Primary hypertension is a vascular disorder characterized mainly by elevated blood pressure. The exact cause of the disease is not yet fully understood, but incidence rates suggest a correlation with age. Data from China indicate that the incidence is 3.11% in those under 20 years old, 3.91% in those aged 20–29, 4.95% in those aged 30–39, and rises significantly after the age of 40. Therefore, primary hypertension is relatively rare among women of childbearing age.

bubble_chart Clinical Manifestations

Repeated blood pressure measurements above 18.7/12 kPa (140/90 mmHg) before 20 weeks of pregnancy, or a confirmed diagnosis of hypertension before pregnancy, is referred to as pregnancy complicated by primary hypertension. Approximately 59% of patients have a family history.

In cases of pregnancy complicated by primary hypertension where blood pressure decreases during the intermediate stage [second stage] of pregnancy or remains below 21.2/13.3 kPa (160/100 mmHg), fetal survival rates are high; if blood pressure exceeds 21.2/13.3 kPa (160/100 mmHg), fetal mortality increases significantly. Among pregnant women with primary hypertension, about 10–20% develop pregnancy-induced hypertension syndrome in the late stage [third stage] of pregnancy. A baseline blood pressure >24/14.6 kPa (180/110 mmHg) results in a fetal mortality rate of 23%; if pregnancy-induced hypertension syndrome is also present, the fetal mortality rate rises to 41.3%. The earlier pregnancy-induced hypertension syndrome appears, the worse the fetal prognosis. For those who develop pregnancy-induced hypertension syndrome before 32 weeks of pregnancy, 75% experience intrauterine fetal death. Additionally, among those with primary hypertension who develop pregnancy-induced hypertension syndrome, the incidence of placental abruption is 2%, which is higher than in cases of pregnancy-induced hypertension syndrome alone.

The blood pressure of normal individuals fluctuates within a certain range under different physiological conditions. It may rise during anxiety, tension, stress, or physical activity. Additionally, systolic blood pressure increases with age, making it difficult to clearly delineate the boundary between hypertension and normal blood pressure. In 1979, China revised its blood pressure measurement methods and diagnostic criteria for hypertension as follows:

1. After resting for 15 minutes, measure the blood pressure of the right arm in a seated position. Repeat the measurement several times until the readings stabilize. The diastolic pressure is determined by the disappearance of the Korotkoff sounds; if the sounds persist, use the value at the point of muffling. Recheck the measurement after an interval of one hour on the same day or on another day.

2. A systolic blood pressure ≥21.2 kPa (160 mmHg) and/or diastolic blood pressure ≥12.6 kPa (95 mmHg), upon verification, confirms the diagnosis. A blood pressure reading of 18.7–21.2/12–12.6 kPa (140–160/90–95 mmHg) is classified as clinical hypertension.

3. Individuals with a history of hypertension who have not received treatment for over three months and currently exhibit normal blood pressure are not classified as hypertensive. However, those who are on medication and show normal blood pressure during the examination should still be diagnosed with hypertension.

Women of childbearing age predominantly present with initial stage [first stage] hypertension, with rare vascular complications. Examinations such as fundoscopy, electrocardiography, cardiac function, and renal function often show no abnormalities. Therefore, the diagnosis must rely solely on elevated stirred pulse pressure. If the first visit occurs during pregnancy intermediate stage [second stage], peripheral vasodilation, hemodilution, and the formation of placental arteriovenous shunts may lead to a 2.7 kPa (20 mmHg) drop in systolic blood pressure in 40% of patients, complicating the diagnosis. If renal impairment is detected during the first visit, it becomes challenging to differentiate whether the condition is symptomatic hypertension caused by chronic glomerulonephritis or chronic pyelonephritis, or renal damage resulting from primary hypertension.

1. Management of Venous Thrombosis

(1) General measures: Bed rest for 1–2 weeks to alleviate limb pain and allow the thrombus to adhere firmly to the venous wall until organization and recanalization occur. Elevate the affected limb to 20–30 cm above the level of the heart and lungs, with slight flexion of the knee joint to facilitate venous return and reduce edema. Maintain bowel regularity to prevent thrombus dislodgement due to straining during defecation. After getting out of bed, wear long elastic stockings for 6–12 weeks to compress superficial veins, enhance venous return, and reduce limb edema.

(2) Thrombolytic therapy: Applicable within 3 days of onset or in cases complicated by pulmonary embolism.

1) Streptokinase: Administer hydrocortisone 25–50 mg or dexamethasone 5–10 mg intravenously 30 minutes prior to use to prevent adverse reactions. Initial dose: 500,000 units of streptokinase mixed with 100 ml of 5% glucose solution or normal saline, infused intravenously over 30 minutes, followed by a maintenance dose of 100,000 units/hour until symptoms resolve, then continue infusion for an additional 3–4 hours. Alternatively, 600,000 units of streptokinase mixed with hydrocortisone 25 mg (or dexamethasone 25 mg) and 250–500 ml of 5% glucose solution can be infused intravenously every 6 hours. Generally, the treatment lasts for 3–5 days.

2) Urokinase: Fewer adverse reactions, eliminating the need for corticosteroids. Initial dose: 30,000–50,000 units mixed with 250–500 ml of 5% glucose solution (or dextran-40), infused intravenously over 1–2 hours, 2–3 times daily. Maintenance dose is adjusted based on daily fibrinogen levels or euglobulin lysis time, and treatment may continue for 1–2 weeks.

4) Plasminogen (fibrinolysinogen) combined with streptokinase: 90 mg or 120 mg of plasminogen mixed with 150 ml of normal saline, infused intravenously over 4–6 hours, followed by 600,000 units of streptokinase mixed with 100 ml of normal saline, infused intravenously over 30 minutes, once daily for 5 days.

(3) Dextran-70 or dextran-40: 500–1000 ml infused intravenously once daily for 10–14 days to improve vascular patency.

(4) Surgical treatment: For large thrombi or when conservative therapy fails, consider thrombectomy or venous ligation of the lower limbs.

2. Treatment of Pulmonary Embolism: For cases complicated by pulmonary embolism, the following measures should also be taken.

(1) Oxygen therapy: To improve arterial oxygen partial pressure.

(2) Analgesia: For chest pain, administer papaverine 30–60 mg or pethidine hydrochloride (Dolantin) 50–100 mg intramuscularly, or morphine 5–10 mg subcutaneously.

(3) Antispasmodics: Atropine 0.5–1 mg intravenously every 1–4 hours to reduce vagal tone and prevent or alleviate reflex spasm of pulmonary vessels and coronary arteries. Aminophylline 0.25–0.5 g mixed with 100–250 ml of 5% glucose solution, infused intravenously to relieve bronchospasm.

(4) Anti-shock therapy: Dopamine 20–40 mg or Aramine 20–40 mg mixed with 200 ml of 5% glucose solution, infused intravenously.

(5) Cardiac support: Deslanoside (Cedilanid) 0.4–0.8 mg or strophanthin K 0.25 mg mixed with 50% glucose solution, administered intravenously by slow injection.