International Journal of Research and Reports in Gynaecology

Pregnancy-induced hypertension (PIH), also referred to as toxaemia of pregnancy(obsolete) is a spectrum of multi-systemic dysfunction in pregnancy, usually seen in the third trimester in approximately 6–8% of pregnancies in the United States, according to the National High Blood Pressure Education Program (NHBPEP). The World Health Organisation reported that this multisystem disorder accounts for 16% of maternal deaths in developed countries and 1.8%-16.7% in most developing countries. This article elucidates the pathophysiological mechanism associated with the spectrum of maternal complications in Pregnancy-induced hypertension. PIH includes a progression of disorders ranging from gestational hypertension to preeclampsia, eclampsia, and in some cases, HELLP syndrome (Hemolysis, Elevated Liver enzymes, and Low Platelet count). Among these, preeclampsia is the most extensively studied and clinically significant due to its potential to evolve into life-threatening eclampsia, leading to seizures, stroke, multi-organ failure, and maternal and fetal death. The spectrum can progress with short and long-term complications that may significantly impact the quality of life of both the fetus and the mother.  Though the pathogenetic mechanisms remain unclear, evidence supporting the roles of genetic, immunologic, and environmental factors is rapidly evolving. The disorder is now recognised as a multifactorial condition, with genetic predisposition, immune maladaptation, and environmental factors (such as diet, obesity, and stress) playing contributory roles. There is also increasing evidence that insulin resistance, preexisting metabolic syndrome, and abnormal immune tolerance to paternal antigens may predispose women to developing PIH. Preeclampsia, an initial spectrum of the disorder, begins with abnormal placentation with failure of adaptation, inflammatory changes, permanent vascular and metabolic damages, and an increasing risk of cardiovascular, renal, endocrine, neurological, haematological, and socioeconomic complications. Regardless of the initiating mechanism, oxidative stress, placental ischemia, hypoxia with release of toxic substances, and endothelial dysfunction play crucial roles. The stressors release antiangiogenic factors (such as soluble fms-like tyrosine kinase-1 or sFlt-1 and endoglin), oxidative stress, and inflammatory cytokines leading to vasoconstriction, capillary leak, coagulation abnormalities, and the release of microparticles into the maternal circulation, essentially culminating in worsening multiple organ damage. American College of Obstetrics and Gynaecology (ACOG) recommends early recognition and regular antenatal screening with early treatment for preeclampsia when the diastolic blood pressure (DBP) is above 105–110 mm Hg. Treatment options include labetalol, nifedipine, and hydralazine as first-line agents. Delivery remains the definitive cure, particularly when severe features develop or gestational age exceeds 37 weeks. In cases of early-onset preeclampsia, expectant management under close monitoring may be considered to improve neonatal outcomes.