| disease | Pregnancy-induced Hypertension Syndrome |
| alias | PIH, Pregnancy-induced Hypertension |
Pregnancy-induced hypertension syndrome (referred to as PIH) is a common yet serious condition that significantly affects the safety of both mother and baby. Improving prenatal care and management can markedly reduce maternal mortality caused by PIH. In selected regions of China from 1984 to 1988, among 7,485 maternal deaths, the top five causes—obstetric hemorrhage, heart disease, PIH, amniotic fluid embolism, and puerperal infection—accounted for 77.4% of all maternal deaths. The prevention and treatment of PIH are therefore critically important.
bubble_chart Etiology
The etiology of pregnancy-induced hypertension (PIH) remains unclear. Below is a brief introduction to the related factors and several major disease cause theories.
1. Related factors of PIH Epidemiological studies suggest that PIH may be associated with the following factors: ① Excessive mental stress or stimulation leading to central nervous system dysfunction; ② Cold seasons or extreme temperature fluctuations, especially during high atmospheric pressure; ③ Young primiparas or advanced-age primiparas; ④ Pregnant women with a history of chronic hypertension, nephritis, or diabetes; ⑤ Malnutrition, such as those with hypoalbuminemia; ⑥ Short and obese body type, with a body mass index [weight (kg)/height (cm)2×100] > 0.24; ⑦ Excessive uterine tension, such as polyhydramnios, twin pregnancy, macrosomia due to diabetes, or hydatidiform mole; ⑧ Family history of hypertension, especially if the pregnant woman’s mother had a history of PIH.
2. Disease cause theories
（1）Uteroplacental ischemia theory: This theory was first proposed by Young (1918), suggesting that PIH is more likely to occur in primiparas, multiple pregnancies, or polyhydramnios due to increased uterine tension, which compromises uterine blood supply, leading to uteroplacental ischemia and hypoxia. Additionally, systemic circulatory insufficiency, such as severe anemia, chronic hypertension, or diabetes in pregnant women, may also predispose to PIH. Some scholars argue that uteroplacental ischemia is not the cause but rather the result of vasospasm.
（2）Neuroendocrine theory: An imbalance in the renin-angiotensin-prostaglandin system may contribute to the pathogenesis of PIH. Previously, it was believed that PIH patients had elevated renin levels, leading to increased angiotensin II (AII), which causes vasoconstriction, elevated blood pressure, and promotes aldosterone secretion, enhancing sodium reabsorption in the renal tubules. However, recent studies have shown that plasma renin and AII levels in PIH patients are lower than in normal pregnancies, especially in severe cases. Thus, the pathogenesis of PIH may involve increased sensitivity to AII.Prostaglandins (PGs) are implicated in PIH. Besides the established roles of prostaglandin E2 (PGE2), which counteracts AII’s vasoconstrictive effects on vascular smooth muscle, and prostaglandin F2a (PGF2a), which has strong vasoconstrictive properties, two new prostaglandin analogs—prostacyclin (PGI2) and thromboxane A2 (TXA2)—have been identified as potentially more significant in PIH. PGI2 inhibits platelet aggregation and enhances vasodilation, while TXA2 promotes platelet aggregation and vasoconstriction. In normal pregnancies, both increase progressively but remain balanced. In PIH, PGI2 levels decrease significantly, while TXA2 levels rise, leading to vasoconstriction, hypertension, and potential coagulation disorders. Evidence suggests that the decline in PGI2 precedes the clinical onset of PIH, indicating its possible role in the disease’s development.
(3) Immunological theory: Pregnancy is considered a successful natural allograft. The maintenance of a normal pregnancy relies on the establishment and stability of immune balance between the fetus and the mother. From an immunological perspective, the cause of pregnancy-induced hypertension (PIH) is attributed to an abnormal immune response to certain antigenic substances from the placenta, which is quite similar to the concept of transplant immunology. Immunological studies on PIH have found that maternal plasma levels of IgG and complement titers are reduced, while the incompatibility of histocompatibility antigens (HLA) between spouses is increased. This HLA incompatibility may be related to the occurrence of PIH. Data indicate that the detection rate of HLA antibodies in PIH patients is significantly higher than in normal pregnancies. However, not every case of PIH can detect HLA antibodies, and even severe cases may show no HLA antibodies. Therefore, the relationship between this disease and immunity remains incompletely understood.
(5) Others: In recent years, new progress has been made in the study of the causes of PIH, such as endothelin, calcium, atrial natriuretic peptide, and trace elements. Among these, the relationship between plasma endothelin and calcium deficiency with PIH has attracted particular attention.
1) PIH and plasma endothelin: Endothelin (ET) is a polypeptide hormone secreted by vascular endothelial cells and is a potent vasoconstrictor. ET and TXA2 and the endothelium-derived relaxing factors (EDRFs) and PGI2 normally maintain a dynamic balance, regulating the body's blood pressure and local blood flow. In PIH, the levels of ET and TXA2, which regulate vasoconstriction, increase, while the levels of EDRFs and PGI2, which regulate vasodilation, decrease, leading to an imbalance in the regulation of vasoconstriction and vasodilation.
2) Calcium deficiency and PIH: Recent studies suggest that the occurrence of PIH may be related to calcium deficiency. Evidence shows that calcium deficiency in both humans and animals can lead to elevated blood pressure. Pregnancy is prone to causing maternal calcium deficiency, which may result in PIH, while calcium supplementation during pregnancy can reduce the incidence of PIH. Therefore, calcium deficiency is considered a potential significant factor in the development of PIH, although the underlying mechanism remains unclear. Additionally, the measurement of urinary calcium excretion can serve as a predictive test for PIH.
Pregnancy-induced hypertension syndrome
1.Grade I Gestational hypertension The main clinical manifestations include Grade I elevated blood pressure, which may be accompanied by Grade I proteinuria and/or edema. This stage can last from several days to weeks, may progress gradually or deteriorate rapidly.
(1) Hypertension: Before pregnancy or before 20 weeks of gestation, the blood pressure (baseline blood pressure) is normal. After 20 weeks of pregnancy, blood pressure begins to rise ≥18.7/12 kPa (140/90 mmHg), or systolic blood pressure increases by 4 kPa (30 mmHg) and diastolic blood pressure by 2 kPa (15 mmHg) compared to the baseline.
(2) Proteinuria: Proteinuria usually appears slightly later than elevated blood pressure, with minimal or initially absent amounts.
(3) Edema: Initially, it may manifest as abnormal weight gain (hidden edema), exceeding 0.5 kg per week. If fluid accumulation is excessive, clinically visible edema occurs. Edema often starts from the ankles, gradually extending to the calves, thighs, vulva, and abdomen, showing pitting upon pressure, known as pitting edema. Significant pitting edema in the ankles and calves that does not subside after rest is marked as "+"; edema extending to the thighs is marked as "++"; "+++" indicates edema extending to the vulva and abdomen; "++++" refers to generalized edema or edema accompanied by ascites.
2.Grade II Gestational hypertension Blood pressure exceeds Grade I but does not surpass 21.3/14.6 kPa (160/110 mmHg); proteinuria (+) indicates urinary protein exceeding 0.5 g in 24 hours; no subjective symptoms are present.
3.Grade III Gestational hypertension Represents further progression of the condition. Blood pressure may rise to 21.3/14.6 kPa (160/110 mmHg) or higher; 24-hour urinary protein reaches or exceeds 5 g; varying degrees of edema may occur, along with a series of subjective symptoms. This stage can be divided into preeclampsia and eclampsia.
(1) Preeclampsia: On the basis of hypertension and proteinuria, the patient develops symptoms such as headache, blurred vision, nausea, epigastric pain, and vomiting. These symptoms indicate worsening of the condition, particularly further progression of intracranial lesions, signaling impending convulsions, hence termed preeclampsia.
(2) Eclampsia: On the basis of preeclampsia, convulsions occur, with or without unconsciousness, known as eclampsia. In rare cases, the condition progresses rapidly with minimal preeclampsia signs before sudden convulsions. A typical eclampsia episode begins with fixed eyeballs, dilated pupils, followed by head turning to one side, clenched teeth, then tremors in the corners of the mouth and facial muscles, progressing within seconds to generalized and limb muscle rigidity, clenched fists, flexed arms, and intense convulsions. Breathing stops during convulsions, and the complexion turns cyanotic. Convulsions weaken after about one minute, muscles relax, followed by deep inhalation and snoring as breathing resumes. Consciousness is lost before and during convulsions. Patients with fewer and longer intervals between convulsions may regain consciousness shortly after; those with frequent and prolonged convulsions often fall into deep unconsciousness. Various injuries may occur during convulsions, such as lip or tongue biting, falls, or even fractures. Vomiting while unconscious can lead to asphyxia or aspiration pneumonia.
Eclampsia mostly occurs in the advanced stages of pregnancy or before labor, termed antepartum eclampsia; a few cases occur during childbirth, termed intrapartum eclampsia; and rarely, within 24 hours postpartum, termed postpartum eclampsia.
Gestational hypertension, especially Grade III, often leads to maternal and fetal complications such as renal dysfunction, placental abruption, intrauterine growth restriction, and fetal distress.
2.Impact on the fetus and newborn
The main pathological change of pregnancy-induced hypertension is systemic small vessel spasm. In severe cases, there is a significant decrease in blood concentration and blood volume, leading to reduced uterine-placental blood perfusion. Acute atherosclerotic changes are present in the placental bed. The placenta shows not only reduced DNA and protein content but also a significant decline in the activity of various enzymes, particularly those involved in glycogenolysis. This results in decreased glucose utilization, severely affecting the fetus's uptake of oxygen and nutrients, leading to fetal growth and developmental disorders. In grade III pregnancy-induced hypertension, the placental reserve function is also greatly diminished. Especially in cases accompanied by intrauterine growth retardation, fetal heartbeats may suddenly disappear during weak uterine contractions, which is related to the reduced placental reserve function. Clinically, the occurrence of premature labor, intrauterine fetal death, stillbirth, and placental abruption are all positively correlated with the severity of pregnancy-induced hypertension.
3. Complications and Their Prevention and Treatment
(1) The clinical manifestations of pregnancy-induced hypertension (PIH) heart disease are: On the basis of grade III PIH, if the preload—i.e., the end-diastolic ventricular volume—is insufficient, symptoms such as reduced urine output and increased pulse rate may occur. Blind volume expansion therapy at this stage can lead to pulmonary hypertension, acute pulmonary edema, and manifestations of total heart failure, such as dyspnea, cyanosis, orthopnea, cough, and expectoration of large amounts of pink frothy sputum. Physical examination may reveal a heart rate of 160–180 beats per minute, a grade II–III systolic murmur or gallop rhythm at the apex, and moist rales in both lungs. Chest X-rays may show cardiomegaly and increased pulmonary markings. Electrocardiograms may indicate ST-segment depression and/or T-wave inversion. The premonitory signs of heart failure include grade I cough or nocturnal choking cough, which are often overlooked by clinicians and mistaken for upper respiratory tract infections. Additionally, there is often a rapid increase in body weight with only mild lower limb edema, and this concealed edema is also easily neglected. These signs must be taken seriously.
(2) The clinical manifestations of cerebrovascular complications are: Patients with PIH complicated by cerebral hemorrhage may experience the following prodromal symptoms days or hours before onset: headache, vertigo, or syncope, motor or sensory disturbances, and blurred vision. Once a cerebrovascular accident occurs, symptoms such as headache and vertigo may worsen, accompanied by projectile vomiting, urinary incontinence, hemiplegia, confusion or unconsciousness, localized or generalized spasms, constricted or unequal pupils, and loss of light reflex. Diagnosis is not difficult when these typical manifestations are present, but early diagnosis is crucial to improve prognosis.
(3) Clinical manifestations and laboratory indicators of HELLP syndrome: The typical clinical manifestations include lack of strength, discomfort or pain in the right upper abdomen, recent excessive weight gain, and other described symptoms and signs. A few patients may exhibit jaundice, blurred vision, hypoglycemia, hyponatremia, and nephrogenic diabetes insipidus. Patients often seek medical attention due to eclampsia spasms, gum bleeding, severe pain in the right upper abdomen or flank, hematuria, as well as nausea, vomiting, upper gastrointestinal bleeding, or hematochezia.
Laboratory findings: Anemia may be mild, moderate, or grade III, but the reticulocyte count is >0.005–0.015. Peripheral blood smears may reveal abnormal red blood cells, helmet cells, acanthocytes, schistocytes, and triangular red cell fragments. The platelet count <100×109 /L; in severe cases, it may drop to <50×109 /L ( <50000/mm3 ). If lactate dehydrogenase (LDH) exceeds 600 IU/L, fibrinogen and fibrin degradation products (FDP) must be measured, along with prothrombin time and partial thromboplastin time. All PIH patients must undergo routine platelet and liver function tests, and abnormalities should prompt consideration of this condition.
4. Characteristics of PIH Complicated by Renal Failure: The typical course can be divided into three stages:
(1) Oliguric stage manifestations include: ① Water retention or edema; ② Hypertension; ③ Heart failure or acute pulmonary edema; ④ Hyperkalemia and corresponding arrhythmias; ⑤ Hypermagnesemia; ⑥ Metabolic acidosis; ⑦ Symptoms of uremia; ⑧ Secondary infections.
(2) Diuretic stage: When transitioning from the oliguric stage to the diuretic stage, the onset is marked by a daily urine output exceeding 400 mL. Urine output may increase gradually or abruptly and can last for 2–3 weeks. Although urine output is high during this stage, symptoms such as nitrogen retention may persist or even worsen. The diuretic stage is often accompanied by severe water and electrolyte imbalances, such as dehydration, hyponatremia, and hypokalemia, which require special attention.
(3) Stage of convalescence: Urine output returns to normal, symptoms improve or disappear, and physical strength and renal function gradually recover, though renal recovery may be slow.
Some patients may present with non-oliguric ARF. These patients generally have milder conditions and higher cure rates. However, due to sometimes inconspicuous clinical manifestations, they may be misdiagnosed as fistula disease, leading to severe complications or even delayed emergency treatment that endangers the patient. Therefore, this should serve as a warning.
In patients with pregnancy-induced hypertension, a sudden drop in blood pressure postpartum, accompanied by pale complexion and profuse sweating. If the mother has no blood loss or birth canal injury, and there are no other causes of shock, yet the above symptoms appear, then this rare postpartum circulatory collapse should be considered.
Table 1
| Classification | Blood Pressure (kPa) | Proteinuria | Edema | Subjective Symptoms |
| Mild | ≥17.3/12.0 or an increase of 4.0/2.0 from baseline blood pressure | + | - | None |
| - | +～++ | None | ||
| Moderate | ≥17.3/12.0 ～<21.3/14.6 or diastolic pressure reaching 13.3 | + | Present or absent | None |
| ± | Present | Present (grade I dizziness) | ||
| Severe | ||||
| Pre-eclampsia | ≥21.3/14.6 or an increase of 8.0/4.0 from baseline blood pressure | ++～+++ | Or with edema | Present |
| - ～ + | ++～+++ | |||
| Eclampsia | With spasms or unconsciousness on the basis of pregnancy-induced hypertension | |||
| Chronic Hypertension Complicated by Pregnancy-Induced Hypertension | History of hypertension before pregnancy, now complicated by proteinuria and edema or with subjective symptoms | |||
bubble_chart Treatment Measures
Since the disease cause of pregnancy-induced hypertension remains unclear to this day, the current treatment principles still involve addressing its predisposing factors and pathophysiological changes, including measures such as antispasmodics, antihypertensives, diuretics, and timely termination of pregnancy.
Application of the antispasmodic drug magnesium sulfate
Magnesium sulfate remains the first-line drug for treating pregnancy-induced hypertension. Clinical practices both domestically and internationally have proven that magnesium sulfate is still the best antispasmodic drug; it remains the preferred treatment for managing and preventing the onset of eclampsia in cases of preeclampsia and eclampsia. The dose and administration route of magnesium sulfate: There is still no consensus on the dosage of magnesium sulfate globally.
(1) Pritchard, when treating eclampsia patients, used an initial dose (loading dose) of 4g intravenously and 5g intramuscularly in each buttock, totaling 14g initially. The maintenance dose was administered intramuscularly, with 5g every 4 hours if urine output was ≥100ml/h and knee reflexes were present. The serum Mg2+ concentration from this maintenance dose was equivalent to that achieved with a continuous IV infusion of 2g/h.
(2) Zuspan used a loading dose of 4g intravenously, followed by a maintenance dose of 1–2g/h, though it is generally considered that 1g/h IV infusion is insufficient as a maintenance dose.
(3) The Obstetrics and Gynecology Hospital of Shanghai Medical University administered magnesium sulfate for preeclampsia or eclampsia patients with an initial dose of 25% magnesium sulfate 10ml mixed with 50% glucose 20ml via slow IV injection, or 5g of magnesium sulfate in 50% glucose 100–200ml infused over 1 hour. Subsequently, 60ml of magnesium sulfate was added to dextran or glucose solution 1,000ml and infused at 1.5–2g/h, with an additional 5g intramuscular injection at night. The total magnesium sulfate dose in the first 24 hours was 20–22.5g. If the initial dose was 10–5g/h, serum magnesium levels rose immediately, peaked at 1 hour, and began to decline after 2 hours. If the initial dose was 10–14g (including IV and IM administration), with a total 24-hour dose of 30–35g, the peak serum magnesium concentration could reach 2.5–3mmol/L, showing significant clinical efficacy. However, Chinese pregnant women generally weigh less than their Western counterparts, particularly those in Europe and America, so caution is warranted when the magnesium sulfate dose for Chinese pregnancy-induced hypertension patients exceeds 30g/day, and it should be used under close observation.
Precautions for using magnesium sulfate: (1) Grade III pregnancy-induced hypertension patients, especially those on long-term low-salt or salt-free diets, may develop hyponatremia. Vomiting during treatment can lead to further sodium loss and acidosis, manifesting as deep and slow breathing, muscle weakness, weakened or absent knee reflexes, reduced urine output, and slowed fetal heart rate, which can be mistaken for magnesium toxicity. In such cases, large doses of magnesium sulfate should not be blindly administered, nor should treatment rely solely on clinical observation. Immediate measurement of serum magnesium and routine electrolytes, along with ECG monitoring, is necessary to determine further management.
(2) Monitor urine output, knee reflexes, and respiration—these three are the primary indicators for observing magnesium toxicity. Chesley also emphasized that during IV magnesium sulfate infusion, in addition to these three indicators, regular auscultation of heart rhythm and rate is essential, as Mg2+ can impair atrioventricular conduction and should not be overlooked.
(3) During the peak effect of magnesium sulfate, respiratory depressants should be used cautiously, and the dose should be reduced if necessary to avoid respiratory depression.
(4) Magnesium sulfate must be used with caution when cardiomyopathy is present, as it may lead to low-output high-resistance heart failure or even cardiac arrest. For pregnant women with hypertensive disorders complicated by valvular heart disease, although magnesium sulfate is not contraindicated, attention must be paid to the intravenous infusion rate and fluid replacement volume.
(5) Intravenous drip is superior to bolus injection. The latter requires diluting the magnesium sulfate concentration to 5-8%, and the injection must be slow, as excessively high concentration per unit time can also cause magnesium toxicity.
(6) The relationship between body weight and dose, as well as the flow rate, must be carefully noted. For individuals with lower body weight, a large dose of magnesium sulfate should not be administered within a short period to avoid toxicity. In Prichard's 1984 data, an eclampsia patient weighing 56kg failed to have spasms controlled after a 2g intravenous bolus. An additional 2g of magnesium sulfate was administered intravenously, totaling 20g within 2 hours. The patient's spasms ceased, but cardiac and respiratory arrest ensued, leading to death. Prichard later encountered two similar cases where the same dose of magnesium sulfate was used, again resulting in cardiac and respiratory arrest. However, due to proper intubation, oxygen administration, and timely intravenous calcium gluconate injection, these two pregnant women were successfully rescued. Through these three cases, Prichard emphasized the critical importance of considering the relationship between body weight, dose, and administration speed when using magnesium sulfate—a lesson that must be heeded.
(7) For patients receiving large doses of intravenous or intramuscular magnesium sulfate, serum magnesium levels must be measured to determine suitability for administration. Although Anderson reported that up to 44g of magnesium sulfate per day for four consecutive days showed no adverse effects and was highly effective, pregnant women in our country generally weigh around 60kg, making a daily dose not exceeding 30g advisable. Dosage reduction may be considered after 24 hours.
(8) During repeated or continuous intravenous magnesium sulfate infusion, in addition to monitoring knee reflexes, urine output must be precisely monitored—at least 100ml/4h (≥25ml/h). Family members should never be entrusted with recording urine output to avoid errors that could compromise patient care.
(9) During continuous intravenous magnesium sulfate infusion, patients often report reduced or absent fetal movement. If this occurs, administration should be paused for 1-2 days for observation. If the reduction is due to magnesium sulfate, fetal movement should resume after discontinuation; otherwise, fetal-placental insufficiency should be considered. When fetal movement weakens, umbilical artery blood flow should be measured to assess fetal hypoxia.
**Volume Expansion Therapy**
Grade III pregnancy-induced hypertension (PIH) patients exhibit varying degrees of hypovolemia. Prichard noted that in normal advanced-stage pregnancy, blood volume increases by 47%, whereas in eclampsia patients, it increases by only 16%. Reduced blood volume is often accompanied by increased blood viscosity and hemoconcentration, leading to poor uteroplacental perfusion. Severe cases may result in preeclampsia or eclampsia, manifesting as low-output, high-resistance heart failure. Thus, volume expansion therapy is warranted for severe cases with elevated plasma and whole-blood viscosity.
**1. Principles of Volume Expansion Therapy**: Can be summarized as: expansion after antispasmodic therapy, dehydration post-expansion, increasing colloid osmotic pressure, and timely delivery to protect both mother and child.
Because PIH, especially in severe cases, is often accompanied by hypoalbuminemia, pulmonary arteriolar spasm, and elevated pulmonary artery wedge pressure (PAWP), pulmonary edema is a risk. Therefore, ECG monitoring, pulse, blood pressure, urine output, and lung auscultation must be observed before and during volume expansion therapy. Administering large volumes of crystalloid solutions without increasing colloid osmotic pressure may paradoxically induce pulmonary edema.
**2. Advantages of Volume Expansion Therapy**
(1) Increases blood volume and improves tissue perfusion.
(2) Improves microcirculatory stasis, increases cerebral blood flow, and alleviates cerebral hypoxia. Improved microcirculation also helps prevent disseminated intravascular coagulation (DIC).
(3) Enhances uteroplacental blood flow, improves fetal-placental function, alleviates fetal hypoxia, and reduces perinatal mortality.
**3. Indications and Contraindications for Volume Expansion Therapy**
(1) Indications for simple volume expansion therapy: According to the criteria of Xinhua Hospital affiliated to Shanghai Second Medical University, volume expansion therapy should be administered when the hematocrit >0.35, whole blood viscosity ratio >3.6, and plasma viscosity ratio >1.6-1.7.
After volume expansion, administer dehydrating agents: For patients showing signs of cerebral edema, such as severe headache, nausea, vomiting, etc., or those with retinal edema accompanied by exudates, if urine output remains <25–30 ml/hour after volume expansion therapy, renal function should be assessed. Generally, 250 ml of 25% mannitol is administered via rapid intravenous drip. If urine output increases, it indicates hypovolemia rather than renal insufficiency or failure, and volume expansion therapy can be continued to replenish blood volume. If urine output does not increase, it suggests renal insufficiency, and fluid intake should be strictly restricted, with treatment for renal failure initiated.
(2) Contraindications for volume expansion therapy: Pulmonary edema, signs of heart failure, or renal insufficiency are absolute contraindications. Additionally, rapid volume expansion should be avoided before hematocrit and urine specific gravity are assessed.
4. Selection of volume expanders: Due to varying severity of pregnancy-induced hypertension, differences in hemoconcentration, and factors such as anemia and proteinuria, different volume expanders are required. Currently, they are categorized into colloid solutions and crystalloid solutions. Specific types are listed in Table 2.
Table 2: Effects of Various Volume Expanders
| Type | Effect | Disadvantages | Indications |
| Colloid | |||
| Albumin, plasma | The ideal volume expander, increases colloid osmotic pressure, absorbs 12 ml/g of water | Expensive, limited availability | Hypoproteinemia, interstitial edema |
| Whole blood | Corrects anemia, increases plasma protein and colloid osmotic pressure | Limited blood supply | Anemia with hypoproteinemia |
| Dextran | Medium molecular weight (75,000) 6% solution absorbs 15 ml/g, effect lasts 4 hours, 50% excreted after 8 hours
Low molecular weight (20,000) 6% solution absorbs 15 ml/g, improves microcirculation, reduces platelet adhesion, prevents DIC |
Short duration of action; requires addition of 1,000 ml of 5% glucose to prolong expansion, termed one expansion unit |
|
| 706 plasma substitute (hydroxyethyl starch), crystalloid | Remains in circulation longer (11 hours), rare allergic reactions, cost-effective | Less effective than dextran | Normal plasma protein and sodium levels |
| Balanced solution | Promotes sodium excretion and diuresis | Hyponatremia, urine specific gravity normal or ≤1.008, hematocrit 0.35 | |
| Sodium bicarbonate | Corrects acidosis, reabsorbs 4 times the tissue fluid, rapid volume expansion | Presence of acidosis |
5. Factors affecting the efficacy of volume expansion therapy
(1) Inappropriate selection of expansion agents: In patients with grade III pregnancy-induced hypertension, there is often high blood viscosity and hemoconcentration. Based on laboratory results, dextran-70 or dextran-40 and balanced solutions can be used to increase and dilute the blood. When the colloid osmotic pressure is <2.7 kPa, treatment should involve colloidal solutions (human albumin or whole blood), and dextran or other crystalloid solutions should not be used.
(2) Insufficient or excessive input speed and volume can both affect the therapeutic efficacy. Therefore, before, during, and after the treatment course, it is necessary to measure hematocrit, urine specific gravity, A/G ratio, and hemorheological indicators, combined with clinical manifestations to evaluate the effectiveness.
Application of Antihypertensive Drugs
1. Principles of Medication: ① The principle is not to affect cardiac output, renal blood flow, or placental perfusion. ② For patients with diastolic blood pressure ≥ 14.7 kPa (110 mmHg), intravenous infusion should be administered.
2. Hydralazine (Apresoline): It blocks α-receptors, causing peripheral vasodilation and lowering blood pressure. Its advantages include increased cardiac output and improved renal and cerebral blood flow. Side effects include tachycardia, facial flushing, nausea, palpitations, and other discomforts. The dose is 12.5–25 mg added to 250–500 ml of glucose solution for intravenous infusion, usually at a rate of 20–30 drops per minute. Once blood pressure stabilizes at 18.6–12.0 kPa (140/90 mmHg), the infusion rate should be slowed to maintain this level.
3. Labetalol: A derivative of salicylamide, it competitively antagonizes α- and β-adrenergic receptors. Its advantages include effective blood pressure reduction, decreased vascular resistance, increased renal blood flow without reducing placental blood flow, promotion of fetal lung maturity, reduced platelet consumption, and increased prostacyclin levels. During intravenous infusion, blood pressure gradually decreases without side effects such as palpitations, flushing, or vomiting, making it more acceptable to patients than hydralazine. The dose is 50 mg or 100 mg added to 500 ml of 5% glucose solution for intravenous infusion at 20–40 drops per minute, adjusted based on blood pressure. The treatment course lasts 5 days. After blood pressure stabilizes, oral administration of 100 mg three times daily can be initiated.
4. Nifedipine: A calcium channel blocker, it prevents extracellular calcium ions from crossing the cell membrane into the cytoplasm and inhibits the release of calcium ions from the sarcoplasmic reticulum. By blocking calcium entry into the cytoplasm, it prevents the activation of myofibrillar ATPase and the breakdown of ATP, interrupting the energy source required for smooth muscle contraction. The pharmacological effect results in systemic vasodilation and blood pressure reduction. Additionally, by inhibiting smooth muscle contraction, it helps prevent threatened premature labor in patients with pregnancy-induced hypertension accompanied by weak uterine contractions. The dose is 10 mg sublingually, three times daily or every 6 hours, with a maximum daily dose of 60 mg. A treatment course lasts 7 days, and 3–5 courses can be administered without intervals.
After the above treatment, the mean arterial pressure can decrease by 1.6–2.8 kPa (12–21 mmHg), demonstrating good efficacy and convenience. A few patients may experience dizziness, flushing, or flusteredness, but these symptoms are generally tolerable and resolve spontaneously within 2–3 days without requiring discontinuation.
5. Captopril: An angiotensin-converting enzyme (ACE) inhibitor, its mechanism involves preventing the conversion of angiotensin I (AT-I) to angiotensin II (AT-II), thereby lowering blood pressure and inhibiting aldosterone. The dose is 12.5–25 mg orally twice daily, with excellent antihypertensive effects. Due to its significant vasodilatory effects, including renal vasodilation and increased renal blood flow, and absence of adverse reactions, it is 10 times more potent than another antihypertensive drug, saralasin. Thus, captopril is simpler and more effective for patients with pregnancy-induced hypertension.
6. Sodium Nitroprusside: In a few cases of grade III pregnancy-induced hypertension with extremely high blood pressure that cannot be controlled by the aforementioned medications, this drug may be used under close observation. Sodium nitroprusside primarily acts on vascular smooth muscle, dilating arteries and veins, reducing peripheral vascular resistance and decreasing end-diastolic pressure in the heart, thereby rapidly lowering blood pressure and improving cardiac function, increasing cardiac output. It must be noted that after intravenous infusion, sodium nitroprusside can quickly cross the placenta into the fetal circulation, with fetal blood concentrations higher than those in the mother. Additionally, the metabolite of sodium nitroprusside (cyanide) can bind to the sulfhydryl groups of red blood cells, exerting toxic effects. Animal experiments have shown that continuous intravenous infusion of sodium nitroprusside in pregnant sheep for 24 hours can lead to intrauterine death of the lamb due to cyanide poisoning. Therefore, for severe cases of pregnancy-induced hypertension, sodium nitroprusside should only be used when other antihypertensive drugs are ineffective, and solely for the safety of the mother. Alternatively, it may be used to control blood pressure in postpartum patients with severe conditions. Dose: 50 mg in 500 ml of 5% glucose solution, equivalent to 100 μg of sodium nitroprusside per milliliter. Start at 6 drops per minute, then increase by 2 drops (i.e., 12 μg) per minute until satisfactory blood pressure reduction is achieved. Generally, blood pressure should be controlled around 18.7/12–13 kPa (140/90–100 mmHg), with measurements taken every 5–10 minutes. The maximum dose is 100 mg per 24 hours.
Precautions:
(1) Sodium nitroprusside is light-sensitive and may turn blue upon exposure to light. Therefore, the injection bottle should be wrapped in black paper or aluminum foil.
(2) The hypotensive effect is very rapid, usually taking effect within 2-3 minutes of infusion. Blood pressure should be measured every 5 minutes initially. Once the infusion rate is adjusted to achieve satisfactory blood pressure control, measurements can be reduced to every 10 minutes. Diastolic blood pressure should be maintained at 12-13 kPa (90-100 mmHg) and should not be too low.
(3) The direct metabolite of sodium nitroprusside can form cyanide. It should be used with caution in patients with severe liver impairment.
(4) Since this drug quickly enters the fetal circulation, childbirth should be completed as soon as possible after the patient's blood pressure drops and symptoms improve, to ensure the safety of both mother and baby.
7. Prazosin: An α-adrenergic receptor blocker that dilates small arteries, reduces peripheral vascular resistance, and lowers blood pressure. It also decreases cardiac preload and afterload, thereby reducing left ventricular end-diastolic pressure and improving cardiac function. The initial dose is 0.5 mg, which can later be adjusted to 0.5-1 mg, taken orally three times daily, with gradual dose increases. The first dose may cause a "first-dose phenomenon," characterized by significant dizziness or discomfort, but this reaction typically does not recur with subsequent doses.
8. Qingxinketong: Chemically known as 3,4-dihydroxyacetophenone, it is an active component extracted from the root and stem of Ilex pubescens. It has vasodilatory effects and regulates the balance of PGI2-TXA2. Both in vivo and in vitro, it inhibits ADP-induced platelet aggregation, with rapid action and minimal side effects. Dose: 100 mg in 500 ml of 5% glucose solution, administered intravenously twice daily.
Use of Sedatives
1. Diazepam (Valium): Has strong sedative, anticonvulsant, hypnotic, and muscle relaxant effects. For eclampsia or preeclampsia patients showing signs of impending convulsions, 10-20 mg of diazepam can be added to 20-40 ml of 25% glucose solution and slowly injected intravenously over 5-10 minutes to quickly control convulsions. If magnesium sulfate has already been administered intravenously, 10 mg of diazepam is preferred. For grade II preeclampsia patients, 2.5 mg of diazepam can be given orally three times daily. Since diazepam rapidly crosses the placenta and even full-term fetuses excrete it slowly, it can accumulate in the fetus and remain in the newborn's system for about a week, potentially affecting sucking and breastfeeding. Therefore, long-term use of diazepam should be avoided.
2. Amobarbital sodium: Has hypnotic and anticonvulsant effects. For convulsions not controlled by magnesium sulfate, 0.2-0.5 g of amobarbital sodium can be added to 20 ml of 50% glucose solution and injected intravenously over 5-10 minutes. Note that if magnesium sulfate has already been used, repeated intravenous injections of amobarbital sodium should be avoided to prevent synergistic respiratory depression. The oral dose is 0.1 g every 8 hours, typically used for only 1-2 days clinically.
3. Morphine: A potent analgesic. For eclampsia convulsions, 10-15 mg administered subcutaneously can provide rapid relief. Due to its respiratory depressant effects, which can lead to respiratory acidosis, reduced urine output, and increased intracranial pressure, it is less commonly used for eclampsia treatment in recent years. However, clinical experience shows that for grade III preeclampsia patients, morphine administered post-cesarean section can help prevent postpartum eclampsia and is still worth using. In rural or mountainous areas, when transferring eclampsia patients for hospital treatment, 10-15 mg of morphine can be given subcutaneously to ensure safety during transport.
4. Phenobarbital and Sodium Barbital: They share the general characteristics of barbiturates. High doses have antispasmodic effects, while excessive doses can produce anesthetic effects and even suppress respiration. The hypnotic effect of this drug is relatively long-lasting, approximately 6 to 8 hours. Common dosage: oral administration of 0.03–0.06g, three times daily, or intramuscular injection of 0.1–0.2g sodium barbital.
Application of Diuretics and Dehydrating Agents
Although patients with pregnancy-induced hypertension syndrome (PIH) often present with edema, recent studies suggest that diuretics should not be routinely used.
1. Disadvantages of Diuretic Use
(1) May lead to electrolyte imbalance and can cause acute pancreatitis in the fetus, resulting in death.
(2) May reduce fetal platelet count, increasing the risk of bleeding.
(3) Although maternal weight may decrease, proteinuria does not improve.
(4) Increases blood concentration in pregnant women, exacerbating microcirculatory disorders, creating a false impression of clinical improvement due to weight loss.
(5) Newborns of mothers who used diuretics have significantly lower birth weights compared to the control group.
(6) Thiazide drugs can inhibit uterine contractions, leading to prolonged labor.
2. Indications for Diuretic Use
(1) Pulmonary edema or heart failure.
(2) Generalized edema.
(3) Hypervolemia or grade III anemia.
Prescribing oral diuretics for PIH patients with only lower limb edema is merely self-reassurance for medical staff and offers no clinical benefit.
3. Selection of Diuretics
(1) Furosemide (Lasix): Used for the above indications. Its primary site of action is the ascending limb of the loop of Henle, though it also affects the proximal tubule. It acts rapidly and has strong sodium and potassium excretion effects, which may lead to electrolyte disturbances and hypokalemic alkalosis.
For PIH patients with heart failure or pulmonary edema, combining furosemide with digitalis yields excellent results. Typically, 20–40mg of furosemide is administered intravenously with 20–40ml of 5% glucose solution. The dose may be repeated as needed or adjusted for intramuscular injection.
(2) Mannitol: This is a dehydrating agent and osmotic diuretic. Intravenous administration increases plasma osmotic pressure, creating a gradient between blood and brain that shifts cerebral fluid into the circulation, thereby reducing intracranial pressure and alleviating cerebral edema. Since mannitol does not enter cells, it generally does not cause rebound intracranial pressure. After rapid IV infusion, it is filtered by the glomeruli with minimal tubular reabsorption, excreting large amounts of water. It may be effective for renal insufficiency or increased intracranial pressure. The dose is 200–250ml of 20% mannitol or sorbitol, administered every 8 hours or twice daily via rapid IV infusion over 15–20 minutes. However, it may cause hyponatremia, so regular monitoring of blood potassium and sodium is essential.
(3) Atrial Natriuretic Peptide (ANP): Has strong sodium excretion, diuretic, and vasodilatory effects. By inhibiting the renin-angiotensin-aldosterone system (R-A-A-S), it improves renal function. Since ANP minimally inhibits renal tubules, its primary effect is increasing renal blood flow, helping correct electrolyte imbalances and acid-base disturbances. It is an important drug for PIH complicated by cardiac or renal dysfunction.
(4) Other Diuretics: Drugs like hydrochlorothiazide or triamterene are less commonly recommended for PIH due to their aforementioned drawbacks. Note that mannitol is contraindicated for PIH with heart failure or pulmonary edema.
In summary, the primary medications for PIH are antispasmodics and antihypertensives. The use of volume expansion and diuretics should be determined based on clinical conditions and laboratory results.
Treatment should be tailored according to different stages of the condition.
1. Grade I Pregnancy-Induced Hypertension: All cases were followed up in outpatient clinics, with appropriate rest and left lateral decubitus position. Sodium intake was not restricted, and phenobarbital could be used at night as needed to aid sleep. Chinese medicinals such as modified Lycium-Chrysanthemum-Rehmannia Decoction could be employed, with the formula as follows: Unprocessed Rehmannia Root 12g, Cornus Officinalis 9g, Chinese Yam 12g, Poria 12g, Stir-fried Moutan Bark 6g, Alisma 12g, Barbary Wolfberry Fruit 9g, Chrysanthemum Flower 12g, Uncaria Stem with Hooks 12-30g (to be decocted later). In the prescription, Unprocessed Rehmannia Root, Cornus Officinalis, and Barbary Wolfberry Fruit nourish liver and kidney yin; Chinese Yam and Poria strengthen the spleen and drain dampness; Moutan Bark cools blood and clears heat; Chrysanthemum Flower and Uncaria Stem with hooks clear liver heat; Alisma promotes diuresis. Treatment with the above Chinese medicinals can alleviate symptoms and reduce blood pressure to varying degrees.
2. Grade II Pregnancy-induced Hypertension: Rest in the left lateral position, and administer antispasmodic, sedative, and oral antihypertensive medications. When using Chinese medicinals, modifications can be made based on the Qi Ju Rehmannia Decoction.
(1) Antispasmodics: Take 300mg of antelope horn powder orally, or use Earthworm 9–12g and scorpion 1.5g (to be decocted later).
(2) Liver-pacifying and yang-subduing medicinals: Fossil Bone 30g, oyster shell 30g, abalone shell 30g, nacre 30g. All four herbs must be decocted first.
(3) Yin-nourishing medicinals: glossy privet fruit 12g, mulberry fruit 12g, Yerbadetajo Herb 12g, asparagus root 12g, Ophiopogon Tuber 9g, Scrophularia Root 12g, tortoise carapace 12–15g.
(4) Blood-activating and stasis-resolving medicinals: Chinese Angelica 9–12g, Salvia 9–12g, red peony root 9g, Japanese thistle herb 15–30g, small thistle 15g.
If outpatient treatment is ineffective, hospitalization should be arranged following the aforementioned principles.
3. Grade III Pregnancy-induced Hypertension: Take immediate and active measures for patients with preeclampsia to prevent the onset of eclampsia and other severe complications.
(1) Absolute bed rest, avoiding auditory and visual stimulation.
(2) Measure blood pressure every 2–4 hours; at night, reduce to one measurement to avoid disrupting rest. Perform a daily urine routine test, accurately record fluid intake and output, and conduct fundus, electrocardiogram, and blood generation and transformation tests. Echocardiography is recommended if available to detect cardiac dysfunction early.
(3) Medication: Follow the aforementioned methods for drug selection and administration. For severe headache, indicating increased intracranial pressure, administer 20% mannitol 250ml via rapid intravenous drip. Additionally, measure hematocrit and urine specific gravity, and if possible, whole blood viscosity and plasma viscosity to determine the need for volume expansion therapy. For patients with anemia, severe edema, and low hematocrit, blood transfusion, component transfusion, or albumin infusion should be given along with diuretics to significantly improve the condition. For preeclampsia complicated by ascites, intravenous infusion of human albumin or placental albumin every other day or daily may be effective. However, the most crucial step is timely termination of pregnancy after short-term conservative treatment, which promotes gradual recovery and ensures maternal and fetal safety. Avoid uniformly waiting until 36–37 weeks of gestation to end childbirth, as this may lead to intrauterine fetal death and worsening maternal condition.
4. Treatment of Eclampsia: According to Iffy, eclampsia-related deaths result from the following seven causes: ① Persistent hypertensive crisis and renal failure; ② Severe placental abruption and dead fetus; ③ Acute pulmonary edema and heart failure; ④ Aspiration of gastric contents due to spasm, causing ventilation impairment; ⑤ Drug overdose leading to toxicity; ⑥ Cardiac arrest during treatment; ⑦ Hypoxic encephalopathy and cerebral hemorrhage.
5. Nursing Care for Eclampsia: Nursing care for eclampsia patients is equally important as treatment. Initially, place the patient in a quiet, well-ventilated single room with family accompaniment. Maintain absolute quietness and avoid all auditory and visual stimuli. During spasms, avoid intramuscular magnesium sulfate injection first, as the pain from the injection may trigger another spasm. All treatments, such as injections and catheterization, should be performed gently to minimize stimulation. The presence of the husband can help alleviate the patient's mental stress.
To prevent falling from the bed during spasm and unconsciousness, bed rails should be used. Dentures should be removed, and a tongue depressor wrapped in gauze should be prepared for timely insertion into the patient's mouth to prevent lip or tongue biting during spasm. The patient should be placed in a head-low lateral position to prevent mucus aspiration or tongue obstruction of the airway. If necessary, use a suction device to remove mucus or vomitus from the throat to avoid suffocation. While the patient remains unconscious, no food, drink, or oral medication should be given to prevent aspiration into the respiratory tract, which could lead to suffocation or pneumonia. Additionally, accurately record intake and output, monitor pupil size, respiration, and heart rate, and document blood pressure, pulse, respiration, limb movement, tendon reflexes, and uterine tension hourly to facilitate early detection of cerebral hemorrhage, pulmonary edema, renal dysfunction, and signs of labor.
Timely termination of pregnancy
1. Indications for labor induction: For patients with pregnancy-induced hypertension, timely termination of pregnancy is one of the important measures after treatment.
（1）Grade III pregnancy-induced hypertension with no significant improvement after active treatment for 48–72 hours.
（2）Grade III pregnancy-induced hypertension with improvement, and gestational age ≥36 weeks.
（3）Pregnancy-induced hypertension lasting more than 8 weeks, especially with primary hypertension or fetal intrauterine growth retardation, and gestational age ≥36 weeks.
（4）Eclampsia controlled for more than 12 hours.
2. Methods of terminating pregnancy
（1）If the cervix is mature, artificial rupture of membranes can be performed for labor induction.
（2）If the cervix is not mature but there is no fetal distress and the condition has improved, dehydroepiandrosterone sulfate 100mg with 20ml of sterile water can be administered intravenously to promote cervical ripening, followed by artificial rupture of membranes or oxytocin-induced labor.
3. Post-induction precautions
（1）Continuous fetal heart rate monitoring should be performed.
（2）For patients with anemia, fetal intrauterine growth restriction, or abnormal liver function, biophysical profile monitoring should be conducted to detect fetal hypoxia early and adjust the delivery method accordingly.
4. Indications for cesarean section
（1）Severe condition, especially with mean arterial pressure ≥18.7kPa (140mmHg).
（2）Severe cases with immature cervix and inability to deliver vaginally within a short period. Neijingvaginal delivery.
（3）Failed labor induction by artificial rupture of membranes.
（4）Significantly impaired fetal-placental function or biophysical profile score ≤6 on ultrasound.
（5）Recurrent eclampsia uncontrolled by adequate antispasmodic, antihypertensive, and sedative medications.
（6）Primipara with pregnancy-induced hypertensive heart disease or pulmonary edema/heart failure, cesarean section is preferable after stabilization.
5. Precautions for cesarean section in pregnancy-induced hypertension
（1）Continuous epidural anesthesia is safer, but the patient should be positioned 15° to the left to prevent reduced uteroplacental blood flow.
（2）Intravenous magnesium sulfate can be continued for 24 hours postoperatively to prevent postpartum eclampsia.
（3）Administer meperidine (Demerol) 50mg every 6 hours for 24 hours postoperatively to manage wound pain, along with oxytocin or low-dose ergometrine intramuscularly. This approach reduces postoperative pain while enhancing uterine contraction and preventing eclampsia.
（4）Most importantly, these patients are in a hypercoagulable state, and elective cesarean section with an unopened uterus increases the risk of intrauterine hematoma. Therefore, postoperative monitoring of pulse, fundal height, and uterine consistency is crucial. Neglecting these signs and relying solely on analgesics may delay treatment and endanger the mother’s life.
Complications of pregnancy-induced hypertension and their management
Pregnancy-induced hypertensive heart disease
1. Management of pregnancy-induced hypertensive heart disease: Based on early diagnosis, the priority is to correct low cardiac output and high resistance (low output-high resistance), control heart failure, and ensure timely delivery.
（1）Common vasodilators for correcting low output-high resistance (Table 3): Phentolamine, an α-receptor blocker, dilates pulmonary arteries, reduces pulmonary hypertension, and improves hypoxia. Concurrently, administer 30–60mg of papaverine in 20ml of 50% glucose intravenously to enhance coronary artery oxygenation.
Table 3: Efficacy of common vasodilators for heart failure in pregnancy-induced hypertension
| Drug | Venous tension | Small arterial resistance | Heart rate | stirred pulse 壓 | Cardiac Output | Left Ventricular Filling Pressure | Administration Method | Adverse Reactions |
| Phentolamine | - | ↓↓ | ↑ | ↓ | ↑↑ | ↓ | 0.1～0.3mg/min, IV Drip | Tachycardia |
| Nitroprusside | ↓↓ | ↓↓ | - | ↓↓ | ↑ | ↓↓ | 0.5～8μg/kg, 500mg+5% Glucose IV Slow Drip | Nausea, Vomiting, Hypotension, Thiocyanate Toxicity |
| Balanced Arteriovenous Dilation | ||||||||
| Prazosin | ↓ | ↓ | - | - | ↑ | ↓ | Oral 0.5mg tid | |
| Balanced Arteriovenous Dilation | ||||||||
| Isosorbide Dinitrate | ↓↓ | - | - | - | - | ↓↓ | 5～10mg, Sublingual, tid | |
| Mainly Venous Dilation | ||||||||
| Captopril | ↓↓ | ↓ | - | - | ↑↑ | ↓↓ | 12.5mg, Oral, q8h | |
| Venous Dilation Greater Than Arterial | ||||||||
| Nifedipine | - | ↓↓ | ↑ | ↓↓ | ↑↑ | ↓↓ | 10～20mg, sublingual, tid | headache, vertigo |
| Dilates veins | ||||||||
| Hydralazine | - | ↓ | ↑ | ↓ | ↑ | ↓ | 12.5～25mg in 250～500ml of 5% glucose IV drip | palpitation, facial flushing |
| Nitroglycerin | ↓↓ | ↓↓ | 20μg/min IV drip, sublingual 0.3mg | |||||
| Mainly dilates veins |
Sodium nitroprusside balances arterial and venous dilation, acts rapidly (effects appear within 2-5 minutes of IV drip), and must be used under strict monitoring. For prenatal use, it is safest not to exceed 24 hours to avoid fetal cyanide poisoning and death. This restriction does not apply to postpartum preeclampsia with heart failure.
Other vasodilators can be used as indicated in Table 18-5 based on the patient's condition.
(2) Controlling heart failure: While using vasodilators, rapid-acting digitalis preparations must be administered to improve myocardial function, starting with a loading dose. However, the loading dose varies for each patient. Indicators of achieving the loading dose include: ① Heart rate slows to 80-90 bpm; ② Decreased lung rales, no orthopnea; ③ Increased urine output; ④ Shrinking of enlarged liver, disappearance or improvement of tenderness; ⑤ Improvement in subjective symptoms. Deslanoside (Cedilanid) is the preferred drug, with 0.4mg in 20ml of 25% glucose administered by slow IV injection, followed by 0.2～0.4mg after 2～4 hours, up to a total dose of 1.2mg.
(3) Use of diuretics: Furosemide (Lasix) is the preferred rapid-acting diuretic for IV injection, with 40～60mg in 25% glucose given by slow IV push. This can rapidly increase urine output, reduce cardiac load, and may be repeated as needed. Electrolyte balance must be closely monitored.
(4) Sedatives: For patients with severe preeclampsia complicated by heart failure, morphine 2mg (1/5 ampule) can be administered with 10% glucose solution 10ml intravenously, with a maximum dose of 5mg via intravenous drip. The patient can quickly become calm because a small dose of morphine can suppress the overexcited respiratory center, dilate peripheral blood vessels, reduce cardiac preload and afterload, and also has antiarrhythmic effects. Therefore, it can achieve good results in the emergency treatment of acute left heart failure with pulmonary edema.
(5) If the above medications have not been applied, rubber strips can be alternately used to ligate the thighs of both lower limbs to reduce venous return and cardiac blood volume. Although this method is outdated, it can achieve temporary effects in emergencies.
2. Regarding childbirth issues: After controlling heart failure in pregnancy-induced hypertension (PIH), some advocate waiting for natural labor without premature intervention. Based on our practical experience, if labor does not occur within 24–48 hours after heart failure is controlled, induction or cesarean section should be performed depending on the specific circumstances. The rationale is that without ending the pregnancy, heart failure may recur. Additionally, since the etiology of PIH remains unclear, delaying pregnancy termination may exacerbate PIH, leading to increased fetal hypoxia, which is unfavorable for both mother and child. Therefore, timely termination of pregnancy is necessary.
(1) Indications for cesarean section: For primiparas with an immature cervix and a moderately sized fetus, even without cephalopelvic disproportion, if childbirth cannot be completed within a few hours, PIH-related cardiac Bingben conditions alone can serve as an indication for cesarean section. According to Ostheimer’s report, during cesarean section under continuous epidural anesthesia, although diastolic and mean arterial pressures decrease by only 0.53–0.67 kPa (4–5 mmHg) compared to pre-anesthesia levels, it can lead to venous dilation in the lower limbs, reduced blood pressure, and decreased cardiac burden. Domestic data indicate that echocardiographic observations of cardiac function changes during vaginal delivery and cesarean section show that vaginal delivery increases cardiac output by 11.1% during the second stage of labor but decreases it by 24.9% at fetal delivery. In contrast, cesarean section increases cardiac output by 9.3% after entering the abdominal cavity, with only a 5.5% decrease at fetal delivery, suggesting cesarean section significantly reduces cardiac function interference compared to vaginal delivery.
(2) Indications for conservative treatment to continue pregnancy: Only in rare cases, such as PIH-related heart failure occurring around 32 weeks of pregnancy that is quickly controlled but the fetus is not yet mature, supportive therapy (e.g., correcting anemia or hypoalbuminemia) may be allowed under close monitoring. Regular fetal surveillance or timely promotion of fetal lung maturation should be performed, and the mode of childbirth should be decided based on subsequent evaluations.
(3) Regardless of the mode of childbirth, attention must be paid to postpartum eclampsia, limiting fluid intake to prevent recurrent heart failure, and closely monitoring postpartum hemorrhage and infection.
3. New drug treatments for PIH-related heart failure: Since the mid-1980s, atrial natriuretic peptide (ANP) has been used to treat hypertension, congestive heart failure, and pulmonary edema. ANP is stored in specialized granules of atrial myocytes and released into the bloodstream, exhibiting strong natriuretic, diuretic, and vasodilatory effects. Yang Menggeng achieved excellent results using synthetic ANP III to treat PIH-related heart failure. Dosage: ANP III 100–300 μg in 5% glucose solution (250 ml), administered intravenously at 5–10 μg/min, completed in 30 minutes, once daily. Heart failure can be fully controlled within 1–3 administrations. Post-treatment, serum superoxide dismutase (SOD) levels significantly decrease, making ANP III an ideal new drug for managing PIH-related heart failure.
Cerebrovascular accidents
1. Treatment: The management of cerebral thrombosis or infarction differs from that of cerebral hemorrhage, so accurate diagnosis is essential, with brain CT scans being indispensable.
(1) Treatment of PIH complicated by cerebral hemorrhage
1) Maintain calm, strict bed rest, and avoid respiratory depressants.
2) Reduce intracranial pressure: Increased intracranial pressure can lead to brain herniation. For cerebral hemorrhage below 30 ml, administer 25% mannitol (250 ml) intravenously every 6 hours for 7–10 days, then reduce to 125 ml intravenously for another week, alongside antispasmodic, antihypertensive, and anti-inflammatory treatments. If the hematoma exceeds 30 ml, immediate craniotomy is required.
3) Application of antispasmodic and antihypertensive drugs: When blood pressure is excessively high, drugs such as magnesium sulfate and labetalol should be used for antispasmodic and antihypertensive purposes; for cerebral hematomas exceeding 30ml with significant brain compression, after antispasmodic, antihypertensive, and dehydration therapy, an immediate cesarean section combined with craniotomy should be performed to facilitate the rescue of the patient's life.
4) Application of hemostatic medicinals: 6-aminocaproic acid, p-aminomethylbenzoic acid, or tranexamic acid (hemostatic acid) can be used. Some oppose the use of antifibrinolytic drugs in pregnant patients with subarachnoid hemorrhage, but calcium channel blockers can be used to relieve vasospasm.
5) For patients with cerebral aneurysms, the safest approach is to perform a cesarean section near full-term pregnancy, followed immediately by neurosurgical intervention for the cerebral vascular condition.
(2) Treatment of pregnancy-induced hypertension complicated by cerebral thrombosis: This condition is caused by increased whole blood and plasma viscosity, leading to blood stasis and thrombosis formation. CT scans may show low-density areas in the posterior superior part of the cerebral hemisphere, occipital lobe, and temporal lobe. Treatment involves intravenous magnesium sulfate for antispasmodic and sedative effects, combined with volume expansion therapy using dextran-40, along with blood-activating and stasis-resolving medicinals such as cinnarizine 25mg or Sichuan Lovage Rhizome 50mg, taken orally three times daily, which has shown good efficacy.
2. Management
(1) Treatment principles: ① Actively treat pregnancy-induced hypertension with antispasmodics, volume expansion, and blood product transfusion to increase osmotic pressure; ② Conservative treatment for 1–2 days, followed by timely termination of pregnancy; ③ Correct coagulation factor deficiencies.
(2) Drug therapy
1) Combined use of magnesium sulfate and antihypertensive drugs to control spasms and lower blood pressure, preventing hypertensive encephalopathy.
2) Application of adrenal corticosteroids: These can reduce capillary permeability, protect cell lysosomes, and decrease platelet destruction in the spleen's endothelial system. Hydrocortisone 200mg can be administered intravenously with glucose solution. For patients with severe edema, methylprednisolone 40mg with 20ml glucose solution can be slowly injected intravenously every 6–8 hours to prevent further water and sodium retention, which is more effective and safer.
3) Antiplatelet aggregation drugs: In 1978, Goodlin proposed that during pregnancy, platelets <75×10/L（7.5萬/mm3 ) Aspirin 85mg daily can normalize platelet aggregation function, increase platelet count, and correct thrombocytopenic purpura, though it carries the risk of fetal intraventricular hemorrhage. Alternatively, intravenous prostacyclin infusion yields good results. The initial dose is 2ng/kg per minute, followed by 8ng/kg per minute to maintain diastolic pressure at 12kPa (90mmHg), counteracting platelet aggregation and strongly relaxing vascular smooth muscle. However, this drug is still in the experimental stage.
4) Fresh frozen plasma transfusion: Rich in clotting factors and antithrombin III, it is highly effective.
5) Fresh blood transfusion: Warm fresh blood, just drawn from the donor, is optimal due to its high content of clotting factors and platelets, yielding excellent results.
6) For those with the means, intravenous antithrombin III can be administered at a dose of 1000–1500u daily, which is beneficial for preventing disseminated intravascular coagulation.
3. Precautions
Clinicians may easily misdiagnose pregnancy-induced hypertension, especially when only edema is present but accompanied by elevated liver enzymes, grade I bilirubin elevation, and right upper quadrant dull pain, as epidemic hepatitis or cholecystitis. Providing liver-protective therapy and symptomatic treatment can delay proper management. Data suggest that pregnant patients with hypertension should routinely undergo liver function tests, platelet counts, and peripheral blood smears. If systemic discomfort, nausea, vomiting, right upper quadrant tenderness, elevated liver enzymes, low platelet counts, or peripheral blood smears reveal serrated, shrunken red blood cells or small irregularly shaped red cell fragments, HELLP syndrome should be promptly diagnosed and aggressively managed.
Disseminated intravascular coagulation
Treatment of Pregnancy-Induced Hypertension Complicated with Disseminated Intravascular Coagulation: The principle is to remove the {|###|}disease cause{|###|}, which is of utmost importance. During antispasmodic and antihypertensive therapy, fresh frozen plasma and warm fresh blood should be intravenously administered to replenish coagulation factors. Suzuki et al. from Japan reported good results with intravenous infusion of antithrombin II at a daily dose of 3000u. Routine high-{|###|}dose{|###|} heparin therapy should not be used for patients with this condition, especially those with an average stirred pulse pressure ≥18.6kPa (140mmHg) accompanied by DIC, as it is more likely to lead to cerebral hemorrhage. Based on our clinical experience, especially immediately after {|###|}childbirth{|###|}, the focus should be on replenishing coagulation factors, and heparin should be used at a low {|###|}dose{|###|}. One case involved a twin {|###|}pregnancy{|###|} with grade III pregnancy-induced hypertension, and {|###|}postpartum metrorrhagia{|###|} with unclottable blood, where all laboratory indicators met the criteria for DIC. While transfusing blood, 25mg of heparin was administered intravenously, and both {|###|}hematuria{|###|} and {|###|}vagina{|###|} bleeding stopped. An additional 12.5mg of heparin was given intravenously, totaling only 37.5mg, but {|###|}hematuria{|###|} and {|###|}vagina{|###|} bleeding recurred. After discontinuing heparin, the bleeding gradually subsided. This case illustrates that in obstetric DIC, the most critical factor is removing the {|###|}disease cause{|###|}, which can lead to rapid improvement. High-{|###|}dose{|###|} heparin therapy should not be used for DIC in pregnancy-induced hypertension after the {|###|}disease cause{|###|} has been removed.
Pregnancy-induced hypertension complicated by renal failure
1. Laboratory diagnosis
(1) Oliguric phase: Oliguria refers to a daily urine output of less than 400ml.
1) Urinalysis: Hematuria, proteinuria, and casts may all be present, with a fixed specific gravity around 1.012.
2) Elevated blood nitrogen levels, with urea nitrogen being the most significantly increased.
3) Electrolyte disturbances: Hyperkalemia, hypermagnesemia, hyperphosphatemia, hyponatremia, and hypocalcemia are commonly observed.
4) Metabolic acidosis
The oliguric phase often needs to be differentiated from functional (prerenal) oliguria. The following laboratory results aid in diagnosing the oliguric phase: ① Urine osmolality <250mmol/L；尿/血滲透濃度比<1.10；②尿/血尿素氮，或尿/血肌酐比<10；③腎衰指數[即尿鈉/（尿/血肌酐）]>2; ④ Urine sodium >40mmol/L; ⑤ Fractional excretion of sodium [i.e., (urine/serum sodium ratio)/(urine/serum creatinine ratio)] multiplied by 100, >2.
(2) Polyuric phase: Urinalysis shows low specific gravity (1.010–1.014), with proteinuria and casts. Nitrogen retention varies in severity, and the initial stage may continue to worsen before gradually declining. Dehydration may lead to increased hematocrit, and hypokalemia may sometimes occur.
(3) Stage of convalescence: Grade I proteinuria, impaired renal concentration and dilution function, and decreased glomerular filtration rate may persist for an extended period.
2. Treatment of ARF complications
First, it is necessary to determine whether the ARF is functional or organic (Table 4). If it is functional renal failure, the priority is to replenish blood volume and relieve vascular spasms. When blood volume has been restored, peripheral blood pressure has normalized, b
