertension such as buffalo hump, wide
purple abdominal striae suggesting glucocorticoid excess, systolic
bruit heard over the abdomen or in the flanks suggesting renal
artery stenosis, and radio-femoral delay or diminished pulses in
the lower versus upper extremities suggesting aortic co-arctation
should be looked for. The presence of a fourth heart sound on
auscultation is not a normal finding in pregnancy and may suggest
left ventricular hypertrophy from chronic hypertension. Carotid
bruits may also reflect atherosclerotic disease due to longstanding
hypertension. In addition, retinal changes of chronic hypertension
may be noted. Retinal vasospasm and retinal oedema, which
may manifest as severely impaired vision, generally reflects pre-
eclampsia.
In pre-eclampsia right upper-quadrant abdominal tenderness
stemming from hepatic swelling and capsular stretch may be
seen. Although brisk or hyperactive reflexes are common during
pregnancy, clonus is a sign of neuromuscular irritability that usually
reflects severe pre-eclampsia.
Laboratory investigations the physician must order
Laboratory investigations to evaluate chronic hypertension include
testing for target-organ damage, and to exclude secondary causes
of hypertension and co-morbid factors. For chronic hypertension
in the first trimester, it is very useful to obtain a full blood count,
electrolyte, urea and creatinine levels, liver enzyme concentrations
and testing for proteinuria. These serve as baseline values to be
referred to later in the pregnancy if there is a concern regarding
superimposed pre-eclampsia.
Serum lipids usually increase during pregnancy and therefore
measurement should be deferred until the postpartum period. Also,
the increase in endogenous corticosteroids levels during normal
pregnancy makes it difficult to evaluate for secondary hypertension
due to adrenal corticosteroid excess.
Useful blood tests when evaluating eclampsia and pre-eclampsia
include urinalysis, a full blood count, serum electrolyte levels, urea
and creatinine 24-hour urinary protein excretion, and serum uric
acid, liver enzyme and bilirubin levels.
Follow up
The long-term implications of having a pregnancy complicated by
pre-eclampsia or hypertension have been highlighted above. It is
important that pregnant women with hypertensive disease be given
every opportunity to attend appropriate follow-up care in order to
prevent long-term premature morbidity and mortality.
References
1. Ebeigbe P, Igberase G, Aziken M. Hypertensive disorders in pregnancy: experience
with 442 recent consecutive cases in Benin city, Nigeria. Niger Med J 2007; 48(4):
94–98.
2. Chowa P, Lin C, Goma F, South-Paul J. Prevalence of hypertension among women
of child bearing age in Zambia. Med J Zambia 2011; 38(3): 3–8.
3. Davey DA, MacGillivray I. The classification and definition of the hypertensive
disorders of pregnancy. Am J Obstet Gynecol 1988; 158(4): 892–898.
4. Sibai B, Dekker G, Kupferminc M. Pre-eclampsia. Lancet 2005; 365(9461): 785–
799.
5. Seely EW, Ecker J. Chronic hypertension in pregnancy. New Engl J Med 2011;
365(5): 439–446.
6. Pijnenborg R, Anthony J, Davey DA, Rees A, Tiltman A, Vercruysse L, et al .
Placental bed spiral arteries in the hypertensive disorders of pregnancy. Br J
Obstet Gynecol 1991; 98(7): 648–655.
7. Lindheimer MD, Taler SJ, Cunningham FG. ASH position paper: hypertension in
pregnancy. J Clin Hypertens 2009; 11(4): 214–225.
8. Sibai BM, Abdella TN, Anderson GD. Pregnancy outcome in 211 patients with
mild chronic hypertension. Obstet Gynecol 1983; 61(5): 571–576.
9. Sibai BM, Lindheimer M, Hauth J, Caritis S, VanDorsten P, Klebanoff M, et al. Risk
factors for preeclampsia, abruptio placentae, and adverse neonatal outcomes
among women with chronic hypertension. New Engl J Med 1998; 339(10): 667–
671.
10. Lie RT, Rasmussen S, Brunborg H, Gjessing HK, Lie-Nielsen E, Irgens LM. Fetal and
maternal contributions to risk of pre-eclampsia: population based study. Br Med
J 1998; 316(7141): 1343.
11. Chappell LC, Enye S, Seed P, Briley AL, Poston L, Shennan AH. Adverse perinatal
outcomes and risk factors for preeclampsia in women with chronic hypertension
a prospective study. Hypertension 2008; 51(4): 1002–1009.
12. Poon LC, Nicolaides KH. First-trimester maternal factors and biomarker screening
for preeclampsia. Prenat Diagn 2014; 34(7): 618–627.
13. Anthony J, Johanson R, Dommisse J. Critical care management of severe pre-
eclampsia. Fetal Matern Med Rev 1994; 6(04): 219–229.
14. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia
and eclampsia. Obstet Gynecol 2001; 97(4): 533–538.
15. Lewis G. Saving mothers’ lives: reviewing maternal deaths to make motherhood
safer: 2006–08. The eighth report on confidential enquiries into maternal deaths
in the United Kingdom. Br J Obstet Gynecol 2007; 118(Suppl 1): 1–203.
16. National Fepartment of Health. Saving Mothers 2011–2013. Sixth report on
confidential enquiries into maternal deaths in South Africa. Short report. 2015.
17. Dekker GA. Management of preeclampsia. Pregnancy Hypertens 2014; 4(3):
246–247.
18. Sircar M, Thadhani R, Karumanchi SA. Pathogenesis of preeclampsia. Curr Opin
Nephrol Hypertens 2015; 24(2): 131–138.
19. Hytten F, Chamberlain G. Clinical Physiology in Obstetrics . Oxford: Blackwell
Scientific, 1980.
20. Easterling TR, Benedetti TJ, Schmucker BC, Millard SP. Maternal hemodynamics in
normal and preeclamptic pregnancies: a longitudinal study. Obstet Gynecol 1990;
76(6): 1061–1069.
21. Sibai BM, Taslimi MM, El-Nazer A, Amon E, Mabie BC, Ryan GM. Maternal–
perinatal outcome associated with the syndrome of hemolysis, elevated liver
enzymes, and low platelets in severe preeclampsia–eclampsia. Am J Obstet
Gynecol 1986; 155(3): 501–507.
22. Belfort M, Anthony J, Kirshon B. Respiratory function in severe gestational
proteinuric hypertension: the effects of rapid volume expansion and subsequent
vasodilatation with verapamil. Br J Obstet Gynecol 1991; 98(10): 964–972.
23. Visser W, Wallenburg H. Central hemodynamic observations in untreated
preeclamptic patients. Hypertension 1991; 17(6 Pt 2): 1072–1077.
24. Belfort MA, Anthony J, Saade GR, Wasserstrum N, Johanson R, Clark S, et al. The
oxygen consumption/oxygen delivery curve in severe preeclampsia: evidence for
a fixed oxygen extraction state. Am J Obstet Gynecol 1993; 169(6): 1448–1455.
25. Belfort M, Akovic K, Anthony J, Saade G, Kirshon B, Moise K. The effect of acute
volume expansion and vasodilatation with verapamil on uterine and umbilical artery
Doppler indices in severe preeclampsia. J Clin Ultrasound 1994; 22(5): 317–325.
26. Khong T, Pearce J, Robertson W. Acute atherosis in preeclampsia: maternal
determinants and fetal outcome in the presence of the lesion. Am J Obstet
Gynecol 1987; 157(2): 360–363.
27. Richards A, Graham F, Bullock R. Clinicopathological study of neurological
complications due to hypertensive disorders of pregnancy. J Neurol Neurosurg
Psychiat 1988; 51(3): 416–421.
28. Gaber LW, Spargo BH, Lindheimer MD. Renal pathology in pre-eclampsia.
Bailliere’s Clin Obstet Gynaecol 1994; 8(2): 443–468.
29. Postma IR, Slager S, Kremer HP, de Groot JC, Zeeman GG. Long-term
consequences of the posterior reversible encephalopathy syndrome in eclampsia
and preeclampsia: a review of the obstetric and nonobstetric literature. Obstet
Gynecol Surv 2014; 69(5): 287–300.
30. O’Dwyer SL, Gupta M, Anthony J. Pulmonary edema in pregnancy and the
puerperium: a cohort study of 53 cases. J Perinatal Med 2015; 43(6): 675–681.