European Journal of Cardiovascular Medicine

Hypertensive disorders of pregnancy (HDP) comprise a heterogeneous group of conditions that include gestational hypertension, preeclampsia, eclampsia, and chronic hypertension with or without superimposed preeclampsia. They complicate a meaningful proportion of pregnancies and continue to be a major cause of preventable maternal and perinatal morbidity and mortality [1-3]. Global estimates suggest that preeclampsia and eclampsia account for a considerable share of maternal deaths, with a disproportionate burden in resource-constrained settings [2,3]. Beyond mortality, HDP contributes to severe maternal complications such as HELLP syndrome, placental abruption, pulmonary edema, acute kidney injury, and postpartum hemorrhage, often requiring high-dependency or intensive care support [4,7,12,13].

The pathophysiology of preeclampsia is multifactorial, involving abnormal placentation, endothelial dysfunction, and an exaggerated maternal inflammatory response, which together culminate in hypertension and end-organ injury [6-8]. Clinically, the condition can evolve rapidly from mild disease to severe features, including neurological symptoms, thrombocytopenia, hepatic dysfunction, renal impairment, and fetal compromise [4,5]. International statements from the International Society for the Study of Hypertension in Pregnancy (ISSHP) and practice guidelines provide standardized definitions for classification and severity assessment, enabling consistent diagnosis and triage [4,5].

HDP is closely linked with adverse perinatal outcomes. Placental insufficiency predisposes to fetal growth restriction, oligohydramnios, and intrapartum fetal distress [14]. In addition, iatrogenic prematurity from medically indicated early delivery remains common when maternal or fetal status deteriorates, contributing to low birth weight, neonatal intensive care unit (NICU) admission, and perinatal death [10,11]. Placental abruption, a feared complication associated with hypertensive disease, further amplifies both maternal hemorrhagic risk and perinatal asphyxia and loss [12].

Evidence-based interventions form the cornerstone of intrapartum management. Magnesium sulfate reduces the risk of eclampsia and is recommended for women with severe preeclampsia and eclampsia [9]. For women with gestational hypertension or mild preeclampsia at term, planned induction of labour improves maternal outcomes compared with expectant monitoring, without unacceptable neonatal compromise [10]. Despite such evidence, implementation gaps persist in real-world settings, especially where referral delays and limited critical care resources intersect.

In India, HDP frequently presents late or as a referred emergency, reflecting gaps in antenatal surveillance and delayed recognition of warning signs. Local outcome data from tertiary care institutions are valuable for auditing intrapartum practices, benchmarking complication rates, and identifying areas for strengthening referral pathways and neonatal preparedness. Against this background, we conducted a hospital-based observational study at Late Bisahu Das Mahant Memorial Medical College, Korba, Chhattisgarh, during March 2023 to March 2024.

Objectives of the study were to (i) describe the spectrum and severity of hypertensive disorders of pregnancy among admitted women and (ii) assess maternal outcomes, delivery characteristics, and perinatal outcomes in this cohort.

Study design and setting: A hospital-based observational study was carried out in the Department of Obstetrics and Gynecology, Late Bisahu Das Mahant Memorial Medical College, Korba, Chhattisgarh, India, over one year (March 2023 to March 2024).

Study population and sample size: The study included 100 pregnant women diagnosed with hypertensive disorders of pregnancy (HDP) who were admitted to the antenatal ward or labour room during the study period. Participants were enrolled consecutively until the required sample size was achieved.

Inclusion and exclusion criteria: Pregnant women at any gestational age with a diagnosis of gestational hypertension, preeclampsia, eclampsia, or chronic hypertension with superimposed preeclampsia were eligible. Women with hypertension due to secondary causes, known chronic renal disease predating pregnancy, or incomplete clinical records for primary outcomes were excluded.

Definitions and classification: HDP subtypes were classified according to standard diagnostic thresholds and consensus recommendations [4,5]. Gestational hypertension was defined as new-onset blood pressure >=140/90 mmHg after 20 weeks of gestation without proteinuria or end-organ dysfunction. Preeclampsia was diagnosed in the presence of hypertension with proteinuria and/or maternal organ dysfunction or uteroplacental dysfunction; severe disease included severe-range blood pressure, neurological symptoms, significant laboratory derangements, pulmonary edema, or other end-organ involvement [4,5]. Eclampsia was defined as new-onset generalized tonic-clonic seizures in a woman with preeclampsia in the absence of other neurological causes.

Data collection: A structured case record form was used to collect socio-demographic details, obstetric history, booking status, gestational age at admission, and HDP subtype. Intrapartum details included onset of labour (spontaneous/induced/no labour), mode of delivery, and indication for cesarean section when performed. Maternal outcomes recorded were need for intravenous antihypertensives, magnesium sulfate administration, HELLP syndrome, abruptio placentae, pulmonary edema, acute kidney injury, postpartum hemorrhage, intensive care unit (ICU) admission, and maternal mortality. Magnesium sulfate was administered for eclampsia and for preeclampsia with severe features as per institutional protocol, supported by evidence from the Magpie Trial [9].

Perinatal assessment: For each birth, gestational age at delivery, birth weight, fetal growth restriction (clinical and/or ultrasonographic assessment), meconium-stained liquor, 5-minute Apgar score, NICU admission, stillbirth, and early neonatal death (within 7 days) were documented. Perinatal mortality was computed as stillbirth plus early neonatal death.

Statistical analysis: Data were entered in a spreadsheet and analyzed using descriptive statistics. Categorical variables were summarized as frequencies and percentages, and continuous variables (where applicable) as mean with standard deviation. Results were presented in tables.

Ethical considerations: The study protocol received approval from the Institutional Ethics Committee of the institute. Written informed consent was obtained from participants or their legally acceptable representatives. Confidentiality was maintained throughout.

A total of 100 pregnant women diagnosed with hypertensive disorders of pregnancy were included. Most participants were aged 21–30 years (74%) and were primigravidae (58%). Nearly half of the women were admitted at term (≥37 weeks, 46%), while 54% were admitted before 37 weeks. Booked cases constituted 62%, and 38% were unbooked or referred (Table 1).

Table 1. Baseline maternal profile of women with HDP (n = 100)

Gestational hypertension was the most frequent diagnosis (44%), followed by preeclampsia without severe features (26%). Severe disease, defined as preeclampsia with severe features, eclampsia, or chronic hypertension with superimposed preeclampsia, was seen in 30% of women (Table 2).

Table 2. Spectrum and severity of hypertensive disorders (n = 100)

Figure 1: Spectrum of Hypertensive Disorders of Pregnancy

Maternal interventions and complications were common. Severe hypertension requiring intravenous antihypertensives was recorded in 34%, and magnesium sulfate was administered in 28%. Major complications included postpartum hemorrhage (9%), abruptio placentae (7%), HELLP syndrome (6%), acute kidney injury (4%), pulmonary edema (3%), ICU admission (10%), and one maternal death (1%) (Table 3).

Table 3. Maternal outcomes and complications (n = 100)

Figure 2: Maternal outcomes and complications in HDP

Regarding delivery, labour was induced in 46%, spontaneous onset occurred in 38%, and 16% underwent elective/emergency cesarean section without labour. Overall, cesarean section was performed in 56% of women (Table 4).

Table 4. Delivery characteristics (n = 100)

Among women delivered by cesarean section (n = 56), the leading indications were non-reassuring fetal status (32.1%) and maternal indications related to severe preeclampsia/eclampsia (25.0%), followed by failed induction (21.4%), previous cesarean section (14.3%), and abruptio placentae (7.1%) (Table 4A).

Table 4A. Indications for cesarean section (n = 56)

Adverse perinatal outcomes were notable. Preterm birth occurred in 40% and low birth weight in 42%. Fetal growth restriction was identified in 24%, meconium-stained liquor in 18%, and 5-minute Apgar score <7 in 14%. NICU admission was required for 28% of neonates. Stillbirth and early neonatal death occurred in 4% and 3%, respectively, resulting in a perinatal mortality of 7% (Table 5).

Table 5. Perinatal outcomes (n = 100 births)

In this hospital-based cohort of 100 women with hypertensive disorders of pregnancy, gestational hypertension constituted the largest subgroup, and severe disease was present in nearly one-third of cases. These patterns are consistent with the recognized spectrum of HDP in tertiary-care settings, where referrals and late presentations increase the proportion of severe preeclampsia and eclampsia [1,2,4]. The predominance of women aged 21-30 years and the higher representation of primigravidae align with established epidemiological observations that first pregnancies carry a higher risk for preeclampsia [5-7].

The burden of maternal complications in the present study underscores the clinical volatility of HDP. Abruptio placentae (7%) and HELLP syndrome (6%) are well-described severe complications linked to placental vascular pathology and systemic endothelial injury [7,12]. Postpartum hemorrhage (9%) and ICU admission (10%) highlight the need for proactive hemodynamic monitoring and readiness for massive obstetric hemorrhage, especially in women with severe features. Large population-based data also show an increased risk of postpartum hemorrhage among women with preeclampsia, reinforcing the relevance of structured third-stage management and access to blood products [13].

Cesarean section was performed in 56% of women, with fetal compromise and maternal indications together accounting for most procedures. High cesarean rates are commonly reported in HDP due to failed induction, non-reassuring fetal status, and the need for expedited delivery in worsening maternal condition [4,5]. Evidence from the HYPITAT trial supports planned induction for women with gestational hypertension or mild preeclampsia beyond 36 weeks, improving maternal outcomes compared with expectant care [10]. In practice, the decision to induce or proceed directly to cesarean is influenced by cervical status, gestational age, fetal well-being, and resource availability.

Perinatal morbidity was substantial, with preterm birth in 40%, low birth weight in 42%, and NICU admission in 28%. These findings reflect both spontaneous and iatrogenic prematurity, as well as fetal growth restriction related to uteroplacental insufficiency [11,14]. The observed fetal growth restriction rate (24%) is compatible with prior reports showing impaired fetal growth in pregnancies complicated by preeclampsia [14]. Placental abruption, although relatively infrequent, carries marked perinatal risk through acute hypoxia and prematurity, which is consistent with epidemiologic evidence [12]. Perinatal mortality of 7% in this cohort further emphasizes the need for coordinated obstetric-neonatal teams, early identification of fetal compromise, and timely delivery planning.

From a systems perspective, our findings reinforce three priorities: strengthening antenatal blood pressure surveillance and counseling, minimizing delays in referral for severe features, and ensuring standardized intrapartum management. Magnesium sulfate remains a key intervention to prevent and treat eclamptic seizures, with robust trial evidence demonstrating risk reduction for eclampsia and probable reduction in maternal death [9]. Improving adherence to evidence-based protocols and ensuring availability of critical care beds and neonatal support can help reduce the avoidable burden of HDP-related complications in similar settings [4,5].

Limitations

This single-center, hospital-based study reflects a referral population with higher clinical acuity, limiting generalizability to community settings. The sample size and descriptive analysis restrict comparisons across HDP subtypes and prevent adjustment for confounders such as body mass index, comorbidities, and timing of disease onset. Several variables relied on routine records, introducing documentation variability. Follow-up was confined to hospital stay and the first 7 neonatal days.

In this observational study gestational hypertension was the most common HDP subtype, while severe disease affected 30% of women. Maternal morbidity remained appreciable, with abruption, HELLP syndrome, acute kidney injury, postpartum hemorrhage, and ICU admission observed, along with one maternal death. Cesarean delivery was frequent, driven by fetal compromise and the need for maternal stabilization. Neonatal outcomes reflected uteroplacental dysfunction and prematurity, with high rates of low birth weight, NICU admission, and a perinatal mortality of 7%. Strengthened antenatal screening, prompt referral for severe features, consistent use of magnesium sulfate, and coordinated obstetric-neonatal care are essential to reduce HDP-related complications. Audit and feedback can sustain protocol adherence.

1. Duley L. The global impact of pre-eclampsia and eclampsia. Semin Perinatol. 2009 Jun;33(3):130-7. doi:10.1053/j.semperi.2009.02.010. PMID:19464502.

1. Abalos E, Cuesta C, Grosso AL, Chou D, Say L. Global and regional estimates of preeclampsia and eclampsia: a systematic review. Eur J Obstet Gynecol Reprod Biol. 2013 Sep;170(1):1-7. doi:10.1016/j.ejogrb.2013.05.005. PMID:23746796.
2. Khan KS, Wojdyla D, Say L, Gülmezoglu AM, Van Look PF. WHO analysis of causes of maternal death: a systematic review. Lancet. 2006 Apr 1;367(9516):1066-74. doi:10.1016/S0140-6736(06)68397-9. PMID:16581405.
3. American College of Obstetricians and Gynecologists' Committee on Practice Bulletins—Obstetrics. Gestational hypertension and preeclampsia: ACOG Practice Bulletin, Number 222. Obstet Gynecol. 2020 Jun;135(6):e237-e260. doi:10.1097/AOG.0000000000003891. PMID:32443079.
4. Brown MA, Magee LA, Kenny LC, Karumanchi SA, McCarthy FP, Saito S, et al. Hypertensive Disorders of Pregnancy: ISSHP classification, diagnosis, and management recommendations for international practice. Hypertension. 2018 Jul;72(1):24-43. doi:10.1161/HYPERTENSIONAHA.117.10803. PMID:29899139.
5. Steegers EAP, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. Lancet. 2010 Aug 21;376(9741):631-44. doi:10.1016/S0140-6736(10)60279-6. PMID:20598363.
6. Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol. 2003 Jul;102(1):181-92. PMID:12850627.
7. von Dadelszen P, Magee LA. Pre-eclampsia: an update. Curr Hypertens Rep. 2014 Aug;16(8):454. doi:10.1007/s11906-014-0454-4. PMID:24915961.
8. Altman D, Carroli G, Duley L, Farrell B, Moodley J, Neilson J, et al; Magpie Trial Collaboration Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002 Jun 1;359(9321):1877-90. doi:10.1016/S0140-6736(02)08778-0. PMID:12057549.
9. Koopmans CM, Bijlenga D, Groen H, Vijgen SMC, Aarnoudse JG, Bekedam DJ, et al; HYPITAT study group. Induction of labour versus expectant monitoring for gestational hypertension or mild pre-eclampsia after 36 weeks' gestation (HYPITAT): a multicentre, open-label randomised controlled trial. Lancet. 2009 Sep 19;374(9694):979-988. doi:10.1016/S0140-6736(09)60736-4. PMID:19656558.
10. Goldenberg RL, Culhane JF, Iams JD, Romero R. Epidemiology and causes of preterm birth. Lancet. 2008 Jan 5;371(9606):75-84. doi:10.1016/S0140-6736(08)60074-4. PMID:18177778.
11. Tikkanen M. Placental abruption: epidemiology, risk factors and consequences. Acta Obstet Gynecol Scand. 2011 Feb;90(2):140-9. doi:10.1111/j.1600-0412.2010.01030.x. PMID:21281325.
12. von Schmidt auf Altenstadt JF, Hukkelhoven CWPM, van Roosmalen J, Bloemenkamp KWM. Preeclampsia increases the risk of postpartum haemorrhage: a nationwide cohort study in the Netherlands. PLoS One. 2013 Dec 17;8(12):e81959. doi:10.1371/journal.pone.0081959. PMID:24367496.
13. Xiao R, Sorensen TK, Williams MA, Luthy DA. Influence of pre-eclampsia on fetal growth. J Matern Fetal Neonatal Med. 2003 Mar;13(3):157-62. doi:10.1080/jmf.13.3.157.162. PMID:12820837.