Hipertensi pada Kehamilan

01Pathophysiology

Normal pregnancy requires extensive remodeling of the uterine spiral arteries. Cytotrophoblasts invade the spiral arteries during the first and early second trimester, replacing the muscular and elastic walls with a low-resistance, high-capacitance vascular bed. This ensures adequate uteroplacental blood flow to support the growing fetus.

In preeclampsia, this trophoblastic invasion is shallow and incomplete. The spiral arteries retain their muscular walls and remain narrow, high-resistance vessels. The result is placental ischemia and hypoperfusion. The ischemic placenta releases a cascade of antiangiogenic factors, most notably soluble fms-like tyrosine kinase 1 (sFlt-1), which binds and neutralizes circulating vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). The depletion of these proangiogenic factors causes widespread maternal endothelial dysfunction.

This endothelial injury is what produces the clinical syndrome. Vasospasm throughout the maternal circulation raises systemic vascular resistance and blood pressure. Endothelial damage in the glomerulus (specifically glomerular endotheliosis, the swelling and vacuolization of glomerular endothelial cells) disrupts the filtration barrier, resulting in proteinuria. Endothelial injury in the hepatic sinusoids causes periportal necrosis and subcapsular hemorrhage, explaining the RUQ pain and elevated transaminases. Microangiopathic injury triggers platelet activation and consumption, producing thrombocytopenia. Red blood cells shearing through damaged microvasculature create schistocytes and elevate LDH, which together with thrombocytopenia and elevated liver enzymes constitute the HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets).

Cerebral endothelial dysfunction and vasospasm impair the blood-brain barrier and cerebral autoregulation. This explains the headache, visual disturbances (scotomata, blurred vision, cortical blindness from posterior reversible encephalopathy syndrome), and ultimately seizures (eclampsia). The seizures in eclampsia are thought to result from cerebral vasospasm, ischemia, and vasogenic edema rather than simply from high blood pressure alone, which is why eclampsia can occur even with only mildly elevated BP.

Understanding this pathophysiology clarifies why delivery of the placenta is the only definitive cure. All other treatments are temporizing measures that address downstream consequences without correcting the underlying placental disease.

02Classification and Clinical Manifestation

Classification of Hypertensive Disorders in Pregnancy

Severe Features of Preeclampsia

This distinction is critical because it dictates whether expectant management is an option or whether delivery must be expedited regardless of gestational age.

HELLP Syndrome Diagnostic Criteria

A critical teaching point: HELLP can present with vague symptoms such as malaise, nausea, vomiting, and RUQ pain that mimic gastroenteritis, hepatitis, or cholecystitis. Approximately 15% of HELLP patients may not have hypertension, and some may lack proteinuria. This is a common exam trap. Any pregnant woman in the third trimester with RUQ pain and abnormal labs should be evaluated for HELLP regardless of her blood pressure reading.

03Diagnostic Workup

When a pregnant patient beyond 20 weeks presents with elevated blood pressure, the first step is to confirm the reading with at least two measurements taken 4 hours apart (unless the BP is in the severe range, in which case it can be confirmed within minutes and treated immediately).

Once hypertension is confirmed, the next step is to determine whether this is isolated gestational hypertension or preeclampsia. The best initial test to evaluate for proteinuria is a spot urine protein-to-creatinine ratio (threshold >0.3). A urine dipstick is rapid but has poor sensitivity and specificity and should not be relied upon in isolation. The 24-hour urine collection remains the gold standard for quantifying proteinuria (>300 mg/24h), but it is time-consuming and often impractical in urgent settings. In clinical practice and on exams, the spot ratio is typically acceptable.

However, proteinuria is no longer required to diagnose preeclampsia. A patient with new-onset hypertension after 20 weeks who has any end-organ dysfunction (thrombocytopenia, elevated transaminases, renal insufficiency, pulmonary edema, or cerebral/visual symptoms) meets the diagnostic criteria for preeclampsia even without proteinuria. This updated diagnostic framework is frequently tested.

After confirming preeclampsia, the next critical determination is whether severe features are present, because this directly dictates management. Order a CBC (looking for thrombocytopenia and hemolysis markers), a comprehensive metabolic panel (AST, ALT, creatinine, LDH), and assess for symptoms (headache, visual changes, RUQ pain, dyspnea). If hemolysis is suspected, add a peripheral smear, haptoglobin, and indirect bilirubin.

If the clinical picture suggests HELLP (RUQ pain, nausea/vomiting, thrombocytopenia, elevated LFTs, elevated LDH with evidence of hemolysis), coagulation studies should be sent to rule out disseminated intravascular coagulation (DIC), which can complicate HELLP and placental abruption.

Fetal surveillance with a nonstress test (NST) and biophysical profile (BPP) should be performed at diagnosis and serially thereafter. Umbilical artery Doppler velocimetry helps assess placental function, particularly in the setting of fetal growth restriction. Absent or reversed end-diastolic flow is an ominous finding that typically prompts delivery.

04Management and Treatment

Prevention. For patients with one or more high-risk factors (prior preeclampsia, chronic hypertension, multifetal gestation, type 1 or 2 diabetes, renal disease, autoimmune disease) or two or more moderate-risk factors (nulliparity, obesity, family history, age >35, prior adverse pregnancy outcome), low-dose aspirin 81 mg daily should be started between 12 and 16 weeks of gestation and continued until delivery. Aspirin inhibits thromboxane A2 synthesis (a vasoconstrictor and platelet aggregator) while relatively preserving prostacyclin (a vasodilator), thereby improving placental perfusion. Calcium supplementation (1.5-2 g daily) is recommended in populations with low dietary calcium intake.

Acute Severe Hypertension (BP >160/110). This is a hypertensive emergency in pregnancy and requires treatment within 30-60 minutes to prevent stroke, placental abruption, and end-organ damage.

The target is to lower BP to <160/110 mmHg but not below 120/80, as aggressive reduction can compromise uteroplacental perfusion.

Seizure Prophylaxis and Treatment. Magnesium sulfate is the drug of choice for both prevention of seizures in severe preeclampsia and treatment of eclamptic seizures. It is superior to phenytoin and diazepam for this indication. The standard regimen is:

• Loading dose: 4-6 g IV over 15-20 minutes

• Maintenance: 1-2 g/hour continuous IV infusion

• Duration: Continue for at least 24-48 hours after delivery or after the last seizure

Magnesium toxicity must be monitored closely:

Monitor for toxicity by checking deep tendon reflexes (loss of patellar reflex is the earliest sign), respiratory rate (must remain >12/min), and urine output (must remain >25 mL/hour, as magnesium is renally excreted). The antidote for magnesium toxicity is calcium gluconate 1 g IV over 2-3 minutes.

Timing of Delivery. Delivery is the only definitive treatment for preeclampsia. The decision of when to deliver depends on gestational age and disease severity:

• >37 weeks with gestational hypertension or preeclampsia without severe features: Deliver. Do not wait.

• 34-37 weeks without severe features: Expectant management is reasonable with close surveillance; deliver at 37 weeks.

• >34 weeks with severe features: Stabilize (magnesium, antihypertensives) and deliver. No benefit to prolonging pregnancy beyond 34 weeks in severe disease.

• <34 weeks with severe features: If the mother and fetus are stable, attempt to prolong pregnancy for 48 hours to administer betamethasone (12 mg IM, two doses 24 hours apart) for fetal lung maturity. Magnesium sulfate at <32 weeks also provides fetal neuroprotection against cerebral palsy. If the patient deteriorates (uncontrolled BP, eclampsia, placental abruption, DIC, nonreassuring fetal status, pulmonary edema), deliver immediately regardless of gestational age or steroid completion.

Route of Delivery. Vaginal delivery is preferred unless obstetric indications for cesarean exist. Preeclampsia alone is not an indication for cesarean section. However, in very preterm gestations with an unfavorable cervix where induction is unlikely to succeed quickly, cesarean may be chosen to minimize prolonged maternal exposure.

Contraindicated Medications. ACE inhibitors (e.g., enalapril, lisinopril) and ARBs (e.g., losartan) are absolutely contraindicated throughout pregnancy due to teratogenicity (renal agenesis, oligohydramnios, pulmonary hypoplasia, skull defects, fetal death). Nitroprusside is avoided due to fetal cyanide toxicity. Atenolol is associated with fetal growth restriction and is not preferred. Diuretics are generally avoided as they can worsen the already contracted intravascular volume in preeclampsia.

Postpartum Considerations. Preeclampsia can develop de novo or worsen in the postpartum period, particularly within the first 48-72 hours but up to 6 weeks after delivery. Patients with severe features should continue magnesium sulfate for 24-48 hours postpartum. Oral antihypertensives (labetalol, nifedipine) are used for persistent postpartum hypertension. NSAIDs should be used cautiously as they can exacerbate hypertension and are avoided in patients with renal impairment or thrombocytopenia. All patients with a history of preeclampsia carry an increased lifetime risk of cardiovascular disease and should receive long-term cardiovascular risk counseling.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on hypertension in pregnancy questions is by failing to classify the disease correctly, which leads to choosing the wrong management. The exam tests whether you can distinguish gestational hypertension from preeclampsia, and preeclampsia without severe features from preeclampsia with severe features, because each category has a different delivery threshold and treatment algorithm. If you see a pregnant patient at 35 weeks with BP of 155/100 and no other abnormalities, that is preeclampsia without severe features and you manage expectantly until 37 weeks. If you add a platelet count of 80,000 or a headache unresponsive to acetaminophen, that now becomes severe disease requiring stabilization and delivery regardless of gestational age.

A second major trap involves HELLP syndrome presenting atypically. The vignette may describe a third-trimester patient with nausea, vomiting, malaise, and RUQ pain, and the answer choices will include cholecystitis, hepatitis, or gastroenteritis. Students who do not check the labs for thrombocytopenia, hemolysis, and elevated transaminases will miss the diagnosis. Remember that HELLP can occur without hypertension or proteinuria in a notable minority of cases.

A third trap is choosing the wrong anti-seizure medication. Magnesium sulfate is the correct answer for both prophylaxis and treatment of eclamptic seizures. Phenytoin, levetiracetam, and benzodiazepines are incorrect in this context even though they are first-line anticonvulsants in other settings. The exam specifically tests whether you know that magnesium sulfate is the standard of care in pregnancy-related seizures.

Fourth, students frequently confuse HELLP with TTP or AFLP. The key discriminators to commit to memory: TTP has severely deficient ADAMTS13 and normal liver enzymes; AFLP has hypoglycemia, markedly prolonged coagulation times, and low antithrombin III; HELLP has the triad of hemolysis, elevated liver enzymes, and low platelets with improvement after delivery.

Fifth, watch for questions on postpartum preeclampsia. A patient who was normotensive during pregnancy presents 3-5 days after delivery with headache, visual changes, and BP of 170/105. This is late-onset postpartum preeclampsia and requires the same workup and treatment (magnesium sulfate, antihypertensives) as antepartum disease. Students who anchor on "delivery is the cure" forget that the disease can appear or worsen after the placenta has already been delivered.

Finally, never choose an ACE inhibitor or ARB for blood pressure management in a pregnant patient, even if it is listed as "the best antihypertensive." These are absolutely contraindicated at any gestational age. The correct oral agents are labetalol, nifedipine, or methyldopa. If the question stem mentions a patient who becomes pregnant while on lisinopril, the next best step is to discontinue the ACE inhibitor immediately and switch to a pregnancy-safe alternative.

The core competency being tested across all variations of this topic is your ability to recognize the clinical syndrome, classify the severity, and match the management to the correct category and gestational age. Every management decision branches from two questions: Does this patient have severe features? And what is the gestational age? If you can answer both, you can answer the question.