Hypertensive Disorders of Pregnancy: A Clinical Guide
Definition
Hypertensive Disorders of Pregnancy (HDP) are a group of conditions characterized by high blood pressure during pregnancy, which are a major cause of maternal and perinatal morbidity and mortality (7). The four main categories are chronic hypertension, gestational hypertension, preeclampsia/eclampsia, and chronic hypertension with superimposed preeclampsia (3). In Malaysia, HDP is defined as a sustained systolic blood pressure (SBP) of >140mmHg or a diastolic blood pressure (DBP) of >90mmHg (1).
Epidemiology
In Malaysia, Hypertensive Disorders of Pregnancy are a significant cause of maternal mortality, second only to obstetric hemorrhage (1). Globally, HDP complicates about 5% to 10% of pregnancies (5). The rising global trend is linked to increasing maternal age and pre-existing conditions like obesity and diabetes (11). [Specific prevalence data for different ethnic groups in Malaysia is not readily available in recent national health surveys and should be interpreted with caution].
Pathophysiology
The development of preeclampsia, a key HDP, is understood through a "two-stage model" (10).
Stage 1: Defective Placentation
In a healthy pregnancy, fetal trophoblast cells invade the mother's spiral arteries, transforming them into wide, low-resistance vessels to ensure ample blood flow to the placenta (9). In preeclampsia, this invasion is shallow and incomplete (9). The spiral arteries remain narrow and muscular, leading to reduced blood flow (hypoperfusion), oxygen deficiency (hypoxia), and oxidative stress in the placenta (9).
Stage 2: Maternal Syndrome
The stressed placenta releases anti-angiogenic factors into the mother's bloodstream (9). These factors cause widespread damage to the mother's vascular endothelium (the cell lining of her blood vessels) (7). This endothelial dysfunction leads to:
Vasoconstriction: Widespread tightening of blood vessels, causing hypertension (7).
Leaky Capillaries: Increased permeability of blood vessels allows fluid and protein to leak into tissues, resulting in proteinuria and edema (7).
Coagulation Activation: Endothelial damage activates platelets, leading to their consumption (thrombocytopenia) and the formation of microthrombi (7).
This cascade explains why the only definitive cure for preeclampsia is the delivery of the placenta (10).
Clinical Presentation
The presentation of HDP can range from asymptomatic high blood pressure detected at a routine check-up to a life-threatening emergency (3).
Diagnostic Clues: The new onset of hypertension (ge140/90textmmHg) after 20 weeks of gestation is the primary clue (3).
Common Symptoms
Headache: Often severe, persistent, and not relieved by simple analgesics (3).
Visual Disturbances: Blurred vision, flashing lights (photopsia), or dark spots (scotomata) indicate central nervous system involvement (3).
Epigastric or Right Upper Quadrant (RUQ) Pain: Caused by the stretching of the liver capsule and is a sign of severe disease (3).
Sudden Swelling (Edema): Rapid weight gain or swelling of the face and hands, although no longer a formal diagnostic criterion (7).
⚠️ Red Flag Signs & Symptoms
Severe Hypertension: SBP ge160textmmHg or DBP ge110textmmHg (1).
New-onset Neurological Symptoms: Severe headache, visual changes, or signs of CNS irritability like hyperreflexia and clonus (3).
Severe RUQ or Epigastric Pain (3).
Shortness of Breath: May indicate pulmonary edema (3).
Oliguria: Decreased urine output, signaling acute kidney injury (3).
Complications
Maternal
Acute: Eclampsia (seizures), stroke, pulmonary edema, acute kidney injury (AKI), HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets), placental abruption, and postpartum hemorrhage (6).
Chronic: Women with a history of preeclampsia have a significantly increased lifetime risk of chronic hypertension, ischemic heart disease, and stroke (7).
Fetal & Neonatal
Intrauterine Growth Restriction (IUGR): Due to chronic placental insufficiency (9).
Preterm Birth: Often medically indicated to protect the mother (9).
Placental Abruption: Premature separation of the placenta, an obstetric emergency (7).
Intrauterine Fetal Demise (Stillbirth): The most severe consequence of placental failure (9).
Prognosis
With timely diagnosis and management, the prognosis for mothers with HDP is generally good. However, severe forms like eclampsia and HELLP syndrome carry significant risks of morbidity and mortality (6). Globally, HDP accounts for a substantial number of maternal deaths (6). The risk of recurrence in a future pregnancy is significant, especially for women with a history of early-onset preeclampsia (7).
Differential Diagnosis
Chronic Hypertension: This is a key differential if high blood pressure is detected early in pregnancy. It is diagnosed if hypertension predates pregnancy or is identified before 20 weeks of gestation and persists 12 weeks postpartum (3). The absence of new-onset proteinuria or end-organ dysfunction helps distinguish it from superimposed preeclampsia.
Renal Disease: Pre-existing kidney disease can present with both hypertension and proteinuria. However, it is less likely if a previous urinalysis was normal and blood pressure was documented as normal before 20 weeks. A renal panel and urine studies can help differentiate (7).
Thrombotic Thrombocytopenic Purpura (TTP) / Hemolytic Uremic Syndrome (HUS): Consider these rare but serious conditions if the patient presents with features of HELLP syndrome (thrombocytopenia, microangiopathic hemolytic anemia). TTP/HUS is often associated with more severe renal failure and neurological symptoms and is not exclusive to pregnancy (7). The absence of significant hypertension might point away from preeclampsia.
Investigations
Immediate & Bedside Tests
Urine Dipstick: A crucial screening test performed immediately to detect proteinuria (1+ or greater) (the rationale), which helps differentiate gestational hypertension from preeclampsia and guides further investigation (the action) (1).
Blood Pressure Measurement: Accurate and repeated measurement is essential to confirm the diagnosis of hypertension and assess its severity (the action), which is critical for preventing complications like stroke (the rationale) (1).
Diagnostic Workup
First-Line Investigations:
Urine Protein-to-Creatinine Ratio (UPCR): This is the preferred method to quantify proteinuria (the rationale); a ratio ge30textmg/mmol confirms significant proteinuria, establishing a diagnosis of preeclampsia without needing a cumbersome 24-hour collection (the action) (1).
Full Blood Count (FBC): Essential to identify thrombocytopenia (platelet count \<100,000times109/textL) or hemoconcentration (the rationale), which are key features of severe disease and HELLP syndrome, respectively (the action) (3).
Renal Function Panel (Urea, Creatinine, Electrolytes): This is performed to detect acute kidney injury (elevated creatinine) (the rationale), a sign of severe end-organ dysfunction that may necessitate urgent delivery (the action) (3).
Liver Function Tests (LFTs): Crucial for detecting elevated liver transaminases (AST/ALT) (the rationale), which signifies hepatocellular injury characteristic of preeclampsia with severe features or HELLP syndrome (the action) (3).
Gold Standard: While clinical criteria define the syndrome, the definitive "cure" and confirmation of placental origin is the resolution of symptoms after delivery of the placenta (the rationale), which underpins all management decisions (the action) (10).
Monitoring & Staging
Serial Blood Tests (FBC, LFTs, Renal Panel): Performed weekly or more frequently in severe cases to monitor for disease progression or the onset of complications like HELLP syndrome (the action), as worsening values indicate increasing endothelial damage and risk (the rationale) (1).
Fetal Ultrasound and Doppler Velocimetry: Serial growth scans are vital to detect Fetal Growth Restriction (FGR), and umbilical artery Doppler studies assess placental resistance (the rationale), providing a direct window into the severity of uteroplacental insufficiency and helping to time delivery (the action) (4).
Management
Management Principles
The management of HDP focuses on controlling maternal hypertension to prevent complications, seizure prophylaxis in severe cases, monitoring for maternal and fetal deterioration, and ultimately, timing the delivery to balance maternal safety with fetal maturity (7).
Acute Stabilisation (The First Hour)
Airway/Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% (the action), which is crucial to prevent tissue hypoxia driven by vasospasm and potential pulmonary edema (the rationale) (3).
Circulation: Secure two large-bore IV cannulas for reliable drug and fluid administration (the action). For severe hypertension (SBP ge160 or DBP ge110textmmHg), administer a stat dose of an antihypertensive agent like IV Labetalol 20mg or Oral Nifedipine 10mg (the action) to lower blood pressure and prevent a stroke (the rationale) (1).
Disability: If signs of impending eclampsia (severe headache, clonus) are present or a seizure has occurred, administer a loading dose of IV Magnesium Sulfate 4-6g over 15-20 minutes (the action) to prevent or treat seizures by stabilising cerebral membranes (the rationale) (1).
Exposure: Assess for signs of end-organ damage such as epigastric tenderness and check deep tendon reflexes (the action) to establish a baseline before starting magnesium sulfate therapy (the rationale) (1).
Definitive Therapy
First-Line Treatment (Severe Hypertension):
Labetalol (IV/Oral): Preferred agent. IV boluses of 20mg, followed by 40-80mg, can be given. Oral dosing is typically 100-200mg TID (1, 12).
Nifedipine (Oral): Immediate-release 10-20mg capsules are effective. Extended-release formulations are used for maintenance (1, 12).
Hydralazine (IV): An alternative, given as 5mg IV boluses, but has more maternal side effects (1, 12).
Second-Line/Escalation: If blood pressure remains uncontrolled despite maximum doses of first-line agents, escalation to a specialist and potential ICU admission is required for consideration of infusions or other agents (1).
Eclampsia Prophylaxis: For all women with preeclampsia with severe features, administer IV Magnesium Sulfate as a loading dose followed by a maintenance infusion of 1-2g/hour (1).
Delivery is the only definitive cure. The timing is based on gestational age and disease severity (7):
With Severe Features: Delivery is recommended at or after 34 weeks of gestation (3).
Without Severe Features: Delivery is recommended at or after 37 weeks of gestation (3).
Supportive & Symptomatic Care
Fluid Management: Administer IV fluids judiciously, often restricting to 80-125 mL/hour (the action) to prevent iatrogenic pulmonary edema in the context of leaky capillaries (the rationale) (1).
Analgesia: Paracetamol can be given for mild headaches. Avoid NSAIDs as they can worsen hypertension and renal function (12).
Antenatal Corticosteroids: Administer a single course of Betamethasone or Dexamethasone if delivery is anticipated before 37 weeks (the action) to accelerate fetal lung maturity and reduce neonatal respiratory distress syndrome (the rationale) (1).
Key Nursing & Monitoring Instructions
Strict hourly input/output chart monitoring to detect oliguria.
Monitor blood pressure every 15-30 minutes during acute stabilization, then hourly.
For patients on Magnesium Sulfate: Check respiratory rate, deep tendon reflexes, and urine output hourly. Ensure calcium gluconate is at the bedside as an antidote (1).
Inform medical staff if systolic BP rises above 160 mmHg, DBP above 110 mmHg, or urine output is <30mL/hr.
Continuous fetal heart rate monitoring (CTG) during acute stabilisation.
Long-Term Plan & Patient Education
Following delivery, blood pressure can peak 3-6 days postpartum, so close monitoring is essential (7). Counsel the patient on her increased long-term risk for cardiovascular disease and the importance of a healthy lifestyle and follow-up with a primary care provider (7). Discuss future pregnancy risks and the need for pre-conception counseling and early antenatal booking (7).
When to Escalate
Call Your Senior (MO/Specialist) if:
The patient has SBP ge160textmmHg or DBP ge110textmmHg unresponsive to initial treatment.
The patient develops any new neurological signs (severe headache, visual disturbance, eclampsia).
There are signs of pulmonary edema (dyspnea, falling SpO2).
Urine output is persistently <30mL/hr.
Laboratory results show evidence of HELLP syndrome or worsening renal failure.
The fetal CTG is non-reassuring.
(All escalation triggers are based on principles from the Malaysian CPG) (1).
Referral Criteria
Refer to the Anesthesia team early for pain management planning and potential epidural, which is safe if platelets are >70,000/µL (3).
Refer to the Nephrology team if acute kidney injury does not resolve postpartum.
Refer to the medical or cardiology team postpartum for ongoing management of chronic hypertension.
References
Ministry of Health Malaysia. (2021). Clinical Practice Guidelines: Management of Hypertensive Disorders in Pregnancy (2nd Edition). Putrajaya: MOH.
World Health Organization. (2018). WHO recommendations: hypertension in pregnancy. Geneva: World Health Organization.
American College of Obstetricians and Gynecologists. (2020). Gestational Hypertension and Preeclampsia. ACOG Practice Bulletin, Number 222. Obstetrics & Gynecology, 135(6), e237-e260. https://www.preeclampsia.org/frontend/assets/img/advocacy_resource/Gestational_Hypertension_and_Preeclampsia_ACOG_Practice_Bulletin._Number_222_1605448006.pdf
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Fox, R., Kitt, J., Leeson, P., Aye, C. Y. L., & Lewandowski, A. J. (2019). Preeclampsia: risk factors, diagnosis, management, and the cardiovascular impact on the offspring. Journal of clinical medicine, 8(10), 1625.
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Roberts, J. M., & Hubel, C. A. (2009). The two stage model of preeclampsia: variations on the theme. Placenta, 30, 32-37.
Ananth, C. V., Keyes, K. M., & Wapner, R. J. (2013). Pre-eclampsia rates in the United States, 1980-2010: age-period-cohort analysis. BMJ, 347, f6564.
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